PREFACE
PURPOSE
We have written Kaufman’s Clinical Neurology for Psychiatrists – a collegial straightforward guide – from our perspective as neurologists at a major, urban academic medical center. In a format combining traditional neuroanatomic correlations with symptom-oriented discussions, the book will assist psychiatrists in learning modern neurology. It emphasizes neurologic conditions that are frequently occurring, common to psychiatry and neurology, illustrative of a scientific principle, or have prominent psychiatric manifestations. It also includes descriptions of numerous neurologic conditions that may underlie aberrant behavior, disturbances in mood, or cognitive impairment – symptoms that prompt patients or medical colleagues to solicit psychiatry consultations. Kaufman’s Clinical Neurology for Psychiatrists does not intend to replace comprehensive neurology textbooks or convert psychiatrists into semiprofessional neurologists; however, this book contains essential information required of psychiatrists.
ORGANIZATION AND CONTENT
The organization and content of Kaufman’s Clinical Neurology for Psychiatrists arose from our experience as faculty at the Albert Einstein College of Medicine, attending physicians at Montefiore Medical Center, and supervisors of numerous neurology and psychiatry residents; consultation with our colleagues, many of whom are worldrenowned physicians; and feedback from many of the 20,000 psychiatrists who have attended the course, “Clinical Neurology for Psychiatrists,” and the more than 50,000 individuals who have purchased previous editions of this book. Learning the material in this book should help readers prepare for examinations, perform effective consultations, and improve their practice and teaching. Section 1 reviews classic anatomic neurology and describes how to approach patients with a suspected neurologic disorder, identify central or peripheral nervous system disease, and correlate physical signs. Section 2 discusses common and otherwise important clinical areas, emphasizing aspects a psychiatrist may encounter. Topics include neurologic illnesses, such as multiple sclerosis, brain tumors, strokes, and traumatic brain injury; and common symptoms, such as headaches, chronic pain, epilepsy, and involuntary movement disorders. For each topic, chapters describe the relevant symptoms including psychiatric comorbidity, easily performed office and bedside examinations, appropriate laboratory tests, differential diagnoses, and some management options.
Many chapters contain outlines for a bedside examination; reproductions of standard bedside tests, such as the Montreal Cognitive Assessment (MoCA) and Abnormal Involuntary Movement Scale (AIMS), references to recent medical literature, and pertinent web sites. One chapter provides a compilation of computed tomography (CT), magnetic resonance imaging (MRI), and positron emission tomography (PET) images that other chapters reference. Appendices contain information pertaining to most chapters: Patient and Family Support Groups (Appendix 1); Costs of Various Tests and Treatments (Appendix 2); Diseases Transmitted by Chromosome or Mitochondria Abnormalities (Appendix 3); and Chemical and Biological Neurotoxins (Appendix 4).
In addition, the book reviews neurologic conditions that have entered the public arena because, willingly or unwillingly, psychiatrists are liable to be drawn into debates involving their own patients or the medical community. Psychiatrists should be well versed in the intricacies of the following conditions that this book describes:
• Amyotrophic lateral sclerosis and multiple sclerosis as battlegrounds of assisted suicide
• Meningomyelocele with Arnold–Chiari malformation as an indication for abortion and the value of spending limited resources on this fatal or severely debilitating condition
• Chronic pain as the fulcrum for legalizing marijuana and heroin
• Parkinson disease, spinal cord injury, and other disorders amenable to research and treatment with stem cells
• Persistent vegetative state and continuing life-support technology
• Cost of medical testing and treatment.
ADDITIONS AND OTHER CHANGES FOR THE EIGHTH EDITION
The first seven editions of Kaufman’s Clinical Neurology for Psychiatrists have enjoyed considerable success in the United States, Canada, and abroad. The book has been translated into Japanese, Italian, Korean, and Spanish. In the eighth edition, written 3 years after the seventh, we have clarified the presentations, discussed recent developments in many areas, and added many clinical, anatomic, and radiologic illustrations. To give the question-andanswer sections greater power, we have increased the number of questions, refined them, expanded the discussions, and provided more illustrations. We have increased the usage of questions based on clinical vignettes because
BOX 1.1 Neurologic Examination
Mental status
Attention
Cooperation
Orientation (to month, year, place, and any physical or mental deficits)
Language
Memory for immediate, recent, and past events
Higher intellectual functions: arithmetic, similarities/ differences
Cranial nerves
I Smell
II Visual acuity, visual fields, optic fundi, pupil size and reactivity (afferent limb)
III, IV, VI Pupil size and reactivity (efferent limb), extraocular movements
V Corneal reflex and facial sensation
VII Strength of upper and lower facial muscles, taste
VIII Hearing
IX–XI Articulation, palate movement, gag reflex
XII Tongue movement
Motor system
Limb strength
Tone (e.g., spasticity, flaccidity)
Abnormal movements (e.g., tremor, chorea, fasciculations)
Reflexes
Deep tendon reflexes
Biceps, triceps, brachioradialis, quadriceps/patellar, Achilles
Pathologic reflexes
Extensor plantar response (Babinski sign), frontal release
Sensation
Position, vibration, stereognosis, light touch
Pain
Cerebellar system
Finger-to-nose and heel-to-shin tests
Rapid alternating movements
Gait
with CNS injury that includes corticospinal tract damage DTRs are hyperactive, whereas with PNS injury DTRs are hypoactive.
