Cranial Vault Size

Because the size of the cranial vault is not controlled genetically, but rather is a function of what is going on inside the braincase, if the newborn's brain does not grow adequately, the cranial vault stays small (microcephaly). If the cranial contents become excessively voluminous, as in hydrocephalus, the cranial vault responds by excessive enlargement.

Sutural Fusion, Both Normal and Otherwise

After adulthood, the sutural connective tissue is no longer essential for growth of the neurocranium. Nevertheless, this tissue usually persists well past puberty (except for the metopic suture). In middle age the bones bordering any given suture may bridge across the connective tissue and fuse. The suture is then said to be fused, or closed. This happens a lot in some people and hardly at all in others. It is of no functional consequence.

In rare instances the metopic suture does not become closed in early childhood. It can then be visualized in anteroposterior Xrays as a wavy radiolucency in the midline of the frontal "bone." It is important to recognize this possibility so that such a wavy midline radiolucency is not mistaken for a fracture (which, by the way, is hardly ever in the midline and never appears wavy). More commonly a bit of the metopic suture just superior to the nasal bones persists well into adult life.

While it makes no difference if a suture closes after its normal period of growth has come to an end, closure significantly prior to this time has profound effects on skull shape. If a suture closes prematurely, expansion of the cranial vault perpendicular to that suture is retarded. The remaining normal sutures will undergo excessive growth in order to keep the size of the vault in pace with intracranial contents. This leads to recognizable deformations of the skull. For example, if the metopic suture closes shortly after birth, the forehead ceases to grow in width, but the back of the skull compensates. The result is a skull that, when viewed from the top, appears triangular, with the apex anteriorly. This is called trigonocephaly. If the sagittal suture closes prematurely, growth in width of most of the cranial vault will be retarded. Compensatory growth in the coronal suture will cause the braincase to become longer than normal, and compensatory growth in the lambdoid and squamosal sutures will lead to excessive skull height. This condition of a narrow, but long and tall skull is called scaphocephaly; it is the most common deformation due to premature sutural closure.

Premature sutural fusion is known as craniosynostosis. It comes in two varieties: simple (one suture fused) or compound (two or more fused sutures). Either variety of craniosynostosis may be primary, meaning there are no other recognizable physical abnormalities, or secondary, meaning there are other obvious developmental defects. In simple primary craniosynostosis, the rate of severe cognitive disability is 3-6% (somewhat higher when the coronal suture is fused than when the sagittal suture is fused). This value is 2 to 3 times greater than would otherwise be expected. Less severe learning disabilities appear in about half the children with a simple primary craniosynostosis. In compound primary craniosynostosis, severe cognitive disability occurs 35-50% of the time.

It has not been determined whether the cognitive problems associated with primary craniosynostoses are caused by an underlying brain malformation, by increased intracranial pressure, or by a distortion of the brain due to the synostosis. Most people believe that the latter possibility is only reasonable when multiple sutures are fused.

Premature sutural fusion is treated surgically. In the simplest case, a strip of bone on either side of the fused suture is removed and some measure taken to prevent regrowth and closure. It has not been possible to demonstrate that surgery to correct the synostosis alters the cognitive development of the patient. One recent study on a small sample of children with simple synostosis, some of whom had surgery to correct it and others of whom did not, found no effect of surgical correction on rate of learning disability. The primary reason for performing such surgery is cosmetic.

The Corrugator Supercilii Muscle and Frontal Migraine Headaches

In the figure associated with Chapter 63, and in Table 19, I reference only those facial muscles I consider to be of particular importance. In 2009, I added corrugator supercilii to that list. Prior to 2009 I had given some thought to mentioning this muscle because it is a target of cosmetic Botox therapy to eliminate the vertical creases above the root of the nose. However, I could never convince myself this was sufficient reason to include corrugtaor supercilii in Core Concepts. What changed my mind in 2009 was an email from Xiaoti Xu, a Stony Brook medical student, telling me about clinicians who believed that irritation of certain peripheral nerves caused by contraction of muscles through which they pass, or which overlie them, can trigger the onset of migraine headaches . It was suggested that compression of the greater occipital nerve by the semispinalis capitis provoked occipital migraines, that compression of the zygomaticotemporal nerve by the temporalis muscle provoked temporal migraines, and that compression of the supraorbital and supratrochlear nerves by the corrugator supercilii provoked frontal migraines, which are the most common type. The origin of this idea was linked to a discovery by plastic surgeons that some patients who underwent forehead rejuvenation by means of Botox injection reported diminution in frequency or disappearance of their frontal migraine headaches. Surgical removal of the corrugator supercilii was said to have the same beneficial effect (Guyuron B et al. 2005 Comprehensive surgical treatment of migraine headaches. Plast. Reconstr. Surg. 115:1-9; Poggi JT et al. 2008 Confirmation of surgical decompression to relieve migraine headaches. Plast. Reconstr. Surg. 122:115-122). Hence, I decided that the corrugator supercilii had earned itself a place in Core Concepts.

Thanks to Kate Corbin, a graduate student in Anatomical Sciences at Stony Brook, I have now learned about a new view of why botulinum toxin injections may be a successful method of prophylaxis for chronic migraines. This new view denies that irritation of nerves caused by muscular contraction is a trigger for migraine headaches, and it asserts that the effect of botulinum toxin to paralyze muscles is irrelevant to its beneficial effect in migraine prophylaxis (e.g., Ramachandran R, Lam C, Yaksh TL. 2015 Botulinum toxin in migraine: Role of transport in trigemino-somatic and trigemino-vascular afferents. Neurobiology of Disease 79:111-122). As pertains to frontal migraines, the research indicates that botulinum toxin is picked up by sensory nerves in the vicinity of the injection site, then transported centrally along sensory axons to the trigeminal ganglion, where it moves out of these sensory nerves and into those coming from the meninges. The action of botulinum toxin on these meningeal nerves diminishes their ability to release the neurotransmitter CGRP (calcitonin gene-related peptide), thereby interfering with transmission of signals from them to the trigeminal nucleus in the brainstem. No transmission of signals from meningeal nerves, no pain. New pharmacological treatment of migraines focusses on blocking CGRP or its receptor (Edvinsson L. 2017 The trigeminovascular pathway: role of CGRP and GCRP receptors in migraine. Headache 57:47-55). The same logic can be applied to the beneficial effect of botulinum toxin injected into the temporalis muscle. To explain any benefit of injection in the vicinity of the greater and lesser occipital nerves, one must resort to a different neuroanatomical pathway, but one that still relies on the uptake of botulinum toxin by sensory nerves. However, as convincing as is this new research, I would be remiss not to mention that there are still numerous and continuing reports of successes in treating migraines by surgical manipulation or removal of muscle tissue around nerves.

If the new views of migraine causation are correct, should I once again deem corrugator supercilli too trivial to merit inclusion in Core Concepts. The answer is no, because this muscle is still a landmark for injection of botulinum toxin by those who believe the toxin acts on sensory nerves (Blumenfeld AM et al. 2017 Insights into the functional anatomy behind the PREEMPT injection paradigm: guidance on achieving optimal outcomes. Headache 57:766-777). For the moment, I stand by my decision to include corrugator supercilii in Core Concepts.

Parotid Gland

Surgeons view the parotid gland as being divided into superficial and deep lobes by the facial nerve. The superficial lobe comprises 70% of the gland. This lobar division is purely descriptive, there being no other anatomical or functional significance to these "lobes". Depending on tumor location, it may be possible to effect a cure by removing only the superficial lobe, rather than performing a total parotidectomy.

Scalp Wounds

In the case of transverse scalp wounds that penetrate the galea, the wound margins are held apart by the opposite pulls of frontalis and occipitalis on the epicranial aponeurosis. This causes extensive bleeding, and such wounds require stitching. Wounds to the scalp that penetrate the galea also present a risk of infectious matter entering the subaponeurotic space and spreading over the entire surface of the cranial vault. The infectious material may even spread through emissary foramina to reach the cranial cavity.

Bilateral Resection of the Internal Jugular Veins

It is stated that when a person is supine almost all venous blood from the brain flows through the internal jugular veins. This is certainly true in the great majority of persons, but there are individuals in whom the internal jugular veins carry less than half the cerebral venous blood even when that individual is supine. In such persons the nonjugular routes are always dominant. This raises the possibility that these nonjugular routes could adapt to become dominant in everyone. Such appears to be the case. Although surgeons try to preserve the internal jugular veins when performing a radical neck dissection to remove cancerous deep cervical nodes, there are cases when it may be necessary to completely remove one or both internal jugular veins. If only one is removed, the circulatory consequences are minimal. If both must be removed, the operations should be separated by at least a month in order to avoid serious problems with inadequate venous return from the head. During the interval between surgeries, collateral channels using the vertebral venous plexus will have opened sufficiently that removal of the second internal jugular vein can be tolerated. Immediately after removing the second IJV, there is swelling and discoloration of the face, and headache, which may be so severe when the patient lies flat that he or she will not do so. (Gius JA, Grier DH. 1950 Venous adaptation following bilateral radaical neck dissection with excision of the jugular veins. Surgery 28:305-321). However, facial discoloration goes away in a few days, and in a few more both the swelling and headache start to dissipate. Ultimately, a persistent puffiness is common, and most patients prefer to sleep with the head a bit elevated, but otherwise, from the perspective of cerebral venous return, they are OK..

Acute and Chronic Subdural Hematomas (I thank my colleague Nate Kley for alerting me to the existence of chronic subdural hematomas and to the most modern method of their treatment.)

The veins on the lateral and superior surfaces of the cerebral hemispheres pass to the superior sagittal sinus. A severe blow to the front or back of the skull that causes large anteroposterior displacements of the brain may cause some cerebral veins to shear off the superior sagittal sinus wall. The likelihood of this happening is less for cerebral veins that are destined for the posterior part of this sinus. This is so because these more posterior veins turn forward while still in the subarachnoid space to approach the dural wall of the sinus at an acute angle. To some degree the oblique course of cerebral veins into the superior sagittal sinus reduces the likelihood that forward and backward motion of the cerebrum will cause these veins to shear off the sinus wall.

When a cerebral vein, or veins, are torn away from superior sagittal sinus, blood spills into the dural border cell (DBC) layer, splitting it into two. As a result, a sheet of DBC lies external to the infiltrating blood and a sheet of DBC lies internal to this blood (Haines DE 1991 On the question of a subdural space. Anat Rec 230:3-21). The accumulation of blood is called an acute subdural hematoma. The sheets of DBC soon develop into a connective tissue that forms what is often referred to as the neomembrane of the hematoma. The layer of this neomembrane abutting the fibrous dura is much thicker and more highly vascularized than the thin layer abutting the arachnoid.

A patient who has undergone a trauma that could give rise to an acute subdural hematoma must be closely monitored, usually by cranial CT scans. If a subdural hematoma has developed, it need not be large enough to cause symptoms of cerebral compression. If it does not grow in size, it will eventually be resorbed without the necessity of surgical intervention. On the other hand, an extensive accumulation of blood may rapidly develop within hours of the trauma. In these cases, the blood must immediately be surgically evacuated. A third scenario is for an initially modest hematoma to increase in size gradually, with symptoms of cerebral compression developing weeks later. In the not too distant past it was believed that such enlargement of a subdural hematoma occurs because the blood within it breaks down and forms a fluid of high osmotic pressure that draws in water from the cerebrospinal fluid. More recently it has been demonstrated that the capillaries of the outer sheet of the neomembrane are "fragile", with poorly developed endothelial cell junctions, thereby allowing blood and fluid to leak into the hematoma (Jafari N et al. 2017 The pathogenesis of chronic subdural hematomas: a study on the formation of chronic subdural hematomas and analysis of computed tomography findings. World Neurosurg 107:376-38; Link TW et al. 2019 Middle meningeal artery embolization for chronic subdural hematoma: a series of 60 cases. Neurosurg 85:801-807). If the acute subdural hematoma is gradually increasing in size, this also necessitates surgical evacuation of the blood.

One hopes that after evacuation of blood constituting an acute subdural hematoma, the problem will be solved. And in most cases this is so. But in a significant percentage of cases, mostly in the elderly and/or those on anticoagulant therapy, the subdural hematoma reforms after evacuation. This is thought to be due to continuous leakage from capillaries of the outer sheet of the neomembrane. When this occurs, the condition is called chronic subdural hematoma.

It has been demonstrated that the vessels of the neomembrane are fed by the middle meningeal artery (Link TW et al. 2018 Middle meningeal artery embolization for chronic subdural hematoma: endovascular technique and radiographic findings. Interv Neuroradiol 24: 455–462). If the redeveloping subdural hematoma has not yet produced neurologic symptoms, a very effective method of treatment is embolization of the middle meningeal artery with tiny polyvinyl alcohol particles (see Link TW references cited above). This deprives the vessels of the neomembrane of their blood supply, and thereby stops further leakage into the hematoma. If the patient has neurologic symptoms, the chronic sudbural hematoma must be surgically evacuated, but then embolization of the middle meningeal artery may be done as a prophylactic procedure to prevent recurrence (Schwarz J et al. 2021 Perioperative prophylactic middle meningeal artery embolization for chronic subdural hematoma: a series of 44 cases. J Neurosurg 135:1627-1635). When embolizing the middle meningeal artery one must keep in mind that there is a small anastomotic vessel (recurrent meningeal a.) between the lacrimal branch of the ophthalmic a. and the anterior branch of the middle meningeal a. (Core Concepts pp. 120 and 221). This recurrent meningeal a. must be spared from embolization. In rare cases, the ophthalmic a. does not arise from the internal carotid a. but instead is completely supplied by the recurrent meningeal artery. Obviously, in such cases embolization of the recurrent meningeal a. would be disastrous. If the ophthalmic a. has a normal origin and the recurrent meningeal a. is relatively large, the standard practice of leaving it patent may result in failure to devascularize the neomembrane of of an anteriorly located subdural hematoma (Link TW et al. 2018 Middle meningeal artery embolizationf or recurrent chronic subdural hematoma: a case series. World Neurosurg 118:e570-e574, https://doi.org/10.1016/j.wneu.2018.06.241). Surgical evacuation then becomes the only option.

Middle Ear Veins

Veins from the middle ear find their way to the superior petrosal sinus. This is of clinical significance as a route of spread of infection from the middle ear to the superior petrosal and transverse sinuses.

Cavernous Sinus Disease

The potential threats to life resulting from cavernous sinus infection are the same as those of any other dural venous sinus. However, before these occur, existence of cavernous sinus thrombosis is betrayed by a series of other symptoms. Many of these will not be understood until you learn more anatomy, but they will all be described here.

First there occurs a swelling of the eyelids and neighboring tissues, owing to retardation of venous flow through the superior and inferior ophthalmic veins. Second, there is dilatation of retinal veins (which may be visualized ophthalmoscopically) and edema of orbital tissues (which causes the eyeball to move forward--a condition known as exophthalmos or proptosis). The optic nerve may or may not become swollen.

Because important nerves run through the cavernous sinus, an inflammatory state within it will soon produce symptoms related to axonal malfunctioning. Thus, pain or tingling over the sensory distribution of the ophthalmic nerve will develop. This will be followed by anesthesia over the same area. In the case that the maxillary nerve has a course through the lower part of the sinus, its areas of sensory distribution may be subject to the same disturbances as those of the ophthalmic nerve. Weakness (paresis) and then paralysis of the muscles supplied by the oculomotor, trochlear, and abducens nerves becomes apparent. Usually, the abducens nerve is the first to be affected because of its central location within the sinus.

As if septic thrombosis of one cavernous sinus were not bad enough, the existence of intercavernous sinuses permits spread from one side to the other. Hopefully, long before this happens, the patient will have been treated with antibiotics. Nerve symptoms will then disappear and collateral routes of venous drainage will expand, or the thrombus will resolve.

Aneurysm of the internal carotid artery with the cavernous sinus may mimic some of the symptoms of sinus thrombosis, especially those related to retardation of superior ophthalmic venous return and compression of the abducens nerve. If the aneurysm ruptures to create an arteriovenous fistula, the exophthalmotic eyeball will pulsate.

Bilateral Inferior Petrosal Sinus Sampling (BIPSS) (I thank Daniel Donoho, a Stony Brook medical student, for drawing this Clinical Sidelight to my attention.)

