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Noxious stimulation to each limb, as described previously, may be useful in looking for BOX Structural Causes of Depressed gross sensory abnormalities. Consciousness Coordination and gait may be tested in patients who are arousable enough. Epidural The cranial nerve exam includes the testing of im- portant brainstem reflexes, including the pupillary, Brain tumor with edema or hemorrhage corneal, and oculocephalic reflexes. Primary The remainder of the examination should be dedi- Metastatic cated to looking for focal abnormalities. The absence of BOX Diffuse Causes of Depressed focal signs suggests a diffuse cause of depressed con- Consciousness sciousness, including metabolic, toxic, or hypoxic- ischemic etiologies Box Examples include coma Metabolic from fulminant hepatic failure, barbiturate overdose, Electrolyte abnormality or anoxia following prolonged cardiac arrest.

Hyponatremia, hypernatremia, hypocalcemia, hypercalcemia, hypomagnesemia, hypermagne- semia, hypophosphatemia KEY POINTS Glucose abnormality In theory, consciousness can be depressed either Hypoglycemia, nonketotic hyperosmolar coma, by dysfunction of the brainstem or dysfunction of diabetic ketoacidosis both cerebral hemispheres simultaneously; in real- Hepatic failure ity, large unilateral hemispheric lesions with pres- Uremia sure on the other side qualify as well.

The presence or absence of brainstem reflexes Thyroid dysfunction Myxedema coma, thyrotoxicosis suggests how deep the coma is. The presence of focal signs suggests a structural Adrenal insufficiency cause of coma. Toxic The absence of focal signs suggests a diffuse cause Alcohol of coma, such as metabolic, toxic, infectious or Sedatives hypoxic-ischemic etiologies. Respiratory failure The presence of focal findings on examination, Cardiac arrest suggesting a structural cause, demands urgent head imaging, almost always a noncontrast computed Other tomography CT scan.

One should be looking for Subarachnoid hemorrhage signs of a large acute stroke, an intracranial hemor- Carcinomatous meningitis rhage, or a mass lesion that may have enlarged rapidly Seizures or postictal state or had hemorrhage within it. Contrast-enhanced CT should be avoided if acute hemorrhage is possible.

Even in cases where focal brainstem signs are found, the initial choice of head imaging may have to be a CT toxicologic screenmay be necessary. If infection is scan rather than magnetic resonance imaging MRI , suspected, a chest x-ray, urinalysis, and blood or despite the poor quality of the former in evaluating the urine cultures may be called for.

There should be a brainstem, because of the possibility of a large cerebral low threshold for obtaining a lumbar puncture LP. Head imaging is gesting a diffuse cause, warrants an extensive workup usually needed even in these cases of suspected for causes of metabolic, toxic, or infectious etiologies. Of course, a head CT 18 for systemic and metabolic disorders, Chapter 19 should be performed before obtaining an LP almost for brain tumors, and Chapter 21 for central nervous without exception in the evaluation of a patient with system CNS infections.

If bac- aimed at lowering ICP should be applied. These terial meningitis is suspected, empiric antibiotic include raising the head of the bed, hyperventilation, treatment can be started if CT scanning is delayed. Frequently, an electroencephalogram EEG is or- Corticosteroids tend to be useful only in cases of dered in patients with coma or altered consciousness. The lowering of Although many of its findings may be nonspecific, ICP may be a neurologic or neurosurgical emergency the EEG can help to assess how deep a coma is based if the patient shows signs of brain herniation, which on the degree of background slowing.

In addition, is discussed in more detail in Chapter Finally, the EEG overdose may recover completely, whereas one with a can rule out nonconvulsive status epilepticus as a severe anoxic injury likely will not. Age is an important cause of coma in cases in which this is or is not clin- prognostic factor as well. One of the most frequent ically suspected. KEY POINTS In these cases the circumstances and duration of the arrest are important, and published studies have corre- If a structural cause of coma is suspected, urgent lated outcome with findings on neurologic examina- head imaging, usually with a noncontrast head CT, tion performed at least 24 hours after the arrest.

If a diffuse cause is suspected, an extensive workup for metabolic, toxic, or infectious causes should be undertaken. KEY POINTS Head imaging in suspected diffuse cases may demonstrate cerebral edema, signs of global The treatment of coma or altered consciousness hypoxic-ischemic injury, or bilateral lesions mimick- depends on etiology. The lowering of intracranial pressure may be a neu- Almost without exception, head CT should be per- rologic emergency if the patient shows signs of formed before LP.

EEG can assess the depth of coma and can occa- Prognostic factors for coma or altered conscious- sionally suggest a specific diagnosis. Metabolic, infectious, or toxic etiologies require mostly medical manage- Persistent vegetative state is a state in which patients ment, while some structural causes of coma may have lost all awareness and cognitive function but require neurosurgical intervention. Specific treat- may remain with their eyes open, exhibit sleep-wake ments for particular conditions are detailed in later cycles, and maintain respiration and other autonomic chapters, in particular Chapter 14 for strokes and functions.

Definition LOCKED-IN SYNDROME The terms confusion, delirium, and encephalopa- thy are often used nonspecifically to indicate a dis- Although a locked-in syndrome can be confused with turbance of mental status in which the patient is coma at first glance, a patient with locked-in syn- unable to carry out a coherent plan of thought or drome is awake and may be intact cognitively, with action. Most neurologists employ the terms confu- no abnormality of consciousness. Usually a conse- sion or encephalopathy, while delirium commonly quence of large lesions in the base of the pons, the used by psychiatrists often implies a state of en- locked-in syndrome leaves patients unable to move cephalopathy characterized by a waxing and waning the extremities and most of the face.