In contrast to DTRs, pathologic reflexes are not normally elicitable beyond infancy. If these are found, they are a sign of CNS damage. The most widely recognized pathologic reflex is the famous Babinski sign. After plantar stimulation, the great toe normally moves downward (i.e., it has a flexor response). With brain or spinal cord damage, plantar stimulation typically causes the great toe to move upward (i.e., to have an extensor response). This reflex extensor movement, which is a manifestation of CNS damage, is the Babinski sign (see Fig. 19.3). Neurologists say that the Babinski sign and other pathologic reflexes are “present,” “found,” or “elicited,” but not “positive” or “negative.” The terminology is similar to a traffic stop sign: It may be present or absent, but not positive or negative.
Frontal release signs, which are also pathologic reflexes, reflect frontal lobe injury. When present they point to an “organic” basis for a change in personality and, to some degree, correlate with cognitive impairment (see Chapter 7).
Unlike abnormal DTRs and Babinski signs, which are reproducible, objective, and difficult to mimic, the sensory examination relies almost entirely on the patient’s report. Its subjective nature has led to the practice of disregarding reports of disturbances inconsistent with the rest of the examination. Under most circumstances, the best approach is to test the major sensory modalities in a clear anatomic order and tentatively accept the patient’s report.
Depending on the nature of the suspected disorder, physicians may first test light touch sensation with their finger-tips or a wood stick cotton swab, and then three sensations carried by the posterior columns of the spinal cord: position, vibration, and stereognosis (appreciation of an object’s form by touching it). Neurologists might test pain (pinprick) sensation, which is carried in the lateral columns, but only in a careful manner with a nonpenetrating, disposable instrument, such as with a broken wood shaft of the cotton swab.
Neurologists evaluate cerebellar function by observing several standard maneuvers that include the finger-to-nose test and rapid alternating movement test (see Chapter 2). These tests may demonstrate intention tremor or incoordination.
If at all possible, neurologists watch the patient walk, because a normal gait requires intact CNS and PNS motor pathways, coordination, proprioception, and balance. Moreover, all these systems must be wellintegrated. Examining the gait is probably the single most valuable assessment of noncognitive functions of the nervous system. Neurologists watch for gait abnormalities that characterize many neurologic illnesses (see Table 2.1). In addition, they should expect certain gait abnormalities to be comorbid with cognitive impairment. Whatever the abnormality, gait impairment is not merely a neurologic sign, but a condition that routinely leads to fatal falls and permanent incapacity for numerous people each year.
FORMULATION
Although somewhat ritualistic, a succinct and cogent formulation remains the basis of neurologic problem solving. A neurologist’s classic formulation consists of an appraisal of the four aspects of the examination: symptoms, signs, localization, and differential diagnosis. A neurologist might also have to support a conclusion that neurologic disease explains the patient’s symptoms and signs or, equally important, does not. For this step, neurologists at least tentatively separate psychogenic signs from neurologic (“organic”) ones.
Localization of neurologic disease requires the clinician not only to determine whether the illness affects the CNS, PNS, or muscles (see Chapters 2–6), but precise localization of lesions within these regions of the nervous system is also generally expected. The physician must also establish whether the illness affects the nervous system diffusely or in a focal, discrete area. The site and extent of neurologic damage generally indicates certain diseases. A readily apparent example is that strokes and tumors usually involve a discrete area of the brain, but
Alzheimer disease usually causes widespread, symmetrical changes.
