Clinical Neurology Flashcards

Question

Memory impairment is caused by discrete bilateral lesions of which of the following st ructures? I. Amygdala II. Hippocampal formation III. Mammillary bodies IV. Dorsomedial nuclei of the thalamus

Answer 1

A. I, II, III B. I, III **C. II, IV** D. IV E. All of the above ## Footnote Discrete, bilateral lesions in the hippocampus (II) and dorsomedial thalamus (IV) impair memory and learning out of proportion to other cognitive functions. Stereotactic lesions of the amygdala (I) and mammillary bodies (III) have failed to produce these symptoms.1

Answer 2

A. 1 and 3 B. 3 and 5 **C. 3 and 7** D. 4 and 5 E. 5 and 7 ## Footnote The gene (CCM1) responsible for familial cavernous malformations has been mapped to 7q11.2–q21. In addition, CCM2 (7p13–15) and CCM3 (3q25.2–27) have been identi ed in pat ients with cavernous malformations

Answer 3

A. It develops over a few hours B. It spares the pupil **C. It is usually painless** D. The lesion involves the center of the nerve E. The prognosis for recovery is good ## Footnote Diabet ic third nerve palsy develops over a few hours (A), and tends to be pupil-sparing (B) because it involves infarction of the center of the nerve (D). Recovery is typical (E) but may take months. Diabetic third nerve palsy is usually painful (C is false).1

Answer 4

**A. Arsenic poisoning** B. Lead poisoning C. Manganese poisoning D. Mercury poisoning E. Phosphorus poisoning ## Footnote Arsenic poisoning (A) may be due to pesticide exposure, may cause transverse white lines in the ngernails, and may be diagnosed based on examination of the hair or urine. Lead poisoning (B) is less common in adults than in children and may present with anemia or peripheral neuropathy. Lead poisoning (B) m ay cause black lines at the gingival margins, increased urinary excretion of coproporphyrin, and may be treated with ethylenediaminetetraacetic acid (EDTA) and dimercaprol (BAL). Chronic manganese poisoning (C) m ay result in extrapyramidal symptoms reminiscent of dystonia or parkinsonism. Mercury poisoning (D) m ay present w ith mood changes, tremors, and a cerebellar syndrome and is treated with penicillamine. Phosphorous poisoning (E) is typically due to exposure to organophosphate insecticides and is manifested by anti cholinesterase e ects in the acute set t ing. Symptoms of phosphorous poisoning (E) can be t reated with atropine and pralidoxime

Answer 5

A. Arsenic poisoning **B. Lead poisoning** C. Manganese poisoning D. Mercury poisoning E. Phosphorus poisoning ## Footnote Arsenic poisoning (A) may be due to pesticide exposure, may cause transverse white lines in the ngernails, and may be diagnosed based on examination of the hair or urine. Lead poisoning (B) is less common in adults than in children and may present with anemia or peripheral neuropathy. Lead poisoning (B) m ay cause black lines at the gingival margins, increased urinary excretion of coproporphyrin, and may be treated with ethylenediaminetetraacetic acid (EDTA) and dimercaprol (BAL). Chronic manganese poisoning (C) m ay result in extrapyramidal symptoms reminiscent of dystonia or parkinsonism. Mercury poisoning (D) m ay present w ith mood changes, tremors, and a cerebellar syndrome and is treated with penicillamine. Phosphorous poisoning (E) is typically due to exposure to organophosphate insecticides and is manifested by anti cholinesterase e ects in the acute set t ing. Symptoms of phosphorous poisoning (E) can be t reated with atropine and pralidoxime

Answer 6

A. Arsenic poisoning B. Lead poisoning **C. Manganese poisoning** D. Mercury poisoning E. Phosphorus poisoning ## Footnote Arsenic poisoning (A) may be due to pesticide exposure, may cause transverse white lines in the ngernails, and may be diagnosed based on examination of the hair or urine. Lead poisoning (B) is less common in adults than in children and may present with anemia or peripheral neuropathy. Lead poisoning (B) m ay cause black lines at the gingival margins, increased urinary excretion of coproporphyrin, and may be treated with ethylenediaminetetraacetic acid (EDTA) and dimercaprol (BAL). Chronic manganese poisoning (C) m ay result in extrapyramidal symptoms reminiscent of dystonia or parkinsonism. Mercury poisoning (D) m ay present w ith mood changes, tremors, and a cerebellar syndrome and is treated with penicillamine. Phosphorous poisoning (E) is typically due to exposure to organophosphate insecticides and is manifested by anti cholinesterase e ects in the acute set t ing. Symptoms of phosphorous poisoning (E) can be t reated with atropine and pralidoxime

Answer 7

A. Arsenic poisoning B. Lead poisoning C. Manganese poisoning D. Mercury poisoning **E. Phosphorus poisoning** ## Footnote Arsenic poisoning (A) may be due to pesticide exposure, may cause transverse white lines in the ngernails, and may be diagnosed based on examination of the hair or urine. Lead poisoning (B) is less common in adults than in children and may present with anemia or peripheral neuropathy. Lead poisoning (B) m ay cause black lines at the gingival margins, increased urinary excretion of coproporphyrin, and may be treated with ethylenediaminetetraacetic acid (EDTA) and dimercaprol (BAL). Chronic manganese poisoning (C) m ay result in extrapyramidal symptoms reminiscent of dystonia or parkinsonism. Mercury poisoning (D) m ay present w ith mood changes, tremors, and a cerebellar syndrome and is treated with penicillamine. Phosphorous poisoning (E) is typically due to exposure to organophosphate insecticides and is manifested by anti cholinesterase e ects in the acute set t ing. Symptoms of phosphorous poisoning (E) can be t reated with atropine and pralidoxime

Answer 8

A. Arsenic poisoning B. Lead poisoning C. Manganese poisoning **D. Mercury poisoning** E. Phosphorus poisoning ## Footnote Arsenic poisoning (A) may be due to pesticide exposure, may cause transverse white lines in the ngernails, and may be diagnosed based on examination of the hair or urine. Lead poisoning (B) is less common in adults than in children and may present with anemia or peripheral neuropathy. Lead poisoning (B) m ay cause black lines at the gingival margins, increased urinary excretion of coproporphyrin, and may be treated with ethylenediaminetetraacetic acid (EDTA) and dimercaprol (BAL). Chronic manganese poisoning (C) m ay result in extrapyramidal symptoms reminiscent of dystonia or parkinsonism. Mercury poisoning (D) m ay present w ith mood changes, tremors, and a cerebellar syndrome and is treated with penicillamine. Phosphorous poisoning (E) is typically due to exposure to organophosphate insecticides and is manifested by anti cholinesterase e ects in the acute set t ing. Symptoms of phosphorous poisoning (E) can be t reated with atropine and pralidoxime

Answer 9

A. Arsenic poisoning B. Lead poisoning C. Manganese poisoning **D. Mercury poisoning** E. Phosphorus poisoning ## Footnote Arsenic poisoning (A) may be due to pesticide exposure, may cause transverse white lines in the ngernails, and may be diagnosed based on examination of the hair or urine. Lead poisoning (B) is less common in adults than in children and may present with anemia or peripheral neuropathy. Lead poisoning (B) m ay cause black lines at the gingival margins, increased urinary excretion of coproporphyrin, and may be treated with ethylenediaminetetraacetic acid (EDTA) and dimercaprol (BAL). Chronic manganese poisoning (C) m ay result in extrapyramidal symptoms reminiscent of dystonia or parkinsonism. Mercury poisoning (D) m ay present w ith mood changes, tremors, and a cerebellar syndrome and is treated with penicillamine. Phosphorous poisoning (E) is typically due to exposure to organophosphate insecticides and is manifested by anti cholinesterase e ects in the acute set t ing. Symptoms of phosphorous poisoning (E) can be t reated with atropine and pralidoxime

Answer 10

A. Arsenic poisoning **B. Lead poisoning** C. Manganese poisoning D. Mercury poisoning E. Phosphorus poisoning ## Footnote Arsenic poisoning (A) may be due to pesticide exposure, may cause transverse white lines in the ngernails, and may be diagnosed based on examination of the hair or urine. Lead poisoning (B) is less common in adults than in children and may present with anemia or peripheral neuropathy. Lead poisoning (B) m ay cause black lines at the gingival margins, increased urinary excretion of coproporphyrin, and may be treated with ethylenediaminetetraacetic acid (EDTA) and dimercaprol (BAL). Chronic manganese poisoning (C) m ay result in extrapyramidal symptoms reminiscent of dystonia or parkinsonism. Mercury poisoning (D) m ay present w ith mood changes, tremors, and a cerebellar syndrome and is treated with penicillamine. Phosphorous poisoning (E) is typically due to exposure to organophosphate insecticides and is manifested by anti cholinesterase e ects in the acute set t ing. Symptoms of phosphorous poisoning (E) can be t reated with atropine and pralidoxime

Answer 11

A. Arsenic poisoning **B. Lead poisoning** C. Manganese poisoning D. Mercury poisoning E. Phosphorus poisoning ## Footnote Arsenic poisoning (A) may be due to pesticide exposure, may cause transverse white lines in the ngernails, and may be diagnosed based on examination of the hair or urine. Lead poisoning (B) is less common in adults than in children and may present with anemia or peripheral neuropathy. Lead poisoning (B) m ay cause black lines at the gingival margins, increased urinary excretion of coproporphyrin, and may be treated with ethylenediaminetetraacetic acid (EDTA) and dimercaprol (BAL). Chronic manganese poisoning (C) m ay result in extrapyramidal symptoms reminiscent of dystonia or parkinsonism. Mercury poisoning (D) m ay present w ith mood changes, tremors, and a cerebellar syndrome and is treated with penicillamine. Phosphorous poisoning (E) is typically due to exposure to organophosphate insecticides and is manifested by anti cholinesterase e ects in the acute set t ing. Symptoms of phosphorous poisoning (E) can be t reated with atropine and pralidoxime

Answer 12

**A. Arsenic poisoning** B. Lead poisoning C. Manganese poisoning D. Mercury poisoning E. Phosphorus poisoning ## Footnote Arsenic poisoning (A) may be due to pesticide exposure, may cause transverse white lines in the ngernails, and may be diagnosed based on examination of the hair or urine. Lead poisoning (B) is less common in adults than in children and may present with anemia or peripheral neuropathy. Lead poisoning (B) m ay cause black lines at the gingival margins, increased urinary excretion of coproporphyrin, and may be treated with ethylenediaminetetraacetic acid (EDTA) and dimercaprol (BAL). Chronic manganese poisoning (C) m ay result in extrapyramidal symptoms reminiscent of dystonia or parkinsonism. Mercury poisoning (D) m ay present w ith mood changes, tremors, and a cerebellar syndrome and is treated with penicillamine. Phosphorous poisoning (E) is typically due to exposure to organophosphate insecticides and is manifested by anti cholinesterase e ects in the acute set t ing. Symptoms of phosphorous poisoning (E) can be t reated with atropine and pralidoxime

Answer 13

A. Degeneration of the ciliary ganglia and postganglionic parasympathetics B. More common in women than in men **C. No reaction to 0.1% pilocarpine solution** D. Paralysis of segments of the pupillary sphincter E. Pupil responds better to near than to light ## Footnote Adie’s syndrome or Adie’s tonic pupil results from degeneration of the ciliary ganglia and postganglionic parasympathetics (A) that are responsible for pupillary constriction. Adie’s pupil responds better to near (accommodation) than to light (E). The condit ion is more common in women (B) and involves paralysis of segments of the pupillary sphincter (D). An Adie’s pupil will respond to 0.1% pilocarpine, whereas a normal pupil would not (denervat ion hypersensit ivity). C is false.1

Answer 14

A. I, II, III B. I, III **C. II, IV** D. IV E. All of the above ## Footnote Infantile seizures or spasms (West’s syndrome) usually begin before 6 months of age and are characterized by sudden exor or extensor spasms of the head, trunk, and limbs and an electroencephalogram (EEG) picture of bilateral high-voltage, slow-wave activity (hypsarrhythmia). Lip smacking and generalized tonic-clonic activity are not features.1

Answer 15

A. Myasthenia gravis **B. Eaton-Lambert myasthenic syndrome** C. Both D. Neither ## Footnote In Eaton-Lambert myasthenic syndrome (B), muscles of the trunk and lower extremities are most frequently involved, there is an incrementing response to stimuli, and there is a poor response to ant icholinesterase drugs. Eaton-Lambert syndrome (B) is associated with antibodies to the presynaptic voltage-dependent calcium channel. These are all features of Eaton-Lambert syndrome (B) and stand in contrast to the features of classic myasthenia gravis (A).1