If all other level of alertness. Thus, a patients fail- ure to answer questions in a coherent manner or to BRAIN DEATH carry out an intended series of actions in an ex- pected way derives from an inability to maintain Death can be declared either when there has been attention for long enough to proceed through the irreversible cessation of cardiopulmonary function or cognitive or motor steps required for the task. On there has been irreversible cessation of all functions formal mental status testing, therefore, patients of the entire brain, including the brainstem.

A decla- with confusion typically do poorly on standard tests ration of death based on the latter criterion is com- of attention, such as spelling the word world in re- monly referred to as brain death. Many institutions verse, reciting the months of the year backward, or have specific guidelines for how brain death must be completing serial subtractions. Such inattention determined, but in general the patient must be com- may be significant enough to make impossible the atose, have absent brainstem reflexes, and have no performance of more detailed mental status testing.

Confounding confusional state, other associated features may be factors such as hypothermia or drug overdose must present on neurologic or general physical examina- not be present. Confirmatory tests most commonly tion as well. Local institutional guidelines for declaration of The differential diagnosis of acute confusion in- brain death should always be consulted. Patients with Wernicke aphasia may appear confused but in fact are atten- A persistent vegetative state may follow prolonged tive and able to carry out coherent series of actions; coma and is characterized by preserved sleep-wake their deficit lies solely in their ability to communi- cycles and maintenance of autonomic functions, cate.

Although patients with psychosis may also with absence of awareness and cognition. Complex paralysis occurs, is often caused by large lesions in partial seizures can be characterized by behavior the base of the pons. Diagnostic Evaluation Treatment and Prognosis An acute confusional state is most commonly caused The treatment and prognosis of acute confusional by an underlying systemic or neurologic disorder, states depend largely on the underlying etiology. Focal brain disorders, particularly disorder is treated appropriately. Confusional states acute right hemispheric lesions, can also lead to con- arising from structural neurologic lesions or more fusion.

The appropriate diagnostic workup in a chronic underlying disturbances may be less likely to patient with confusion is therefore potentially quite improve spontaneously. Blood work and urinalysis to search for infectious or metabolic disturbances are often war- ranted. Neuroimaging should be obtained if the An acute confusional state, also sometimes called neurologic history or examination suggests the possi- delirium, is characterized by an inability to carry out bility of an acute focal lesion.

An EEG can help to a coherent plan of thought or action. It is unlikely problem with attention. An understanding of visual impairment, pupillary dis- to many higher-order centers in the posterior parietal turbances, and oculomotor control is essential in the and inferior temporal cortices, where the perception of diagnosis of neurologic disorders. Maximal interpre- motion, depth, color, location, and form takes place. This chapter covers the first two; the third consti- The most common neuro-ophthalmologic symptoms tutes part of higher cortical function, discussed else- are loss of vision and diplopia.

Other symptoms in- where see Chapter Two important signs discussed in this chapter are the abnormal optic disc and anisocoria unequal pupils. Positive visual phenomena in- optic nerve to centers in the brain for further pro- clude brightness, shimmering, sparkling, hallucina- cessing and visual perception.

The visual pathway tions, shining, flickering, or colors, often suggesting with various field defects is shown in Figure Negative visual phenomena The more posterior parts of the cerebral hemi- can be described as blackness, grayness, dimness, or spheres are involved in seeing and analyzing visual in- shade-obscuring vision, as seen in patients with formation, including written language, and the more strokes or transient ischemic attacks.

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Is this a monocular or binocular problem? Does principal subcortical structure that carries visual infor- the problem go away when one eye is closed? Does it affect a portion or the entire visual field? The primary visual cortex is visual area 1 V1 , 3. Is it transient or persistent? Are there associated symptoms, such as headache, which receives information from the contralateral vi- visual auras, motor or sensory disturbances, changes sual hemifield. This information is then transferred to in mentation, seizures, or eye pain e.

Localization Visual field defect 1. Optic nerve 1. Right eye blindness 2. Chiasm 2. Bitemporal visual field defect 3. Optic tract 3. Left homonymous hemianopia 4. Optic radiations parietal 4. Left inferior homonymous quadrantonopia 5. Optic radiations temporal or Meyers loop 5. Left superior homonymous quadrantonopia 6. Optic radiations both 6. Left homonymous hemianopia 7. Occipital cortex 7. Left homonymous hemianopia with macular sparing. Impairment of VA with determining whether the problem is at the level is usually a problem in the refractive apparatus of the of the eye, optic nerve, chiasm, optic tract, lateral eye or the optic nerve, or both.

Rarely, chiasmal or geniculate nuclei LGN , optic radiation, or occipital retrochiasmal lesions cause changes in VA. Once the site of dysfunction is determined, Color vision is tested by using Ishihara plates. Another method is looking for red desaturation de- The diagnostic evaluation includes assessment of creased perception of red color , which can be seen visual acuity and color vision, test for afferent pupil- early in optic nerve problems particularly optic lary defects, testing of visual fields, and ophthalmo- neuritis.

The ophthalmoscopic evaluation When testing pupils, report their size and reac- looks for damage to the retinal nerve fiber layer, optic tion to light, both consensually and in accommoda- atrophy, swollen disc, abnormal optic disc hypoplas- tion. Use a bright light. Look for a relative afferent tic, tilted, etc. To perform this test, place the patient with good illumination. At the bedside, the near in a dimly illuminated room and ask for fixation in chart handheld Snellen chart is often enough.

If the the distance. A bright light is flashed alternately for VA is poor, try using a pinhole one can be created 2 to 3 seconds in each eye. If the light is directed by making small holes in a blank card. If the pinhole toward one eye and the ipsilateral pupil appears to test improves the VA, the problem is in refraction.