When I first heard of this procedure, which involves threading fine catheters into the right and left inferior petrosal sinuses, I was incredulous, but it turns out that BIPSS is considered the most accurate method of diagnosing Cushing's disease. Cushing's disease is defined as excess production of ACTH (adrenocorticotrophic hormone) by the pituitary gland. It is almost always caused by a tiny benign pituitary tumor (microadenoma), frequently too small to be seen on CT or MRI. The excess ACTH causes the adrenal gland cortex to produce excess glucocorticoids (principally cortisol), leading to a set of symptoms that comprise Cushing's syndrome. (Cushing's syndrome arises whenever the adrenal cortex produces excess glucocorticoids. About 20% of the time the disease is in the gland itself, and not to due to excess ACTH production. The latter can be assessed by measuring plasma ACTH levels.) If every time a person had too much ACTH in their blood it was due a problem in the pituitary gland, then diagnosis would be simple. However, in about 15% of patients with excess plasma ACTH, the hypersecretion comes not from a tumor in the pituitary gland, but from a tumor in some other organ (most often the lung). This is referred to as ectopic ACTH syndrome. How can you decide if the excess ACTH is coming from the pituitary (Cushing's disease), or is of ectopic origin? This is where BIPSS comes in. It is based on the following facts: (1) venous drainage from the pituitary gland goes to the cavernous sinus, (2) the right half of the gland drains to the right cavernous sinus and the left half of the gland drains to the left cavernous sinus, and (3) a substantial portion of cavernous sinus blood drains via the inferior petrosal sinus into the jugular bulb. Without going into details (which you can read in Miller DL & Doppman JL. 1991 Petrosal sinus sampling: technique and rationale. Radiology 178:37-47), the BIPSS procedure consists of inserting a small catheter into the right common femoral vein, threading it all the way up to the right IJV, and (under fluoroscopic guidance) manipulating it into the right inferior petrosal sinus. A second catheter is then inserted into the left common femoral vein and threaded all the way up into the left IJV and left inferior petrosal sinus. This is a bit trickier because of the changes in direction from the SVC into the left brachiocephalic vein, and from the latter into the left IJV. The catheters placed in the two inferior petrosal sinuses are said to sample "central" venous blood.

	from Lad SP et al. 2007 The role of inferior petrosal sinus sampling in the diagnostic localization of Cushing's disease. Neurosurg Focus 23(3): http://thejns.org/doi/pdfplus/10.3171/foc.2007.23.3.3

A third catheter is inserted into a peripheral vein, like the median cubital. Levels of ACTH in the venous blood of each inferior petrosal sinus and in the peripheral vein are measured. If the source of the excess ACTH is a pituitary adenoma, the level of ACTH in one or both of the inferior petrosal sinuses will be much greater than in the peripheral vein. If the source of the ACTH was a tumor in some other organ, then the level of ACTH in the central venous blood will not be significantly different from that in the peripheral venous blood. Both inferior petrosal sinuses are sampled because a small tumor in one half of the pituitary gland will generally cause excess ACTH only in the ipsilateral cavernous and inferior petrosal sinuses, so if you were to sample only one side, you could miss a contralateral tumor. (There are also instances when the entire gland drains only to one cavernous sinus. In these instances you would miss the diagnosis entirely if you had decided to sample only one inferior petrosal sinus and, by chance, you chose the wrong side.) If the BIPSS procedure proves the source of excess ACTH is in the pituitary gland, the patient is scheduled for pituitary resection. In many cases, one can be pretty sure about the side of the gland in which the tumor resides, and the surgeon may choose to remove only that side of the gland. Finally, it is also possible to thread the central catheters through the inferior petrosal sinuses into the cavernous sinuses. Some authors advocate this technique, but most authors find it to be no more accurate than BIPPS, and two cases of transient abducens nerve palsies have been reported.

Added September 28, 2018 - Daniel Donoho, the medical student who first brought BIPSS to my attention, is now Dr. Daniel Donoho, a neurosurgery fellow training in pituitary surgery at Brigham and Women's Hospital in Boston. He sent me an email reporting that his group regularly uses BIPSS to evaluate patients. He also drew my attention to a small modification in the procedure I describe. After the venous-sampling catheters have been placed in the two central and one peripheral locations, the patient is administered a dose of ovine Corticotropin Releasing Hormone (oCRH). As its name suggests, this hormone causes release of ACTH by the pituitary gland. In Dr. Donoho's words "ACTH is a fickle molecule even in cushing disease, levels not necessarily being that high all of the time and our patience is limited with a catheter in the IPS." A few minutes after administration of oCRH, the blood level of ACTH rises, much more markedly in the inferior petrosal sinus on the side of any ACTH secreting pituitary adenoma.

CHAPTER 66 - Emissary Veins, Cranial Pia/Arachnoid, and Arteries of the Brain

Spread of Infection

An example of how the state of superficial structures may provide information about dural sinuses is the dilatation of veins and swelling of tissue over the mastoid process when there is thrombosis at the junction of the transverse and sigmoid sinuses secondary to a middle ear infection. The venous dilatation and tissue edema is due to blockage of blood flow in the mastoid emissary vein. It is also possible for the intracranial thrombus and infection to spread via the mastoid emissary vein to the tissue over the mastoid region.

Infections of the face pose the very serious threat of passage to the cavernous sinus. One route is via the communication established between the facial vein and the cavernous sinus by the superior ophthalmic vein. Another, more complicated, route uses the facial vein's connection to the pterygoid plexus via the deep facial vein. Once the infection has reached the pterygoid plexus, it may spread to the cavernous sinus via an emissary vein through the foramen ovale, or via an emissary vein that runs through the inferior orbital fissure to join the inferior ophthalmic vein, which in turn empties into the cavernous sinus (see figure for Chapter 74).

(Vertebral) Subclavian Steal

In normal circulation, some fraction of the blood entering a subclavian artery will find its way into the vertebral artery (a branch of the subclavian) and be carried to the beginning of basilar artery, formed by junction of the right and left vertebrals. If there should develop a stenosis (narrowing of the lumen) in one subclavian artery proximal to the origin of its vertebral branch, then quite obviously a reduced amount of blood reaches its vertebral branch and, indeed, the entire upper limb on that side. When you measure the blood pressure in each arm, it is lower on the affected side (usually the left) by >20 mm Hg. What then happens is that the body takes advantage of the fact that the formation of the basilar artery by the right and left vertebrals represents a normal right-left anastomosis between the two subclavian arteries. Blood passing through the contralateral open subclavian artery and its vertebral branch will reach the beginning of the basilar artery, where some of this blood will continue into the basilar to supply the brain, but some travels retrograde down the vertebral artery whose subclavian parent is stenotic (so little blood is getting into that vertebral artery by the normal route that there is minimal resistance to retrograde flow). The arterial blood flowing backward in the vertebral artery of the affected side reaches the diseased subclavian artery distal to its narrowing. This is called a subclavian steal phenomenon because the stenotic subclavian is stealing blood from the brain. In the past, subclavian steal was thought to lead often to symptoms (dizziness and a sense that one is about to faint, problems with coordination, and more rarely visual disturbances) arising from ischemia of the part of the brain fed by the basilar artery. When these symptoms arose, the patient was said to have a subclavian steal syndrome. If the patient with subclavian steal did not regularly experience neurologic symptoms, it was believed that such symptoms could be elicited by exercise of the affected upper limb, because arteriolar dilatation in the limb increases the retrograde flow in the vertebral artery and thus steals more blood from the brain. Furthermore, if the blood flow to the limb was still insufficient to meet its demands, it would experience ischemic pain. (Ischemic pain in an exercising limb is called claudication, and often occurs in the lower limb of people with bad arteriosclerosis.) In recent years, the ease of determining the direction of arterial blood flow by means of duplex ultrasound has led to the observation that >90% of patients characterized by reversed flow in a vertebral artery (i.e., subclavian steal phenomenon) are asymptomatic under all circumstances (Labropoulos N et al. 2010 Prevalence and impact of the subclavian steal syndrome. Ann Surg 252:166-170). Those few that do experience symptoms are characterized by large differentials in blood pressure between the two upper limbs. In these patients, neurologic symptoms are more common than upper limb pain, and there is no good evidence that exercise of the affected limb brings on neurologic symptoms (Bornstein NM and Morris JW 1986 Subclavian steal: a harmless hemodynamic phenomenon. Lancet 186;2:303-305). A person with subclavian steal phenomenon will probably only develop neurologic symptoms if atherosclerosis in other cranial arteries prevents adequate collateral flow. If such patients cannot be managed conservatively, they can be treated by percutaneous transluminal angioplasty (PTA) of the stenosed subclavian artery, or by surgically shunting blood from the ipsilateral common carotid artery into the affected subclavian artery distal to the narrowing.

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CHAPTER 67 - The Orbit and Eyeball

Eye Color

The posterior (retinal) layer of the iris normally always contains pigment. If the anterior (uveal) layer of the iris is unpigmented, one will have blue eyes. If the anterior layer of the iris contains lots of pigment, the eyes will be brown. Variants between blue and brown depend on the amount of pigment in the anterior layer.

Episcleral Space

Because Tenon's capsule intervenes between the bulbar conjunctiva and the visible part of the sclera, blood or infectious matter that accumulates in the episcleral space (i.e., between the sclera and Tenon's capsule) may reveal themselves by elevation of the bulbar conjunctiva.

Glaucoma

Glaucoma must be treated because the increased intraocular pressure presents a threat to the optical retina. Some cases can be treated medically, others are treated by surgically creating a path of egress of aqueous humor or altering the structure of the trabecular meshwork with a laser (I thank David Fell, a Stony Brook medical student, for alerting me to this last treatment modality.)

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CHAPTER 68 - Blood Vessels of the Orbit

It is branches of the central artery of the retina, and tributaries of the central vein, that are seen when looking into the eye with an ophthalmoscope.

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CHAPTER 69 - Extraocular Muscles

Range of Ocular Motion

An eyeball can be abducted or adducted a maximum of 50 degrees in either direction. It can be elevated or depressed a maximum of 45 degrees in either direction. However, in normal use the eyeball rarely deviates from its primary position more than 15 degrees in any direction (von Noorden, GK. 1990 Binocular Vision and Ocular Motility, 4th ed., CV Mosby, St. Louis).

Cyclovertical Muscles

Each vertical rectus and each oblique muscle produces significant rotations of the eyeball around two axes - optic and horizontal. For this reason, ophthalmologists group these four muscles together under the rubric "cyclovertical muscles". As the eye abducts, the vertical recti become increasingly better at producing vertical excursions and increasingly poor at producing torsions (cyclorotations), whereas the obliques become better cyclorotators and worse at elevation/depression. In contrast, during adduction of the eye the opposite changes occur - the vertical recti becoming increasingly good at cycloductions and worse at producing vertical motions, while the obliques become increasingly better at producing vertical excursions and worse at producing torsions. At maximum adduction, the obliques are almost pure elevator/depressors whereas the vertical recti are primarily cyclorotators. However, in more commonly used states of adduction, the strong vertical recti are able to make a very significant (some say even predominant) contribution to vertical excursion. Indeed, persons with both obliques nonfunctioning can still elevate and depress the adducted eye (von Noorden, pers. comm.).

Cyclovertical Muscles as Adductors/Abductors

Cyclovertical muscles also have an effect around the vertical axis to produce either adduction or abduction. However, it is known from experiments on monkeys that no combination of the vertical recti and obliques is able to adduct an eye whose medial rectus is paralyzed but whose lateral rectus is intact, nor can the cyclovertical muscles abduct an eye whose lateral rectus is paralyzed but medial rectus is intact. It is true that if both horizontal recti are eliminated, the vertical recti have the ability to adduct the eye somewhat, and the obliques have the ability to abduct it somewhat. It has been said that in the normal eye the vertical recti can be significant as adductors once the eye has already been brought to 35° of adduction by the medial rectus, but such a position is uncommon.

Normal Cyclorotation

There is one behavior in which cyclorotation of the eyeball normally occurs. When a person laterally flexes the neck so that his or her ear approaches the shoulder, the eyes cyclorotate in the opposite direction by several degrees. For example, if you tilt your head so your right ear approaches your right shoulder, your right eye will incycloduct (intort) and your left eye will excycloduct (extort), in a seeming attempt to minimize your perception of environmental spinning. The right eye's intorsion is brought about by the SR and SO, whose vertical effects nullify one another; the left eye's extorsion is brought about by the IR and IO, whose vertical effects nullify one another. This normal cyclorotation during head tilt is the basis of the Bielschowsky Head-Tilt Test, a very important diagnostic maneuver described below.

More About Strabismus

As stated in this chapter, strabismus is defined as divergence of the optic axes (more precisely, the condition in which the optic axis of one eye is no longer directed at the object fixated by the other eye). If one eye aims higher than its partner, this is called hypertropia. For example, if the right eye points higher than the left, this is called right hypertropia. There are two possibilities for why the right eye might point higher than the left. Either the right eye is abnormally elevated and the left eye is just fine, or the left eye is abnormally depressed and the right eye is just fine. The way the term is used, hypertropia of an eye may be due to pathology on either side. Right hypertropia can be produced either by a weak depressor of the right eye or a weak elevator of the left eye. It's the job of the diagnostician to figure out if the problem is ipsilateral or contralateral to the hypertropic eye.

An eye that is abnormally deviated inward is said to be esotropic; one that is abnormally deviated outward is said to be exotropic. In these cases, you can tell which eye is affected just by asking the patient to look straight ahead.

During significant strabismus of any kind, diplopia (double vision) will occur, because the image of an object falls on noncorresponding parts of the right and left retinae and, consequently, cannot be fused by the brain.

With complete paralysis of an extraocular muscle, strabismus and diplopia will often occur when the patient is simply trying to look straight ahead. For example, paralysis of the SO (a depressor) usually causes the affected eye to point slightly upward when the patient is looking straight ahead. Strabismus gets even worse when the patient moves the eye into a position that would require greater participation of the paralyzed muscle, and the strabismus will diminish when the eye is placed in a position that would require little or no participation by the paralyzed muscle. Since the superior and inferior oblique muscles play a significant role in determining the vertical position of an adducted eye, but almost no role in determining the vertical position of an abducted eye, any observable strabismus caused by a paralyzed oblique muscle will get worse when the affected eye is adducted, and the strabismus is likely to go away when the affected eye is abducted. In our example of a paralyzed SO, any hypertropia will become worse when the affected eye looks medially, whereas it may virtually disappear when the affected eye abducts. By similar reasoning, since the superior and inferior recti play a dominant role in determining the vertical position of an abducted eye, but a much smaller role in determining the vertical position of an adducted eye, any observable strabismus caused by a paralyzed vertical rectus muscle will get worse when the affected eye is abducted, and will diminish or go away when the affected eye is adducted.

With only weakness (paresis) of a muscle, strabismus and diplopia may not be noticeable until the patient actually attempts to move the affected eye in a direction that requires extra effort by the weak muscle. For example, weakness of the SO may lead to a noticeable strabismus only upon looking downward, or downward and inward. The chart on page 111 indicates the motions of the eye that should be elicited in order to look for strabismus resulting from a paretic extraocular muscle.

Bielschowsky Head-Tilt Test for Testing the Superior and Inferior Obliques

Testing for weakness of an oblique muscle by eliciting elevation and depression of the adducted eye may sometimes be unrevealing. This is so because the vertical recti contribute to elevation/depression of an eye that is moderately adducted (and there are other complicated reasons relating to changes in the intact extraocular muscles after one of their colleagues has been paralyzed for a long time). The best way to examine the strength of the superior and inferior oblique muscles relies on understanding the cyclorotation that normally occurs when someone laterally flexes his/her neck. You know that if you ask a patient to tilt the head to the right, he or she will incycloduct the right eye and excycloduct the left eye. The incycloduction is brought about by the SO and SR, the excycloduction by the IO and IR. If a person performing a head tilt to the right has a weak right SO, the depressor action of that SO will be unable to counteract the elevating action of the normal right SR. Hence, the right eye will deviate upwards during the head tilt. Similar reasoning reveals that if a patient had a weak left IO, its elevation action would not be able to overcome the depressor action of the left IR, and the left eye would move downward during the head tilt to the right. A head-tilt to the left serves to test the left SO and right IO.

The attempt to observe abnormal vertical deviation of an eye during head-tilts is called the Bielschowsky Head-Tilt Test. Although logic would suggest that weakness of a vertical rectus muscle could be revealed by this test (e.g., upon a head-tilt to the right, a weak right SR should lead to depression of the eye by a normal SO), it has been observed that strabismus upon head-tilt is a consistent observation when an oblique muscle is weak, but inconsistently present in the case of weak vertical recti. This is probably related to the fact that the obliques are predominantly cyclorotators when the eye is the primary position.

Head Posture With Strabismus

In strabismus, the two optic axes fail to converge on the object being looked at. However, in some cases it may be possible for the patient to get the optic axes to point in the same direction by adopting a head position that calls upon the good eye to point in the same direction as the affected eye. One example is illustrated in Core Concept 70: if a lateral rectus is paralyzed and, as a consequence, the affected eye is adducted, the patient can get both optic axes to point in the same direction by adopting a head position that calls upon the normal eye to abduct.

Paralysis of one or the other oblique muscles is frequently associated with an abnormal head position. Since, in the primary position of the eye, these muscles are mainly cyclorotators, the paralysis of either one causes a cyclodeviation (torsion) of the affected eye producing a peculiar kind of strabismus called cyclotropia. Paralysis of the SO leads to an excyclodeviation (excyclotropia) of the affected eye; paralysis of the IO leads to an incyclodeviation (incyclotropia) of the affected eye.

Take the case of a patient who has an excyclotropia of the right eye due to SO paralysis. She can avoid diplopia by adopting a head position in which excycloduction of the right eye would normally occur, i.e., one in which the head is tilted to the left (see image below on the left). Such a position induces the unaffected left eye to incycloduct, resulting in comparable torsions of the two eyes and corresponding positions of their retinal images. (By the way, a head-tilt to the left will mask any right hypertropia seen with right SO paralysis. The patient "chose" this head position precisely because it does not require use of the right eye's incycloductors, including the SR that causes the hypertropia.) Head-tilts used to avoid diplopia are referred to as ocular torticollis.