Answer 16

A. Myasthenia gravis **B. Eaton-Lambert myasthenic syndrome** C. Both D. Neither ## Footnote In Eaton-Lambert myasthenic syndrome (B), muscles of the trunk and lower extremities are most frequently involved, there is an incrementing response to stimuli, and there is a poor response to ant icholinesterase drugs. Eaton-Lambert syndrome (B) is associated with antibodies to the presynaptic voltage-dependent calcium channel. These are all features of Eaton-Lambert syndrome (B) and stand in contrast to the features of classic myasthenia gravis (A).1

Answer 17

A. Myasthenia gravis **B. Eaton-Lambert myasthenic syndrome** C. Both D. Neither ## Footnote In Eaton-Lambert myasthenic syndrome (B), muscles of the trunk and lower extremities are most frequently involved, there is an incrementing response to stimuli, and there is a poor response to ant icholinesterase drugs. Eaton-Lambert syndrome (B) is associated with antibodies to the presynaptic voltage-dependent calcium channel. These are all features of Eaton-Lambert syndrome (B) and stand in contrast to the features of classic myasthenia gravis (A).1

Answer 18

A. Myasthenia gravis **B. Eaton-Lambert myasthenic syndrome** C. Both D. Neither ## Footnote In Eaton-Lambert myasthenic syndrome (B), muscles of the trunk and lower extremities are most frequently involved, there is an incrementing response to stimuli, and there is a poor response to ant icholinesterase drugs. Eaton-Lambert syndrome (B) is associated with antibodies to the presynaptic voltage-dependent calcium channel. These are all features of Eaton-Lambert syndrome (B) and stand in contrast to the features of classic myasthenia gravis (A).1

Answer 19

A. I, II, III B. I, III **C. II, IV** D. IV E. All of the above ## Footnote The dorsal scapular nerve arises from the anterior ramus of C5 and pierces the middle scalene to innervate the rhomboid muscles (II) and levator scapulae muscle (IV). The supraspinatus muscle (I) is innervated by the suprascapular nerve, which arises from the superior t runk of the brachial plexus and receives cont ribut ions from C5, C6, and C4. The subscapularis muscle (III) is innervated by the upper and lower subscapular nerves that are branches of the posterior cord receiving bers from C5 and C6, respect ively.3

Answer 20

A. Axillary nerve B. Dorsal scapular nerve **C. Subscapular nerve** D. Suprascapular nerve E. None of the above ## Footnote The axillary nerve (A) is one of the two terminal branches of the posterior cord and innervates the teres minor and deltoid muscles. The dorsal scapular nerve (B) arises from the anterior ramus of C5 and innervates the levator scapulae and rhomboid muscles. The subscapular nerve (C) has upper and lower components that come o the posterior cord to innervate the teres major and subscapularis muscles. The suprascapular nerve (D) arises from the superior trunk to innervate the supraspinatus and infraspinatus muscles.3

Answer 21

**A. Axillary nerve** B. Dorsal scapular nerve C. Subscapular nerve D. Suprascapular nerve E. None of the above ## Footnote The axillary nerve (A) is one of the two terminal branches of the posterior cord and innervates the teres minor and deltoid muscles. The dorsal scapular nerve (B) arises from the anterior ramus of C5 and innervates the levator scapulae and rhomboid muscles. The subscapular nerve (C) has upper and lower components that come o the posterior cord to innervate the teres major and subscapularis muscles. The suprascapular nerve (D) arises from the superior trunk to innervate the supraspinatus and infraspinatus muscles.3

Answer 22

A. Axillary nerve B. Dorsal scapular nerve **C. Subscapular nerve** D. Suprascapular nerve E. None of the above ## Footnote The axillary nerve (A) is one of the two terminal branches of the posterior cord and innervates the teres minor and deltoid muscles. The dorsal scapular nerve (B) arises from the anterior ramus of C5 and innervates the levator scapulae and rhomboid muscles. The subscapular nerve (C) has upper and lower components that come o the posterior cord to innervate the teres major and subscapularis muscles. The suprascapular nerve (D) arises from the superior trunk to innervate the supraspinatus and infraspinatus muscles.3

Answer 23

A. Axillary nerve **B. Dorsal scapular nerve** C. Subscapular nerve D. Suprascapular nerve E. None of the above ## Footnote The axillary nerve (A) is one of the two terminal branches of the posterior cord and innervates the teres minor and deltoid muscles. The dorsal scapular nerve (B) arises from the anterior ramus of C5 and innervates the levator scapulae and rhomboid muscles. The subscapular nerve (C) has upper and lower components that come o the posterior cord to innervate the teres major and subscapularis muscles. The suprascapular nerve (D) arises from the superior trunk to innervate the supraspinatus and infraspinatus muscles.3

Answer 24

A. Axillary nerve B. Dorsal scapular nerve C. Subscapular nerve **D. Suprascapular nerve** E. None of the above ## Footnote The axillary nerve (A) is one of the two terminal branches of the posterior cord and innervates the teres minor and deltoid muscles. The dorsal scapular nerve (B) arises from the anterior ramus of C5 and innervates the levator scapulae and rhomboid muscles. The subscapular nerve (C) has upper and lower components that come o the posterior cord to innervate the teres major and subscapularis muscles. The suprascapular nerve (D) arises from the superior trunk to innervate the supraspinatus and infraspinatus muscles.3

Answer 25

A. Axillary nerve B. Dorsal scapular nerve C. Subscapular nerve **D. Suprascapular nerve** E. None of the above ## Footnote The axillary nerve (A) is one of the two terminal branches of the posterior cord and innervates the teres minor and deltoid muscles. The dorsal scapular nerve (B) arises from the anterior ramus of C5 and innervates the levator scapulae and rhomboid muscles. The subscapular nerve (C) has upper and lower components that come o the posterior cord to innervate the teres major and subscapularis muscles. The suprascapular nerve (D) arises from the superior trunk to innervate the supraspinatus and infraspinatus muscles.3

Answer 26

A. Axillary nerve **B. Dorsal scapular nerve** C. Subscapular nerve D. Suprascapular nerve E. None of the above ## Footnote The axillary nerve (A) is one of the two terminal branches of the posterior cord and innervates the teres minor and deltoid muscles. The dorsal scapular nerve (B) arises from the anterior ramus of C5 and innervates the levator scapulae and rhomboid muscles. The subscapular nerve (C) has upper and lower components that come o the posterior cord to innervate the teres major and subscapularis muscles. The suprascapular nerve (D) arises from the superior trunk to innervate the supraspinatus and infraspinatus muscles.3

Answer 27

**A. Decreased voltage and decreased duration** B. Decreased voltage and increased duration C. Decreased voltage and normal duration D. Normal voltage and decreased duration E. Normal voltage and increased duration ## Footnote The motor unit potential of myopathy tends to be of decreased voltage and decreased duration because in these conditions there is a reduced number of motor bers per motor unit.

Answer 28

A. Frontal balding occurs only in men. B. Lens abnormalities are rare. **C. The congenital form is inherited only from the maternal line.** D. The inheritance is autosomal recessive. E. Weakness always predates the myotonia. ## Footnote Frontal balding occurs in both men and women a icted with myotonic dystrophy (A is false). Lens opacities are found by slit lamp in 90% of patients (B is false). The inheritance is autosomal dominant, and the defective gene segregates on chromosome 19 (D is false). Myotonia may precede weakness by several years (E is false). Answer C is correct: In the congenital (neonatal) form of myotonic dyst rophy, the a ected parent is always the mother

Answer 29

**A. Cobalamin** B. Folic acid C. Nicotinic acid D. Pyridoxine E. Thiamine ## Footnote Subacute combined de ciency of the cord occurs from failure to t ransfer cobalamin (vitamin B12) across the interstit ial mucosa because of lack of int rinsic factor. Folic acid de ciency typically causes hematologic e ects, and while folic acid is involved in B12 metabolism, it is rarely implicated in neurologic disease states (B is incorrect). Nicot inic acid de ciency has been associated with encephalopathy (C is incorrect). Pyridoxine (vitamin B6) de ciency is associated with isoniazid therapy for tuberculosis and causes polyneuropathy (D is incorrect). Thiamine de ciency is associated with the Wernicke-Korsako syndrome seen in chronic alcoholism (E is incorrect).1

Answer 30

**A. 4** B. 11 C. 17 D. 22 E. None of the above ## Footnote The marker linked to the Hunt ington gene is localized to the short arm of chromosome 4 (A). Neuro bromatosis t ype I is linked to chromosome 17 (C is incorrect). Neuro bromatosis t ype II is linked to chromosome 22 (D is incorrect).1

Answer 31

**A. Left geniculocalcarine tract and corpus callosum** B. Left geniculocalcarine tract and Wernicke’s area C. Left geniculocalcarine tract, corpus callosum, and Wernicke’s area D. Right geniculocalcarine tract and corpus callosum E. Right geniculocalcarine tract and Wernicke’s area ## Footnote The lesion described in A would render the patient blind in the right half of the visual eld. Visual information reaches only the right occipital lobe but cannot be transferred to Wernicke’s area across the callosum. Thus the ability to read aloud and to understand the writ ten word is lost, but the ability to understand the spoken language, speak, write, dictate, and converse is retained.1

Answer 32

A. Calcarine artery bilaterally B. Calcarine artery on the contralateral side **C. Contralateral paramedian branch of the basilar artery** D. Ipsilateral superior cerebellar artery E. Superior division of the contralateral middle cerebral artery ## Footnote Deviation of the eyes away from the lesion occurs in brainstem syndromes, for example, the medial midpontine syndrome (occlusion of the paramedian branch of the midbasilar artery [C]). Answers B, D, and E would cause deviation of the eyes to the left .1

Answer 33

A. Carbamazepine B. Ethosuximide C. Phenobarbital D. Phenytoin **E. Valproate** ## Footnote Of the antiepileptic drugs listed, phenobarbital (C) has the longest half-life of 96 6 12 hours, followed by ethosuximide (B), 40 6 6 hours; phenytoin (D), 24 6 12 hours; carbamazepine (A), 12 6 4 hours; and valproate (E), 8 6 2 hours.1

Answer 34

A. Amyotrophic lateral sclerosis B. Syringomyelia **C. Both** D. Neither ## Footnote Despite the at rophy of the hands and forearms in amyotrophic lateral sclerosis (ALS), di use hyperre exia is seen, with absence of sensory change.1

Answer 35

A. Amyotrophic lateral sclerosis **B. Syringomyelia** C. Both D. Neither ## Footnote Despite the at rophy of the hands and forearms in amyotrophic lateral sclerosis (ALS), di use hyperre exia is seen, with absence of sensory change.1

Answer 36

**A. Amyotrophic lateral sclerosis** B. Syringomyelia C. Both D. Neither ## Footnote Despite the at rophy of the hands and forearms in amyotrophic lateral sclerosis (ALS), di use hyperre exia is seen, with absence of sensory change.1

Answer 37

A. Increased levels of extracellular potassium in glial scars near seizure foci B. Decreased rate of binding and removing acetylcholine in the foci C. De ciency of -aminobutyric acid (GABA) **D. Decreased glycine levels** E. Decreased taurine levels ## Footnote Increased glycine levels have been found in neurons in seizure foci (D is false).