If dilate, an RAPD is present i. Toxic: ethambutol Sphenoid mucocele. Degenerative: macular degeneration, retinitis Internal carotid artery aneurysm pigmentosa Trauma Ischemic: embolic Demyelination Optic disc Vascular AION: vasculitic and nonvasculitic Toxic Optic neuritis Retrochiasmal Glaucoma Tumor: glioma, meningioma, metastasis Papilledema late Stroke involving the visual pathway Sarcoidosis Demyelination Tumor Degenerative diseases Optic nerve Demyelination Tumor, including meningioma, glioma, etc.

Thyroid ophthalmopathy Trauma. Unequal pupil size anisocoria is common. The chal- Visual field testing at the bedside is done by con- lenge is to distinguish a physiologic from a pathologic frontation. Cover one eye at a time. Move your fin- anisocoria. Light activates retinal ganglion cells, which send their axons through the optic nerve, chiasm, and optic tract to synapse in the pretectal midbrain nuclei, also KEY POINTS known as Edinger-Westphal nuclei EWN in the rostral portion of the third nerve nucleus.

Efferent Organize your exam when examining vision. In the cavernous sinus, Examine one eye at a time. The iris optic nerve, or chiasm. Binocular visual loss implies contains two muscles that regulate pupil size. The a chiasmal or retrochiasmal lesion. The dilator tion of the site of the lesion see Fig. If the anisocoria is not physiologic, neuron and projects down the brainstem to the the next question to be answered is which pupil is ab- intermediolateral cell column at the C8T1 spinal normal, the dilated or the constricted one. The second-order neurons synapse in the supe- First, examine the pupils in the dark turn the lights rior cervical ganglion and represent the preganglionic off and look at the pupils during the first 5 to 10 sec- neurons.

Third-order neurons postganglionic travel onds. A dilation lag in the small pupil and anisocoria along the internal carotid artery into the cavernous greater in darkness means a sympathetic defect in that sinus and from there into the orbit to the pupil- pupil. Horners syndrome HS is characterized by uni- lodilator muscles. If the cocaine test is negative, hydroxyampheta- Document pupil reactivity and size in bright and dim mine eyedrops will help to distinguish a preganglionic illumination. In physiologic anisocoria, the amount of The different causes of HS are summarized in Box Usually both pupils are small and irreg- First-order Horners, or central Horners: ular, with impaired light reaction and intact near re- Hypothalamic infarcts, tumor sponse light-near dissociation ; pupils also dilate Mesencephalic stroke poorly to mydriatic agents.

Pulmonary apical tumor: Pancoast tumor An Adies pupil is dilated, with segmental contrac- Third-order Horners, or postganglionic: tion and light-near dissociation. Superior cervical ganglion tumor, iatrogenic, etc. Argyll Robertson pupils are small and poorly reac- tive to light but have preserved near response; they Internal carotid artery: dissection, trauma, are typically associated with syphilis.

Light-near dissociation LND : Normally the pupil- Base of skull: tumor, trauma lary constriction to light is greater than to a near Middle ear problems stimulus. The opposite is called LND. It implies a de- Cavernous sinus: tumor, inflammation Tolosa- fect in light response, as in optic neuropathy, or the Hunt syndrome , aneurysm, thrombosis, fistula presence of aberrant regeneration, as in the Adie pupil.

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Other causes of LND include dorsal midbrain lesions and severe bilateral visual loss. The term papilledema implies optic disc swelling re- Third nerve palsy is characterized by ptosis, di- sulting from increased ICP. Other forms of optic disc lated pupil, and ophthalmoplegia. Because the swelling due to local or systemic causes should just be parasympathetic fibers run in the outer part of the called optic disc swelling ODS.

The clinical pupil without compromising eye movements. On the symptoms depend on the underlying cause pain on other hand, vascular problems producing third nerve eye movements with demyelinating optic neuritis, ischemia e. The most common symptom of ODS is nervated by the third nerve. They are usually precipitated by changes in cell bodies or postganglionic fibers. Symptoms in- posture bending or straightening and can occur many clude anisocoria, photophobia, and blurred near vision times per day.

The exam The most common causes of unilateral optic disc shows a dilated pupil, poor light reaction with the edema are optic neuritis, AION, and orbital compres- typical segmental contraction , and light-near dissoci- sive lesions. As a rule, optic nerve function is abnormal ation. It can be confirmed by demonstrating supersen- in each. The appearance of the optic disc may be sitivity of the affected pupil to 0. Disc hemor- pupil than in the normal pupil. AION than in optic neuritis or compressive lesions. An abnormal optic disc has many possible causes Table summarizes abnormalities of the optic see Table No RAPD, central acuity spared the cause Idiopathic No color loss; enlarged blind spot IIH: acetazolamide, nerve intracranial Fundi show bilateral disc decompression, shunt hypertension IIH , hyperemia also known as pseudotumor cerebri Drusen calcified Small hyaline Asymptomatic Clinical; CT and orbital hyaline bodies or concretions Enlarged blind spot with normal ultrasound to see calcified pseudopapilledema familial, autosomal visual acuity initially hyaline bodies dominant Fundi: glistening hyaline bodies VP No disc hyperemia or exudates Optic neuritis Usually indicates Painful visual loss Clinical; MRI looking for demyelination Uhthoffs phenomenon demyelination; LP MS, SLE, worsening visual function Visual evoked potentials adrenoleukodystrophy, during exercise, hot baths, etc.