If you see a person with left torticollis that you believe might be ocular in origin, say to yourself "This person chose to have an excycloducted right eye and an incycloducted left eye." Therefore, they must have either a weak right SO or a weak left IO. Do other tests to determine which is the case. If you see a person with a right torticollis that you believe might be ocular in origin, say to yourself "This person chose to have an excycloducted left eye and an incycloducted right eye. Therefore, they must have either a weak left SO or a weak right IO. Again, do other tests to determine which is the case.

Check Ligaments

In the words of von Noorden (1990, Binocular Vision and Ocular Motility, 4th ed., CV Mosby, St. Louis), "there are numerous extensions from all the sheaths of the extraocular muscles, which form an intricate system of fibrous attachments interconnecting the muscles, attaching them to the orbit, supporting the globe, and checking the ocular movements." This intricate system is thought to prevent certain muscles from overshortening, to support the eyeball against the pull of gravity, and to keep the eyeball from being pulled backward into the depth of the orbit by contraction of the rectus muscles. It is said that developmental anomalies of the fascial system are more common than those of the extraocular muscles and are clinically more significant. Thus, ophthalmologists put a lot of effort into naming and describing various parts of the fascial system. If that becomes your chosen field, be forewarned.

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CHAPTER 71 - Olfactory and Optic Nerves

Olfactory Nerve

In a routine neurologic examination, olfaction is tested with the simple goal of determining if the ability to smell through one nostril is the same as the ability to smell through the other nostril, i.e., to determine if there has been unilateral damage to the olfactory pathway. A nonirritating odoriferous substance is placed beneath one nostril while the other nostril is compressed. The patient is asked if an odor is detected, and to identify it. Coffee, oil of peppermint, wintergreen, cloves, or camphor are commonly used. The test is then repeated on the other side. A difference between sides raises the suspicion of a tumor (e.g., a meningioma) compressing the olfactory bulb or tract on the side with the poorer sense of smell. This is a treatable condition. A fracture through one cribriform plate that damages fila olfactoria will also produce unilateral impairment of smell, but this is not treatable.

With the exception noted below, the observation that a patient has bilateral impairment of olfaction is not very significant. Some people are born with no ability to smell (anosmia). In people born with normal olfaction, the ability to detect odors declines past middle age (i.e., odor thresholds progessively rise in old people). Common nasal infections can lead to temporary (or more rarely, permanent) loss of smell, as can exposure to toxic chemicals. Blows to the front or back of the head that cause large anteroposterior excursions of the brain can lead to shearing off of the fila olfactoria as they pass through holes in the cribriform plate on their way to the olfactory bulb. If all the fila are torn, the result will be untreatable anosmia.

The important exceptions to the insignificance of bilateral olfactory impairment are patients with Alzheimer's disease or Parkinson's disease. Alzheimer's patients have unusually high odor thresholds for their age, and they suffer an even more dramatic reduction in their ability to identify and discriminate different odors. Patients with Parkinson's disease also experience olfactory deficits, but their impairment in odor identification is less severe, and their impairment in odor detection is more severe, than in Alzheimer's patients (Rahayel S et al. 2012 The effect of Alzheimer's disease and Parkinson's disease on olfaction: a meta-analysis. Behavioural Brain Res 231:60-74). There is evidence that the olfactory deficits in Alzheimer's disease precede the cognitive impairment, and that that the olfactory deficits in Parkinson's disease precede motor impairment. One may get information about the course of one these diseases by using sophisticated tests of odor detection, identification, and discrimination. Patients in the early stages of either disease, but with severe olfactory impairment, have a poorer prognosis. (I wish to acknowledge Chelsea Dahl, a Stony Brook medical student, for alerting me to the impairment of olfaction occuring in Alzheimer's and Parkinson's diseases, and to the role of olfactory assessment in predicting the courses of these diseases.)

Testing the Optic Nerve

Neuro-ophthalmologists have ways of accurately assessing visual field defects. In the more typical physical exam, the exploration of visual fields is usually done simply by bringing a wiggling finger into view of the patient from the sides, from above, and from below. The patient looks straight ahead and is requested to state when the finger can first be seen.

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CHAPTER 72 - Oculomotor, Trochlear, and Abducens Nerves

Routine testing of extraocular muscles involves asking the patient to look at your finger as you move it in directions that should elicit adduction and abduction of the eye, elevation and depression of the eye when it is adducted, and elevation and depression of the eye when it is abducted. Chapter 69 discusses which muscles (and therefore which nerves) are required for these motions. The clinical comments for Chapter 69 provide additional information on testing extraocular muscles. Test of the levator palpebrae superioris is as simple as asking the patient to look upward so you can observe if elevation of the eyelid accompanies this effort.

Testing the parasympathetic pathway to the constrictor pupillae is done by shining a light in the patient's eye. The pupil should constrict. Note that this pupillary light reflex is consensual, which means that shining a light into only one eye causes both pupils to constrict. Testing the sympathetic pathway to the dilator pupillae is done by shielding an eye from light; its pupil should dilate. This reflex is also consensual.

A second test for the parasympathetic pathway to the constrictor pupillae relies on the accommodation reflex that causes the pupil to constrict when one attempts to focus on an object very close to the eye. Normally this involves convergence of the eyes, i.e., rotation so that their optic axes converge on a nearby point. The test is performed by asking the patient to follow your finger as you bring it toward the bridge of his/her nose. One assumes that the ciliary muscle is also contracting, but there is no easy way of determining this. Paralysis of the ciliary muscle should cause focusing problems, but these may be unnoticed by the patient.

While damage to the oculomotor nerve affects both the pupillary light and pupillary accommodation reflexes, some central nervous system diseases (e.g., neurosyphilis) produce a pupil that constricts on accommodation but not in response to light. This is called an Argyll-Robertson pupil (mnemonic: the initials AR correspond to Accommodation Reactive).

Isolated lesions of the trochlear nerve are uncommon. The abducens is the most frequently damaged of all nerves feeding extraocular muscles. It is the first nerve to be affected by septic thrombosis of the cavernous sinus. Aneurysm of the internal carotid artery within the cavernous sinus may put pressure on the abducens. A variety of tumors at the base of the brain will tend to compress the nerve against the clivus.

The Swinging Flashlight Test

This is really a test to discover if one of a patient's eyes has a diminished ability to perceive light (by virtue of a retinal disease) or has a diminished ability to tell the brain it has perceived light (by virtue of an optic nerve disease). Although the swinging flashlight test is a test of retinal or optic nerve function, it cannot be understood until one has a knowledge of the pupillary light reflex, so I am presenting it here.

If you shine a light in one eye, hold it there for about a second to allow the pupils to constrict, then quickly move the light to the other eye and hold it there for about a second, there are three possible outcomes.

(a) If both eyes are equal in their ability perceive the light and transmit this information to the brain, there will be no change in pupil size as the light impacts on the second eye. Both pupils will maintain the same degree of constriction as they had acquired when the light was shown in the first eye.

(b) If the second eye perceives the light as dimmer than did the first eye, or cannot fully transmit its information to the brain, then both pupils will dilate even as the light is shown in the second eye. They will dilate until the pupil of the second eye reaches the size appropriate for the amount of light the brain believes is being shown to that eye. This second eye is said to have a relative afferent pupillary defect (RAPD).

(c) If the second eye perceives the light as brighter than did the first eye (because the first eye has retinal disease), or more fully transmits its information to the brain (because the first eye has optic nerve disease), then both pupils will constrict further as the light is shown in the second eye. They will constrict until the pupil of the second eye reaches the size appropriate for the amount of light the brain believes is being shown to that eye.

Hence, by swinging a light back and forth between the eyes, holding it in front of each for about a second, you will be able to get information about differences between the eyes in optic nerve or retinal functioning. If the pupils do not change in size after a swing, then both eyes are operating at the same level. If the pupils dilate after a swing, then the second eye is functioning more poorly; if both eyes constrict after the swing, then the second eye is functioning better. (Obviously, the swinging flashlight test only works if there is no oculomotor nerve disease, and it cannot reveal instances of disease that affects both optic nerves or both retinas equally.)

Click here to see the swinging flashlight test in action. What this video shows is a swinging flashlight test performed on a patient with left optic neuritis. Using increasingly dark filters, the physician will attempt to find out how much light must be stopped from reaching the right eye in order to make it as "bad" as the left eye. He will have succeeded when the pupils of the eyes no longer change size as light is swung between them.

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CHAPTER 75 - Maxillary Division of C.N. V, and Clinical Consderations for the Trigeminal Nerve

75 lists some symptoms of trigeminal palsy. No mention was made of problems arising from paralysis of nonmasticatory muscles innervated by the trigeminal. That's because I have not encountered a description of middle ear problems in adult humans arising from paralysis of the tensor veli palatini, nor have I discovered reports of difficulties in swallowing resulting from paralysis of the mylohyoid or of auditory symptoms resulting from paralysis of the tensor tympani.

For your information, extirpation of the tensor veli palatini in experimental animals does lead to severe middle ear pressure dysfunction. Also, human children born with cleft palate almost always accumulate fluid in the middle ear cavity, which interferes with their hearing and frequently leads to middle ear infections. The most commonly accepted explanation is that cleft of the soft palate, by removing the fixed point of insertion of the tensor veli palatini, greatly diminishes the ability of this muscle to open the Eustachian tube. This is treated by placing a tiny drainage tube ("myringotomy tube") through the eardrum. Interestingly, even in children whose cleft palate is not repaired, middle ear problems tend to get better by age 3 or 4, probably because the Eustachian tube inclines a bit downward as one matures. (I wish to acknowledge Dr. Alexander Dagum, Chief of Plastic Surgery at Stony Brook University, for this information.)

Testing the Trigeminal Nerve

Damage to the ophthalmic nerve is tested by determining the responsiveness of the skin of the forehead (frontal nerve) to touch and prick with a sharp object (like a broken Q-tip). A second test involves the corneal reflex. When the cornea is touched, the sensation travels via V1 back to the trigeminal nerve and thence to the brain. Here fibers synapse with facial neurons innervating the palpebral portion of orbicularis oculi, which is caused to contract, producing a blink. Like the pupillary light reflex, the corneal reflex is consensual, i.e., both eyelids blink when either cornea is touched. Obviously, disturbances of the corneal reflex will occur if either the sensory or motor limb is damaged. If the sensory limb is damaged, neither eyelid will blink when the affected cornea is touched. On the other hand, if touching the cornea of one eye produces a blink in the opposite eye, the examiner knows that V1 is working and that the defect is in the ipsilateral facial nerve.

Damage to the maxillary nerve is usually tested only by assessing the responsiveness of the skin over the front of the cheek (infraorbital nerve) to touch and pain. Nasal, palatal, and upper dental sensation are affected by damage to maxillary nerve, but these are not tested for routinely.

During a routine exam, the test for sensory fibers that run in V3 is usually confined to the skin over the chin (mental nerve) and side of the cheek (buccal nerve). General sensation to the front of the tongue (lingual nerve) may also be tested. Obviously, a thorough neurological exam can involve tests over other regions (e.g., temple, upper part of external ear).

Tests for strength of the masseter and pterygoids are often made in routine physical examinations. The examiner places one hand over the left masseter and the other hand over the right masseter, and then asks the patient to clench his or her teeth. An assessment is made about the degree to which one side may be contracting less strongly than the other. (The test can also be done with the hands placed over the temporalis muscles, but these are less easily palpable.) The lateral pterygoid, medial pterygoid, and superficial masseter, when acting together on one side, protract that side of the mandible and cause the chin to deviate toward the opposite side. The left protractors push the chin toward the right; the right protractors push the chin to the left. If the examiner places a hand on the right side of the chin and attempts to push the jaw to the left, the patient must use the left protractors to resist this. If the examiner places a hand on the left side of the chin and attempts to push the jaw to the right, the right muscles must be used to resist this. By asking the patient to resist such pushes on the jaw, an assessment of strength of the jaw protractors on one side compared with those on the other may be made.

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CHAPTER 76 - Facial Nerve

The symptoms of damage to the facial nerve within the posterior wall of the tympanic cavity are summarized in Chapter 76. Additionally, some patients with damage to the chorda tympani also complain of partial numbness of the tongue on the ipsilateral side. It is not known whether this is simply the way persons perceive disruption of sensory input for taste from the tongue, or if some of the sensory axons within the chorda tympani of humans are connected to mechanoreceptors, as occurs in cats.

Surgery on the middle ear may damage the facial nerve within the labyrinthine wall of the tympanic cavity, leading to all the symptoms mentioned in Chapter 76. Tumors within the petrous temporal may affect the facial nerve at the site of the geniculate ganglion. This leads to the symptoms mentioned in Chapter 76, plus loss of tearing on the affected side. Lesions of the facial nerve between the brain and the facial canal may affect one root and not the other, because the two roots are actually separate during this part of their courses.

There is a peculiarity about the cortical input to the facial nuclei of the brainstem that is useful in diagnostics. You will learn in neuroanatomy that, in general, a cerebral hemisphere controls muscles on the contralateral side of the body. As one would expect, the facial motoneurons projecting to the lower two thirds of the face receive cortical input only from the opposite cerebral hemisphere. Surprisingly, however, facial motoneurons going to the upper third of the face receive cortical control from both the right and left cerebral hemispheres. Thus, if there is a unilateral interruption of the pathway from the cerebral cortex to the brainstem, paralysis of the opposite side's mouth and cheek muscles will be will be full-blown, but the orbicularis oculi and frontalis of that side will still be able to weakly contract.

Testing the Facial Nerve

Testing the facial nerve during a routine physical examination begins with observing the appearance of the face to assess the normality of skin creases, width of the palpebral fissures, and position of the corners of the mouth. Then, the patient is asked to raise the eyebrows or wrinkle the forehead (frontalis) and the examiner looks to see if this is done symmetrically. The patient may be asked to close the eyes very tightly (orbicularis oculi) and the examiner tries to pry them open by pushing up on the eyebrows. A broad smile is requested (several muscles) and assessed for symmetry. The patient is asked to puff out the cheeks. Puffing out one's cheeks is made possible by the action of orbicularis oris to prevent escape of air between the lips. If one side is very weak, air escapes on that side. If air does not escape, the examiner may apply a test of strength by pushing in on both cheeks to see if the orbicularis oris on one side can be overwhelmed.

Only if these tests of facial muscles reveal a deficit does the examination progress to a test of taste or lacrimation. Taste on the anterior two thirds of the tongue can be evaluated by applying a strong tasting solution (e.g., salt, sugar, citric acid, quinine) to its right and left edges, where most of the taste buds are concentrated. There exist special absorbent paper strips that can be applied to the surface of the eye for assessing tear production.

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CHAPTER 77 - Prevertebral Muscles and Pharynx

Zenker's Diverticulum

As stated in Core Concepts, the cricopharyngeus (also known as the Upper Esophageal Sphincter, or UES) must relax so that swallowed food can enter the esophagus. If this doesn't happen properly, pressure build-up proximal to the UES may cause an outpocketing of pharyngeal mucosa at the site of relative muscle weakness between the cricopharyngeal and thyropharyngeal portions of the inferior constrictor. The site of relative weakness is called Killian's triangle. Such an outpocketing through Killian's triangle is called a Zenker's diverticulum. If large it can be symptomatic, requiring surgical treatment that involves cutting the cricopharyngeus (i.e., a cricopharyngeal myotomy).

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CHAPTER 79 - The Two Extrinsic Muscles of the Soft Palate

The dilator tubae portion of the tensor veli palatini is often called into action by the same behaviors that require the rest of the muscle to tighten the soft palate. Thus, during the descent of an airplane, passengers are advised to swallow or yawn (behaviors that induce soft palate tightening)in order to equalize pressure between the external environment and middle ear cavity. These maneuvers often fail to work, indicating that it is possible to contract the bulk of the tensor veli palatini without simultaneous recruitment of dilator tubae. Eventually, however, a reflex swallow or yawn occurs in which the auditory tube is opened.

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CHAPTER 80 - Nasal Cavities and Paranasal Sinuses

Vomeronasal Organ, Vomeronasal Nerve (?), and the Nervus Terminalis (Cranial Nerve 0)

What I am about to discuss doesn't actually constitute a "Clinical Sidelight", but it's so interesting I wanted to include it anyway. It has now been demonstrated conclusively that adult humans possess a vomeronasal organ (VNO), once thought to have been lost during higher primate evolution. The VNO is present bilaterally as a small epithelial tubular sac lying submucosally in the antero-inferior part of the nasal septum. Each VNO has a tiny opening into the antero-inferior region of the nasal cavity. In many mammals, a subpopulation of cells within the VNO are chemoreceptive neurons that respond to stimulation by pheromones. These cells give rise to axons that form a few vomeronasal nerves, which travel up the nasal septum and through the cribriform plate to synapse on an accessory olfactory bulb next to the main one. Human adults do not have an accessory olfactory bulb. Furthermore, most researchers have not been able to find chemosensory cells in the human VNO, nor have vomeronasal nerves been found in adult humans (Bhatnagar KP, Smith TD. 2001 The human vomeronasal organ. III. Postnatal development from infancy to the ninth decade. J Anat 199:289-302; Witt M et al. 2002 On the chemosensory nature of the vomeronasal epithelium in adult humans. Histochem Cell Biol 117:493-509). Genes that in other mammals produce receptor molecules for the chemosensory cells of the VNO are almost entirely nonfunctional in humans (Mombaerts P. 2004 Genes and ligands for odorant, vomeronasal and taste receptors. Nature Reviews Neuroscience 5:263-278). Still, it must be said that some researchers believe the human VNO is a functioning pheromone sensitive organ that communicates with the brain via vomeronasal nerves (see Monti-Bloch L, et al. 1998 The human vomeronasal system. A review. Ann NY Acad Sci 855:373-389).