Answer 38

A. Low vitamin B12 on a m icrobiologic assay B. Low vitamin B12 on a radioisotope dilution assay C. Low vitamin B12 on a Schilling test D. The nding of hypersegmented polymorphonuclear neutrophil leukocytes (PMN) in bone marrow smears **E. The finding of increased serum concentration of methylmalonic acid and homocysteine** ## Footnote Although microbiologic assay (A) is the most accurate way to measure serum cobalamin (B12) levels, the serum level is not a measure of total body cobalamin (B12). High serum concentrations of cobalamin (B12) metabolites (methylmalonic acid and homocysteine [E]) are the m ost reliable indicators of an intracellular cobalamin de ciency.1

Answer 39

A. Absence of pain is typical early in the course B. It occurs 12 to 15 months after radiation C. Magnetic resonance imaging (MRI) shows abnormal signal intensity; decreased on T1 and increased on T2 **D. Sensory changes usually develop after motor changes** E. The most severe parenchymal changes are typical of infarction ## Footnote In radiation myelopathy, sensory changes usually precede the weakness (D is false). The other responses are characteristics of radiation myelopathy (delayed progressive type).1

Answer 40

**A. Motor nerve fiber irritability** B. Motor nerve ber destruction C. Motor unit denervation D. Muscle atrophy E. Reinnervation of muscle units ## Footnote Fasciculation potent ials are a sign of motor nerve fiber irritability (A). Fibrillation potentials are associated with motor nerve ber destruction (B). Insertional act ivit y is t ypically seen with denervating processes (C). Muscle atrophy (D) results in motor unit potentials of lower voltage and shorter duration. Reinnervation of muscle units (E) may result in “giant” motor unit potentials of unusually high amplitude.1

Answer 41

A. Fasciculation potential **B. Fibrillation potential** C. Both D. Neither

Answer 42

**A. Fasciculation potential** B. Fibrillation potential C. Both D. Neither

Answer 43

A. Fasciculation potential **B. Fibrillation potential** C. Both D. Neither

Answer 44

A. Fasciculation potential B. Fibrillation potential **C. Both** D. Neither

Answer 45

A. Fasciculation potential B. Fibrillation potential C. Both D. **Neither**

Answer 46

**A. Fasciculation potential** B. Fibrillation potential C. Both D. Neither ## Footnote Fibrillation potentials last from 1 to 5 milliseconds, may take the form of positive sharp waves, and are seen 10 to 25 days after the death of an axon. Fasciculation potentials have three to ve phases. Both can be seen in poliomyelitis.1

Answer 47

A. Prolonged, high amplitude, and polyphasic **B. Prolonged, low amplitude, and polyphasic** C. Shortened, high amplitude, and polyphasic D. Shortened, low amplitude, and polyphasic E. None of the above ## Footnote In early denervation, motor unit potentials may increase in size and amplitude and become longer in duration and polyphasic (A). These so-called “giant” potentials are a result of motor units containing more than the usual number of motor bers. In early reinnervation the motor units are low in amplitude, prolonged, and polyphasic (B), representing a transit ional con gurat ion.1

Answer 48

**A. Abnormal pupillary response to accommodation** B. Normal pupillary response to light C. Weakness of extraocular muscles D. Weakness of eye closure E. Weakness of eye opening ## Footnote Normal pupillary response to light and accommodation (A is false, B is true), together with ext raocular (C) and orbicularis oculi (D) muscle weakness, is highly suggestive of myasthenia gravis.

Answer 49

A. I, II, III B. I, III C. II, IV D. IV **E. All of the above** ## Footnote Acromegaly (I), amyloidosis (II), hypothyroidism (III), and pregnancy (IV) are all risk factors for the carpal tunnel syndrome (median nerve entrapment neuropathy at the wrist).1

Answer 50

A. Cranial nerve VI is most frequently involved. B. Sarcoidosis occurs in 25% of cases of sarcoid. **C. Polydipsia, polyuria, somnolence, and obesity are common features.** D. The granulomatous in ltration is most prominent over the hemispheres. E. Visual disturbances are usually secondary to lesions in the occipital cortex. ## Footnote Neurologic involvement in sarcoidosis occurs in 5% of cases (B is false). A granulomatous in ammator y response most prevalent at the base of the brain is seen (D is false). Visual disturbances (due to lesions in and around the optic nerves and chiasm [E is false]) and polydipsia, polyuria, somnolence, or obesity (due to involvement of the pituitary and hypothalamus) are the usual features (C is true). The facial nerve is the most common cranial nerve involved (A is false).1

Answer 51

**A. Increased total number of hours per day spent sleeping** B. Cataplexy C. Hypnagogic hallucinations D. Sleep paralysis E. Sleep patterns beginning with the rapid eye movements (REM) stage ## Footnote The nocturnal sleep of a narcolept ic is often reduced, but frequent naps are taken during the day; hence, the total number of hours spent sleeping is similar to a normal individual (A is false). The other responses are associated with narcolepsy.1

Answer 52

**A. Bilateral internuclear ophthalmoplegia** B. Gait ataxia C. Lhermitte’s sign D. Optic neuritis E. Vertigo ## Footnote The init ial manifestat ion of MS in 25% of all pat ients is optic neuritis (D), and 50% of patients who present with optic neuritis will eventually develop MS. Bilateral internuclear ophthalmoplegia occurring in a young person (A), however, is virtually diagnost ic of MS.1

Answer 53

**A. Inferior, superior, and medial recti** B. Inferior rectus and superior oblique C. Lateral and superior recti D. Lateral rectus and superior oblique E. Medial rectus and inferior oblique ## Footnote Upgaze or downgaze is usually more limited than lateral gaze. These de cits are caused by an in ammatory in ltrat ion of the inferior and medial rect i, leading to contractures of these muscles.1

Answer 54

**A. Ephaptic transmission** B. Hypersensitivity of facial muscles C. Hypocalcemia D. Psychiatric disorders E. Recurrence of latent viral infection ## Footnote The spasm is thought to be caused by nerve root compression and segmental demyelination, which leads to impulses conducted in one motor ber being transmit ted to neighboring bers (ephapt ic t ransmission [A]).1

Answer 55

**A. Biopsy evidence of sarcoid granulomas in non–central nervous system (CNS) tissue and neurologic findings** B. Computed tomography (CT) scan showing meningeal involvement C. Increased sedimentation rate and hyperglobulinemia D. Increased serum levels of angiotensin-converting enzyme E. MRI ndings of periventricular and white matter changes ## Footnote Although all of the options are seen in act ive neurosarcoidosis, the diagnosis is made on the basis of answer A.1

Answer 56

A. Limbic encephalitis B. Eaton-Lambert syndrome C. Moersch-Woltman (stiff -man) syndrome **D. Opsoclonus-myoclonus** E. Sensory neuropathy ## Footnote The IgG antibody in patients with Eaton-Lambert syndrome (B) (associated with small-cell carcinoma of the lung) reacts with presynaptic voltagegated calcium channels. The Moersch-Woltman syndrome (C) is characterized by involuntary muscle rigidity and spasms, and 60% of pat ients have autoantibodies to glutamic acid decarboxylase. Underlying tumors are often found. Most cases of paraneoplastic sensory neuropathy (E) are associated with small-cell carcinoma of the lung or lymphoma, and an antinuclear antibody (anti-Hu) is found in 70% of these patients. Paraneoplastic opsoclonus (D) in adults is associated w ith breast cancer and an antineuronal ant ibody (anti-Ri).4

Answer 57

A. Limbic encephalitis B. Eaton-Lambert syndrome C. Moersch-Woltman (stiff -man) syndrome D. Opsoclonus-myoclonus **E. Sensory neuropathy** ## Footnote The IgG antibody in patients with Eaton-Lambert syndrome (B) (associated with small-cell carcinoma of the lung) reacts with presynaptic voltagegated calcium channels. The Moersch-Woltman syndrome (C) is characterized by involuntary muscle rigidity and spasms, and 60% of pat ients have autoantibodies to glutamic acid decarboxylase. Underlying tumors are often found. Most cases of paraneoplastic sensory neuropathy (E) are associated with small-cell carcinoma of the lung or lymphoma, and an antinuclear antibody (anti-Hu) is found in 70% of these patients. Paraneoplastic opsoclonus (D) in adults is associated w ith breast cancer and an antineuronal ant ibody (anti-Ri).4

Answer 58

A. Limbic encephalitis B. Eaton-Lambert syndrome C. Moersch-Woltman (stiff -man) syndrome **D. Opsoclonus-myoclonus** E. Sensory neuropathy ## Footnote The IgG antibody in patients with Eaton-Lambert syndrome (B) (associated with small-cell carcinoma of the lung) reacts with presynaptic voltagegated calcium channels. The Moersch-Woltman syndrome (C) is characterized by involuntary muscle rigidity and spasms, and 60% of pat ients have autoantibodies to glutamic acid decarboxylase. Underlying tumors are often found. Most cases of paraneoplastic sensory neuropathy (E) are associated with small-cell carcinoma of the lung or lymphoma, and an antinuclear antibody (anti-Hu) is found in 70% of these patients. Paraneoplastic opsoclonus (D) in adults is associated w ith breast cancer and an antineuronal ant ibody (anti-Ri).4

Answer 59

A. Limbic encephalitis **B. Eaton-Lambert syndrome** C. Moersch-Woltman (stiff -man) syndrome D. Opsoclonus-myoclonus E. Sensory neuropathy ## Footnote The IgG antibody in patients with Eaton-Lambert syndrome (B) (associated with small-cell carcinoma of the lung) reacts with presynaptic voltagegated calcium channels. The Moersch-Woltman syndrome (C) is characterized by involuntary muscle rigidity and spasms, and 60% of pat ients have autoantibodies to glutamic acid decarboxylase. Underlying tumors are often found. Most cases of paraneoplastic sensory neuropathy (E) are associated with small-cell carcinoma of the lung or lymphoma, and an antinuclear antibody (anti-Hu) is found in 70% of these patients. Paraneoplastic opsoclonus (D) in adults is associated w ith breast cancer and an antineuronal ant ibody (anti-Ri).4

Answer 60

A. Limbic encephalitis B. Eaton-Lambert syndrome **C. Moersch-Woltman (stiff -man) syndrome **D. Opsoclonus-myoclonus E. Sensory neuropathy ## Footnote The IgG antibody in patients with Eaton-Lambert syndrome (B) (associated with small-cell carcinoma of the lung) reacts with presynaptic voltagegated calcium channels. The Moersch-Woltman syndrome (C) is characterized by involuntary muscle rigidity and spasms, and 60% of pat ients have autoantibodies to glutamic acid decarboxylase. Underlying tumors are often found. Most cases of paraneoplastic sensory neuropathy (E) are associated with small-cell carcinoma of the lung or lymphoma, and an antinuclear antibody (anti-Hu) is found in 70% of these patients. Paraneoplastic opsoclonus (D) in adults is associated w ith breast cancer and an antineuronal ant ibody (anti-Ri).4

Answer 61

A. Basilar syndrome B. Lateral medullary syndrome (vertebral artery [VA] or posteroinferior cerebellar artery [PICA] occlusion) C. Lateral superior pontine syndrome (superior cerebellar artery [SCA] occlusion) **D. Medial medullary occlusion** E. None of the above ## Footnote **Medial medullary occlusion (D) is associated w ith contralateral hemiparesis sparing the face, cont ralateral loss of posit ion and vibration sense, ipsilateral paralysis, and at rophy of the tongue. Lateral medullary syndrome (VA or PICA occlusion [B]) is associated w ith contralateral pain and temperature loss in the body, ipsilateral Horner’s syndrome, ipsilateral ataxia, ipsilateral paralysis of the palate and vocal cords, and ipsilateral pain and numbness in the face. Lateral superior pontine syndrome (SCA occlusion [C]) is associated with ipsilateral cerebellar ataxia, contralateral loss of pain and temperature in the body, partial deafness, and nausea and vomiting. Basilar syndrome (A) is associated with bilateral motor weakness in all extremities, bilateral cerebellar ataxia, and diplopia.1**

Answer 62

A. Basilar syndrome **B. Lateral medullary syndrome (vertebral artery [VA] or posteroinferior** cerebellar artery [PICA] occlusion) C. Lateral superior pontine syndrome (superior cerebellar artery [SCA] occlusion) D. Medial medullary occlusion E. None of the above ## Footnote Medial medullary occlusion (D) is associated w ith contralateral hemiparesis sparing the face, cont ralateral loss of posit ion and vibration sense, ipsilateral paralysis, and at rophy of the tongue. Lateral medullary syndrome (VA or PICA occlusion [B]) is associated w ith contralateral pain and temperature loss in the body, ipsilateral Horner’s syndrome, ipsilateral ataxia, ipsilateral paralysis of the palate and vocal cords, and ipsilateral pain and numbness in the face. Lateral superior pontine syndrome (SCA occlusion [C]) is associated with ipsilateral cerebellar ataxia, contralateral loss of pain and temperature in the body, partial deafness, and nausea and vomiting. Basilar syndrome (A) is associated with bilateral motor weakness in all extremities, bilateral cerebellar ataxia, and diplopia.1

Answer 63

A. Basilar syndrome B. Lateral medullary syndrome (vertebral artery [VA] or posteroinferior cerebellar artery [PICA] occlusion) **C. Lateral superior pontine syndrome (superior cerebellar artery [SCA] occlusion)** D. Medial medullary occlusion E. None of the above ## Footnote Medial medullary occlusion (D) is associated w ith contralateral hemiparesis sparing the face, cont ralateral loss of posit ion and vibration sense, ipsilateral paralysis, and at rophy of the tongue. Lateral medullary syndrome (VA or PICA occlusion [B]) is associated w ith contralateral pain and temperature loss in the body, ipsilateral Horner’s syndrome, ipsilateral ataxia, ipsilateral paralysis of the palate and vocal cords, and ipsilateral pain and numbness in the face. Lateral superior pontine syndrome (SCA occlusion [C]) is associated with ipsilateral cerebellar ataxia, contralateral loss of pain and temperature in the body, partial deafness, and nausea and vomiting. Basilar syndrome (A) is associated with bilateral motor weakness in all extremities, bilateral cerebellar ataxia, and diplopia.1