If MRI of the meningitis, Behet, Loss of color discrimination head shows more than Whipple, and Crohn Central scotoma is classic three demyelinating lesions, diseases Fundi: variable: from normal the probability of optic disc to optic atrophy or developing MS is up to papillitis. TABLE Some Terms Used to Define Eye Misalignment Strabismus Misalignment of the eyes Comitant Misalignment is constant in all directions of gaze, and each eye has full range of movement usually an ophthalmologic problem Incomitant The degree of misalignment varies with the direction of gaze usually a neurologic problem Phoria Misalignment of the eyes when binocular vision is absent Tropia Misalignment of the eyes when both eyes are opened and binocular vision is possible.

Patients compensate with a DIPLOPIA contralateral head tilt in other words, the diplopia improves with head tilt away from the side of the Double vision usually arises from a misalignment of lesion. Abnormal eye movements can gaze. Sixth nerve palsy can be a nonlocalizing sign of result from lesions in individual extraocular muscles, increased ICP.

Some useful concepts for clusion and ischemia, commonly associated with hy- understanding eye movements are summarized in pertension, diabetes mellitus, and atherosclerosis. Its dysfunction produces ptosis, mydriasis, and ophthal- Is it monocular or binocular? If binocular, is it hori- moparesis with the eye deviated down and out when zontal or vertical? Is it worse at near or at far? In addition, depend- nally, is the problem localized to an extraocular mus- ing on the site of the lesion, there may be one of the cle paresis or fatigue , brainstem MLF internuclear following patterns: ophthalmoplegia , or the orbit itself?

Lesions of the MLF contralateral superior rectus; failure of eye elevation produce an internuclear ophthalmoplegia INO. Subarachnoid space: Meningismus, constitutional The clinical characteristics of a right INO include in- symptoms, and other CN defects ability to adduct the right eye in left lateral gaze plus Tentorial edge compression: Depressed level of nystagmus of the abducting left eye. Adduction dur- consciousness, hemiparesis, and history of trauma ing convergence is preserved because this action does or supratentorial mass lesion not depend on the MLF.

Bilateral INOs can be seen CN IV innervates the superior oblique muscle in Wernicke encephalopathy along with gait ataxia that intorts and depresses the adducted eye. Fourth or confusional state , botulism, myasthenia gravis, nerve lesions produce oblique diplopia, worse on brainstem strokes, and demyelination. The only eye movement present in the horizontal plane in this case is the abduc- tion of the left eye. These produce an ation of the pupils.

It is generally produced by a ipsilateral gaze palsy and INO on the contralateral pineal tumor compressing the dorsal midbrain. The hy- Vertical eye movements are controlled by the ros- potropic lower eye is often on the side of the lesion. The diplopia include the following: downgaze pathway is less well understood but does not travel in the posterior commissure. Abnormal Cover test: Ask the patient to fixate on a small tar- vertical gaze movements can be found in dorsal mid- get. Cover one eye and watch the other eye. If the brain syndromes.

Parinaud syndrome is characterized eye makes a refixation movement, this means that by upgaze disturbance, convergence-retraction nys- it was not aligned on the target. For example, a third nerve palsy produces exotropia and hypotropia of Saccades are rapid eye movements to redirect the the paretic eye. Abducens palsy produces eso- eyes to a new fixation object. In general, voluntary tropia of the affected eye. Phorias do not cause diplopia be- gaze.

These areas have a direct connection with the cause the eyes are aligned when both are open contralateral PPRF and participate in saccadic simultaneously. Other areas that contribute to saccadic Parks three-step test: Detects a fourth-nerve palsy: control include the dorsolateral prefrontal cortex, 1. Hypertropia relative upward deviation of the supplementary eye field, and parietal lobe.

Vertical paretic eye. Hypertropia increases when the patient looks superior colliculi and connect to the contralateral to the opposite side. Inability to produce saccades is called oculo- 3. Hypertropia increases when the patient tilts the motor apraxia. Abnormal saccades include those that overshoot Oculocephalic maneuver dolls-eye test : Useful hypermetric or undershoot hypometric and un- in unconscious patients to evaluate the integrity of wanted saccades or saccadic intrusions square wave the vestibular and oculomotor apparatus. It is jerks, ocular flutter, and opsoclonus.

The vestibulo-ocular reflex rotates the track a moving visual target to keep it in focus. The eyes in the direction opposite to head movement. Visual cortex Saccades: Rapid, conjugate movement of the eyes inputs reach the temporo-occipital region. The oc- between objects e. In general, dis- cipitoparietotemporal junction is responsible for in- orders of eye movement will produce slowness of tegrating the movement data.

The fibers course into saccades in the direction of the paretic muscle. Then they travel se- Periocular signs or proptosis quentially to the cerebellar vermis, nucleus preposi- tus hypoglossi, medial vestibular nuclei, and finally to the abducens nuclei for horizontal pursuit. Neurologic diseases such as Parkinson disease, pro- gressive supranuclear palsy, drugs, and aging can slow The abducens nucleus contains motor neurons and down pursuits. Deep parietal lobe lesions produce internuclear neurons that travel with the MLF to the contralateral oculomotor nuclei in the midbrain.

Slow, passive head movements can elicit the PPRF for horizontal gaze. The pathway involves the semicircular canals ro- A gaze palsy may indicate a supranuclear or nuclear tation and otoliths linear acceleration and travels dysfunction. The dolls-eye maneuver or caloric to the vestibular nuclei. From there, it proceeds to testing will distinguish them. Abnormalities of the VOR result in nystagmus see following section. Vestibulo-ocular By rotations of the subjects head. Also irrigation of the ear caloric test.