A different set of axons beginning in the vicinity of the VNO (and also a nearby area of the nasal septum mucosa) collect into a few nerve bundles that constitute the nervus terminalis, another structure once thought to be absent in adult humans. The bundles of the nervus terminalis course up the nasal septum and through the cribriform plate, but then pass along the medial aspect of the olfactory bulb and olfactory tract into the brain (Fuller GN, Burger PC. 1990 Nervus terminalis (cranial nerve zero) in the adult human. Clin Neuropath 9:279-283). The cell bodies of these axons are scattered along their path to the brain. They are immunoreactive for luteinizing hormone releasing hormone (LHRH), and in development some cells from the same embryologic source migrate along the nervus terminalis into the hypothalamus to become the cells that secrete LHRH. Aside from playing the role of a "highway" in development, the function of the human nervus terminalis is unknown (Schwanzel-Fukuda M, Pfaff DW. 2003 The structure and function of the nervus terminalis. Pp. 1001-1026 in Handbook of Olfaction and Gustation, RL Doty, ed., Marcel Dekker, NY).

Sinusitis

Because the ostia (i.e., openings) of the paranasal sinuses into the nasal cavities are small and surrounded by easily swollen mucous membrane, the flow of air between the paranasal sinuses and nasal cavity is highly restricted. Mucous secreted by the epithelium lining each sinus normally flows into the nasal cavity unless the mucous membrane lining its ostium becomes swollen to the point of occlusion. Then the patient will want to take decongestants to reduce this swelling, open the ostium, and thereby "decompress" the sinus. Infectious organisms may pass from the nasal cavity into the sinuses, leading to the well-known condition of sinusitis.

Epistaxis

Nosebleeds (epistaxis) are classified as anterior or posterior. Anterior bleeds usually stop by themselves; if not, packing is usually successful. Posterior bleeds are harder to control. If all conservative measures fail, the surgeon enters the pterygopalatine fossa through the maxillary sinus and ties off the inner division of the maxillary artery. A newer approach entails catheterization and embolization of the sphenopalatine and descending palatine arteries under radiographic guidance. However, regardless of the technique used to occlude the branches of the maxillary artery to the nose, many surgeons recommend simultaneous ligation of the anterior ethmoidal artery because it anastomoses with such branches. Even this procedure may fail and posterior ethmoidal artery ligation also be necessary.

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CHAPTER 81 - Oral Cavity, Oropharynx, and Tongue

Genioglossus and Sleep

It has been suggested that some persons are subject to respiratory distress during sleep (sleep apnea) because they have periods of inactivity of the genioglossus, with the result that the tongue falls backward into the oropharynx. Certainly during general anesthesia, one must guard against the tongue falling backward and obstructing the air passageway. (See Clinical Sidelights to Chapter 86 for the description of a new method for treating sleep apnea caused by genioglossus insufficiency.)

Lingual Frenulum

One cause of speech impediments is a short lingual frenulum, which may then be incised.

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CHAPTER 82 - Vestibulocochlear Nerve and Glossopharyngeal Nerve

Vestibulocochlear Nerve

The assessment of the sense of equilibrium, or of auditory sensitivity by sound frequency, is left to specialists. However, a routine physical examination may attempt to judge general hearing acuity, particularly as it depends on adequate operation of the middle ear mechanism.

A first test - the Weber test - can be done to determine if there is unilateral hearing diminution due either to sensorineural (cochlea or nerve) or conductive (eardrum and ossicular chain) problems. The stem of a vibrating tuning fork (256 or 512 Hz) is placed in contact with the vertex of the skull so that sound is sent directly through the bone to reach both the right and left cochleae. If hearing is normal, the sound will be reported as being equally loud in both ears. As you might expect, if a cochlea or its nerve is damaged on one side, the sound of the tuning fork will be heard as louder on the opposite, normal side. On the other hand, you might be surprised to learn that if there is a problem on one side with the conductive mechanism, the tuning fork will actually be heard as louder on that abnormal side. This is because the sound of the tuning fork transmitted through the bone of the skull competes with room noise transmitted through the eardrum and ossicular chain. Such room noise becomes a poorer competitor if the conductive mechanism that brings it to the cochlea is defective, with the consequence that the tuning fork sounds louder in that ear. To summarize, in a Weber test, lateralization of the tuning fork's sound to a particular side occurs if there is a problem either with that side's conductive mechanism or the opposite side's sensorineural mechanism. The inherent ambiguity of this result should be resolved by the application of the Rinne test, described below.

Although the Weber test is described in most physical diagnosis and neurology texts, there is evidence that it has a high risk both of giving false positive and false negative results (Miltenburg, DM, J. Otolaryngology, 23:254-259, 1994). My neurology colleagues don't use it. They simply whisper a number into one ear while rubbing their thumb and fingers next to the opposite ear so as to shield it from hearing the whispered number. They repeat this on the opposite side. If the patient can identify a whispered sound equally well in both ears, then he or she is considered to have acceptable hearing.

If a patient has an abnormal Weber test, or can't hear a whispered sound, the Rinne test is considered a pretty good (though not perfect) method for determining if the hearing loss is due to a conductive or sensorineural problem. The Rinne test is applied to each side separately. Various neurology and physical diagnosis texts describe it as consisting of three steps: (1) apply the stem of a vibrating tuning fork to the patient's mastoid process so that the vibrations reach the cochlea via bone conduction, (2) ask the patient to report when the sound is no longer heard, (3) then place the tines of the tuning fork near the external auditory meatus and inquire if the sound can once again be heard. If the patient's middle ear on the tested side is operating normally, the sound will once again be heard, usually for an additional period of time that equals the duration of the audible bone conduction through the mastoid process.

Otolaryngologists seem to agree that the accuracy of the Rinne test can be improved by performing it somewhat differently than just described. They recommend the following method:
1) strike a 256 or 512 Hz tuning fork and hold its tines about one inch from the external auditory meatus for a few seconds;
2) move the stem of the tuning fork onto the patients mastoid process for a few seconds;
3) ask the patient whether the sound was louder in the front or the back.
If the patient reports that the front (i.e., air conduction) sounded louder than the back (i.e., bone conduction), the test indicates that nothing is wrong with the conductive mechanism and that any hearing loss is probably sensorineural in origin. If the bone conduction sounded louder than the air conduction, there is a significant likelihood of a problem with the conductive mechanism. The Rinne test is not considered very useful as a general screening tool for hearing loss because a normal test is often found in people with hearing impairment (Bagai A, Thavendiranathan P, Detsky AS. 2006 Does this patient have hearing impairment? JAMA 295:416-428.).

Glossopharyngeal Nerve

The routine test of glossopharyngeal function is the gag reflex. This reflex consists of pharyngeal constriction when the back wall of oropharynx is touched. The glossopharyngeal nerve is supposed to be the sensory limb of the gag reflex; the vagus is the motor limb. However, since some authors state that the gag reflex is not lost after glossopharyngeal nerve section, the vagus may participate in conducting pharyngeal sensation. If this is true, then the standard test for glossopharyngeal function is not informative.

Taste on the posterior third of the tongue can be assessed by applying a small electrical current between copper electrodes placed on the back of the tongue. An acid or metallic taste is elicited. This is not a common procedure. Applying solutions of strong taste to the back of the tongue is not a good method because of the rapid spread of the solution to the other side. Another reason not to bother with such a test is that some authors report that intracranial transection of the glossopharyngeal nerve does not lead to loss of taste or general sensation from the tongue. It would seem that more remains to be learned about the complete pathway of such modalities.

Frey's Syndrome

As you know, the glossopharyngeal nerve carries the preganglionic parasympathetic axons responsible for stimulating salivary secretion by the parotid gland. These axons synapse on cells of the otic ganglion, whose postganglionic axons travel through the auriculotemporal nerve to reach the gland. Partial or total parotidectomy is a treatment for parotid tumors (which fortunately are usually benign). Several months (sometimes longer) following such surgery, when patients are eating they often experience sweating in the skin over the site of removed glandular tissue. Gustatory sweating (i.e, sweating that occurs when you taste something) arising as a consequence of parotid injury is called Frey's syndrome. It is sometimes accompanied by facial flushing in the same region. Frey's syndrome is thought to arise when transected postganglionic parasympathetic axons grow into the skin and aberrantly innervate sweat glands and blood vessels. Some surgeons try to prevent the development of Frey's syndrome by interposing a barrier between the cut surface of the parotid tissue and the undersurface of the skin. Flaps from the sternocleidomastoid, SMAS, temporoparietal fascia, or vascularized fat have been used. So has acellular dermis that can be purchased commercially. These barriers may also reduce the sunken appearance of the face that would otherwise occur at the site of the removed parotid tissue. However, their success in preventing Frey's syndrome is debated (Witt RL, Pribitkin EA. 2013 How can Frey's Syndrome be prevented or treated following parotid surgery? Laryngoscope 123:1573-1574). What appears to be most successful in treating Frey's syndrome is intradermal injection of botulinum toxin, which usually has a beneficial effect that lasts well past the time when the physiological action of the toxin has dissipated. It can also be repeated if necessary.

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CHAPTER 83 - Vagus Nerve

Vagus Nerve

The first edition of Core Concepts in Anatomy presented a discussion of how vocal fold position following injury to the recurrent laryngeal nerve (RLN) will be different from vocal fold position following injury to the vagus proximal to its superior laryngeal (SL) branch. That discussion was based on the Wagner-Grossman hypothesis, which had nearly universal acceptance prior to 1993. Since that time (and largely initiated by the research of Dr. Gayle E. Woodson, Southern Illinois University School of Medicine) evidence has accumulated that no such difference exists. The second edition of Core Concepts reflects the current view, but I will discuss it in a bit more detail here.

First and foremost, it seems that except under the experimental circumstance of electrically induced maximum contraction, the cricothyroid muscle does not produce vocal fold adduction. Consequently, even though the cricothyroid muscle remains intact after complete injury to an RLN, the affected vocal fold does not immediately assume a taut paramedian position. Instead, immediately after complete injury to an RLN, the ipsilateral vocal fold is flaccid and lies the intermediate position. The symptoms associated with such a paralyzed vocal fold are (1) hoarse and breathy voice (dysphonia), (2) weak cough, (3) risk of aspiration of fluids (which risk arises not only because the folds cannot be tightly approximated but also because sensation is diminished on one side of the glottis), and (4) exertional dyspnea (breathing during normal activities is not a problem since the intact cord can compensate for the mildly narrowed glottis by wider abduction; only during exertion is there likely to be any difficulty breathing). If the vagus is injured proximal to its SL branch, the ipsilateral vocal fold appears the same as just described for an RLN injury. In other words, one cannot diagnose the site of nerve injury based on vocal fold position.

Regardless of the site of nerve injury, after several months the paralyzed vocal fold may move medially, sometimes actually reaching the paramedian position. This is the usual occurrence in cases of RLN injury. One explanation offered for why a paralyzed vocal fold might move medially is reinnervation by axonal regrowth from the part of the nerve proximal to the injury. Animal experiments have demonstrated a remarkable ability of RLN axons to cross surgically created gaps in the nerve and eventually reach the internal laryngeal muscles on the affected side. The axons do not end up going to the same muscles they had originally innervated, so useful control of the reinnervated vocal fold is not regained. However, since there are four times as many adductor muscle motor units as posterior cricoarytenoid motor units, the statistically favored effect is to cause a more adducted position of the cord. Additionally, reinnervation of the thyroarytenoid muscle reverses atrophy of this muscle and leads to increased bulk of the paralyzed fold. As a result, there is a diminution of symptoms, because the intact fold is now better able to make firm contact with the fuller, tauter paralyzed fold.

By itself, reinnervation does not always happen. Consequently, one approach to treating unilateral vocal fold paralysis caused by nerve injury is to surgically anastomose one of the major branches of the ansa cervicalis to the distal stump of the RLN (reviewed in Paniello RC. 2004 Laryngeal reinnervation. Otolaryngol Clin N Am 37:161-181), or to the branch of the RLN that goes to the adductor muscles (Zheng H et al. 1996 Update: laryngeal reinnervation for unilateral vocal cord paralysis with the ansa cervicalis. Laryngoscope 106:1522-1527). This results in partial denervation of the infrahyoid strap muscles, but the loss is barely noticeable. There has also been a study in which the hypoglossal nerve was cut and then anastomosed to the distal part of the RLN. As stated on p. 155 of Core Concepts, speech, chewing, and swallowing are affected only slightly when half the tongue is denervated. If the surgeon opts against reinnervation of the laryngeal muscles, or if the procedure fails to produce the desired result, other surgical treatments to "medialize" the paralyzed fold can be attempted. [I want to acknowledge Wai Lee, a Stony Brook medical student, for bringing the technique of laryngeal reinnervation to my attention.]

Bilateral RLN injury requires the patient to be intubated. This is not because the two vocal folds are fixed in the paramedian position (although this may happen with time). Intubation is required because air moving past the flaccid vocal folds experiences a pressure drop (due to Bernoulli's Principle) that causes them to be "sucked" closer together. Thus, the airway becomes compromised on any but the slowest inspirations. (I thank my colleague Dr. Ghassan Samara, Dept. of Surgery, Stony Brook University, for this tidbit.)

Testing the Vagus Nerve

If the patient presents no symptoms attributable to vagal damage, routine testing of the vagus nerve consists of observing of the soft palate at rest and while the patient says "Ah". If the soft palate droops on one side, or it does not rise on one side when the patient says "Ah", paralysis of the levator veli palatini is indicated and damage to the ipsilateral vagus must be suspected. Failure of the paralyzed half of the palate to rise when the patient says "Ah" may cause the uvula to shift to the intact side, and this might be easier to assess than how high the soft palate rises. The gag reflex may also be elicited to test for the vagus. If the contraction of the pharynx that is elicited by touching its back wall is absent on the same side as the drooping soft palate, this is further indication of vagal malfunction.

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CHAPTER 84 - Autonomic Innervation of the Head

More on Horner's Syndrome

The mild ptosis of Horner's syndrome can be easily distinguished from the more marked ptosis due to levator palpebrae superioris paralysis simply by asking the patient to direct the gaze upward, which will elicit elevation of the upper lid if the LPS is intact.

One anatomically interesting phenomenon is the occurrence of a reversible Horner's syndrome in some persons who experience migraine headaches. Regardless of what might trigger a migraine, the actual headache is believed to be caused by vasodilation of meningeal branches of the external carotid artery. However, in some persons the vasodilation may also involve the internal carotid artery. Since this vessel passes through the inexpansible carotid canal of the petrous temporal, expansion of the ICA can compress and temporarily damage the sympathetic nerves that surround it. The result is a partial Horner's syndrome (affecting the eye and forehead) that resolves itself over the course of the next few months.

Excessive Frequency and Extent of Facial Blushing (I wish to thank Peter Yoo, a Stony Brook medical student, for drawing my attention to this Clinical Sidelight.)

Some persons blush intensely at the slightest provocation. This can lead to dread of social situations and be psychologically debilitating. Since emotional vasodilation of facial vessels is controlled by preganglionic sympathetic cells lying predominantly in the T2 level of the spinal cord, interrupting the course of their axons can cure the condition. Surgeons perform an endoscopic procedure in which the sympathetic trunk is cut just superior to the T2 ganglion, or the T2 ganglion (and sometimes also T3) may be removed entirely. This operation was initially developed to treat excess sweating in the palm, but a somewhat different technique is now recommended for that condition. Sympathicotomy (cutting the sympathetic trunk) or sympathectomy (excising a portion of the trunk) at the T2 level has also been used to treat complaints of excessive facial sweating.

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CHAPTER 86 - Accessory and Hypoglossal Nerves

Testing the Accessory Nerve

Assessing the strength of the sternocleidomastoid and trapezius is done as a part of any routine test for the integrity of the accessory nerve. The patient is asked to turn the head to one side against resistance from the examiner. A resisted turn to the right tests the left sternocleidomastoid, and vice versa. Again, the examiner is trying to discover weakness of one side relative to the other. Another way to judge strength of the sternocleidomastoids is to have the patient attempt to flex the neck against resistance applied to the forehead. In this case, the examiner compares strength of the right and left muscles by palpating the rigidity of each tendon that comes from the manubrium.