Answer 64

**A. Basilar syndrome** B. Lateral medullary syndrome (vertebral artery [VA] or posteroinferior cerebellar artery [PICA] occlusion) C. Lateral superior pontine syndrome (superior cerebellar artery [SCA] occlusion) D. Medial medullary occlusion E. None of the above ## Footnote Medial medullary occlusion (D) is associated w ith contralateral hemiparesis sparing the face, cont ralateral loss of posit ion and vibration sense, ipsilateral paralysis, and at rophy of the tongue. Lateral medullary syndrome (VA or PICA occlusion [B]) is associated w ith contralateral pain and temperature loss in the body, ipsilateral Horner’s syndrome, ipsilateral ataxia, ipsilateral paralysis of the palate and vocal cords, and ipsilateral pain and numbness in the face. Lateral superior pontine syndrome (SCA occlusion [C]) is associated with ipsilateral cerebellar ataxia, contralateral loss of pain and temperature in the body, partial deafness, and nausea and vomiting. Basilar syndrome (A) is associated with bilateral motor weakness in all extremities, bilateral cerebellar ataxia, and diplopia.1

Answer 65

A. Brachium conjunctivum B. Caudate nucleus C. Dorsomedial nucleus of the thalamus D. Substantia nigra **E. Subthalamic nucleus** ## Footnote The lesion in hemiballismus is localized to the contralateral subthalamic nucleus (E). Cerebellar incoordination and intent ion tremor are associated with damage to the brachium conjunctivum (A). Huntington’s chorea is associated with damage to the caudate nucleus (B). Dysfunct ion of the substantia nigra (D) is involved in the pathogenesis of Parkinson’s disease.1

Answer 66

A. Latissimus dorsi B. Levator scapulae C. Rhomboids **D. Serratus anterior** E. Teres minor ## Footnote The long thoracic nerve arises from the posterior aspect of the anterior rami of C5, C6, and C7 and innervates the serratus anterior muscle (D); lesions to the long thoracic nerve result in winging of the scapula. The levator scapulae (B) and rhomboids (C) are innervated by the dorsal scapular nerve, which is a branch o the posterior aspect of the anterior ramus of C5. The latissimus dorsi (A) is innervated by the thoracodorsal nerve, a side branch of the posterior cord. The teres minor (E) is innervated by the axillary nerve along with the deltoid muscle.3

Answer 67

A. Abnormal presynaptic vesicles B. Antibodies to the acetylcholine receptor C. Decreased numbers of acetylcholine receptors **D. Defect in release of acetylcholine quanta** E. None of the above ## Footnote In Eaton-Lambert syndrome, the presynaptic vesicles are normal (A is false), ant ibodies to the acetylcholine receptor are not present (B is false), and the extent of receptor surface is actually increased (C is false). There is, however, a defect in the release of acetylcholine quanta from the nerve terminals (D)

Answer 68

A. A defect on chromosome 3 B. Dominant inheritance **C. Iris hamartomas** D. Pancreatic cysts E. Renal cell carcinoma ## Footnote Von Hippel-Lindau disease is associated with a defect on chromosome 3 (A), dominant inheritance (B), pancreatic cysts (D), and renal cell carcinomas (E). Iris hamartomas (Lisch nodules [C]) are seen in neuro - bromatosis type 1.1

Answer 69

A. Dominant frontal lobe **B. Dominant parietal lobe** C. Dominant temporal lobe D. Nondominant parietal lobe E. Nondominant temporal lobe ## Footnote Gerstmann’s syndrome consists of nger agnosia, left–right confusion, acalculia, and agraphia. It is associated with lesions of the dominant parietal lobe (B), usually in the inferior parietal lobule, angular gyrus, or subjacent white matter.1

Answer 70

A. Homovanillic acid is a metabolite. B. It is derived from phenylalanine. C. It is metabolized by monoamine oxidase (MAO). D. The activation of the D2 receptor decreases the release of transmitter at synaptic terminals. **E. The rate-limiting step in its synthesis is dopa decarboxylase.** ## Footnote The rate-limiting step in dopamine synthesis is t yrosine hydroxylase (converts L-t yrosine to L-hydroxyphenylalanine [L-dopa]). The other responses regarding dopamine pharmacology are true.1,5

Answer 71

A. Amantadine B. Artane (trihexyphenidyl) C. Bromocriptine D. Eldepryl (selegiline) **E. Sinemet (carbidopa-levodopa)** ## Footnote Amantadine (A) is an antiviral agent that may release dopamine from striatal neurons. Artane (trihexyphenidyl [B]) is an anticholinergic agent w ith side effects that include dry mouth and blurred vision. Bromocriptine (C) is an ergot derivative that agonizes D2 receptors. Eldepryl (selegiline [D]) is a m onoamine oxidase B inhibitor and slows progression of disability. Sinemet (carbidopalevodopa [E]) combines L-dopa w ith a dopa decarboxylase inhibitor.1

Answer 72

A. Amantadine B. Artane (trihexyphenidyl) C. Bromocriptine **D. Eldepryl (selegiline)** E. Sinemet (carbidopa-levodopa) ## Footnote Amantadine (A) is an antiviral agent that may release dopamine from striatal neurons. Artane (trihexyphenidyl [B]) is an anticholinergic agent w ith side effects that include dry mouth and blurred vision. Bromocriptine (C) is an ergot derivative that agonizes D2 receptors. Eldepryl (selegiline [D]) is a m onoamine oxidase B inhibitor and slows progression of disability. Sinemet (carbidopalevodopa [E]) combines L-dopa w ith a dopa decarboxylase inhibitor.1

Answer 73

A. Amantadine B. Artane (trihexyphenidyl) **C. Bromocriptine** D. Eldepryl (selegiline) E. Sinemet (carbidopa-levodopa) ## Footnote Amantadine (A) is an antiviral agent that may release dopamine from striatal neurons. Artane (trihexyphenidyl [B]) is an anticholinergic agent w ith side effects that include dry mouth and blurred vision. Bromocriptine (C) is an ergot derivative that agonizes D2 receptors. Eldepryl (selegiline [D]) is a m onoamine oxidase B inhibitor and slows progression of disability. Sinemet (carbidopalevodopa [E]) combines L-dopa w ith a dopa decarboxylase inhibitor.1

Answer 74

A. Amantadine **B. Artane (trihexyphenidyl)** C. Bromocriptine D. Eldepryl (selegiline) E. Sinemet (carbidopa-levodopa) ## Footnote Amantadine (A) is an antiviral agent that may release dopamine from striatal neurons. Artane (trihexyphenidyl [B]) is an anticholinergic agent w ith side effects that include dry mouth and blurred vision. Bromocriptine (C) is an ergot derivative that agonizes D2 receptors. Eldepryl (selegiline [D]) is a m onoamine oxidase B inhibitor and slows progression of disability. Sinemet (carbidopalevodopa [E]) combines L-dopa w ith a dopa decarboxylase inhibitor.1

Answer 75

A. Amantadine B. Artane (trihexyphenidyl) C. Bromocriptine **D. Eldepryl (selegiline)** E. Sinemet (carbidopa-levodopa) ## Footnote Amantadine (A) is an antiviral agent that may release dopamine from striatal neurons. Artane (trihexyphenidyl [B]) is an anticholinergic agent w ith side effects that include dry mouth and blurred vision. Bromocriptine (C) is an ergot derivative that agonizes D2 receptors. Eldepryl (selegiline [D]) is a m onoamine oxidase B inhibitor and slows progression of disability. Sinemet (carbidopalevodopa [E]) combines L-dopa w ith a dopa decarboxylase inhibitor.1

Answer 76

A. 17 B. 19 **C. 22** D. 41 and 42 E. 44 ## Footnote Wernicke’s area corresponds most closely to Brodmann’s area 22 (C). Area 17 (A) corresponds to primary visual cortex located on the banks of the calcarine ssure. Area 19 (B) represents tertiary visual function. Areas 41 and 42 (D) represent primary and secondary auditory cortex in Heschl’s gyri and the superior temporal gyrus. Area 44 (E) corresponds to Broca’s area located in the frontal operculum.1,6

Answer 77

**A. I, II, III** B. I, III C. II, IV D. IV E. All of the above ## Footnote The progressive sensorimotor polyneuropathy (IV) associated w ith diabetes mellitus is generally (but not universally) thought to be metabolic in origin. The pathophysiology of ophthalmoplegia (I), acute mononeuropathy (II), and mononeuritis multiplex (III) are generally thought to be vascular in origin.1,4

Answer 78

A. Bradycardia B. Diarrhea **C. Increased strength after the Tensilon test** D. Miosis E. Sweating ## Footnote In a myasthenic patient present ing with acutely worsening weakness and respiratory failure, the di erential includes myasthenic crisis and cholinergic crisis (due to anticholinesterase therapy). Muscarinic symptoms include bradycardia (A), diarrhea (B), miosis (D), and sweating (E). Increased strength following the administration of Tensilon (edrophonium [C]) does not support the diagnosis of cholinergic crisis. Edrophonium is an ant icholinesterase drug, which would increase the availability of acetycholine on administ ration. The weakness of a cholinergic crisis is una ected by Tensilon (edrophonium).1

Answer 79

A. Autosomal dominant B. Autosomal recessive **C. Maternal inheritance** D. Sporadic E. X-linked recessive ## Footnote The MELAS syndrome (mitochondrial myopathy, encephalopathy, lact ic acidosis, and strokelike episodes) is a mitochondrial disease associated with a maternal inheritance.1

Answer 80

A. Anterior cord syndrome B. Brown-Séquard syndrome **C. Central cord syndrome** D. A and B E. None of the above ## Footnote The anterior cord syndrome (A) is associated with hypesthesia and hypalgesia due to injury of the anterior and lateral spinothalamic tracts and is associated with hyper exion injuries. Posterior column function is generally preserved. The Brown-Séquard syndrome (B) is associated with cont ralateral pain and temperature loss, ipsilateral dorsal column dysfunct ion, and ipsilateral hemiplegia. It is usually due to penet rat ing t rauma and has the best prognosis of the incomplete syndromes. Central cord syndrome (C) is thought to be due to hyperextension in the set t ing of cervical stenosis. Central cord injuries cause decreased sensation over the upper limbs and shoulders and decreased motor function that is worse in the upper extremit ies.2

Answer 81

**A. Anterior cord syndrome** B. Brown-Séquard syndrome C. Central cord syndrome D. A and B E. None of the above ## Footnote The anterior cord syndrome (A) is associated with hypesthesia and hypalgesia due to injury of the anterior and lateral spinothalamic tracts and is associated with hyper exion injuries. Posterior column function is generally preserved. The Brown-Séquard syndrome (B) is associated with cont ralateral pain and temperature loss, ipsilateral dorsal column dysfunct ion, and ipsilateral hemiplegia. It is usually due to penet rat ing t rauma and has the best prognosis of the incomplete syndromes. Central cord syndrome (C) is thought to be due to hyperextension in the set t ing of cervical stenosis. Central cord injuries cause decreased sensation over the upper limbs and shoulders and decreased motor function that is worse in the upper extremit ies.2

Answer 82

**A. Anterior cord syndrome** B. Brown-Séquard syndrome C. Central cord syndrome D. A and B E. None of the above ## Footnote The anterior cord syndrome (A) is associated with hypesthesia and hypalgesia due to injury of the anterior and lateral spinothalamic tracts and is associated with hyper exion injuries. Posterior column function is generally preserved. The Brown-Séquard syndrome (B) is associated with cont ralateral pain and temperature loss, ipsilateral dorsal column dysfunct ion, and ipsilateral hemiplegia. It is usually due to penet rat ing t rauma and has the best prognosis of the incomplete syndromes. Central cord syndrome (C) is thought to be due to hyperextension in the set t ing of cervical stenosis. Central cord injuries cause decreased sensation over the upper limbs and shoulders and decreased motor function that is worse in the upper extremit ies.2

Answer 83

A. Anterior cord syndrome **B. Brown-Séquard syndrome** C. Central cord syndrome D. A and B E. None of the above ## Footnote The anterior cord syndrome (A) is associated with hypesthesia and hypalgesia due to injury of the anterior and lateral spinothalamic tracts and is associated with hyper exion injuries. Posterior column function is generally preserved. The Brown-Séquard syndrome (B) is associated with cont ralateral pain and temperature loss, ipsilateral dorsal column dysfunct ion, and ipsilateral hemiplegia. It is usually due to penet rat ing t rauma and has the best prognosis of the incomplete syndromes. Central cord syndrome (C) is thought to be due to hyperextension in the set t ing of cervical stenosis. Central cord injuries cause decreased sensation over the upper limbs and shoulders and decreased motor function that is worse in the upper extremit ies.2