Endpoint nystagmus Few beats of nystagmus in eccentric gaze. Congenital nystagmus Jerk or pendular, present after birth and remains throughout life. Pathologic or acquired nystagmus Periodic alternating nystagmus Horizontal jerk nystagmus that changes direction every 2 to 3 minutes. Acquired forms are associated with craniocervical junction abnormalities, multiple sclerosis, bilateral blindness, and toxicity from anticonvulsants. Downbeat nystagmus Present in primary position. Also seen in disorders of the craniocervical junction Chiari malformation , spinocerebellar degeneration, multiple sclerosis, familial periodic ataxia, and drug intoxication.

Upbeating nystagmus In primary position is associated with lesions of the anterior cerebellar vermis and lower brainstem. Also occurs with drug intoxication and Wernicke encephalopathy. See-saw nystagmus One eye elevates and intorts while the other depresses and extorts. Associated with third ventricle tumors and bitemporal hemianopsia, trauma, and brainstem vascular disease. Gaze-evoked nystagmus Similar to endpoint nystagmus but amplitude is greater and it occurs in a less eccentric position of the eyes. Most common cause is drug intoxication. Also seen in cerebellar disease and brainstem or hemisphere pathology.

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Rebound nystagmus Seen as a transient, rapid, horizontal jerk when eyes are moving to or from eccentric position. Usually associated with cerebellar or posterior fossa lesions. Vestibular nystagmus Usually horizontal with a rotatory component. Associated with peripheral inner ear disorders, Mnire disease, vascular disorder, and drug toxicity.

It can be either pendular or jerking. In jerk nys- ited by fixation. The direction of the nystagmus is named hibited by fixation. Table Saccades are fast eye movements that redirect the gives a brief description of physiologic and acquired fovea to a new target. Horizontal saccades are initi- nystagmus and possible causes. It is very common to be called to the ER Vertical saccades originate from bilateral frontal to evaluate a patient with the acute onset of vertigo; eye fields or the superior colliculus. Table describes a few the frontal lobe with destruction of the frontal eye characteristics to help differentiate central from pe- field; the eyes deviate toward the side of the lesion.

During a seizure, the eyes often turn away from the frontal focus. Weakness is one of the most common presenting which muscles in the left leg are weak or, if they are neurologic complaints. Many patients may tolerate all diffusely weak, which are weaker than others. Determine the pattern of weakness. This is fre- often it is when weakness sets in that medical atten- quently the crux of the entire diagnosis. It is the tion is finally sought. Similarly, friends or family pattern of weakness that will reveal when left leg members will not notice a patients sensory prob- weakness is due to a peroneal nerve problem and lems, but significant weakness will be obvious to all.

Needless to say, At the same time, weakness can be one of the most one must be familiar with the different patterns of difficult neurologic problems to sort out, because the weakness and their implications. Look for associated signs and symptoms. If a leg is axis of the nervous system. Left leg weakness can arise weak, determine whether it is also numb, tingling, from a peripheral nerve lesion, a lumbosacral plexus or painful. Check the reflexes carefully.

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Often the problem, or a stroke in the right cerebral hemisphere. Use laboratory and electrophysiologic tests wisely. The key steps in the clinical approach peripheral nervous system. Tests are most useful are outlined below. Make sure that true weakness is the complaint. Sometimes patients will use the term weak to mean a general sense of fatigue; others will say a limb is weak when it is clumsy or numb.

Likewise, a limb that is painful Weakness can be caused by lesions along the entire to move may seem weak; whether there is true neuraxis, from brain to muscle. The diagnosis rests on determining what the pat- 2. Identify which muscles are weak. This seems like an tern of weakness is, searching for associated signs obvious point but must be emphasized. It is not suf- and symptoms, and using laboratory tests and ficient to know that a patient has left leg weakness. Testing must be done in enough detail to know.

Make sure true weakness is the complaint. Are they consistent with your localization? Consider the differential diagnosis of disorders within your localization. Pattern of Weakness Below, each anatomic category is presented with the clues that might lead a clinician to suspect a disorder Primary muscle problems tend to cause weakness in that location. Distal muscles are affected later or not as change from hour to hour. Depending on the specific severely.

In addition, neck flexors and extensors, disease, strength may be worse after using the muscles which are not affected in most nerve or brain lesions, or toward the end of the day; it may improve after may be weak in a muscle disorder. Alternatively, strength may paradoxically improve after exercise in Associated Signs and Symptoms other conditions. Associated signs and symptoms may occasionally Associated Signs and Symptoms include muscle pain if the muscle disorder is inflam- matory, such as polymyositis.

By their nature, pri- By their nature, NMJ problems, which affect only the mary disorders of muscle should not cause sensory junction between the motor axon terminal and the signs or other symptoms. Reflexes are characteristi- muscle, should not lead to sensory signs or symp- cally preserved unless the process is so severe that the toms. Some NMJ disorders may have associated muscles are nearly paralyzed. The demon- findings for certain NMJ disorders on specialized stration of characteristic myopathic changes on an testing.

Some of the diseases in this category have EMG can help confirm a primary muscle disorder. Differential Diagnosis Differential Diagnosis Primary muscle disorders, discussed in Chapter 24, include both acquired problems myopathies , which NMJ disorders are discussed in Chapter 24; they can result from inflammatory or toxic etiologies include myasthenia gravis and Lambert-Eaton myas- among other causes, and congenital problems mus- thenic syndrome, among others. Sensory signs and symptoms are not present in The key to diagnosing NMJ disorders is fluctuation myopathies.

Pattern of Weakness Pattern of Weakness Neuromuscular junction NMJ problems can vary in Each muscle in the upper or lower extremity is inner- the pattern of weakness they cause, though most affect vated by an individual peripheral nerve Table Some NMJ disorders A lesion involving a particular peripheral nerve will can lead to ptosis as well as weakness of extraocular, lead to weakness in the muscles innervated by that bulbar, and neck muscles.