To test for strength of the trapezius, the patient is asked to shrug the shoulders against resistance by the examiner. Both sides are tested simultaneously so that a weakness of one side relative to the other can be detected. Clearly this test informs one only about strength of the upper fibers of the muscle, but these are the ones that receive most of their innervation from the accessory nerve.

Cerebral control of the sternocleidomastoids is unusual. Whereas the general rule is that one side of the cerebral cortex controls muscles on the opposite side of the body (but see discussion of superior facial muscles above), the sternocleidomastoids get cortical input from both cerebral hemispheres. As would be predicted from the general rule, the contralateral hemisphere stimulates the sternocleidomastoid when you use it to flex or laterally flex your neck. For example, a right hemisphere lesion causes weakness in the left sternocleidomastoid that can be revealed when you try to touch your left ear to your left shoulder. Unexpectedly, the ipsilateral hemisphere stimulates the sternocleidomastoid when the muscle is used to turn the head. For example, when you want to turn your head to the right, use of your left sternocleidomastoid is initiated by the left cerebral cortex. Since the left cortex also causes your eyes to turn to the right, ipsilateral cerebral control of sternocleidomastoid during head turning behaviors is functionally sound.

Testing the Hypoglossal Nerve

Routine examination of the hypoglossal nerve consists of a request that the patient stick out the tongue and wiggle it from side to side. In theory, the left genioglossus is primarily responsible for shoving the tongue to the right, while the right genioglossus is chiefly responsible for shoving the tongue to the left. If the tongue can only be wiggled to one side, the muscles of that side are paralyzed. The patient may also be asked to push first one, and then the other, cheek out with the tongue while the examiner resists the movement. Again, in theory, the left genioglossus is primarily responsible for pushing out the right cheek while the right genioglossus is chiefly responsible for pushing out the left cheek. This test is entirely analogous to resisting sideways deviations of the chin in order to assess mandibular protractors.

Stimulation of the Hypoglossal Nerve to Treat Obstructive Sleep Apnea

It was mentioned in Chapter 81 that the genioglossus, a protractor of the tongue, plays a significant role in keeping the airway open during both wakefulness and sleep. Persons with obstructive sleep apnea (OSA) have a problem keeping the airway open during sleep. The blockage occurs at the level of the oropharynx. The cause for this blockage is probably multifactorial, but it has been shown that in sleeping apneic patients, spontaneous prominent contractions of genioglossus are associated with moments of airway patency. The standard treatment for OSA is continuous positive airway pressure (CPAP), but some patients cannot tolerate this procedure, and others simply fail to adhere to its requirements. A new treatment for such patients entails stimulation of the nerve that supplies genioglossus timed to inspiratory efforts (Mauer JT et al. 2012 Operative technique of upper airway stimulation: an implantable treatment of obstructive sleep apnea. Oper Tech Otolaryngol 23:227-233). The hypoglossal nerve is identified in the digastric triangle as it passes onto the surface of the hyoglossus. The free posterior edge of mylohoid is retracted anteriorly, allowing the nerve to be followed forward. Before reaching the halfway point of its course across hyoglossus, the hypoglossal nerve gives off a branch to geniohyoid and one or more lateral branches that go to hyoglossus, styloglossus, and some intrinsic longitudinal muscles. After that, the continuation of the nerve is called its medial branch, which innervates genioglossus and the remaining intrinsic muscles. This medial branch is identified, a stimulating cuff placed around it, and the surgeon verifies that stimulation protrudes the tongue. The stimulating cuff is connected to an implantable pulse generator that also receives input from a small pressure-sensing device placed between the external and internal intercostal muscles of the 4th interspace. When this device senses that inspiration begins, it tells the pulse generator to stimulate the medial branch of the hypoglossal nerve. The patient turns the system on at bedtime, but leaves it off during wakefulness. The procedure is performed only on the right side, but a study of over 100 patients demonstrated that this method of treating OSA "resulted in significant and clinically meaningful reductions in the severity of obstructive sleep apnea" (Strollo PJ Jr et al. 2014 Upper-airway stimulation for Obstructive Sleep Apnea. N Engl J Med 370:139-149).

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CHAPTER 87 - The Larynx

The valleculae and piriform recesses are places where fish bones and the like may lodge.

Anesthesia of the Airway for Orotracheal Intubation in a Conscious Patient (I want to acknowledge Dr. Michael M. Todd, Professor of Anesthesiology, University of Iowa, for assistance with this topic.)

Whereas many patients are given intravenous anesthesia prior to airway intubation, selected patients (e.g., those with cervical spine fractures) are intubated while awake. It is then necessary to anesthetize the oropharynx and larynx to provide comfort and eliminate the risk of injury associated with coughing and gagging. A solution of lidocaine sprayed into the back of the mouth is often sufficient for oropharyngeal anesthesia, but this may be supplemented with an injection of lidocaine into the middle of the palatopharyngeal fold (posterior faucial pillar), where it will block the glossopharyngeal nerve prior to its branches to the tongue and adjacent region of the pharynx. Anesthesia of the larynx is accomplished using two approaches. Sensation from the supraglottic larynx is eliminated by administering lidocaine adjacent to the internal laryngeal nerve (although this technique is usually referred to as "superior laryngeal nerve block"). It will be recalled that the internal laryngeal nerve enters the larynx by piercing the posterior portion of the thyrohyoid membrane. Thus, one may either aim the needle to hit the greater cornu of the hyoid bone just anterior to its tip, then inject anesthesia as you walk the needle inferiorly, or one may aim for the superior border of the thyroid lamina in front of its superior horn and inject anesthesia as you walk the needle upward. In either case, the needle is also pushed through the thyrohyoid membrane (which offers a palpable resistance) and anesthetic solution injected around the nerve deep to this structure. The lower part of the larynx is made insensate by spraying lidocaine through a catheter that has been inserted either through the median cricothyroid ligament or through the trachea above or below the first tracheal ring.

Position of Larynx at Birth

It is interesting that the larynx actually sits higher in the newborn than in the adult. At birth, the superior tip of the epiglottis lies just behind the soft palate. The oropharynx exists only as a small region anterior to the epiglottis. An oropharynx of significant dimensions develops concomitantly with descent of the larynx in early childhood. As a result of the high position of the larynx in the newborn, the food and air passageways are separate, enabling liquid food to be swallowed at the same time as breathing occurs. This is good for suckling. Newborns tend to breathe solely through their noses, although they outgrow this habit before the larynx descends.

Intubation of Children

Long term intubation of children is prone to lead to a condition called subglottic stenosis, which is a narrowing of the air passage at the level of the cricoid cartilage. It develops because the cricoid is a complete ring and cannot yield around the tube. This can lead to formation of scar tissue at the site of contact between the endotracheal tube and the mucous membrane lining of the cricoid cartilage.

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CHAPTER 89 - Relationships in the Head

Facial Nerve

In surgery on the parotid gland, it is important to see the facial nerve so that it be preserved. There are a variety of ways to locate it just below the stylomastoid foramen. One is to find the posterior belly of the digastric and trace this upward; the facial nerve is anterior to it near the base of the skull. Sometimes surgeons find it the way we do in dissection. That is, they locate a small branch crossing the masseter and trace this proximally.

The skin incision for parotid surgery usually sacrifices the anterior branch of the great auricular nerve.

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CHAPTER 90 - Surface Anatomy of the Head

Parotid Duct

The rule of thumb is that a vertical laceration of the face below the zygomatic arch and posterior to the lateral canthus of the eye threatens the parotid duct. This is so because the duct lies on the relatively unyielding masseter here.

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CHAPTER 95 - Muscles moving the shoulder Girdle

Winging of the Scapula

When the serratus anterior is paralyzed, the inferior angle of the scapula moves posteriorly away from the chest wall to make a noticeable ridge beneath the skin of the back, a condition known as winging of the scapula. Paralysis of the trapezius yields a similar change in appearance of the back. At first look, the examiner may be unable to decide whether winging of the scapula is due to a serratus anterior or a trapezius paralysis. The determination is then made by requiring the patient to perform a motion for which one of the muscles is significantly more important than the other. If that important muscle is damaged, the winging will become worse; if that important muscle is intact, the winging will become less noticeable. For example, when the patient abducts the arm, a motion for which trapezius action on the scapula is particularly important, trapezius-winging will become more prominent but a serratus-winging will lessen (or remain unchanged). When the patient flexes the arm, a motion for which serratus action on the scapula is particularly important, a serratus-winging will worsen but any winging caused by a paralyzed trapezius will diminish.

The serratus anterior is not only a rotator of the scapula, but it also protracts (pulls anteriorly) this bone. Consequently, winging due to a paralyzed serratus anterior will be accentuated by applying a dorsally directed force to the scapula that the paralyzed serratus is unable to resist. In diagnosis, this is accomplished by asking the patient to hold his or her hands stretched out in front of the body and then lean against a wall supported by the outstretched hands. This maneuver stresses the protracting ability of the serratus and causes a serratus-winging to become even worse. Had the appearance of winging at rest been due to a weak trapezius, the winging would virtually disappear when the patient performed such a test.

Posterolateral Thoracotomy

In the standard posterolateral thoracotomy, the serratus anterior is divided transversely. Many surgeons prefer to make this cut lower than the intercostal space to be entered so as to preserve as much as possible of the long thoracic nerve (nerve to serratus anterior).

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CHAPTER 97 - Muscles Acting on the Glenohumeral Joint II

Quadrangular Space

During surgery on the shoulder from the anterior approach, one eventually reaches a point where the subscapularis must be transected. In so doing, the surgeon must take care not to extend the incision into the quadrangular space, wherein reside some important things.

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CHAPTER 98 - Organization of the Upper Limb Musculature and the Brachial Plexus

Erb-Duchenne Syndrome

Falls that cause the head and shoulder to be pushed apart may result in tearing, or actual avulsion from the spinal cord, of the upper roots (C5 and C6) of the brachial plexus. The same damage may occur in a newborn if the person "assisting" a normal head-first delivery tries to promote passage of the shoulders by laterally flexing the child's neck and pulling. The motor symptoms of brachial plexus upper root damage are said to constitute the Erb-Duchenne syndrome. Since these roots predominantly innervate muscles proximal to the elbow, motions at the shoulder and elbow joints are most affected. There occurs paralysis of abduction and lateral rotation of the upper arm, paralysis of elbow flexion, and weakness of supination of the forearm. The upper limb hangs limply at the side with the upper arm in medial rotation and the forearm pronated (the so-called waiter's tip position). There is also a characteristic sensory deficit associated with injury to C5 and C6. As might be expected, the skin over the pre-axial side of the limb is without feeling.

To a certain extent one can predict which muscles will be paralyzed in Erb-Duchenne syndrome from a knowledge of brachial plexus formation and the distribution of specific nerves. The upper roots form the superior trunk, which is the sole source of axons to the suprascapular nerve. The superior and middle trunks (C5, C6, C7) are the sole source of axons to the lateral cord, from which the musculocutaneous nerve is derived. Unfortunately, there are other paralyses that cannot be deduced in this way.

Avulsion of C5 and C6 leads to paralysis of some trunk muscles attaching to the shoulder girdle (e.g., subclavius, rhomboids, and most of serratus anterior). However, Erb-Duchenne syndrome is defined by the consequences of limb muscle denervation and can occur by damage to the superior trunk of the brachial plexus, which will not affect trunk muscles innervated by C5 and C6.

Klumpke Syndrome

Damage to the lower roots (C8 and T1) of the brachial plexus can occur during strong upward traction on the upper limb. This might occur if a person attempts to stop a fall by grabbing onto an overhead support. It also may occur during delivery of a neonate if an attempt is made to facilitate passage of the trunk by pulling on the upper limb. The motor deficits that result from damage to the lower roots of the brachial plexus constitute the Klumpke syndrome. Since these roots innervate predominantly muscles distal to the elbow, motions of the wrist and hand are most affected.

We can predict certain of the deficits in Klumpke syndrome by realizing that C8 and T1 are the sole source of axons to the medial cord and ulnar nerve. Thus, all the ulnar innervated muscles of the forearm and hand will be paralyzed. It just so happens that those axons of the median nerve destined for intrinsic hand muscles and for the deep extrinsic digital flexors are also derived from C8 and T1. The sensory deficit in Klumpke's syndrome is characterized by loss of sensation in the skin along the postaxial aspect of the upper limb.

Anastomoses Between Median and Ulnar Nerves

The ventral division axons for muscles distal to the elbow are carried by either the median or ulnar nerve. Interestingly, nerve fibers that normally run with the ulnar nerve may sometimes leave the brachial plexus in the median nerve, and vice versa. Such fibers may stay with their abnormal carrier all the way to the muscle for which they are destined, in which case that muscle has an anomalous innervation from the "wrong" nerve. More frequently, these fibers cross from the abnormal carrier to their proper carrier somewhere below the elbow. The most common form of such a median/ulnar communication is called the Martin-Gruber anastomosis, which occurs in about 15% of limbs. It arises when motor axons that should have left the brachial plexus with the ulnar nerve to innervate certain muscles of the hand, instead leave with the median nerve. Then in the forearm, these misdirected axons correct their mistake by crossing from the median nerve to join the ulnar nerve, thereby creating the anastomosis.

The significance of Martin-Gruber anastomosis is that injury to the median nerve proximal to the anastomosis will lead to specific hand muscle paralyses expected from ulnar nerve damage, and damage to the ulnar nerve proximal to the anastomosis fails to yield these expected symptoms.

Sympathectomy (or Sympathicotomy, or Sympathetic Chain Clipping) for Palmar Hyperhidrosis

The upper limb receives its sympathetic innervation through gray rami that join the ventral rami of the brachial plexus. The postganglionic axons in these gray rami come from cells in the middle cervical sympathetic ganglion, the inferior cervical sympathetic ganglion, and the first thoracic ganglion. For many years people believed that these postganglionic cells are controlled by preganglionic axons that arise in the T2-T3 spinal cord segments, travel in the 2nd and 3rd white rami communicantes to the T2 and T3 paravertebral ganglia, then ascend in the sympathetic chain to the ganglia of synapse. As a result, surgical removal or destruction of the T2 and T3 sympathetic ganglia, or simply cutting the sympathetic trunk (i.e., sympathicotomy) at one or more sites just below the T1 ganglion, became an accepted procedure to treat a distressing condition in which the patient is plagued by excessive sweating of the palm (i.e., palmar hyperhidrosis). As long as the T1 ganglion and its white ramus are left unscathed, no ocular symptoms of a Horner's syndrome are produced. However, since the sweat glands and vasculature of the face are innervated mainly by the T2 level of the spinal cord, functions of these structures are affected by such surgery. Indeed, this surgery may be done as a means to treat excessive facial sweating or blushing .

Recently, it has been discovered that one can effectively treat palmar hyperhidrosis by interrupting the sympathetic trunk between the T3 and T4 ganglia (Lin CC & Telaranta T. 2001 Annales Chirurgiae et Gynaecologie 90:161-166). This means that the preganglionic cells for the upper limb reside predominantly in the T4 and lower (T5, T6?) segments of the intermediolateral column (although it does seem that T3 provides a small amount of sympathetic innervation to the palms.) Leaving the sympathetic trunk intact above the T4 ganglion has the distinct advantage of preserving the sympathetic input to the face. Also, this newer procedure is less often associated with excessive compensatory sweating elsewhere in the body, which is one of the most unpleasant side effects of transection of the sympathetic trunk above the T3 or T2 ganglia.

There are some people who experience hyperhidrosis of the armpit. If this occurs along with palmar hyperhidrosis, interrupting the sympathetic trunk just above the T4 ganglion is often effective in treating both conditions, although the success rate for eliminating the axillary hyperhidrosis is lower than that for eliminating the palmar hyperhidrosis (Neumayer C et al. 2005 Arch. Surg. 140:676-680). The fact that the axillary apocrine glands (which produce the odiferous secretion) are not under nervous control may account for the higher failure rate of sympathicotomy in treating axillary hyperhidrosis. I have read that if a person's sole complaint is axillary hyperhidrosis, interrupting the sympathetic trunk between T4 and T5 helps as much as interrupting it above T4. However, since surgery for this condition may or may not produce the desired result, and since it is possible to surgically remove the glands of the armpit without major disfigurement, some physicians do not recommend sympathicotomy if axillary hyperhidrosis is the sole complaint.

As an aside, some surgeons now espouse placing surgical clips across the sympathetic trunk as a means of blocking transmission of nerve signals. This technique is said to be as effective as cutting the trunk, and if the side effects of the surgery are intolerable to the patient, removal of the clips restores function to the presurgery state.

Pancoast (Superior Sulcus) Tumor and Syndrome

You will recall that the apex of the lung rises as high as the neck of the first rib. The ventral ramus of T1 crosses in front of the neck of the first rib (hence behind the apex of the lung) to reach the superior surface of the rib just posterior to the subclavian artery. At this site, the ventral ramus of T1 is joined by the ventral ramus of C8 to form the inferior trunk of the brachial plexus. You should also recall that lying on the head of the first rib is the first thoracic sympathetic ganglion (called stellate ganglion if it is joined to the inferior cervical ganglion). From these relationships you can deduce that tumors of the apex of the lung, particularly those located posteriorly in the apex, may compress or involve the lower trunk of the brachial plexus and the first thoracic sympathetic ganglion. Such tumors often produce pain (and later numbness and weakness) in those regions of the upper limb served by C8 and T1. About 20% of the time a Horner's syndrome is also produced [Detterbeck FC 1997 Pancoast (Superior Sulcus) Tumors. Ann Thor Surg 63:1810-1818]. Tumors in the apex of the lung producing these symptoms are called Pancoast tumors (after a radiologist named Henry Pancoast), and the suite of symptoms due to nerve involvement are said to constitute a Pancoast syndrome. Although other diseases involving the apex of the lung can produce a Pancoast syndrome, they are rare compared to Pancoast tumor.