Answer 84

A. REM sleep B. Non–rapid eye movement (NREM) sleep **C. Both** D. Neither

Answer 85

A. REM sleep **B. Non–rapid eye movement (NREM) sleep** C. Both D. Neither

Answer 86

**A. REM sleep** B. Non–rapid eye movement (NREM) sleep C. Both D. Neither

Answer 87

A. REM sleep **B. Non–rapid eye movement (NREM) sleep** C. Both D. Neither

Answer 88

A. REM sleep **B. Non–rapid eye movement (NREM) sleep** C. Both D. Neither

Answer 89

**A. REM sleep** B. Non–rapid eye movement (NREM) sleep C. Both D. Neither

Answer 90

A. Glycogen storage disease type II (acid maltase de ciency) **B. Glycogen storage disease type V (McArdle’s disease)** C. Both D. Neither

Answer 91

**A. Glycogen storage disease type II (acid maltase de ciency)** B. Glycogen storage disease type V (McArdle’s disease) C. Both D. Neither ## Footnote Glycogen storage disease type II (A) results from acid maltase (a -1,4-glucosidase) de ciency and has three forms: infantile (classic Pompe’s disease), juvenile, and adult forms. Glycogen accumulates in lysosomes throughout the body. Glycogen storage disease type V (McArdle’s disease [B]) results from myophosphorylase de ciency. Glycogen cannot be converted to glucose-6-phosphate, and the blood lactate does not rise after ischemic exercise. Both types are autosomal recessive. Rarely, type V may be autosomal dominant.1

Answer 92

**A. Glycogen storage disease type II (acid maltase de ciency)** B. Glycogen storage disease type V (McArdle’s disease) C. Both D. Neither ## Footnote Glycogen storage disease type II (A) results from acid maltase (a -1,4-glucosidase) de ciency and has three forms: infantile (classic Pompe’s disease), juvenile, and adult forms. Glycogen accumulates in lysosomes throughout the body. Glycogen storage disease type V (McArdle’s disease [B]) results from myophosphorylase de ciency. Glycogen cannot be converted to glucose-6-phosphate, and the blood lactate does not rise after ischemic exercise. Both types are autosomal recessive. Rarely, type V may be autosomal dominant.1

Answer 93

A. Glycogen storage disease type II (acid maltase de ciency) B. Glycogen storage disease type V (McArdle’s disease) C. Both D. **Neither** ## Footnote Glycogen storage disease type II (A) results from acid maltase (a -1,4-glucosidase) de ciency and has three forms: infantile (classic Pompe’s disease), juvenile, and adult forms. Glycogen accumulates in lysosomes throughout the body. Glycogen storage disease type V (McArdle’s disease [B]) results from myophosphorylase de ciency. Glycogen cannot be converted to glucose-6-phosphate, and the blood lactate does not rise after ischemic exercise. Both types are autosomal recessive. Rarely, type V may be autosomal dominant.1

Answer 94

A. I, II, III **B. I, III** C. II, IV D. IV E. All of the above ## Footnote Wilson’s disease is characterized by an increased urinary copper excretion (I), low serum copper levels (II is false), and low ceruloplasmin levels (III). The computed tomography (CT) scan sometimes shows hypodense areas in the lenticular nuclei (IV is false).1

Answer 95

**A. A marked in ammatory response with destruction of nerve cells in the pons is seen.** B. It is associated with rapid correction of hyponatremia. C. It is associated with chronic alcoholism. D. Quadriplegia, pseudobulbar palsy, and a locked-in syndrome can occur. E. Some patients have no signs or symptoms referable to the pontine lesion. ## Footnote Central pont ine myelinolysis (CPM) occurs in the set ting of rapid correction of chronic hyponatremia (B), as is somet imes seen in chronic alcoholism (C). Quadriplegia, pseudobulbar palsy, and locked-in syndrome (D) can occur with CPM. Microscopically, destruct ion of the medullated sheaths with relative sparing of the axis cylinders and preservation of nerve cells in the pons is seen. An in ammatory response is absent (A is false).1

Answer 96

A. Homocystinuria B. Marfan’s syndrome C. **Both** D. Neither ## Footnote Pat ients with homocystinuria (A) and those with Marfan’s syndrome (B) have a tall, thin frame and arachnodactyly. Pat ients with homocyst inuria (cystathione synthase de ciency) also show evidence of mental retardation and are prone to strokes.1

Answer 97

A. **Homocystinuria** B. Marfan’s syndrome C. Both D. Neither ## Footnote Pat ients with homocystinuria (A) and those with Marfan’s syndrome (B) have a tall, thin frame and arachnodactyly. Pat ients with homocyst inuria (cystathione synthase de ciency) also show evidence of mental retardation and are prone to strokes.1

Answer 98

A. **Homocystinuria** B. Marfan’s syndrome C. Both D. Neither ## Footnote Pat ients with homocystinuria (A) and those with Marfan’s syndrome (B) have a tall, thin frame and arachnodactyly. Pat ients with homocyst inuria (cystathione synthase de ciency) also show evidence of mental retardation and are prone to strokes.1

Answer 99

A. Dominant frontal lobe B. Dominant parietal lobe C. Nondominant frontal lobe **D. Nondominant parietal lobe** E. Nondominant temporal lobe ## Footnote Dressing apraxia is a special type of anosognosia that is t ypically at t ributed to dysfunction of the nondominant parietal lobe (D).1

Answer 100

A. Coracobrachialis B. Rhomboids C. Supraspinatus D. Teres major **E. Teres minor** ## Footnote The axillary nerve innervates the teres minor (E) and deltoid muscles. Coracobrachialis (A) is innervated by the musculocutaneous nerve. The rhomboids (B) are innervated by the dorsal scapular nerve. The suprascapular nerve innervates the supraspinatus (C) and infraspinatus muscles. The subscapular nerves innervate the teres major (D) and subscapularis m uscles.3

Answer 101

**A. Calcified cortical vessels** B. Facial nevus contralateral to seizure activity C. Hemisensory de cit contralateral to facial nevus D. Meningeal venous angiomas E. Tramline calci cations outlining the convolution of the parieto-occipital cortex ## Footnote Sturge-Weber syndrome is characterized by a facial vascular nevus (B) that is present at birth, with seizures, hemisensory de cit (C), and hemiparesis contralateral to the side of the nevus. Meningeal venous angiomas (D) are also present ipsilateral to the skin lesion. Skull lms may reveal tramline calci cation is present in the parieto-occipital cortical substance (E), not the vessels (A is false).1

Answer 102

A. 10 meters per second (m/s) B. 25 m/s **C. 50 m/s** D. 100 m/s E. 150 m/s ## Footnote The normal sensory conduction velocit y in the median and ulnar nerves is approximately 50 m/s (C). The other answer choices are incorrect.

Answer 103

A. Autosomal dominance is the usual mode of inheritance. B. Distal muscle atrophy is prominent. C. It can a ect the upper extremities. D. Steroids have no e ect on disease progression. **E. The autonomic nervous system is usually involved.** ## Footnote Charcot-Marie-Tooth disease, or peroneal muscular atrophy, is a slowly progressive, symmetric, inherited demyelinat ing condition of the peripheral nervous system. The usual pat tern of inheritance is autosomal dominant (A), and the disease may cause weakness, at rophy, and ataxia of both the upper and lower extremities (C), part icularly of the distal muscle groups (B)—foot drop is common. No speci c medical therapy is available at this time, and steroids do not appear to have an e ect on disease progression (D). The autonomic nervous system is usually not involved in Charcot-Marie-Tooth disease (E is false).1

Answer 104

A. I, II, III B. I, III C. II, IV D. IV **E. All of the above** ## Footnote Clival chordomas may cause palsies of multiple cranial nerves. All of the cranial nerves listed could potent ially be a ected by a destruct ive lesion of the skull base (II, V, X, and XII).1

Answer 105

A. Glucose of 30 mg/dL B. Lymphocytic predomination after 1 week of illness C. Opening pressure of 200 mm CSF **D. Protein of 35 mg/dL** E. White blood cell count (WBC) of 200 cells/mm3 ## Footnote Lumbar puncture and CSF ndings in tuberculous meningitis t ypically include glucose less than 40 mg/dL (A), although glucose levels are typically not as low as those found in pyogenic meningitis. CSF tends to be under increased pressure (C), and a leukocytosis is usually present (E) w ith a predominance of lymphocytes after several days of the illness (B). The protein level is elevated in tuberculous meningitis and is usually 100 to 200 mg/dL (D is false).1

Answer 106

**A. Contralateral Horner’s syndrome** B. Contralateral loss of pain and temperature over the body C. Ipsilateral ataxia D. Ipsilateral numbness of the limbs ## Footnote PICA occlusion may result in Wallenberg’s lateral medullary syndrome, which is characterized by contralateral pain and temperature loss over the body (due to disruption of spinothalamic bers [B]), ipsilateral numbness over half of the face (due to descending tract and nucleus of the t rigeminal nerve), ipsilateral ataxia (etiology uncertain [C]), ipsilateral numbness of the limbs (due to injury to the cuneate and gracile nuclei [D]), ipsilateral paralysis of the palate (E), and ipsilateral Horner’s syndrome (due to injury of descending sympathetic bers; A is incorrect).1

Answer 107

**A. K complexes** B. Delta waves C. Desynchronization of the EEG D. REM sleep E. Somnambulism ## Footnote K complexes (A) are a characteristic of stage 2 sleep. Delta waves (B) are prevalent in stage 3 and 4 sleep. Desynchronization of the EEG (C) occurs in REM sleep (A), and somnambulism (E) occurs almost exclusively in stage 4 sleep.1

Answer 108

A. Becker’s muscular dystrophy **B. Duchenne’s muscular dystrophy** C. Emery-Dreifuss muscular dystrophy D. Landouzy-Dejerine (facioscapulohumeral) dystrophy E. Myotonic dystrophy

Answer 109

A. **Becker’s muscular dystrophy** B. Duchenne’s muscular dystrophy C. Emery-Dreifuss muscular dystrophy D. Landouzy-Dejerine (facioscapulohumeral) dystrophy E. Myotonic dystrophy ## Footnote Duchenne’s (B) and Becker’s (A) muscular dystrophies are X-linked recessive disorders characterized by the absence of the gene product dyst rophin in the former and the presence of a structurally abnormal form of the product in the lat ter. Weakness and pseudo-hypertrophy of certain muscles (notably the calf) occur. The onset is later and the course more benign in the Becker’s type (A). Myotonic dystrophy (E) is the most common adult form of muscular dystrophy and is characterized by an autosomal dominant inheritance, with the defective gene localized to chromosome 19q. Features include dystrophic changes in nonmuscular tissues (e.g., lens opacit ies) and a characteristic facies. Landouzy-Dejerine dystrophy (D) is usually transmitted by autosomal dominant inheritance, and the abnormal gene has been localized to chromosome 4. Congenital absence of a pectoral, brachioradialis, or biceps femoris muscle occasionally occurs. Characteristics of Emery-Dreifuss dystrophy (C), a benign X-linked dyst rophy, include cont ractures of the elbow exors, neck extensors, and posterior calf muscles.1

Answer 110

A. Becker’s muscular dystrophy B. Duchenne’s muscular dystrophy C. Emery-Dreifuss muscular dystrophy D. Landouzy-Dejerine (facioscapulohumeral) dystrophy **E. Myotonic dystrophy** ## Footnote Duchenne’s (B) and Becker’s (A) muscular dystrophies are X-linked recessive disorders characterized by the absence of the gene product dyst rophin in the former and the presence of a structurally abnormal form of the product in the lat ter. Weakness and pseudo-hypertrophy of certain muscles (notably the calf) occur. The onset is later and the course more benign in the Becker’s type (A). Myotonic dystrophy (E) is the most common adult form of muscular dystrophy and is characterized by an autosomal dominant inheritance, with the defective gene localized to chromosome 19q. Features include dystrophic changes in nonmuscular tissues (e.g., lens opacit ies) and a characteristic facies. Landouzy-Dejerine dystrophy (D) is usually transmitted by autosomal dominant inheritance, and the abnormal gene has been localized to chromosome 4. Congenital absence of a pectoral, brachioradialis, or biceps femoris muscle occasionally occurs. Characteristics of Emery-Dreifuss dystrophy (C), a benign X-linked dyst rophy, include cont ractures of the elbow exors, neck extensors, and posterior calf muscles.1