Finally, neurologists create a differential diagnosis that lists the disease or diseases most consistent with the patient’s symptoms and signs. They should include unlikely but potentially life-threatening conditions. In addition, many neurologists, in a flourish of intellectualism, conclude with unlikely but fascinating explanations. However, even at tertiary care institutions, common conditions arise commonly. Just as “hoof beats are usually from horses, not zebras,” patients are more likely to have hemiparesis from a stroke than a mitochondrial disorder.
A typical formulation might be as follows: “Mr. Jones, a 56-year-old right-handed bartender, has had left-sided headaches for 2 months and, on the day before admission, had a generalized seizure. He is lethargic. He has papilledema, a right hemiparesis with hyperactive DTRs, and a Babinski sign. The lesion is probably situated in the left cerebral hemisphere. It is most likely a tumor or stroke, but possibly a bacterial abscess.” This formulation briefly recapitulates the salient elements of the history and physical findings. In this case, neurologists would tacitly assume that neurologic disease is present because of the obvious, objective physical findings. The history of seizures, the right-sided hemiparesis, and abnormal reflexes localize the lesion. Neurologists would base their differential diagnosis on the high probability that a discrete cerebral lesion is causing these abnormalities.
A house officer presenting a case to a superior is well advised to separate the wheat from the chaff and complete the presentation within 2 minutes, which is the limit of most listeners’ attention spans. The clinician should also practice the presentation before rounds, bearing in mind Benjamin Franklin’s proverb, “By failing to prepare, you are preparing to fail.”
In summary, the neurologist should present a succinct, well-rehearsed formulation that answers The Four Questions of Neurology:
• What are the symptoms of neurologic disease?
• What are the signs of neurologic disease?
• Where is the lesion?
• What is the lesion?
RESPONDING AS A NEUROLOGIST TO CONSULTATIONS
During their training, psychiatry residents often rotate through a neurology service where they are required to answer requests for neurology consultations. Consultants at all levels must work with a variation of the traditional summary-and-formulation format. While the patient’s interests remain paramount, the consultant’s “client” is the referring physician. Both the referring physician and consultant should be clear about the reason for the consultation. Reasons for consultations typically concern a neurologic symptom, the significance of a neuroimaging report, or a treatment recommendation. Sometimes physicians request a broad review, such as when they ask the consultant to provide a second opinion or offer a prognosis. On the other hand, the referring physicians may not want to know the diagnosis or treatment options, but
simply want the neurology service to assume the primary care of the patient.
Without belaboring the obvious, the consultation note must be organized, succinct, and practical. The primary physician in an acute care hospital should be able to digest it in 2 minutes. Long notes are usually boring and inadvertently hide useful information. Cutting and pasting information and conclusions in computerized medical records by a consultant is redundant, liable to repeat errors, and, if a previous physician made an astute diagnosis, appears to take credit for someone else’s idea. Notes that are bad, for whatever reason, reflect poorly on the consultant and the consultant’s service, and they hamper the patient’s care. At least in an academic setting, the consultant should offer at least one teaching point about the case and provide general guidelines for handling similar inquires.
Finally, consultants should show an awareness of the entire situation, which often contains incomplete and conflicting elements. They should also be mindful of the situation of the referring physician and patient. Consultants in emergency situations might help by ordering –not merely suggesting – routine tests, such as blood studies, and important but innocuous treatments, such as thiamine injections. Except in unusual circumstances, consulting residents should not suggest hazardous tests or treatments without first presenting the case to their supervisor. Consultants should not divert the primary physicians’ efforts from the patient’s most important medical problems. They should not suggest embarking on elaborate, time-consuming testing for obscure, unlikely diagnoses when the patient’s illness is obvious and requires the primary medical team’s full attention. The consultant should ask, “How can I help?”
NEUROLOGIC DIAGNOSIS
Neurologists confirm a clinical diagnosis using different frames of reference. For some diseases, such as migraine and chronic pain, neurologists rely almost entirely on a patient’s symptoms. For others, such as Parkinson disease, they base their diagnosis on physical abnormalities or constellations of findings. For many other diseases, regardless of the patient’s symptoms and signs, their diagnosis rests on an abnormal test result. For example, the diagnosis of stroke or a brain tumor requires imaging studies, and confirmation of seizures often necessitates an EEG. Neurologists diagnose many asymptomatic individuals as having a neurologic disease on the basis of a single test, such as genetic analysis or MRI (see Chapter 20).
The clinical formulation remains the mainstay of neurologic diagnosis, but abnormal findings on MRI or other studies routinely trump clinical impressions. For example, the clinical examination may indicate the presence, location, and etiology of a cerebral lesion, but if an MRI indicates a different process, neurologists generally forsake their clinical formulation and accept the MRI findings as the diagnosis.