The characteristic feature of nerve while sparing other, often neighboring muscles. NMJ disorders is not the pattern of weakness, how- Disorders affecting a single peripheral nerve are ever, but the fluctuation. The degree of weakness may known as mononeuropathies. Finally, when pe- ripheral nerves are all affected diffusely, in a poly- Differential Diagnosis neuropathy, dysfunction typically occurs in the longest nerves first.

Thus, weakness from a polyneu- Mononeuropathies most commonly occur as a result ropathy usually appears first in the distal muscles, of entrapment as in carpal tunnel syndrome. Mononeuropathy multiplex is associated with systemic vasculitis and other metabolic or rheumatologic dis- eases. Demyelinating polyneuropathies can be heredi- Associated Signs and Symptoms tary such as Charcot-Marie-Tooth disease or acquired Mononeuropathies may cause sensory symptoms as in Guillain-Barr syndrome , while axonal polyneu- such as numbness, tingling, or painin the distribu- ropathies have many potential underlying causes.

Mononeu- Peripheral nerve disorders are discussed in Chapter Mononeuropathies lead to weakness in muscles innervated by a single peripheral nerve. Pattern of Weakness Single radiculopathies usually require MRI of the spine to rule out structural causes, whereas polyradicu- Each nerve root relevant to the upper or lower lopathies usually require lumbar puncture LP to look extremity exits the spinal cord and eventually traverses for infectious or inflammatory conditions.

The result is that most muscles Single radiculopathies can be caused by herniated discs are innervated by fibers that originate from more than or by reactivation of varicella-zoster virus shingles , one nerve root, although some muscles are predomi- for example. Polyradiculopathies are often inflamma- nantly innervated by fibers from one nerve root see tory or infectious. These disorders are discussed in Table In any case, a lesion of a single nerve root Chapter Some processes lead to dysfunction of A radiculopathy causes weakness in the muscles multiple nerve roots at once polyradiculopathy , innervated predominantly by fibers from one nerve leaving a pattern of weakness that may be more diffuse root.

If the nerve root subserves a particular muscle stretch reflex, that reflex may be depressed or absent. Associated Signs and Symptoms A polyradiculopathy may lead to weakness of multiple muscles related to multiple nerve roots Radiculopathies often have associated tingling or bilaterally. Objective sensory loss is rare in disorders affecting a single nerve root because there is overlap from neigh- boring roots. Pattern of Weakness The intricacies of brachial and lumbosacral plexus Laboratory Studies anatomy Fig.

Put sim- ply, if multiple muscles in a limb are weak and do not TABLE Commonly Tested Muscle Stretch conform to the pattern of a particular nerve root or pe- Reflexes ripheral nerve, a plexus problem should be suspected. In the leg, for example, weakness in both hip flex- Reflex Root ors and hip adductors would have to involve the L1, Biceps C5 L2, and L3 roots or both the nerve to the iliopsoas Brachioradialis C6 and the obturator nerve see Table ; a much Triceps C7 more likely explanation is a lesion in the upper part of the lumbosacral plexus.

Roots Trunks Cords Nerves. C5 Musculocutaneous. Upper Lateral. C6 Median. C7 Middle Medial Ulnar. C8 Axillary. Lower Posterior. Figure Brachial plexus anatomy. T1 Radial. Spinal cord disorders cause weakness in two ways. First, the anterior horn cells located at the level of the Laboratory Studies lesion are affected, leading to weakness of the muscles innervated by the nerve root at that level.

Second, there is weakness below the tion to the plexus, given the less than straightforward level of the lesion due to interruption of the anatomy. MRI of the brachial plexus or pelvis or descending corticospinal tracts. This weakness occurs lumbosacral plexus may be necessary to rule out in an upper motor neuron UMN pattern Fig.

Associated Signs and Symptoms Differential Diagnosis Depending on the extent of the lesion, there may be Plexopathies can be caused by idiopathic inflamma- sensory findings due to interruption of the ascending tion, radiation, infiltration by metastases, hemor- tracts. There may be a sensory level loss of sensation rhage, or trauma. They are discussed in Chapter Diabetic patients are prone to develop a character- Typically, reflexes below the level of a spinal cord istic lumbosacral plexopathy known as diabetic lesion are increased, and there may be Babinski signs.

Bladder and bowel incontinence may occur. There may be associated sensory signs or reflex loss in plexus disorders. Amyotrophic lateral sclerosis causes degeneration of both the corti- cospinal tracts and anterior horn cells. There may be sensory loss below the level of the lesion due to interruption of ascending tracts. Reflexes below the level of the lesion are typically increased, and Babinski signs may be present.

Imaging of the brain is important to evaluate almost Knowledge of the homunculus of the motor all of the potential etiologies in this category. The strip Fig. Deep hemispheric lesions, as in the internal capsule, may lead to weakness of all three parts of The differential diagnosis includes such diverse eti- the contralateral body face, arm, and leg , because ologies as stroke Chapter 14 , demyelinating disease motor fibers from all areas of the motor strip join Chapter 20 , traumatic injury Chapter 17 , brain together as they travel toward the brainstem.

Lesions in the base of the pons may lead to weak- ness of the ipsilateral face and contralateral arm and leg crossed signs , because descending motor fibers KEY POINTS to the face have crossed at that level but those to the body have not. Cerebral hemispheric lesions lead to weakness of the contralateral side in a UMN pattern.

Parasagittal lesions lead primarily to leg weakness, Associated Signs and Symptoms more lateral lesions lead primarily to face and arm Lesions of the cerebral hemispheres frequently have weakness, and deep lesions may lead to weakness associated cognitive signs, such as those described in of all three parts. Chapter Left hemispheric lesions may cause apha- Cerebral hemispheric lesions may have accompa- sia or apraxia, while right hemispheric lesions may nying cognitive signs, such as aphasia or neglect.