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CHAPTER 99 - The Axilla, and Nerves to Proximal Upper Limb Muscles

Suprascapular Nerve

The suprascapular nerve is not often injured by itself, although trauma to the posterior triangle of the neck, or falls on the shoulder, may do so. In addition to the symptoms mentioned in this chapter, right-handed persons usually experience difficulty in writing, since movement of the hand across the page involves lateral rotation of the humerus.

Although a test of abduction strength would reveal weakness of supraspinatus in the case of suprascapular nerve injury, the examiner would be unable to distinguish this from weakness of deltoid due to axillary nerve injury without further observations. Thus, the least ambiguous test for the suprascapular nerve is for strength of lateral rotation of the arm. The patient is instructed to hold the arms at the sides with the elbows flexed. The examiner attempts to push the hands inward against resistance by the patient. The teres minor is too weak a lateral rotator to confound results of this test.

Pectoral Nerves

Specific injuries to the pectoral nerves are rare. To assess function of the pectoral nerves, one asks the patient to hold the arms out in front of the body, and the examiner attempts to push the elbows apart against the patient's resistance.

Subscapular Nerves

The subscapular nerves are rarely injured. One can theorize that such injury would greatly affect medial rotation of the arm, and also affect combined extension/adduction of the arm. The test for strength of medial rotation is to ask the patient to hold the arms at the side, with the elbows flexed, and then resist the attempt of the examiner to push the hands apart. If the patient is able to offer only weak resistance to this movement, and palpation of the pectoralis major indicates it is working, one can suspect injury to subscapular nerves. The test for strength of combined extension/adduction of the arm consists of asking the patient to hold the arm straight out to the side and resist the examiner's attempt to lift it upward and forward.

Axillary Nerve

The test for the axillary nerve consists of asking a patient to hold the arms straight out to the side while the examiner attempts to push them down. In this way, weakness of one deltoid relative to the other may be easily assessed. The motion will be weak if the supraspinatus is paralyzed, so one must use his/her powers of observation, or palpation, to determine that the weakness is due to a paralyzed deltoid.

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CHAPTER 100 - Branches of the Subclavian Artery to the Upper Limb, and the Axillary Artery

Warm Ischemia Time

An organ or structure deprived of its blood supply will die. The length of time it can remain alive at room temperature without irreversible tissue damage is called its "warm ischemia time". For limb muscles and nerves this is 4 hours (Whitesides TE Jr, Heckman MM. 1996 Acute compartment syndrome: update on diagnosis and treatment. J Am Acad Orthop Surg 4::209- 218). After 8 hours of warm ischemia, irreversible damage has occurred. In between these times, the damage is variable. If the affected segment is cooled to 4 °C the ischemic lifetime can be greatly extended (doubled or more). Major causes of limb ischemia are arterial occlusion and, more dramatically, accidental amputation.

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CHAPTER 102 - Major Nerves of the (Upper) Arm

Musculocutaneous Nerve

The musculocutaneous nerve is rarely injured alone. Fractures of the humerus, direct wounds to the axilla, or even axillary artery aneurysm may affect it. One must make sure not to damage the musculocutaneous nerve in an anterior approach to surgery on the shoulder. This is done by staying on the lateral side of the conjoint tendon of origin of coracobrachialis and short head of biceps brachii. The motor test for function of the musculocutaneous nerve is no more complicated than asking the patient to flex the elbow against resistance by the examiner.

Radial Nerve

Tests for motor function of the radial nerve consist of assessing strength of elbow extension, wrist extension, and finger extension (at the MCP joint). Sensory examination involves choosing a spot of skin whose innervation by the radial nerve is rarely, if ever, altered by variations in nerve distribution. Such a spot is the web of skin overlying the 1st dorsal interosseous muscle on the back of the hand. This skin is stimulated by soft and sharp objects to determine the patient's response.

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CHAPTER 103 - Radial and Ulnar Arteries in the Forearm

Superficial Ulnar Artery

Core Concepts states that injections meant for the median cubital vein may have dire consequences if put in a superficial ulnar artery. The reason is that solutions of drugs meant for intravenous injection are usually highly concentrated in anticipation of the fact that they will become diluted with venous blood from other parts of the body when they reach the heart. If such a solution is injected into an artery by mistake, it reaches the capillary bed of that artery without significant dilution. The result may be serious injury to capillary walls and to the tissues supplied by these capillaries.

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CHAPTER 107 - Radial and Ulnar Arteries at the Wrist and Hand

Arterial Anastomoses in the Hand and the Modified Allen Test (I wish to thank Scott McGovern, a Stony Brook medical student, for drawing my attention to this Clinical Sidelight.)

In the hand there are two major anastomotic routes between the radial and ulnar arteries:

(1)

the superficial palmar arch, which in roughly a third of people is structurally complete (i.e., formed by a visible anastomosis between the superficial ulnar artery and the superficial palmar branch of the radial artery), and in another third of people is often called "complete" if the superficial ulnar artery sends a branch to the thumb but does not visibly connect to a branch of the radial artery;

(2)

the deep palmar arch, which is structurally a complete arch in almost everybody.

As a result of these anastomotic routes, if either the ulnar or radial artery is injured at the wrist, patients tolerate ligation of the injured vessel very well. Does this mean you need not worry about damaging one of these arteries during the course of another medical procedure?

This issue has come to fore because (a) the radial artery is becoming increasingly popular as a substitute for the great saphenous vein during coronary artery bypass grafting, (b) the radial artery is becoming increasingly popular as a substitute for the common femoral artery as the route for inserting the catheter needed to perform coronary angiography, (c) the radial artery is often cannulated for the purpose of monitoring blood pressure and blood gasses during anesthesia or in an ICU, and (d) hemodialysis usually involves establishing an arteriovenous fistula between the radial artery and a vein at the wrist. Before one removes the radial artery, or risks occluding it, or diverts its blood, it would be nice to know if the patient's ulnar artery can take over complete supply of the hand, particularly of the thenar eminence and thumb, which rely most heavily on the radial artery for their supply of blood.

There are some sophisticated ways (measurement of blood pressure within the thumb, Doppler ultrasound measurement of blood flow in the princeps pollicis artery, pulse oximetry of the thumb) to assess the ability of the unlar artery to keep the entire hand alive, but many physicians recommend starting out with a very simple test called the modified Allen test. The examiner puts pressure on both the radial and ulnar arteries at the wrist, then either asks the patient to make and release a tight fist several times (YouTube Video), or to make a tight fist, hold it for 15 -30 seconds, then open the hand (YouTube Video). In either case, the making of the fist drives most of the blood out of the hand so that after the last opening, the palm and the palmar surfaces of the digits are pale. Now the real test begins. The examiner releases the pressure on the ulnar artery and observes if and how long it takes for the hand to turn red. If the collateral circulation between the ulnar and radial arteries is adequate, the hand will turn from pale to red within 5 seconds even though the radial artery remains compressed. If it takes longer than 10 seconds to become red, then the ulnar artery is considered unable to supply the entire hand all by itself. Failure to turn red within 10 seconds is said to constitute a positive (or abnormal) Allen test. It is important that the patient be instructed not to overextend the wrist nor completely extend the digits, because doing so places tension on the skin and palmar aponeurosis that may compress the cutaneous vessels and give a false positive result.

Many physicians believe that if a patient has a positive (abnormal) modified Allen test, you shouldn't perform any procedure on that patient that compromises the radial artery's blood supply to the hand. However, there is evidence that even when carefully done, modified Allen tests tend to give a fair number of false positive results. As a result, some physicians believe that in the case of a positive modified Allen test, the patient should undergo more sophisticated assessments of blood supply to the hand so as not to be excluded from a procedure on the radial artery that will actually be well tolerated.

The problem posed by the relatively high frequency of false positive modified Allen tests has recently been addressed by a paper proposing a new, but equally simple, method of assessing the ulnar artery's ability to supply the entire hand. This method uses a smartphone app able to measure blood circulation to the index finger (Di Santo P et al. 2018 Photoplethysmography using a smartphone application for assessment of ulnar artery patency: a randomized clinical trial. CMAJ 190:E380-E388). The app, called Instant Heart Rate (by Azumio), is available for both iPhones and Android phones. When the phone's camera lens is placed on the pad of one's index finger and the pad is illuminated by the camera light, the phone uses color and brightness changes of the reflected light to measure volume changes in the finger pad due to blood flow. While advertised as as a means to measure heart rate, the app also presents a graphical representation of blood volume change. When this graphical record is assessed during radial artery compression, a determination can be made of the how well the ulnar artery can take over blood supply to the index finger. This new method was found to be as good as the modified Allen test for detecting an inadequate collateral circulation to the hand, and to have many fewer false positive results than the modified Allen test. Time will tell if it becomes widely accepted.

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CHAPTER 109 - Carpal Tunnel, Guyon's Canal;, Palmar Aponeurosis, Palmaris Brevis, Fibrous and Synovial Digital Flxor Sheaths

Synovial Sheaths

A penetrating wound of a finger or thumb may introduce infectious material into its synovial digital flexor sheath. The sheath then provides a passageway for this infectious material to travel proximally into the palm. Because the synovial sheaths do not extend to the tips of the digits, wounds here run less risk of proximal spread of infection. The synovial sheath of the little finger is connected to the synovial bursa in the carpal tunnel. Consequently, an infection of the little finger's synovial sheath can spread into the carpal tunnel. Similarly, an infection of the thumb's synovial digital flexor sheath can spread into the carpal tunnel.

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CHAPTER 111 - Median Nerve in the Hand

Median Nerve

In routine physical examinations, one motor and one sensory test for the median nerve are performed. The motor test consists of asking the patient to make a circle by opposing the pads of the thumb and little finger, whereupon the examiner attempts to pull the thumb away by applying a force to its proximal phalanx. This is a test of strength for the thenar eminence muscles. The sensory test consists of assessing cutaneous sensation at the tip of the index finger. This is the part of the median's cutaneous distribution least susceptible to variation in nerve supply. Obviously, other tests can be performed (e.g., of wrist flexion and finger flexion) if these two standard tests produce suspicious results.

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CHAPTER 112 - Ulnar Nerve in the Hand

Ulnar Nerve - How to Test

In routine physical examinations, assessment of the ulnar nerve is usually confined to one sensory and one motor test. The skin over the tip of the little finger is chosen for the sensory test, because its innervation by the ulnar nerve is rarely, if ever, altered by variations in nerve distribution. To assess ulnar-innervated muscles the patient is asked to spread apart his or her fingers while the examiner tries to squeeze the index and little fingers together. This tests the strength of the first dorsal interosseous and abductor digiti minimi (with flexor carpi ulnaris used as a synergist to prevent pisiform displacement).

Ulnar Nerve - Motor Symptoms If Damaged

It is stated that injury to the ulnar nerve at the wrist is characterized by clawing of the ring and little fingers. This is true in most people, but not in persons whose MCP joint capsules are so tight as to prevent hyperextension of the MCP joints. (I happen to be such a person.) In ulnar-nerve-injured patients with tight MCP joint capsules, the fingers can be completely extended by the extrinsic digital extensors. It is in this group (and in patients with high ulnar nerve injuries, where clawing is not so prominent anyway) that "falling away" of the little finger from the ring finger is most obvious. In Core Concepts, I describe this persistent abduction of the little finger (known as Wartenberg's sign) as being caused by paralysis of its palmar interosseous muscle. This is true, but another factor is needed to actually produce the abduction of the little finger. Most authors believe this factor is provided by tension within the tendon of extensor digiti minimi. In about half of people the extensor digiti minimi has an abductor leverage at the little finger MCP joint. Obviously, in the half of people in which the extensor digiti minimi cannot abduct the little finger, Wartenberg's sign is not a feature of ulnar nerve injury.

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CHAPTER 114 - Anatomic Snuffbox, Dorsal Wrist Compartments, and the Mechanisms of Finger Extension and Flexion

Snuffbox

It is significant that the scaphoid is in the floor of the snuffbox, since fractures of the scaphoid are indicated by tenderness or swelling in the snuffbox.

De Quervain's Disease and Finkelstein's Test (This section is being added at the suggestion of Jeffrey Jacobson, a Stony Brook medical student, and with his help.)

As stated in 114, septa extend from the deep surface of the extensor retinaculum of the wrist to the distal radius and ulna, thereby dividing the space beneath the retinaculum into compartments for the different carpal and digital extensor tendons. Tendons of the abductor pollicis longus and extensor pollicis brevis pass through the first, most radial, of these compartments, which lies along the lateral aspect of the styloid process of the radius. Sometimes, for reasons unknown (but far more commonly in women than in men), the retinacular tissue of this compartment becomes thickened, thereby impinging upon the tendons passing beneath it. Movements of the thumb or wrist produced by the APL and/or EPB then become painful. This state of affairs is called De Quervain's disease. It may be accompanied by an inflammation of the synovial sheaths of the APL and EPB tendons (i.e., tenosynovitis).

Finkelstein's test is used to determine if painful motion of the thumb is from De Quervain's disease or has some other cause. The patient is asked to make a fist, but one in which the fingers curl over the thumb, just as we were taught to avoid when we were children. The examiner then grasps the hand and moves it into adduction (i.e., ulnar deviation) at the wrist. In De Quervain's disease, this maneuver causes severe pain over the radial styloid process. One may also find a positive Finkelstein's test in arthritis of the first carpometacarpal joint. These two conditions are then differentiated by pushing the first metacarpal proximally while twisting it back and forth. Such a "grind test" elicits pain in pollical CMC joint disease but not in De Quervain's disease.

Muscle Interaction During Finger Flexion and Extension

This paragraph of Core Concepts states that contraction of an extrinsic finger extensor (EDC, extensor indicis, or extensor digiti minimi) by itself produces hyperextension at the MCP joint and, because of increased passive tension within the stretched FDP, flexion at the IP joints. This is true in the majority of persons, who require active contribution by some intrinsic hand muscles in order to straighten out their fingers. (A hand in which all the fingers are clawed is said to be intrinsic-minus.) However, in some people the ventral portion of an MCP joint capsule is so tight as to stop hyperextension of the joint. In such cases, an extrinsic finger extensor can fully extend the finger without any assistance from intrinsic hand muscles. Patients with tight ventral MCP joint capsules of the little and ring fingers will not present with the typical ulnar claw hand.

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CHAPTER 116 - Anatomy of the Shoulder, Elbow, and Radiolulnar Joints

Repeated strenuous movements of the shoulder may lead to painful inflammation of the subacromial bursa, or even injury to the rotator cuff muscles, particularly supraspinatus. Furthermore, not everybody's scapula is shaped precisely the same. Notably, the acromion process can be bent into a sort of hook. Orthopaedists classify acromions according to how hooked they are.

There is evidence that subacromial bursitis and supraspinatus injury are more likely to occur in persons with Type 3 acromions. Someone experiencing symptoms from impingement of the acromion on the underlying soft tissues may be treated by acromioplasty, i.e., reshaping it so it is less hooked-shaped. (For more information, see Campbell's Operative Orthopaedics, S. T. Canale, ed., Mosby, St. Louis.)

In older persons with arthritis of the shoulder, the intracapsular part of the biceps long head tendon may erode, so that the biceps long head then arises from the intertubercular sulcus of the humerus.

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CHAPTER 117 - Relationships of Nerves in the Upper Limb

Carpal Tunnel Syndrome

Carpal tunnel syndrome is treated by surgical transection of the transverse carpal ligament. In the old days, a skin incision was made in the palm starting at a point just proximal to the projected position of the superficial palmar arch and extending proximally to the distal carpal flexion crease. The incision was positioned along a line corresponding to the radial edge of the ring finger because this minimizes the chance of cutting the palmar cutaneous branch of the median nerve which lies subcutaneously between the tendons of the palmaris longus and flexor carpi radialis. The transverse carpal ligament was cut near its ulnar attachment so as to minimize the possibility of damaging the median nerve.

Nowadays, unless contraindicated, surgery to incise the transverse carpal ligament is almost always done endoscopically and requires only a small transverse skin incision through one of the carpal flexion creases (again avoiding damage to the palmar cutaneous branch of the median nerve). There are a number of ways to perform the actual cutting of the ligament; two are shown in https://www.youtube.com/watch?v=B2HEQvBr03k and https://www.youtube.com/watch?v=OcCW064Gg6k&t=76s. Because the skin incision used in an endoscopic carpal tunnel release is small and does not go through the palm, recovery from surgery is much quicker and is associated with far less pain.

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CHAPTER 121 - Tibia, Fibula, Ankle and Foot Bones

A human who sustains a minor fracture of the fibula will not generally require a cast because the bone bears minimal loads.