Overall, neurologists’ and psychiatrists’ diagnoses routinely differ in several respects. Neurologists shift the basis of their diagnosis from clinical constellation, to
BOX 2.1 Signs of Common CNS Lesions
Cerebral hemisphere*
Hemiparesis with hyperactive deep tendon reflexes, spasticity, and Babinski sign
Hemisensory loss
Homonymous hemianopia
Focal (partial) seizures
Aphasia, hemi-inattention, and dementia
Pseudobulbar palsy
Basal ganglia*
Movement disorders: parkinsonism, athetosis, chorea, and hemiballismus
Postural instability
Rigidity
Brainstem
Cranial nerve palsy with contralateral hemiparesis
Internuclear ophthalmoplegia (MLF# syndrome)
Nystagmus
Bulbar palsy
Cerebellum
Tremor on intention^
Impaired rapid alternating movements (dysdiadochokinesia)^
Ataxic gait
Scanning speech
Spinal cord
Paraparesis or quadriparesis
Spasticity
Sensory loss up to a “level”
Bladder, bowel, and sexual dysfunction
*Signs contralateral to lesions
#MLF, Medial longitudinal fasciculus
^Signs ipsilateral to lesions
BOX 2.2 Signs of Common Cerebral Lesions
Either hemisphere*
Hemiparesis with hyperactive deep tendon reflexes and a Babinski sign
Hemisensory loss
Homonymous hemianopia
Focal seizure
Dominant hemisphere
Aphasia: fluent, nonfluent, conduction, or isolation
Gerstmann syndrome: acalculia, agraphia, finger agnosia, and left–right confusion
Alexia without agraphia
Nondominant hemisphere
Hemi-inattention
Anosognosia
Constructional apraxia
Both hemispheres
Dementia
Pseudobulbar palsy
*Signs contralateral to lesions
paresis. When they have left hemiparesis, patients may not appreciate it (anosognosia). Many patients lose their ability to arrange matchsticks into certain patterns or copy simple forms (constructional apraxia, Fig. 2.8).
As opposed to signs resulting from unilateral cerebral hemisphere damage, bilateral cerebral hemisphere
Midbrain Pons
Internal capsule
Medulla
Spinal cord
FIGURE 2.1 ■ Each corticospinal tract originates in the cerebral cortex, passes through the internal capsule, and descends into the brainstem. The tracts cross in the pyramids, which are protuberances on the inferior portion of the medulla, to descend in the spinal cord mostly as the lateral corticospinal tract. The corticospinal tracts synapse with the anterior horn cells of the spinal cord, which give rise to peripheral nerves. Neurologists often call the corticospinal tract the pyramidal tract because it crosses in the pyramids. The extrapyramidal system, which modulates the corticospinal tract, originates in the basal ganglia and cerebellum, and remains within the brain.
damage produces several important disturbances that psychiatrists are likely to encounter in their patients. One of them, pseudobulbar palsy, best known for producing emotional lability, results from bilateral corticobulbar tract damage (see Chapter 4). The corticobulbar tract, like its counterpart the corticospinal tract, originates in the motor cortex of the posterior portion of the frontal lobe. It innervates the brainstem motor nuclei, which in turn innervate the head and neck muscles. Traumatic brain injury (TBI), multiple cerebral infarctions (strokes), and frontotemporal dementia (see Chapter 7), are apt to strike the corticobulbar tract, as well as the surrounding frontal lobes, and thereby cause pseudobulbar palsy. Damage to both cerebral hemispheres – from large or multiple discrete lesions, degenerative diseases, or metabolic abnormalities – also causes dementia (see Chapter 7). In addition, because CNS damage that causes dementia must be extensive and severe, it usually also produces at least subtle physical neurologic findings, such as hyperactive DTRs, Babinski signs, mild gait impairment, and frontal lobe release reflexes. However, many neurodegenerative illnesses that cause dementia, particularly
TABLE 2.1 Gait Abnormalities Associated With Neurologic Disorders
bodies disease, and Parkinson disease dementia (see Chapter 7). Several distinct gait abnormalities are clues to specific neurologic disorders, such as normal pressure hydrocephalus (Table 2.1). As a general rule, slow gait speed, e.g., 0.7 m/sec or less, is associated with an increased risk of dementia, stroke, falls, disability, hospitalization, and death.