Lesions of Brainstem lesions may have accompanying CN the brainstem may cause cranial nerve problems, such findings. The sensory system includes somatosensory and spe- Spinothalamic tract: At the level of the spinal cial senses: smell, vision, taste, hearing, and vestibu- cord, sacral segments are located laterally, lumbar lar sensation.

The common characteristic in all is the fibers more medially, and cervical segments in the presence of a receptor, an afferent nerve, and a dor- most medial locations. At the level of Somatosensory abnormalities may be character- the medial lemniscus, the upper body fibers ized by increase, alteration, impairment, or loss of become medial and those of the lower body lateral.

The diagnosis of these problems includes Facial sensation is carried to the brainstem by the analysis of the nature, location, characteristics, and trigeminal nerve.

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The STT and the trigeminal tract distribution of symptoms. Information the lowest area and the leg in the parasagittal area. Pain and temperature functioning of the sensory cortex. Proprioception, requires the patients cooperation. The evaluation of vibration, and light touch run ipsilaterally in heavily different primary sensory modalities temperature, myelinated fibers A-alpha and A-beta fibers in the pain [pinprick], light touch, vibration, and propio- dorsal column system, reaching the second-order ception is necessary to characterize sensory loss and neuron at the level of the medulla in the nuclei gra- its extent.

In some instances, it is difficult to demon- cilis and cuneatus. Axons from these nuclei cross at strate sensory abnormalities in a patient with sensory the lower medulla to form the medial lemniscus symptoms; in others, the exam shows sensory find- Fig. Whatever the situa- There is a somatotopic arrangement of fibers in tion, the sensory examination must be organized and these tracts. Figure Anterolateral system. Figure Posterior columnmedial lemniscal system. Touch sensation is tested with a wisp of cotton, The next step is to record the sensory abnormali- using a very soft stimulus.

Pain sensation is tested ties using accepted definitions. It is important to reg- with a pin. Thermal modalities are tested using ob- ister the patients own words rather than using the jects with a temperature range between 10 and terms below. Not only the presence or absence of 50C, because beyond those limits the stimulus be- sensation but also slight differences and gradations comes painful. Moving the great toe up and down should be recorded. The following list defines some and asking the patient to indicate the direction of of the terminology used to describe sensory abnor- movement test joint position sense.

Proprioception malities: can also be tested by moving an object up or down on Paresthesias are abnormal sensations described the skin and asking the patient the direction of the by the patient as tingling, prickling, pins, and nee- movement. The testing of vibration sense requires a dles, etc.

TABLE Patterns of Sensory Loss According to Localization Other Neurologic Site of the Lesion Sensory Findings Abnormalities Examples Peripheral nerve Loss of LT, T, PP, and proprio- Distal muscle weakness, Peroneal neuropathy; ception in the influenced area; atrophy, areflexia median and ulnar associated weakness in muscles neuropathies innervated by that nerve Root Loss of all sensory modalities in Weakness in a myotomal L5 radiculopathy; cervical a dermatomal distribution distribution, atrophy, radiculopathy segmental hyporeflexia Plexus Sensory loss in the distribution Muscle weakness that Brachial plexopathy due to of two or more peripheral cannot be localized to a trauma, inflammation, nerves single nerve or root infiltration, etc.

Hyperesthesia is increased sensitivity to sensory to light touch and normal proprioception. This stimuli. The opposite is hypesthesia. The former malities is to establish the cause.

There are many pri- usually means disruption of nerve excitation; the latter mary neurologic diseases as well as systemic diseases in general means excitation or disinhibition. They are In a patient complaining of sensory disturbances, explored in more detail in Chapter 23 on peripheral the first goal is to establish the presence or absence of neuropathies. Sometimes the sensory problems accompany tion of the respective neurologic problem are repre- other symptomssuch as weakness, neglect, visual sented in Table This table provides a guide to the field cuts, behavioral problems, or seizuresthat may process of diagnosis based on clinical symptoms and help to determine the lesions location.

Although in theory it is easy to distinguish peripheral nerve from segmental nerve or root, spinal cord, or other CNS locations, this is in fact often not possible or at best imprecise. It is important to obtain a good history of the Root problems give a dermatomal pattern of loss sensory abnormalities and direct the exam accord- Fig. Spinal cord disease leads to a characteris- ing to it. In brain- Nerve damage produces sensory problems in the stem lesions, the sensory abnormalities may occur on distribution of the damaged nerve; root damage the ipsilateral side of the face and contralateral side produces sensory problems in a dermatome; and of the body.

Central sensory loss involving the tha- plexus damage produces sensory problems in a lamus or sensory cortex will generally affect the con- group of nerves in the same limb. Spinal cord lesions produce a sensory level; brain- Once the location of sensory loss has been charac- stem lesions cause a crossed sensory loss; and thal- terized, it is important to determine what sensory amus and cortex lesions produce sensory loss in the modality is involved, because different pathologic contralateral face, arm, and leg. Chapter Dizziness, Vertigo, and 7 Syncope. Because dizziness means different things to differ- cause, whereas diplopia, dysarthria, dysphagia, or ent people, it is not a useful term in describing ones other symptoms of brainstem dysfunction indicate a symptoms.

Broadly speaking, the possibilities in- central process. Accompanying nausea and vomiting clude vertigo, light-headedness, dysequilibrium, and is often more prominent with peripheral causes of a fourth category of ill-defined dizziness. Vertigo is vertigo, and the ability to walk or maintain posture an illusion or hallucination of movement that is usu- may be more impaired with central disease. Neither ally rotatory but may be linear.