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CHAPTER 122 - Veins of the Lower Limb

Varicose Veins

Varicose superficial veins of the lower limb are not an uncommon result of pregnancy, since the enlarged uterus compresses the common iliac veins and thereby elevates venous pressure within the lower limb.

Great Saphenous Vein

Probably everyone knows that the great saphenous vein has particular clinical significance for coronary bypass surgery. Being long and easily located, it is resected so that segments of it may be used as grafts extending from the ascending aorta to various coronary arteries beyond the sites of their occlusion. It also used for femoropopliteal bypass surgery (connecting the common femoral artery to the popliteal artery so that blockage on the superficial femoral artery may be bypassed). During femoropopliteal bypass, the great saphenous vein may be excised and turned around so that the valves permit distal flow of blood, or it may be left in situ and all the valves stripped out. If left in situ, its tributaries must be sutured so that arteriovenous fistulae do not develop.

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CHAPTER 127 - Muscles of the Anterior and Medial Thigh

Q Angle

In clinical practice, the Q angle is estimated by angle between two lines: one between the anterior superior iliac spine and the center of the patella, the other between the center of the patella and the tibial tuberosity. So estimated, the Q angle averages 13° in males and 16° in females. Lateral patellar dislocation occurs more often in women than men because of this difference, a reflection of women's higher femoral bicondylar angles.

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CHAPTER 129 - Nerves of the Anterior and Medial Thigh

NOTE: For information on causes of injury to these nerves I have relied heavily on the text Focal Peripheral Neuropathies by JD Stewart, 1993, Raven Press, NY.

Femoral Nerve

The femoral nerve may be inadvertently cut during pelvic, groin, or hip surgeries. It may be stretched by a retractor during pelvic surgery. It may be compressed against the inguinal ligament during prolonged lithotomy position. Pelvic tumors, pelvic fractures, anterior hip dislocations, and penetrating injuries to the groin also place the nerve at risk. Motor tests require the patient to extend the lower leg against resistance and, for the purpose of testing the rectus femoris and iliopsoas, to flex the thigh against resistance.

Obturator Nerve

The anterior division of the obturator nerve is of particular clinical significance in the symptomatic treatment of cerebral palsy. Children with this disorder may experience a severe impairment of gait due to spastic medial rotation and adduction of the thigh. Transection of the anterior division of the obturator nerve will paralyze gracilis, adductor longus, and adductor brevis; such paralysis actually has a salutatory effect on locomotion. Elimination of spasticity in the gracilis has the additional positive result of reducing the tendency of the knee to be held in a partly flexed posture.

Like the femoral nerve, the obturator is not often injured. Intrapelvic tumors may compress the obturator nerve. Sometimes the pressure exerted by the fetal head during parturition may damage the maternal obturator nerve. Fracture of the superior pubic ramus, or hernia of bowel through the obturator canal are other potential sources of injury. One tests for damage to the obturator nerve by requiring the patient to adduct the thigh against resistance.

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CHAPTER 131 - Nerves of the Gluteal Region

Superior Gluteal Nerve

The Trendelenburg test is described in Chapter 131. Another test for damage to the superior gluteal nerve requires the patient to lie on his or her side and attempt to elevate the lower limb against resistance.

Inferior Gluteal Nerve

The inferior gluteal nerve is tested by requiring the prone patient to flex the knee and then raise the thigh off the examining table against resistance. The gluteus maximus should be palpated as the test is performed. Flexion of the knee is necessary because it causes the hamstring muscles to operate in unfavorable regions of their length-tension curves and, therefore, enables a purer test of gluteus maximus strength.

Piriformis Syndrome

Many persons who experience sciatica (i.e., pain along some part of the distribution of the sciatic nerve) are found to have a slipped disc, but other patients with sciatica have myelograms or MRIs that show no evidence of disc (or other spinal) disease. After many years of debate, it is now believed that another common cause of sciatica is something called "piriformis syndrome" (Filler AG, et al. 2005 Sciatica of nondisc origin and piriformis syndrome: diagnosis by magnetic resonance neurography and interventional magnetic resonance imaging with outcome study of resulting treatment. J Neurosurg Spine 2:99-115). Folks with piriformis syndrome typically present with buttock pain that may or may not radiate down the back of the lower limb. When it does so radiate, it less commonly goes into the foot than in cases of disc disease. If it does go into the foot, the pain affects all five toes, whereas a radiculopathy due to a herniated disc affects only the toes innervated by the compressed spinal nerve (medial toes if L5, lateral toes if S1). Numbness and muscle weakness are rare in cases of piriformis syndrome, and the SLR (straight leg raise) test is usually negative. The pain is made worse by sitting, and also becomes worse when an examiner places the thigh in a flexed, adducted, and internally rotated position, especially if the patient is then asked to abduct or externally rotate the thigh against resistance. In its early stages, the pain of piriformis syndrome is believed to be caused by irritation of the sciatic nerve due to a spastically contracting piriformis muscle. Subsequently, the nerve may be affected by hypertrophy of the piriformis, or atrophy and tightness of the muscle, or secondary adhesions to the muscle and surrounding tissues. What initially causes spasm of a piriformis is uncertain, but it may be set off by a back injury or trauma to the buttock. Although a study of possible piriformis syndrome patients has been performed to see if visual abnormalities of the muscle or sciatic nerve can be detected by MRI, the best proof of the condition is that it is relieved either by MR guided injection of anesthetic and steroid into the muscle, or if this fails, by surgical resection of a segment of the piriformis overlying the sciatic nerve.

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CHAPTER 135 - Sciatic Nerve in the Thigh and Popliteal Fossa, Common Peroneal Nerve and Sural Nerve

Sciatic Nerve

Damage to the entire sciatic nerve may occur in major traumatic injury to the buttock or thigh, fractures or dislocations of the hip, and during hip surgery. Intrapelvic tumors and very poorly placed injections in the buttock can produce partial injuries. Compression of the nerve can arise from sitting for a long time wedged in a toilet seat (usually associated with inebriation), or in emaciated patients that lie supine on an operating table for a long time, or during bicycling, or from prolonged sitting on one's thick wallet (usually associated with being a professor). Paralysis of lower leg muscles supplied by both the common peroneal and tibial nerves should cause one to think of damage to the sciatic, rather than separate damage to its branches. Paralysis of the hamstrings is a sign of damage above the proximal thigh.

Some tests for motor function of the sciatic nerve are the same as those for its common peroneal and tibial branches (see further on). However, assessing the strength of knee flexion addresses the sciatic's innervation of the hamstrings and short head of biceps femoris, branches to which are given off before the sciatic splits into the common peroneal and tibial nerves. So that the examiner can distinguish weakness of knee flexion due to sartorius or gracilis paralysis from that due to muscles innervated by the sciatic nerve, palpation of the hamstrings is essential.

Sural Nerve

Posterior to the lateral malleolus lies the small saphenous vein, and posterior to the vein lies the sural nerve. The nerve is easily located here. It can be traced upward from this point and removed virtually in its entirety to supply bridging segments during attempts to repair damage to more important nerves of the body.

Common Peroneal Nerve

As stated in Chapter 147, the common peroneal nerve is the most frequently injured nerve of the lower limb. In addition to the listed causes of injury, plaster casts, or the supports used to hold up the legs in the lithotomy position, can also compress the nerve. Signs of injury are a combination of those resulting from malfunctioning of both the deep and superficial peroneal nerves.

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CHAPTER 137 - Muscles of the Posterior Leg, and the Tibial nerve

Tibial Nerve

The tibial nerve may be injured by wounds to the popliteal fossa or back of the lower leg, fractures at the knee, or dislocations of the knee. It can be compressed by a Baker's cyst, which is a fluid-filled pouch derived either from one of the bursae at the back of the knee or from an outpocketing of synovial membrane through the posterior capsule of the joint. Testing the motor functions of the tibial nerve is done by requiring the patient to plantarflex the foot, to invert the foot, and to flex the toes against resistance. Asking the patient to walk on his/her toes is another good test for the strength of the triceps surae. Some physicians ask the patient to spread the toes apart in an attempt to assess the intrinsic muscles of the foot, however, many of us perfect persons cannot perform this maneuver.

Plantaris

The very small plantaris muscle gives rise to a long thin tendon that is separate from the Achilles tendon. It is a clinically significant structure for two reasons: (a) rupture of the plantaris tendon is a highly painful condition, (b) the plantaris tendon may be removed to be used as a graft for repair of badly damaged tendons in the hand.

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CHAPTER 138 - Anterior and Lateral Regions of Leg, and Dorsum of Foot

Compartment Syndromes

The anterior tibial, peroneal, and deep posterior compartments of the calf are inexpansible. Buildup of pressure within any of these compartments is a potentially serious problem because the small veins in that compartment become compressed. As this happens, venous pressure rises and, consequently, the arteriovenous pressure gradient falls (Matsen FA III. 1980 Compartmental Syndromes. Grune & Stratton, NY). The result is diminished capillary flow and ischemia of the structures within the compartment. Nerves are most sensitive to such ischemia, and the first sign that compartmental pressure has reached dangerous levels is tingling or diminished sensation in the areas of skin supplied by intracompartmental nerves. Pain upon passive stretching of the involved muscles is also a sign for concern. The compartmental ischemia leads to increased capillary permeability and further swelling, so that the pressure buildup becomes increasingly worse. When the intracompartmental pressure rises to within 25 - 30 mm Hg of the average arterial pressure (diastolic + 1/3[systolic-diastolic]), capillary blood flow stops.

The diminished capillary blood flow of a compartment syndrome leads to tissue damage even before all capillary flow stops. If the high intracompartmental pressure goes untreated, all the compartmental contents will die. Muscles killed in this way become fibrotic and shortened. Not only are they nonfunctional, but the shortening results in deformities.

One cause of compartment syndrome is an unaccustomed period of strenuous exercise. Muscles become swollen and tender after such exercise. For muscles like the deltoid or pectoralis major, which are not within confined spaces, this swelling presents no particular problem and will resolve with time. If the overused muscles lie within an inexpansible compartment, such as found in the lower leg, it is still possible for the swelling to resolve itself without complication. However, it is also possible for the pressure buildup to lead to an "exertional" compartment syndrome. One example of this is anterior tibial syndrome, which may occur after a long walk by an otherwise sedentary person. Anterior tibial syndrome (like any other compartment syndrome) is accompanied by pain in the compartment. However, the first sign that intervention may be necessary is malfunctioning of the deep peroneal nerve, revealed by tingling or diminished sensation in the dorsal web of skin between the first and second toes. The treatment for this, and most other compartment syndromes, is to make a long incision through the fascia bounding the compartment. Such a "fasciotomy" relieves the intracompartmental pressure.

More common than exertional compartment syndromes are those that arise following trauma (like a broken bone) that causes bleeding into the compartment. A third cause of compartment syndrome is reperfusion injury. When a structure is deprived of blood, the capillaries become more permeable. If blood flow is suddenly restored, the reperfused structure will swell. The general rule is that if a limb has been ischemic for 6 hours, whatever the reason, you should do a prophylactic fasciotomy prior to restoring circulation. Obviously, if a limb has been ischemic for significantly more than six hours, it must be amputated (see Warm Ischemia Time).

Medial Tibial Stress Syndrome ("Shin Splints")

The term "shin splints" has been applied to so many different conditions characterized by exertional leg pain (e.g., incipient anterior tibial syndrome, incipient deep posterior compartment syndrome, stress fracture) that most clinicians now advise against its use. However, it seems that the majority of persons who present with what they believe to be shin splints are actually suffering from a condition more properly called "medial tibial stress syndrome" (MTSS). The symptom of MTSS is a diffuse pain along the posteromedial border of the tibia, usually bridging the junction of its middle and distal thirds. This pain is brought about by exercise, most commonly running or jumping, and is to be distinguished from a stress fracture, the pain of which is more focal. At one time it was widely believed that MTSS was essentially an inflammation of the tibial periosteum (i.e., a periostitis) along the site where the medial edge of the soleus has a fascial attachment to the posteromedial edge of the tibia (below the actual origin of the soleus from the soleal line of the tibia). Among the appealing aspects of this theory was the increased incidence of MTSS in persons who experience an unusually high range (or possibly speed) of subtalar joint pronation during running. It is believed that such persons overuse the soleus, which is both a plantarflexor and supinator of the subtalar joint. Also, MRI on patients with posteromedial tibial pain frequently reveals periosteal edema in the affected region. The theory that MTSS is a periostitis even guides surgical treatment when more conservative approaches fail. The surgery primarily involves cutting the fascial attachment of the soleus to the posteromedial edge of the distal tibia. It does not always work.

The problem with attributing the pain of MTSS to periostitis is that most studies have found no evidence of periosteal inflammation in persons undergoing surgery for this condition. The pendulum is swinging toward the belief that basic pathology of MTSS is a decreased bone density (i.e., greater bone porosity) due to an incomplete remodeling effort as the bone attempts to respond to exceptionally high and/or frequent loads (Jones BH, et al. 1989 Exercise-induced stress fractures and stress reactions of bone: epidemiology, etiology, and classification. Exerc Sports Sci Rev 17:379-422). There is certainly evidence to support the existence of metabolic and histologic changes in the bone of the affected region. However, the link between having a zone of porous bone and being in pain is not clear (Gaeta M, et al. 2005 High resolution CT grading of tibial stress reaction in distance runners. AJR 187:789-793). It may be that the porous bone responds to heavy loading with microcracks that are painful, but the issue has yet to be resolved. One would like to reconcile the "porous bone" explanation of MTSS with a role for soleus overuse in causing this syndrome. The only suggestion of which I am aware is that contraction of the soleus may add to the bending loads on the tibia (Beck BR. 1998 Tibial stress injuries: an aetiological review for the purposes of guiding management. Sports Med 26:265-279).

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CHAPTER 139 - Superficial and Deep Peroneal Nerves

Specific motor test of the superficial peroneal nerve requires the patient to evert the foot against resistance; the strength of this motion is due far more to lateral compartment muscles than to peroneus tertius.

A specific test of the deep peroneal nerve requires the patient to dorsiflex the foot and toes against resistance. Another test is to ask patient to walk on his or her heels, a behavior that requires strong anterior tibial compartment muscles.

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CHAPTER 144 - Knee Joint

Isolated injuries of the anterior cruciate ligament do occur, but there is no consensus on what motion produces them. Excessive axial rotation, which involves injury to one of the collateral ligaments, is often accompanied by an anterior cruciate tear. One clinical test for the anterior cruciate ligament involves the examiner placing the knee of a supine patient in 90° of flexion, then attempting to the pull the tibia forward off the undersurface of the femur.

Very little motion is allowed in a normal knee. Some books say that more than 3 mm is abnormal. If significant movement does occur, this constitutes a positive anterior drawer sign, and indicates an injured anterior cruciate ligament. Before using this test to gain information on the anterior cruciate ligament, you should be sure that the tibia has not fallen posteriorly relative to the femoral condyles because of a torn posterior cruciate ligament. If it had, you would be able to pull it forward into its normal position, but this would tell you nothing about the ACL. For this very reason, many orthopaedists don't like to assess ACL integrity by the anterior drawer test. They use a test described in the next paragraph.

A more sensitive test for anterior cruciate injury is the Lachman test, but it requires greater skill to interpret. The difference is that the knee is placed is placed in only 20-30° of flexion. Now when the examiner tries to pull the tibia forward he or she will normally be able to elicit a few millimeters of movement, but this movement should have a firm stopping point. If the stopping point is "mushy", this is a sign of anterior cruciate ligament damage.

It possible for one bundle of the ACL to be injured while the other remains functionally intact, or the two bundles may both be injured but each at a different site along its length. If both bundles are seriously damaged, as is often the case, the entire ACL is replaced by a graft. There is an active debate about whether a single graft is sufficient or the surgeon should use two grafts, with each attempting to replicate the path of one bundle of the ACL. The "single-bundle" technique restores adequate resistance to anterior sliding of the tibia on the femur but, because the ACL also functions in stabilizing other motions at the knee, some orthopaedists believe that the more complicated "double-bundle" technique better reproduces the overall function of the ACL.

The posterior cruciate ligament is not as often injured as is the ACL. Isolated injuries of the PCL are usually the result of a posteriorly directed force applied to the proximal tibia when the knee is flexed. A classic example is an automobile passenger who, as the result of a car accident, is thrust forward so that the lower leg bangs into the dashboard. Falling down forward so that one lands on a flexed knee may also create the requisite force. The clinical test for the posterior cruciate ligament involves the examiner attempting to the push the flexed tibia backward off the undersurface of the femur. Virtually no motion is allowed in a normal knee; if significant movement does occur because of an injured posterior cruciate ligament, this constitutes a positive posterior drawer sign. The use of a double-bundle technique for repair of a seriously damaged PCL is even more controversial than use of this technique to treat ACL injuries.

A blow to the lateral aspect of the knee (not uncommon in football) may very well rupture both the superficial and deep fibers of the medial collateral ligament. Because the latter are adherent to the capsule, it and the attached medial meniscus may also be torn.