Answer 111

A. Becker’s muscular dystrophy **B. Duchenne’s muscular dystrophy** C. Emery-Dreifuss muscular dystrophy D. Landouzy-Dejerine (facioscapulohumeral) dystrophy E. Myotonic dystrophy ## Footnote Duchenne’s (B) and Becker’s (A) muscular dystrophies are X-linked recessive disorders characterized by the absence of the gene product dyst rophin in the former and the presence of a structurally abnormal form of the product in the lat ter. Weakness and pseudo-hypertrophy of certain muscles (notably the calf) occur. The onset is later and the course more benign in the Becker’s type (A). Myotonic dystrophy (E) is the most common adult form of muscular dystrophy and is characterized by an autosomal dominant inheritance, with the defective gene localized to chromosome 19q. Features include dystrophic changes in nonmuscular tissues (e.g., lens opacit ies) and a characteristic facies. Landouzy-Dejerine dystrophy (D) is usually transmitted by autosomal dominant inheritance, and the abnormal gene has been localized to chromosome 4. Congenital absence of a pectoral, brachioradialis, or biceps femoris muscle occasionally occurs. Characteristics of Emery-Dreifuss dystrophy (C), a benign X-linked dyst rophy, include cont ractures of the elbow exors, neck extensors, and posterior calf muscles.1

Answer 112

A. Becker’s muscular dystrophy B. Duchenne’s muscular dystrophy **C. Emery-Dreifuss muscular dystrophy** D. Landouzy-Dejerine (facioscapulohumeral) dystrophy E. Myotonic dystrophy ## Footnote Duchenne’s (B) and Becker’s (A) muscular dystrophies are X-linked recessive disorders characterized by the absence of the gene product dyst rophin in the former and the presence of a structurally abnormal form of the product in the lat ter. Weakness and pseudo-hypertrophy of certain muscles (notably the calf) occur. The onset is later and the course more benign in the Becker’s type (A). Myotonic dystrophy (E) is the most common adult form of muscular dystrophy and is characterized by an autosomal dominant inheritance, with the defective gene localized to chromosome 19q. Features include dystrophic changes in nonmuscular tissues (e.g., lens opacit ies) and a characteristic facies. Landouzy-Dejerine dystrophy (D) is usually transmitted by autosomal dominant inheritance, and the abnormal gene has been localized to chromosome 4. Congenital absence of a pectoral, brachioradialis, or biceps femoris muscle occasionally occurs. Characteristics of Emery-Dreifuss dystrophy (C), a benign X-linked dyst rophy, include cont ractures of the elbow exors, neck extensors, and posterior calf muscles.1

Answer 113

A. Becker’s muscular dystrophy B. Duchenne’s muscular dystrophy C. Emery-Dreifuss muscular dystrophy **D. Landouzy-Dejerine (facioscapulohumeral) dystrophy** E. Myotonic dystrophy ## Footnote Duchenne’s (B) and Becker’s (A) muscular dystrophies are X-linked recessive disorders characterized by the absence of the gene product dyst rophin in the former and the presence of a structurally abnormal form of the product in the lat ter. Weakness and pseudo-hypertrophy of certain muscles (notably the calf) occur. The onset is later and the course more benign in the Becker’s type (A). Myotonic dystrophy (E) is the most common adult form of muscular dystrophy and is characterized by an autosomal dominant inheritance, with the defective gene localized to chromosome 19q. Features include dystrophic changes in nonmuscular tissues (e.g., lens opacit ies) and a characteristic facies. Landouzy-Dejerine dystrophy (D) is usually transmitted by autosomal dominant inheritance, and the abnormal gene has been localized to chromosome 4. Congenital absence of a pectoral, brachioradialis, or biceps femoris muscle occasionally occurs. Characteristics of Emery-Dreifuss dystrophy (C), a benign X-linked dyst rophy, include cont ractures of the elbow exors, neck extensors, and posterior calf muscles.1

Answer 114

A. Becker’s muscular dystrophy B. Duchenne’s muscular dystrophy C. Emery-Dreifuss muscular dystrophy D. Landouzy-Dejerine (facioscapulohumeral) dystrophy **E. Myotonic dystrophy** ## Footnote Duchenne’s (B) and Becker’s (A) muscular dystrophies are X-linked recessive disorders characterized by the absence of the gene product dyst rophin in the former and the presence of a structurally abnormal form of the product in the lat ter. Weakness and pseudo-hypertrophy of certain muscles (notably the calf) occur. The onset is later and the course more benign in the Becker’s type (A). Myotonic dystrophy (E) is the most common adult form of muscular dystrophy and is characterized by an autosomal dominant inheritance, with the defective gene localized to chromosome 19q. Features include dystrophic changes in nonmuscular tissues (e.g., lens opacit ies) and a characteristic facies. Landouzy-Dejerine dystrophy (D) is usually transmitted by autosomal dominant inheritance, and the abnormal gene has been localized to chromosome 4. Congenital absence of a pectoral, brachioradialis, or biceps femoris muscle occasionally occurs. Characteristics of Emery-Dreifuss dystrophy (C), a benign X-linked dyst rophy, include cont ractures of the elbow exors, neck extensors, and posterior calf muscles.1

Answer 115

A. Becker’s muscular dystrophy B. Duchenne’s muscular dystrophy C. Emery-Dreifuss muscular dystrophy **D. Landouzy-Dejerine (facioscapulohumeral) dystrophy** E. Myotonic dystrophy ## Footnote Duchenne’s (B) and Becker’s (A) muscular dystrophies are X-linked recessive disorders characterized by the absence of the gene product dyst rophin in the former and the presence of a structurally abnormal form of the product in the lat ter. Weakness and pseudo-hypertrophy of certain muscles (notably the calf) occur. The onset is later and the course more benign in the Becker’s type (A). Myotonic dystrophy (E) is the most common adult form of muscular dystrophy and is characterized by an autosomal dominant inheritance, with the defective gene localized to chromosome 19q. Features include dystrophic changes in nonmuscular tissues (e.g., lens opacit ies) and a characteristic facies. Landouzy-Dejerine dystrophy (D) is usually transmitted by autosomal dominant inheritance, and the abnormal gene has been localized to chromosome 4. Congenital absence of a pectoral, brachioradialis, or biceps femoris muscle occasionally occurs. Characteristics of Emery-Dreifuss dystrophy (C), a benign X-linked dyst rophy, include cont ractures of the elbow exors, neck extensors, and posterior calf muscles.1

Answer 116

A. Becker’s muscular dystrophy B. Duchenne’s muscular dystrophy C. Emery-Dreifuss muscular dystrophy D. Landouzy-Dejerine (facioscapulohumeral) dystrophy **E. Myotonic dystrophy** ## Footnote Duchenne’s (B) and Becker’s (A) muscular dystrophies are X-linked recessive disorders characterized by the absence of the gene product dyst rophin in the former and the presence of a structurally abnormal form of the product in the lat ter. Weakness and pseudo-hypertrophy of certain muscles (notably the calf) occur. The onset is later and the course more benign in the Becker’s type (A). Myotonic dystrophy (E) is the most common adult form of muscular dystrophy and is characterized by an autosomal dominant inheritance, with the defective gene localized to chromosome 19q. Features include dystrophic changes in nonmuscular tissues (e.g., lens opacit ies) and a characteristic facies. Landouzy-Dejerine dystrophy (D) is usually transmitted by autosomal dominant inheritance, and the abnormal gene has been localized to chromosome 4. Congenital absence of a pectoral, brachioradialis, or biceps femoris muscle occasionally occurs. Characteristics of Emery-Dreifuss dystrophy (C), a benign X-linked dyst rophy, include cont ractures of the elbow exors, neck extensors, and posterior calf muscles.1

Answer 117

A. Becker’s muscular dystrophy B. Duchenne’s muscular dystrophy C. Emery-Dreifuss muscular dystrophy D. Landouzy-Dejerine (facioscapulohumeral) dystrophy **E. Myotonic dystrophy** ## Footnote Duchenne’s (B) and Becker’s (A) muscular dystrophies are X-linked recessive disorders characterized by the absence of the gene product dyst rophin in the former and the presence of a structurally abnormal form of the product in the lat ter. Weakness and pseudo-hypertrophy of certain muscles (notably the calf) occur. The onset is later and the course more benign in the Becker’s type (A). Myotonic dystrophy (E) is the most common adult form of muscular dystrophy and is characterized by an autosomal dominant inheritance, with the defective gene localized to chromosome 19q. Features include dystrophic changes in nonmuscular tissues (e.g., lens opacit ies) and a characteristic facies. Landouzy-Dejerine dystrophy (D) is usually transmitted by autosomal dominant inheritance, and the abnormal gene has been localized to chromosome 4. Congenital absence of a pectoral, brachioradialis, or biceps femoris muscle occasionally occurs. Characteristics of Emery-Dreifuss dystrophy (C), a benign X-linked dyst rophy, include cont ractures of the elbow exors, neck extensors, and posterior calf muscles.1

Answer 118

A. Brainstem **B. Cortex** C. Internal capsule D. Peripheral nerve E. Spinal cord

Answer 119

A. I, II, III B. I, III **C. II, IV** D. IV E. All of the above ## Footnote Subacute spongiform encephalopathy, or Creut zfeldt-Jakob disease, is a progressive neurologic illness characterized by dementia and myoclonic jerks. The disease is thought to be due to a prion protein that is resistant to formalin (I), alcohol (III), boiling, and ultraviolet radiation. The protein can be inactivated by autoclaving at 132°C under pressure for 1 hour (II), or by immersion in bleach for 1 hour (IV).1

Answer 120

A. Flat loss **B. High-frequency loss** C. Low-tone loss D. Normal audiogram E. Trough-shaped loss

Answer 121

A. Lateral cord lesion B. Lower trunk lesion C. Medial cord lesion **D. Middle trunk lesion** E. Upper trunk lesion ## Footnote Although lower trunk lesions (B) resemble medial cord lesions (C), abnormalities of radially innervated C8 muscles are seen with the former, but not with the lat ter. Low-amplitude act ion potentials in the deltoid and biceps are seen in upper trunk lesions (E). Median sensory responses from the index and middle nger are abnormal, and motor conduction velocities of the hand muscles are normal in middle trunk lesions (D). Lateral cord lesions (A) cause weakness of the muscles supplied by the musculocutaneous nerve and the lateral root of the median nerve (innervates the forearm muscles). The int rinsic hand muscles innervated by the medial root of the median nerve are spared.7

Answer 122

A. Lateral cord lesion **B. Lower trunk lesion** C. Medial cord lesion D. Middle trunk lesion E. Upper trunk lesion ## Footnote Although lower trunk lesions (B) resemble medial cord lesions (C), abnormalities of radially innervated C8 muscles are seen with the former, but not with the lat ter. Low-amplitude act ion potentials in the deltoid and biceps are seen in upper trunk lesions (E). Median sensory responses from the index and middle nger are abnormal, and motor conduction velocities of the hand muscles are normal in middle trunk lesions (D). Lateral cord lesions (A) cause weakness of the muscles supplied by the musculocutaneous nerve and the lateral root of the median nerve (innervates the forearm muscles). The int rinsic hand muscles innervated by the medial root of the median nerve are spared.7

Answer 123

A. Lateral cord lesion B. Lower trunk lesion **C. Medial cord lesion** D. Middle trunk lesion E. Upper trunk lesion ## Footnote Although lower trunk lesions (B) resemble medial cord lesions (C), abnormalities of radially innervated C8 muscles are seen with the former, but not with the lat ter. Low-amplitude act ion potentials in the deltoid and biceps are seen in upper trunk lesions (E). Median sensory responses from the index and middle nger are abnormal, and motor conduction velocities of the hand muscles are normal in middle trunk lesions (D). Lateral cord lesions (A) cause weakness of the muscles supplied by the musculocutaneous nerve and the lateral root of the median nerve (innervates the forearm muscles). The int rinsic hand muscles innervated by the medial root of the median nerve are spared.7

Answer 124

A. Lateral cord lesion B. Lower trunk lesion C. Medial cord lesion D. Middle trunk lesion **E. Upper trunk lesion** ## Footnote Although lower trunk lesions (B) resemble medial cord lesions (C), abnormalities of radially innervated C8 muscles are seen with the former, but not with the lat ter. Low-amplitude act ion potentials in the deltoid and biceps are seen in upper trunk lesions (E). Median sensory responses from the index and middle nger are abnormal, and motor conduction velocities of the hand muscles are normal in middle trunk lesions (D). Lateral cord lesions (A) cause weakness of the muscles supplied by the musculocutaneous nerve and the lateral root of the median nerve (innervates the forearm muscles). The int rinsic hand muscles innervated by the medial root of the median nerve are spared.7