Light-headedness of these latter features, however, is very reliable.


This chapter focuses on these source of the vertigo. Vertical and direction-changing two categories. Dysequilibrium is a sensation of imbalance or Unidirectional nystagmus may arise from either cen- unsteadiness that is usually referable to the legs rather tral or peripheral dysfunction. The neurologic ab- Vestibular neuronitis presents as an acute unilat- normalities responsible for this symptom are outlined eral complete or incomplete peripheral vestibu- in detail in Chapter 8.

Finally, there are people who lopathy. The designation neuronitis is inaccurate simply cannot define their symptoms accurately, as because there is no evidence of inflammation, but well as those with anxiety. Patients develop a sudden and spontaneous onset of vertigo, nausea, and vomiting. The onset is VERTIGO usually over minutes to hours; symptoms peak within 24 hours and then improve gradually over Most vertigo is caused by an acute asymmetry or several days or weeks. Complete recovery may not imbalance of neural activity between the left and occur for months.

Nystagmus is strictly unilateral right vestibular systems. Vertigo does not result from and may be suppressed by visual fixation. Recovery symmetric bilateral loss of vestibular function as represents central compensation for the loss of pe- with ototoxic drugs or from a slow unilateral loss of ripheral vestibular function. A injury irrespective of whether there is an associated useful approach Box to sorting out the etiology skull fracture.

Vertigo is sometimes accompanied by is to determine the periodicity and duration of the hearing loss and tinnitus. A determination should also be made as to lum. The blood supply to the central and peripheral whether the vertigo is of peripheral or central origin; vestibular apparatus and the cerebellum is via the the most helpful features in this regard are the pres- vertebrobasilar system posterior and anterior infe- ence and nature of the associated symptoms and rior cerebellar arteries and the superior cerebellar ar- signs. Tinnitus or hearing loss suggests a peripheral tery.

Attacks occur most frequently Vertigo when the individual is reclining in bed at night or upon awakening in the morning. There may be asso- Spontaneous vertigo ciated severe nausea and vomiting. Attacks may Single prolonged episode occur in clusters, with patients remaining asympto- Vestibular neuronitis matic for months or years in between. BPPV results from freely moving crystals of cal- Labyrinthine concussion cium carbonate within one of the semicircular canals.

Lateral medullary or cerebellar infarction When the head is stationary, these crystals settle in Recurrent episodes the most dependent part of the canal usually poste- Mnire disease rior. With head movements, the crystals move more slowly than the endolymph within which they lie; Perilymph fistula once the head comes to rest, their inertia causes Migraine ongoing stimulation of the hair cells, resulting in the Posterior circulation ischemia illusion of movement vertigo. Diagnosis is estab- Positional vertigo lished by demonstrating the characteristic downbeat- ing and torsional nystagmus with the Dix-Hallpike Peripheral test Fig.

The offending ear is the one Benign positional paroxysmal vertigo BPPV that is toward the ground when vertigo occurs during Central the test. A positioning Epley maneuver Fig. The head is turned in auditory artery, a branch of the anteroinferior cere- the direction of the offending ear. The illustration bellar artery. Infarction of the inner ear presents with demonstrates treatment for BPPV originating from a sudden onset of deafness, vertigo, or both.

Brainstem or cerebellar stroke is the most impor- tant differential diagnosis in patients with suspected acute vestibular neuronitis. A central-type nystagmus from acute unilateral vestibular dysfunction. Isolated vertigo is almost never caused by brain- Mnire disease is characterized by episodic stem ischemia. It is caused by an typical of benign positional paroxysmal vertigo.

A perilymph fistula results from disruption of the lining of the endolymphatic system. Typically, the patient reports hearing a pop at the time of a sud- SYNCOPE den increase in middle ear pressure, with sneezing, nose-blowing, coughing, or straining. This is followed Syncope is a transient loss of consciousness and pos- by the abrupt onset of vertigo.

Patients with benign positional paroxysmal ver- Prior to losing consciousness, patients often report tigo BPPV have episodes of vertigo that are precip- light-headedness and a variety of visual symptoms itated by changes in position, such as turning over in blurred or tunnel vision, graying or blacking out.

The attacks are brief, usually The term presyncope is used when patients experi- lasting seconds to minutes, and symptoms typically ence this prodrome of symptoms but do not subse- begin after a few seconds latency following the quently lose consciousness. Figure The Dix-Hallpike maneuver is illustrated in the first two frames of the figure. The patients head is rotated 45 degrees to one side and then extended 30 degrees over the edge of the bed. The examiner looks for a rotatory and down-beating nystagmus.

The Epley positioning maneuver begins with the positioning used for the Dix-Hallpike maneuver and continues with a series of other positions, as illustrated. Syncope is charges from arterial including cardiac or great ves- most commonly a manifestation of hypotension due sel or visceral mechanoreceptors. Afferent impulses to cardiac causes, low intravascular volume, or exces- via the vagus nerve lead to cardioinhibition and sive vasodilation.

Cardiac causes include asystole, vasodepression, resulting in hypotension and brady- third-degree heart block, tachyarrhythmias, outflow cardia. Expanded review questions and detailed explanations correct and incorrect answers to equip students for success on shelf exams and the USMLE. Updated case-based vignettes help students translate concepts to a clinical context and confidently prepare for clerkship. Newly added 4-full color highlights key content for a faster, more efficient review. Subscribe now to be the first to hear about specials and upcoming releases. Title Author. Blueprints Neurology.

Description of this Book Succinct, logically organized, and supported by more than board-style review questions, Blueprints Neurology delivers a complete review of key topics and concepts optimized for clerkship, shelf review, and USMLE preparation. Author's Bio There is no author biography for this title. This preview is indicative only.

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