SIGNS OF BASAL GANGLIA LESIONS
The basal ganglia, located subcortically in the cerebrum, consist of the caudate and putamen (together constituting the striatum), globus pallidus, substantia nigra; and subthalamic nucleus (corpus of Luysii) (see Fig. 18.1). They give rise to the extrapyramidal motor system, which modulates the corticospinal (pyramidal) tract. It controls muscle tone, regulates motor activity, and generates postural reflexes. Its efferent fibers play on the cerebral cortex, thalamus, and other CNS structures. Because its efferent fibers are confined to the brain, the extrapyramidal tract does not act directly on the spinal cord or LMNs. Signs of basal ganglia disorders include a group of fascinating, often dramatic, involuntary movement disorders (see Chapter 18):
• Parkinsonism is the combination of resting tremor, rigidity, bradykinesia (slowness of movement) or akinesia (absence of movement), and postural abnormalities. It usually results from Parkinson disease and related neurodegenerative illnesses, exposure to dopamine receptor-blocking antipsychotic medications, or toxins.
• Athetosis is the slow, continuous, writhing movement of the fingers, hands, face, and throat. Kernicterus or other perinatal basal ganglia injury usually causes it.
• Chorea is intermittent, randomly located, jerking of limbs and the trunk. The best-known example occurs in Huntington disease (previously called “Huntington chorea”), in which the caudate nuclei characteristically atrophy.
• Hemiballismus is the intermittent flinging of the arm and leg of one side of the body. It is classically associated with small infarctions of the contralateral subthalamic nucleus, but similar lesions in other basal ganglia may be responsible.
In general, when damage is restricted to the extrapyramidal system, patients have no paresis, DTR abnormalities, or Babinski signs – hallmarks of corticospinal (pyramidal) tract damage. More important, in many of these conditions, such as hemiballismus and athetosis, patients have no cognitive impairment or other neuropsychologic disorder. On the other hand, several conditions – such as Huntington disease, Wilson disease, and advanced Parkinson disease – affect the cerebrum as well as the basal ganglia. In them, dementia, depression, and psychosis frequently accompany involuntary movements (see Box 18.4).
With unilateral basal ganglia damage, signs develop in the contralateral limbs. For example, an infarction of the subthalamic nucleus causes contralateral hemiballismus, and degeneration of the substantia nigra causes contralateral parkinsonism (“hemiparkinsonism”).
SIGNS OF BRAINSTEM LESIONS
The brainstem contains, among a multitude of structures, the cranial nerve nuclei, the corticospinal tracts, other “long tracts” that travel between the cerebral hemispheres and the limbs, and cerebellar afferent (inflow) and efferent (outflow) tracts. Combinations of cranial nerve and long tract signs, and the absence of signs of cerebral injury, such as visual field cuts and neuropsychologic deficits, indicate the presence and location of a brainstem lesion. For example, brainstem injuries cause diplopia (double vision) because of cranial nerve impairment, but visual acuity and visual fields remain normal because the visual pathway, which passes from the optic chiasm to the cerebral hemispheres, does not travel within the brainstem (see Fig. 4.1). Similarly, a right hemiparesis associated with a left third cranial nerve palsy localizes the lesion to the brainstem (particularly the left midbrain). Moreover, that pair of findings indicates that further examination will reveal neither aphasia nor dementia.
Several brainstem syndromes illustrate critical anatomic relationships, such as the location of the cranial nerve nuclei or the course of the corticospinal tract; however, none of them involves neuropsychologic abnormalities. Although each syndrome has an eponym, for practical purposes it is only necessary to identify the clinical findings and, if appropriate, attribute them to a lesion in one of the three major divisions of the brainstem: midbrain, pons, or medulla (Fig. 2.9). Whatever the localization, most brainstem lesions result from occlusion of a small branch of the basilar or vertebral arteries.
In the midbrain, where the oculomotor (third cranial) nerve fibers pass through the descending corticospinal
hypotonia and pendular DTRs. However, cerebellar lesions do not cause paresis, hyperactive DTRs, or Babinski signs.
Although several technically sophisticated studies have shown that the cerebellum contributes to cognition and emotion, it does not play a discernible role in these functions in everyday endeavors. For example, lesions restricted to the cerebellum do not lead to dementia, language impairment, or other cognitive impairment. A good example is the normal intellect of children and young adults despite having undergone resection of a cerebellar hemisphere for removal of an astrocytoma (see Chapter 19).
On the other hand, several conditions damage the cerebrum as well as the cerebellum. For example, alcohol, phenytoin (Dilantin), lithium, and toluene may cause prominent ataxia and cognitive impairment.