Answer 125

**A. Lateral cord lesion** B. Lower trunk lesion C. Medial cord lesion D. Middle trunk lesion E. Upper trunk lesion ## Footnote Although lower trunk lesions (B) resemble medial cord lesions (C), abnormalities of radially innervated C8 muscles are seen with the former, but not with the lat ter. Low-amplitude act ion potentials in the deltoid and biceps are seen in upper trunk lesions (E). Median sensory responses from the index and middle nger are abnormal, and motor conduction velocities of the hand muscles are normal in middle trunk lesions (D). Lateral cord lesions (A) cause weakness of the muscles supplied by the musculocutaneous nerve and the lateral root of the median nerve (innervates the forearm muscles). The int rinsic hand muscles innervated by the medial root of the median nerve are spared.7

Answer 126

**A. Equal to that of the high-risk zone** B. Equal to that of the low-risk zone C. Intermediate between the two zones D. Lower than that of the low-risk zone E. Unpredictable ## Footnote Several studies indicate that a person migrating from a high-risk to a low-risk zone of MS before age 15 will develop a risk that is similar to the low-risk zone (B). If the migrat ion takes place after age 15, the risk is similar to that of natives of the high-risk zone (A).1

Answer 127

A. I, II, III B. I, III C. II, IV D. IV **E. All of the above**

Answer 128

A. Broca’s aphasia B. Conduction aphasia C. Global aphasia D**. Transcortical sensory aphasia** E. Wernicke’s aphasia ## Footnote Transcortical motor and sensory aphasias (D) are manifested by preserved repetit ion. Broca’s aphasia (A) is characterized by a disrupt ion of expressive speech with relative preservation of comprehension—repetition is impaired. Wernicke’s aphasia (E) is characterized by uent, articulate speech that lacks meaning with signi cant impairment of comprehension—repetition is impaired. Conduction aphasia (B) is characterized by uent speech and a relat ive preservation of comprehension, but with signi cant impairment of repetit ion. Global aphasia (C) is characterized by impairment of speech, comprehension, and repetition.1

Answer 129

A. Stage 1 B. Stage 2 C. Stage 3 D. Stage 4 E. **REM** ## Footnote Narcoleptic sleep at tacks tend to begin with REM sleep (E), rather than with non-REM (A–D) sleep as in the general population. This nding suggests that narcolepsy is not a condition of excessive dayt ime

Answer 130

A. **Enterovirus** B. Human immunode ciency virus (HIV) C. Leptospirosis D. Lymphocytic choriomeningitis E. Mumps ## Footnote The enteroviruses (A), which include echovirus, Coxsackie, and polio, represent the most common cause of viral meningitis. HIV (B) may cause a mononucleosis-like syndrome, and mumps (E) can be associated with meningitis, although this is not as common as enterovirus meningitis. Leptospirosis (C) is a spirochete and therefore not a cause of viral m eningitis.1

Answer 131

A. Meningitis B. Sarcoidosis C. Tumors of the brainstem D. Tumors of the cavernous sinus **E. Tumors of the clivus** ## Footnote Garcin’s (hemibasal) syndrome has been reported with chondromas or chondrosarcomas of the clivus.1

Answer 132

A. Distention of the endolymphatic duct occurs B. Hearing loss is usually unilateral **C. High-tone loss occurs early in the disease** D. Horizontal nystagmus occurs during an acute attack E. Low-pitched tinnitus is typical ## Footnote Ménière's disease is characterized by recurrent at tacks of vertigo and unilateral tinnitus and deafness (B). Distention of the endolymphatic duct is a characteristic pathologic change (A). Horizontal nystagmus may occur during an acute attack (D), and low-pitched tinnitus is typical (E). Early in Ménière's disease, deafness a ects mainly the low tones and uctuates in severity. Later in the disease, high tones are a ected (C is false).1

Answer 133

**A. Are more fatigable** B. Fire more tonically C. Have slower contraction and relaxation rates D. Have more mitochondria E. Have more oxidative enzymes ## Footnote Type I (red) muscle bers are richer in oxidative en zymes (E), poorer in glycolytic enzymes, contain more mitochondria (D) and myoglobin, re more tonically (B), have slower rates of contraction and relaxation (C), and are less fat igable (A is false) than type II (white) bers.1

Answer 134

A. Autonomic disturbances are seen B. Fasciculations are not seen C. It has been associated with carcinoma of the stomach and colon D. Temporary increase in muscle power may occur during the rst few contractions **E. Women are more frequently a ected than men** ## Footnote The Eaton-Lambert syndrome is due to decreased calcium-dependent release of acetylcholine quanta at the neuromuscular junct ion. A temporary increase in muscle power may be observed during the rst few contractions (D), in cont rast to myasthenia gravis. The disease process has been associated with carcinoma of the stomach and colon (C); autonomic disturbances are often observed (A), but fasciculations are not a presenting feature (B). Men are more often a ected than women (5:1; E is false).1

Answer 135

A. Anterior cerebral artery **B. Anterior choroidal artery** C. Middle cerebral artery D. Posterior communicating artery E. Recurrent artery of Huebner ## Footnote Infarction of the anterior choroidal artery may result in contralateral hemiplegia, hemihypesthesia, and homonymous hemianopia with sparing of cognitive and language funct ions. Historically, ligat ion of the anterior choroidal artery (B) was an early surgical treatment for pat ients with unilateral tremor and rigidity from Parkinson’s disease.1

Answer 136

A. Lower extremities are more commonly a ected than upper extremities B. Painful neuropathy C. Proximal extremities are more commonly a ected than distal extremities D. Recovery is usual **E. Symmetric neuropathy** ## Footnote Mononeuropathy multiplex of diabetes is classically asymmet ric (E is false). In pract ice, however, a con uence of mult iple mononeuropathies may lead to a symmet ric picture. The other answer choices are characterist ics of diabetic mononeuritis mult iplex: lower extremities are more commonly a ected than upper extremities (A), neuropathy tends to be painful (B), proximal extremities are more commonly a ected than distal extremities (C), and recovery is usual (D).1

Answer 137

A. Adrenocorticotropic hormone (ACTH) B. Ethosuximide **C. Lorazepam** D. Tegretol E. Valproic acid F. D or E ## Footnote Ben zodiazepines such as lorazepam (C) are the rst-line agents for the treatment of status epilepticus. Ethosuximide (B) is typically used for the treatment of absence seizures. ACTH (A) is employed in the t reatment of infantile spasms. Tegretol (D) and valproic acid (E) are acceptable alternatives for the t reatment of complex part ial seizures. Valproic acid (E) is sometimes used in the atypical petit mal syndrome of Lennox-Gastaut.1

Answer 138

A. Adrenocorticotropic hormone (ACTH) **B. Ethosuximide** C. Lorazepam D. Tegretol E. Valproic acid F. D or E ## Footnote Ben zodiazepines such as lorazepam (C) are the rst-line agents for the treatment of status epilepticus. Ethosuximide (B) is typically used for the treatment of absence seizures. ACTH (A) is employed in the t reatment of infantile spasms. Tegretol (D) and valproic acid (E) are acceptable alternatives for the t reatment of complex part ial seizures. Valproic acid (E) is sometimes used in the atypical petit mal syndrome of Lennox-Gastaut.1

Answer 139

A. Adrenocorticotropic hormone (ACTH) B. Ethosuximide C. Lorazepam D. Tegretol E. Valproic acid **F. D or E** ## Footnote Ben zodiazepines such as lorazepam (C) are the rst-line agents for the treatment of status epilepticus. Ethosuximide (B) is typically used for the treatment of absence seizures. ACTH (A) is employed in the t reatment of infantile spasms. Tegretol (D) and valproic acid (E) are acceptable alternatives for the t reatment of complex part ial seizures. Valproic acid (E) is sometimes used in the atypical petit mal syndrome of Lennox-Gastaut.1

Answer 140

**A. Adrenocorticotropic hormone (ACTH)** B. Ethosuximide C. Lorazepam D. Tegretol E. Valproic acid F. D or E ## Footnote Ben zodiazepines such as lorazepam (C) are the rst-line agents for the treatment of status epilepticus. Ethosuximide (B) is typically used for the treatment of absence seizures. ACTH (A) is employed in the t reatment of infantile spasms. Tegretol (D) and valproic acid (E) are acceptable alternatives for the t reatment of complex part ial seizures. Valproic acid (E) is sometimes used in the atypical petit mal syndrome of Lennox-Gastaut.1

Answer 141

A. Adrenocorticotropic hormone (ACTH) B. Ethosuximide C. Lorazepam D. Tegretol **E. Valproic acid** F. D or E ## Footnote Ben zodiazepines such as lorazepam (C) are the rst-line agents for the treatment of status epilepticus. Ethosuximide (B) is typically used for the treatment of absence seizures. ACTH (A) is employed in the t reatment of infantile spasms. Tegretol (D) and valproic acid (E) are acceptable alternatives for the t reatment of complex part ial seizures. Valproic acid (E) is sometimes used in the atypical petit mal syndrome of Lennox-Gastaut.1

Answer 142

A. Carcinoma a ects 9% of patients with polymyositis. B. It is most commonly associated with lung and prostate cancer in men. **C. It is usually painful.** D. Muscle biopsies show no evidence of tumor cells. E. Proximal muscles are initially a ected more than distal ones. ## Footnote Pain with polymyositis occurs in only 15% of patients and often suggests an additional disorder, such as rheumatoid arthritis (C is false). The other responses regarding polymyositis associated with carcinoma are true: carcinoma a ects 9% of patients with polymyositis (A), it is most commonly associated with lung and prostate cancer in men (B), muscle biopsies show no evidence of tumor cells (D), and proximal muscles are initially a ected more than distal ones (E).1

Answer 143

A. Associated with lacrimation and rhinorrhea **B. Bilateral location** C. Daily occurrence for 2 months D. Male predominance E. Orbital location ## Footnote Cluster headaches t ypically are recurrent for 6 to 12 weeks (C) in a unilateral (B is false) orbital (E) location. The male-to-female ratio is 4.5:1 to 6.7:1 (D). Lacrimation, rhinorrhea (A), ushing of the face, and other such parasympathet ic-type responses often accompany the headache

Answer 144

A. Bronchial spasms **B. Dry mouth** C. Miosis D. Sweating E. Vomiting

Answer 145

A. Decreased dopamine **B. Decreased GABA** C. Decreased norepinephrine D. Decreased somatostatin E. Increased acetylcholine ## Footnote Decreased glutamic acid decarboxylase (hence, decreased g-aminobutyric acid [GABA] [B]) and choline acetyltransferase (hence, decreased acetylcholine; E is false) have been found in the striatum and lateral pallidum in Hunt ington’s disease. Also reported has been increased norepinephrine and somatostatin in the striatum (C and D are false). An excess of dopamine or an increased sensitivity of striatal dopamine receptors has been postulated in the pathogenesis of Huntington’s disease (A is false).1

Answer 146

A. Anterior corpus callosum B. Bilateral anteroinferior temporal lobes **C. Bilateral medial temporo-occipital lobes** D. Occipital poles E. Posterior corpus callosum ## Footnote Prosopagnosia refers to the inability to identify a familiar face while retaining the ability to ident ify its features and is associated with injury to the bilateral medial temporo-occipital lobes (C).1

Answer 147

A. Echolalia B. Palilalia **C. Poverty of spontaneous speech** D. Receptive aphasia E. No speech abnormalities ## Footnote Injuries to the supplementary motor cortex are associated with mutism, contralateral motor neglect , and impairment of coordinat ion (C is correct).1

Answer 148

A. Abductor hallucis and gastrocnemius B. Extensor digitorum longus and brevis and abductor hallucis C. Gastrocnemius and exor hallucis longus **D. Tibialis anterior and extensor digitorum longus and brevis** E. Tibialis anterior and exor digitorum brevis ## Footnote Lesions of the peroneal nerve produce weakness of the tibialis anterior and extensor digitorum longus and brevis (D). The t ibialis anterior is innervated by the deep peroneal nerve, while the exor digitorum brevis is innervated by the medial plantar nerve, a branch of the tibial nerve (E is incorrect). The abductor hallucis is innervated by the medial plantar nerve (a branch of the tibial nerve), and the gastrocnemius is innervated by the t ibial nerve (A is incorrect). The extensor digitorum longus and brevis are innervated by the deep peroneal nerve, whereas the abductor hallucis is innervated by a branch of the t ibial nerve (B is incorrect). C is incorrect because the gast rocnemius and exor hallucis longus are innervated by the tibial nerve.3

Answer 149

**A. Corticospinal tract dysfunction** B. Dysnomia C. Korsako ’s amnesic state D. Personality change E. Spatial disorientation ## Footnote Corticospinal and corticosensory functions, visual acuit y, and visual elds are relatively preserved throughout the course of Alzheimer’s disease (A is false).1