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CHAPTER 145 - Tibiofibular and Ankle Joints

The lateral ligaments of the ankle are more frequently sprained than is the deltoid ligament. A physician tests for the integrity of these ligaments by manually trying to move the foot in a way that an intact ligament would resist. For example, the test for the anterior talofibular ligament is for the examiner to place one hand on the front of the leg and then attempt to pull the foot forward by pressure applied to the heel. If the foot can be pulled forward relative to the leg, this is said to be a positive anterior drawer sign of the ankle, indicating a torn anterior talofibular ligament.

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CHAPTER 146 - The Longitudinal Arch of the Foot

Posterior Tibial Tendon Insufficiency (PTTI) ( I thank Matt Gotlin, a Stony Brook medical student, for drawing my attention to this condition.)

Some people are born with a predisposition to develop bilateral flat feet in childhood. This may be due to ligament laxity, or an underdeveloped sustentaculum tali, or other reasons I don't fully understand. However, unilateral development of a flat foot in an adult (called Adult Acquired Flatfoot Deformity, AAFD) is very frequently associated with degeneration or rupture of the tendon of the tibialis posterior muscle. Indeed some authors treat AAFD as if it were synonymous with PTTI. The tibialis posterior is an extrinsic muscle that provides support for the longitudinal arch. Although not active when a person is simply standing, the muscle comes into play during the stance phase of locomotion. It makes sense that if the muscle cannot do its job because its tendon has undergone a degenerative process or has ruptured, then the ligaments that support the longitudinal arch, particularly the spring ligament, are placed under greater stress and will eventually fail. However, there is a bit of the chicken and egg controversy surrounding the cause of AAFD. Some evidence exists that laxity of, or damage to, the spring ligament may precede the development of PTTI. The logic here is that ligamentous malfunction places extra stress on the tibialis posterior to serve as an active supporter of the arch, leading over time to PTTI. Regardless, people with AAFD usually show not only damage to the tibialis posterior tendon but also to the spring ligament (Deland JT et al. 2005 Posterior tibial tendon insufficiency: which ligaments are involved? Foot Ankle Intl 26:427-435). If AAFD has progressed beyond the point where it can be managed by conservative treatment, but has not yet reached the stage when correction can only be achieved by realigning and fusing ankle bones to one another, most experts believe surgical treatment should entail, among other things, an attempt to repair or reconstruct the spring ligament.

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CHAPTER 149 - Surface Anatomy of Lower Limb Structures

Common Femoral Artery

The ability to compress the common femoral artery against the head of the femur has significance beyond taking the pulse of this vessel. Radiologists frequently use the common femoral artery as a site to gain entry into the arterial system. A hypodermic needle is inserted through the anterior wall of the vessel where it lies anterior to head of the femur. A guide wire is threaded through the needle, the needle is withdrawn, a catheter is threaded over the guide wire into the artery, and finally the guide wire is withdrawn. Catheters inserted in this manner may be passed superiorly into the aorta or one of its branches for the purpose of angiography or selective arterial embolization. At the end of the procedure, when the catheter is withdrawn, bleeding from the common femoral artery is controlled by compressing it against the femoral head for 10 minutes. Following this compression, the patient must lie immobile for at least 2 hours to ensure cessation of external bleeding. If, by mistake, the puncture needle had been directed too obliquely upward, with the result that it entered the common femoral artery proximal to the femoral head or, worse, entered the external iliac artery, one is left with a hole in a vessel that has no posterior structure against which it can be compressed. The result may a considerable hematoma in the proximal thigh and/or pelvis. An example of this is found at http://jackstern.org/RadiologySelfTest/indexanompath.html, case 7.

Some physicians prefer to perform a femoral stick by passing the needle through both the anterior and posterior walls of the artery, then partially withdrawing the needle so its opening lies in the arterial lumen. The site of arterial puncture should be the same as described above. If the puncture site is located too far distally, it may enter the superficial femoral artery where this vessel lies anterior to the superficial femoral vein. After piercing the back wall of the artery, the needle may inadvertently enter the vein, creating the risk that an arteriovenous fistula will develop.

The common femoral artery is large and provides a fairly direct route to the ascending aorta, but there are a few factors that mitigate against using the common femoral artery as the site of insertion for cardiac catheterization. In obese patients it is particularly difficult to hit the femoral artery. If a patient has advanced iliac atherosclerotic disease, this may hinder passage of the catheter into the abdominal aorta. As mentioned above, after the procedure is concluded the patient must remain supine and immobile for at least 2 hours, and if the stick was too high, internal bleeding is a real risk. For all these reasons, use of the radial artery as the insertion site for cardiac catheterization has grown in popularity. Though the radial artery is considerably smaller than the common femoral artery, it still may be easier to hit in an obese patient. In everyone, after the catheter has been withdrawn, external bleeding is easily controlled by a compression wrist band, allowing the patient immediately to walk and eat. Finally, there is no risk of internal bleeding from a radial artery stick. You will probably have deduced that the radial artery is not a suitable candidate for catheter insertion unless the hand can be kept alive by the ulnar artery during the period of the procedure. Hence performing an Allen test, or some more sophisticated assessment of blood supply to the hand, is a prerequisite. (I thank Derek Nelsen, a Stony Brook medical student, for alerting me to the increasing popularity of the radial artery as a site of insertion for cardiac catheterization.)

CHAPTER 150 - Lymphatics of the Body

Uterine Cancer

It is generally true that pelvic organs drain to internal iliac nodes, but lymph from the fundus of the uterus and uterine tubes also drains via channels that accompany ovarian vessels back to lumbar nodes. As mentioned in Table 98, when the normal routes of uterine lymphatic drainage become blocked, lymph may drain through channels that accompany the round ligament through inguinal canal, and then to the superficial inguinal nodes. If the latter are sites of metastatic uterine cancer, this is a bad sign, because it implies that intrapelvic nodes are heavily loaded with tumor.

Tongue Cancer

Any region of the tongue near its midline will send lymph to both the ipsilateral and the contralateral sides. For example, the tip of the tongue drains to both right and left submental nodes, as well as directly to both right and left jugulo-omohyoid nodes. It is also the case that regions of the lower lip near the midline send lymph to both the ipsilateral and contralateral submental nodes. Consequently, paramedian cancer of the tongue or lower lip is far more serious than cancer of these structures' lateral edges, because of the potential for metastases to both the right and left deep cervical chains.

Sampling Axillary Nodes for Spread of Breast Cancer

Breast surgeons use a different terminology for naming groups of axillary nodes than do anatomists. Surgeons usually speak of level 1 nodes, defined as those lateral to the pectoralis minor muscle (i.e., the pectoral, subscapular, lateral, and a few central nodes), level 2 nodes, defined as those deep to the pectoralis minor (i.e., most of the central nodes), and level 3 nodes, defined as those medial to pectoralis minor (i.e., the apical axillary nodes). The lower the number of the level, the more likely is the node group to be a recipient of mammary carcinoma spread. (However, spread to level 2 nodes can occur with negative level 1 nodes and, although unlikely, there can be positive level 3 nodes without tumor detected in either level 1 or level 2 nodes).

For obvious reasons, lymphatic drainage of the breast is the subject of much research. I summarize some of this research below, but even this summary contains far more detail than I would expect a first-year student to learn. I have highlighted in bold type what I think you should know.

Most surgeons accept that 75% of the lymph from the breast goes to the axillary nodes, while 25% goes to the internal mammary nodes (IMN). In fact, recent studies indicate that if breast cancer has spread to the axillary nodes, there is about a 25% chance it will also have spread to the IMN (Purushotham AD, Cariati M. 2005 Br. J. Surg. 92:131-132). On the other hand, among patients who have negative axillary nodes, only 5-15% (depending on the study) will prove to have tumor in the IMN. There is some indication that the superficial part of the breast drains almost entirely to axillary nodes, whereas the deeper portion drains to both the axillary nodes and the IMN (Shimazu K et al. 2003 Ann. Surg. 237:390-398). There is also some evidence that, although all quadrants of the breast send lymph to the IMN, the incidence of metastases to these nodes is somewhat higher if the tumor is in the medial half of the breast. Surgical sampling of lymph nodes draining the breast is generally confined to the axillary nodes, recognizing the pretty small chance of isolated IMN metastases and the greater difficulty of surgical access to the IMN.

One can identify the lymph node most likely to house metastatic breast cancer by combining a technique called lymphoscintigraphy with injection of a blue dye that is picked up by breast lymphatic vessels. Lymphoscintigraphy entails the injection of radiocolloid into the breast around the site of the tumor. After an hour or so, a blue dye is injected at the same site. An incision is made in the axilla and the surgeon looks for a lymph node that has picked up the blue dye and/or (using a Geiger counter) a lymph node that is radioactive. In either case, such a node is called a "sentinel node". Sometimes the blue node is also the radioactive node, sometimes they are different, sometimes there are two or three nodes that satisfy one or both of the criteria for being called a sentinel node. Regardless, a sentinel node is viewed as the first in the series of nodes that receives lymph from the breast. For many years after the development of the sentinel node procedure for breast cancer, the practice was to send identified sentinel nodes for immediate frozen section to determine if there were microscopic foci of tumor in these nodes. If tumor was found, the surgeon removed many more axillary nodes in a procedure simply referred to as an axillary node dissection. This was believed to improve survival rates and to help in planning future treatment.

Axillary node dissection is not without risks. Removing certain nodes along the axillary vein may interrupt lymphatic drainage from the upper limb. When lymphatic drainage from any region of the body wall is significantly blocked, that region tends to swell - a condition called lymphedema. Because breast lymph rarely goes to lymph nodes that lie along the convexity (i.e., superior surface) of the axillary vein, whereas most lymph from the upper limb goes to these nodes, breast surgeons will preserve them in hopes of minimizing the incidence of postoperative upper limb lymphedema. Also, crossing near the floor of the axilla is the intercostobrachial nerve. It is often sacrificed during axillary node dissection, although in recent years surgeons are making a greater attempt to preserve this nerve because cutting it leaves the patient with unpleasant numbness on the posteromedial aspect of the upper arm. The surgeon should also look out for the thoracodorsal nerve, the nerve to serratus anterior (i.e., long thoracic n.), and the thoracodorsal artery. Preservation of the latter is especially important because the latissimus dorsi may be used later for breast reconstruction.

To reach apical axillary nodes (level 3), which are usually only removed if there is to be a mastectomy, the surgeon will cut ("take down") the pectoralis minor at its origin in order to improve exposure of the relevant region. Effort should be made to preserve the medial pectoral nerve, which often pierces the pectoralis minor. If this nerve is cut, the sternocostal pectoralis major becomes atrophic.

Because an axillary node dissection may have undesirable consequences, and patients with microscopic tumor in a sentinel node will generally receive radiation and chemotherapy whether or not tumor has spread to other axillary nodes, a major study was conducted to determine if removal of numerous axillary nodes really helps (Giuliano AE et al. 2011 Axillary dissection vs. no axillary dissection in women with invasive breast cancer and sentinel node metastasis. A randomized clinical trial. JAMA 305:569-575). The findings were that axillary node dissection does not improve survival rates, or diminish rates of local tumor recurrence, in patients with positive sentinel nodes who received postoperative radiation and chemotherapy. As a result, many breast surgeons no longer send sentinel nodes for immediate frozen section. Instead, the removed sentinel nodes will be sent for standard pathological assessment over the next few days. The results guide details of future radiation and chemotherapy. However, axillary node dissections are usually still performed if the surgeon sees obvious tumor in axillary nodes.

As implied above, the overwhelming majority of sentinel nodes are found in the axilla. However, in a large series of patients with breast cancer, it was shown that about 15% of patients have sentinel nodes in both the axilla and the IMN (Hong J et al. 2005 Eur. J. Surg. Oncol. 31:942-948). (Other studies give higher percentages for sentinel nodes in both locations.) Only 2% of patients had a sentinel node in the IMN without having one in the axilla. There is active research on the value of attempting to identify metastatic disease in the IMN, but for the moment, standard procedure calls only for looking in the axilla to find sentinel nodes.

Variability in Lymphatic Drainage of the Skin (The new information presented below is my summary of Uren RF, Howman-Giles R, Thompson JF. 2003 Patterns of lymphatic drainage from the skin in patients with melanoma. J Nucl Med 44:570-582).

The figure accompanying Chapter 150 depicts a human torso with one horizontal line drawn at the level of the clavicles and another at the level of the umbilicus. Arrows indicate the following: (1) lymphatic drainage from skin and subcutaneous tissue above the transclavicular plane goes to deep cervical nodes, (2) lymphatic drainage from skin and subcutaneous tissue between the transclavicular and transumbilical planes goes primarily to axillary nodes, but also to internal mammary nodes, and (3) lymphatic drainage from skin and subcutaneous tissue below the transumbilical plane goes to superficial inguinal nodes. These arrows also indicate that lymphatic drainage from skin and subcutaneous tissue to the right of the median sagittal plane goes to right-sided nodes, and lymphatic drainage from skin and subcutaneous tissue to the left of the median sagittal plane goes to left-sided nodes. All these "facts" are oversimplifications of the truth.

In cases of cutaneous melanoma it has become standard practice to look for sentinel nodes using lymphoscintigraphy (injection of radiocolloid into the skin around the site of the tumor) followed by imaging that reveals where radioactivity has concentrated. Observations have been made of drainage to lymph nodes in completely unexpected places, and in some cases to nodes not previously known to drain the skin. First, skin within a 10 cm region straddling either the transclavicular or transumbilical plane can drain to regions above that plane, below that plane, or both. Similarly, skin within a 10 cm region straddling the median sagittal plane can drain ipsilaterally, contralaterally, or both. Second, Uren and colleagues discovered that in 10-15% of patients the first nodes to drain skin of the back above the transumbilical plane are found in the triangular intermuscular space of the shoulder (i.e., that space bounded by teres major, teres minor, and long head of triceps brachii - see figure to Chapter 97). This nodal group had not been previously known. Third, skin of the back in the vicinity of the transumbilical plane may drain to para-aortic nodes in addition to axillary or superficial inguinal nodes. For those of us who just want to memorize a simple pattern, the only good news is that drainage from the skin of the anterior trunk more often goes to predicted nodes, and less often crosses the midline, than lymphatic drainage from the back. The authors describe various other incidences of unexpected lymphatic drainage involving skin of the head and upper limbs. The bottom line is that one should memorize the lymphatic drainage patterns of the skin shown in the figure for Chapter 150, but they are not chiseled in stone.

Surgical Nomenclature for Nodes Draining the Lungs

Surgeons use a nomenclature for lymph nodes draining the lungs that differs from what you will find in most anatomy texts. The American Joint Committee on Cancer and the Prognostic Factors TNM Committee of the Union Internationale Contre le Cancer have adopted the scheme shown in the figure (modified from Mountain CF and Dresler CM. 1997 Regional lymph node classification for lung cancer staging. Chest 111:1718-1723). I have been told that a new standard nomenclature is in the works. Regardless, I cannot recommend that a first-year medical student commit this memory, except for a few terms I will mention below.

Of all the terms used by surgeons to describe mediastinal nodes, the ones you should know are

hilar nodes - lie around the mainstem bronchi within the lung
subcarinal nodes - lie in the inferior angle of the tracheal bifurcation
paratracheal nodes - lie alongside the trachea

Also, one often hears the intrapulmonary nodes distal to the hilar nodes referred to as "peribronchial nodes". The hilar and peribronchial nodes are not accessible via mediastinoscopy without breaking the parietal pleura and risking pneumothorax.

The right lung drains almost entirely to right paratracheal nodes. The left upper lobe drains almost entirely to left paratracheal nodes. The left lower lobe drains to both right and left sides. If there is evidence of left lower lobe cancer, surgeons want to know if the cancer has spread to the right paratracheal nodes, because such spread is a counterindication for surgical treatment of the cancer. One way to get the necessary information is to perform a mediastinoscopy. Some facilities have supplanted this with a PET (Positron Emission Tomography) scan of the superior mediastinum, which is as sensitive, or more so, in revealing tumor involvement of relevant nodes. Finally, T. J. Santo, a student at Stony Brook, has drawn my attention to the existence of a relatively new technique - ultrasound guided transbronchial needle aspiration, in which a flexible bronchoscope fitted with an ultrasound transmitter/receiver and biopsy needle is passed into the trachea and mainstem bronchi, where the needle is jabbed through the wall of the air passageway to take cytologic samples from suspicious nodes identified on CT. This technique does give access to hilar and peribronchial nodes.

Iliac Node Dissection

When removing external iliac lymph nodes, the surgeon must be careful not to damage the genitofemoral nerve lying lateral to these nodes. When removing the obturator nodes, it is the obturator nerve that is in danger.

Cloquet's Node

Cloquet's node is variously described at the most superior of the deep inguinal nodes or the most inferior of external iliac nodes. It lies in the femoral ring (i.e., the entrance to the femoral canal). Deep inguinal nodes are sampled for spread of cancer from the lower limb, or from any superficial tissue below the umbilical plane. If Cloquet's node is negative, it is often considered unnecessary to go higher and sample external iliac and obturator nodes. If Cloquet's node is positive for cancer, the surgery is extended into the abdomen and pelvis to take out external iliac and obturator nodes.

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