For practical purposes, neurologists assess cerebellar function in tests of coordinated motor function. Thus, intention tremor, demonstrable in the finger-to-nose (Fig. 2.11) and heel-to-shin tests (Fig. 2.12), characterizes cerebellar dysfunction. This tremor is evident when the patient moves to a target but is absent when the patient rests. In a classic contrast, Parkinson disease causes a
resting tremor that is present when the patient sits quietly and reduced or even abolished when the patient moves (see Chapter 18). Physicians should not confuse the neurologic term “intention tremor” with “intentional tremor,” which would be a self-induced or psychogenic tremor.
Another sign of incoordination due to a cerebellar lesion is dysdiadochokinesia, impaired rapid alternating movements of the limbs. When asked to slap the palm and then the back of the hand rapidly and alternately on his or her own knee, for example, a patient with dysdiadochokinesia will do so with uneven force and irregular rhythm, and lose the alternating pattern.
Damage to either the entire cerebellum or the vermis alone causes incoordination of the trunk (truncal ataxia). This manifestation of cerebellar damage forces patients to place their feet widely apart when standing and leads to a lurching, unsteady, and wide-based pattern of walking (gait ataxia) (Table 2.1 and Fig. 2.13). A common example is the staggering and reeling of people intoxicated by alcohol. In addition, such cerebellar damage prevents people from walking heel-to-toe, i.e., performing “tandem gait.” Another common example of ataxia occurs in individuals who have inherited genetic mutations that cause combinations of cerebellar and spinal cord degeneration. In several disorders, patients have abnormalities beyond the nervous system (Fig. 2.14). Extensive damage of the cerebellum causes scanning speech, a variety of dysarthria. Scanning speech, which reflects incoordination of speech production, is characterized by poor modulation, irregular cadence, and
2.11 ■ This young man has a multiple sclerosis plaque in the right cerebellar hemisphere. During the finger-to-nose test, his right index finger touches his nose and then the examiner’s finger by following a coarse, irregular path. The oscillation in his arm’s movement is an intention tremor, and the irregularity in the rhythm is dysmetria
2.13 ■ Because this man has developed cerebellar degeneration from alcoholism, he has a typical ataxic gait His stance is broad-based. His gait is unsteady, and he is uncoordinated.
FIGURE
FIGURE 2.12 ■ In the heel-to-shin test, the patient with the rightsided cerebellar lesion in the previous sketch displays limb ataxia as his right heel wobbles when he pushes it along the crest of his left shin.
FIGURE
FIGURE 2.18 ■ Left, A syringomyelia (syrinx) is an elongated cavity in the spinal cord. Its expansion disrupts the lateral spinothalamic tract as it crosses, and compresses the anterior horn cells of the gray matter. It does not impair the function of the posterior columns and corticospinal tracts. Right, The classic finding is a shawl-like pattern of loss of pain and temperature sensation in the arms and upper chest (in this case, C4–T4) that is accompanied by weakness, atrophy, and areflexia in the arms.
FIGURE 2.19 standard spinal cord preparation stains (white matter) black central H-shaped column gray. B, In combined system degeneration (vitamin B12 deficiency), posterior column and corticospinal tract demyelination causes their lack of stain. C, In tabes dorsalis (tertiary syphilis), damage to the posterior column leaves them unstained. D, MS leads to asymmetric, irregular, demyelinated unstained plaques.
dentists, causes a pronounced myelopathy by inactivating vitamin B12 (see Chapter 5). Copper deficiency, often from excess consumption of zinc by food faddists or inadvertently ingested from excess denture cream, leads to myelopathy. Also, unless physicians closely monitor and replace vitamins and nutrients following gastric bypass surgery, patients remain at risk of developing myelopathy for up to several years after the surgery.
FIGURE 2.20 ■ The steppage gait consists of the patient’s raising each knee excessively, as if perpetually climbing a staircase. This maneuver compensates for a loss of position sense by elevating the feet to ensure that they will clear the ground. Although the steppage gait is a classic sign of posterior column spinal cord damage from tabes dorsalis, peripheral neuropathies that impair position sense are a more frequent cause of this gait abnormality.
Most important, dementia accompanies myelopathy in several illnesses because of concomitant cerebral damage. Examples of this association include tabes dorsalis, vitamin B12 deficiency, AIDS, and, when disseminated throughout the cerebrum, MS.
Fasciculus cuneatus
Spinothalamic tract