Answer 150

**A. Abnormal startle response** B. Autosomal recessive inheritance C. Cherry red spots in the retina D. De ciency of sphingomyelinase E. Macrocephaly ## Footnote Tay-Sachs disease is characterized by macrocephaly (E), abnormal startle response (A), and cherry red spots in the retina (C). It is t ransmit ted via autosomal recessive inheritance (B). De ciency of hexoaminidase A characterizes Tay-Sachs disease (D is false), while sphingomyelinase de ciency is present in Niemann-Pick disease types A and B.1

Answer 151

A. Disturbances of autonomic function are common **B. High-dose steroids form the mainstay of therapy** C. Hypo- or are exia is characteristic D. The mortality rate is 3% E. The peak severity is 10 to 14 days after onset in 80% of cases ## Footnote Neither conventional dose nor high-dose steroids have been shown to be helpful in the treatment of Guillain-Barré syndrome (B is false). The other statements regarding the Guillain-Barré syndrome are true: disturbances of autonomic function are common (A), hypo- or are exia is characteristic (C), the mortality rate is 3% (D), and the peak severity is 10 to 14 days after onset in 80% of cases.1

Answer 152

A. Ciliary ganglion to the iris B. Edinger-Westphal nucleus to the ciliary ganglion C. Hypothalamus to the lateral horn cells at C8 to T3 **D. Lateral horn cells at C8 to T3 to the superior cervical ganglion** E. Superior cervical ganglion to the iris ## Footnote The pathway from the lateral horn cells at C8 to T3 to the superior cervical ganglion (D) constitutes the second-order neuron (preganglionic) in the sympathetic pathway to the pupil. Neurons from the hypothalamus to the lateral horn cells at C8 to T3 (C) constitute the rst-order neurons (central), and neurons projecting from the superior cervical ganglion to the iris (E) const itute the third-order neurons (postganglionic) in the sympathetic innervation of the pupil. Projections from the Edinger-Westphal nucleus to the ciliary ganglion (B) represent the parasympathet ic system

Answer 153

A. Penicillin B. Praziquantel **C. Pyrimethamine and sulfadiazine** D. Rifampin and nafcillin E. Thiabendazole ## Footnote The t reatment of choice for toxoplasmosis is oral sulfadiazine and pyrimethamine (C) for at least 4 weeks. Leucovorin is sometimes given as an adjuvant to counteract the antifolate e ects of pyrimethamine. Penicillin and nafcillin (A and D) are b-lactam ant ibiotics and are not an appropriate treatment for toxoplasmosis. Praziquantel (B) is used for the treatment of cysticercosis; albendazole is another option for cysticercosis treatment. Thiabendazole (E) is m ost commonly employed in the treatment of trichinosis.1

Answer 154

A. Intracytoplasmic but not intranuclear inclusions are found. B. It is more common in patients . 18 years of age. C. Lesions are con ned to the white matter. **D. The EEG shows characteristic periodic waves that occur every 2 to 3 seconds.** E. The CSF protein is normal ## Footnote Subacute sclerosing panencephalit is (SSPE), characterized by a progressive mental decline with seizures, myoclonus, and ataxia, mainly a ects children and adolescents (B is false). SSPE is thought to be the result of chronic measles infect ion. The lesions are found in both the cerebral cortex and white matter (C is false). Eosinophilic inclusions are found in both the cytoplasm and nuclei of neurons and glial cells (A is false). Elevated gamma globulin in the CSF is typical—that is, CSF protein tends to be increased (E is false). The EEG shows characteristic 2 to 3 per second waves (D is true).1

Answer 155

A. Intrathecal prednisolone **B. Intravenous methylprednisolone followed by oral prednisone** C. Oral prednisone only D. Oral prednisone followed by intravenous methylprednisolone E. Plasmapheresis ## Footnote Treatment with oral prednisone (C) alone actually increased the risk of new episodes of opt ic neuritis in a large randomized controlled study of optic neuritis t reatment. Intravenous methylprednisolone therapy followed by oral prednisone speeds recovery of visual loss (B is correct).1

Answer 156

A. Duchenne’s muscular dystrophy B. Krabbe’s disease **C. Multiple sclerosis** D. Trisomy 13 E. Tuberous sclerosis ## Footnote Schilder’s disease (C) is a demyelinat ing illness of children and young adults that has several features in common with chronic relapsing MS

Answer 157

**A. External branch of the superior laryngeal nerve** B. Internal laryngeal branch of the superior laryngeal nerve C. Ninth cranial nerve D. Recurrent laryngeal nerve E. Seventh cranial nerve ## Footnote The cricothyroid, supplied by the external laryngeal nerve (A), is the only in t rinsic laryngeal muscle not supplied by the recurrent laryngeal nerve (D). Cranial nerves VII (E) and IX (C) do not provide m otor innervat ion to the larynx.3

Answer 158

**A. Defect in learning and loss of past memories** B. Global confusional state C. Manic-depressive state D. Paranoid ideation E. Stupor or coma ## Footnote In Korsako ’s psychosis, retent ive memory is impaired out of proport ion to other cognitive functions in an otherwise alert pat ient.1

Answer 159

A. Are exia B. Autosomal recessive inheritance C. Hypotonia D. Involvement of chromosome 5q **E. Mental retardation** ## Footnote Werdnig-Ho mann disease is infantile spinal muscular atrophy, or SMA type I. SMA type I is characterized by neonatal hypotonia (C) and are exia (A). Inheritance is autosomal recessive (B) and has been linked to chromosome 5q (D). Mental retardation is not a feature of the spinal muscular atrophy of infancy and childhood (E), but may be associated with late-onset varieties of spinal muscular at rophy.1

Answer 160

A. I, II, III **B. I, III** C. II, IV D. IV E. All of the above ## Footnote Tricyclic antidepressants such as imipramine and amit ript yline block the reuptake of both norepinephrine and serotonin (I and III). Selective serotonin reuptake inhibitors such as citalopram or uoxetine prevent the reuptake of serotonin only (III). Monoamine oxidase inhibitors such as iproniazid and phenelzine prevent the oxidative deamination of monoamines (II).5

Answer 161

A. Amyotrophic lateral sclerosis (ALS) B. Cervical spondylosis **C. Both** D. Neither

Answer 162

A. Amyotrophic lateral sclerosis (ALS) B. Cervical spondylosis C. Both **D. Neithe**r

Answer 163

A. Amyotrophic lateral sclerosis (ALS) B. Cervical spondylosis C. **Both** D. Neither

Answer 164

**A. Amyotrophic lateral sclerosis (ALS)** B. Cervical spondylosis C. Both D. Neither

Answer 165

A. Amyotrophic lateral sclerosis (ALS) B. Cervical spondylosis **C. Both** D. Neither

Answer 166

A. Cogan’s syndrome B. Polyarteritis nodosa C. Systemic lupus erythematosus D. Takayasu’s syndrome E. Temporal arteritis **F. Wegener’s granulomatosis**

Answer 167

A. Cogan’s syndrome B. Polyarteritis nodosa **C. Systemic lupus erythematosus** D. Takayasu’s syndrome E. Temporal arteritis F. Wegener’s granulomatosis

Answer 168

A. Cogan’s syndrome B. Polyarteritis nodosa C. Systemic lupus erythematosus D. Takayasu’s syndrome E. Temporal arteritis **F. Wegener’s granulomatosis**

Answer 169

A. Cogan’s syndrome B. Polyarteritis nodosa C. Systemic lupus erythematosus **D. Takayasu’s syndrome** E. Temporal arteritis F. Wegener’s granulomatosis

Answer 170

A. Cogan’s syndrome **B. Polyarteritis nodosa** C. Systemic lupus erythematosus D. Takayasu’s syndrome E. Temporal arteritis F. Wegener’s granulomatosis

Answer 171

**A. Cogan’s syndrome** B. Polyarteritis nodosa C. Systemic lupus erythematosus D. Takayasu’s syndrome E. Temporal arteritis F. Wegener’s granulomatosis

Answer 172

**A. Defect in retentive memory out of proportion to other cognitive functions** B. Gait ataxia C. Gaze palsy D. Mental confusion E. Nystagmus

Answer 173

A. Astereognosis B. Lossofpositionsense **C. Loss of temperature sensation** D. Loss of two-point discrimination E. Atopognosia

Answer 174

A. Left calcarine cortex B. Left superior occipitotemporal region **C. Right inferior occipitotemporal region** D. Right occipital cortex and angular gyrus E. Right superior calcarine cortex

Answer 175

A. First-order Horner’s syndrome B. Second-order Horner’s syndrome **C. Third-order Horner’s syndrome** D. First- or second-order Horner’s syndrome E. Second- or third-order Horner’s syndrome

Answer 176

A. Stage 1 B. Stage 2 **C. Stage 4** D. REM E. Allof the above

Answer 177

A. Klonopin B. Clonidine C. Haloperidol (Haldol) **D. Imipramine (Tofranil)** E. Methylphenidate (Ritalin)

Answer 178

A. Apraxia of both hands to command **B. Apraxia of the left hand to command** C. Apraxia of the right hand to command D. Object agnosia E. Nodecit

Answer 179

A. Good comprehension, fluent speech, poor repetition B. Good comprehension, nonfluent speech, good repetition **C. Good comprehension, nonfluent speech, poor repetition** D. Poor comprehension, fuent speech, good repetition E. Poor comprehension, fuent speech, poor repetition F. Poor comprehension, nonfluent speech, poor repetition

Answer 180

**A. Good comprehension, fluent speech, poor repetition** B. Good comprehension, nonfluent speech, good repetition C. Good comprehension, nonfluent speech, poor repetition D. Poor comprehension, fuent speech, good repetition E. Poor comprehension, fuent speech, poor repetition F. Poor comprehension, nonfluent speech, poor repetition

Answer 181

A. Good comprehension, fluent speech, poor repetition B. Good comprehension, nonfluent speech, good repetition C. Good comprehension, nonfluent speech, poor repetition D. Poor comprehension, fuent speech, good repetition E. Poor comprehension, fuent speech, poor repetition **F. Poor comprehension, nonfluent speech, poor repetition**

Answer 182

A. Good comprehension, fluent speech, poor repetition **B. Good comprehension, nonfluent speech, good repetition** C. Good comprehension, nonfluent speech, poor repetition D. Poor comprehension, fuent speech, good repetition E. Poor comprehension, fuent speech, poor repetition F. Poor comprehension, nonfluent speech, poor repetition

Answer 183

A. Good comprehension, fluent speech, poor repetition B. Good comprehension, nonfluent speech, good repetition C. Good comprehension, nonfluent speech, poor repetition **D. Poor comprehension, fuent speech, good repetition** E. Poor comprehension, fuent speech, poor repetition F. Poor comprehension, nonfluent speech, poor repetition

Answer 184

A. Good comprehension, fluent speech, poor repetition B. Good comprehension, nonfluent speech, good repetition C. Good comprehension, nonfluent speech, poor repetition D. Poor comprehension, fuent speech, good repetition **E. Poor comprehension, fuent speech, poor repetition** F. Poor comprehension, nonfluent speech, poor repetition

Answer 185

A. Dermatomyositis B. Polymyositis **C. Both** D. Neither

Answer 186

A. Dermatomyositis B. Polymyositis C. Both **D. Neither**

Answer 187

A. Dermatomyositis **B. Polymyositis** C. Both D. Neither

Answer 188

**A. Dermatomyositis** B. Polymyositis C. Both D. Neither

Answer 189

A. Dermatomyositis **B. Polymyositis** C. Both D. Neither

Answer 190

**A. Dermatomyositis** B. Polymyositis C. Both D. Neither

Answer 191

A. Dermatomyositis B. Polymyositis C. Both **D. Neither**

Answer 192

**A. Carbamazepine** B. Gabapentin C. Levetiracetam D. Phenytoin E. Topiramate

Answer 193

A. Both ictal and interictal SPECT studies can be acquired and compared for seizure localization B. Ictal SPECT scans are generally easier to acquire than ictal PET scans **C. Ictal SPECT scans show decreased tracer signal in the seizure focus** D. Perfusion follows changes in metabolism during seizures E. Tracer needs to be injected within 1–2 minutes of seizure onset for an ictal SPECT study

Answer 194

A. Diabetes B. HIV **C. Neurocysticercosis** D. Polyarteritis nodosa E. Sarcoidosis

Answer 195

A. 1,3 **B. 3,4.5** C. 4.5,6 D. 6,8 E. 8,10

Answer 196

A. 3 B. 4.5 **C. 6** D. 8 E. 12

Answer 197

A. 3 B. 4.5 C. 6 **D. 8** E. 12

Answer 198

A. Contraindication to intravenous tPA B. Di usion-perfusion mismatch C. Failure to improve with intravenous tPA **D. NIH stroke score of . 20** E. Patient presents outside the therapeutic window for intravenous tPA