clinical neurology 100-130 Flashcards
Wernicke's area corresponds most closely to Brodmann's area(s) A. 17 B. 19 C. 22 D. 41 and 42 E. 44
C 22
Complications of diabetes generally thought to be vascular in origin include I. ophthalmoplegia 11. acute mononeuropathy 111. mononeuritis multiplex IV. distal sensorimotor polyneuropathy A. I, 11,111 B. I, I11 C. 11, IV D. IV E. all of the above
A.I. ophthalmoplegia
11. acute mononeuropathy
111. mononeuritis multiplex
Mer p. 624, V&A pp. 1396-1398. The progressive sensorimotor polyneuro- pathy is generally (but not universally) thought to be metabolic in origin.
Each of the following is consistent with a cholinergic crisis in a patient with myasthenia gravis being treated with pyridostigmine (Mestinon) except
A. bradycardia
B. diarrhea
C. increased strength after the Tensilon test
D. miosis
E. sweating
C.increased strength after the Tensilon test
V&A p. 1544. The weakness of a cholinergic crisis is unaffected by Tensilon (edrophonium).
The genetic transmission of the MELAS syndrome is A. autosomal dominant B. autosomal recessive C. maternal inheritance D. sporadic E. X-linked recessive
C. maternal inheritance
V&A p. 985. The MELAS syndrome is a mitochondria1 disease associated with a maternal inheritance.
acute hyperextension A. anterior cord syndrome B. Brown-Sequard syndrome C. central cord syndrome D. AandB E. none of the above
C. central cord syndrome
flexion injury A. anterior cord syndrome B. Brown-Sequard syndrome C. central cord syndrome D. AandB E. none of the above
A. anterior cord syndrome
dissociated sensory loss A. anterior cord syndrome B. Brown-Sequard syndrome C. central cord syndrome D. AandB E. none of the above
A. anterior cord syndrome
Among the incomplete syndromes, this has the best prognosis. A. anterior cord syndrome B. Brown-Sequard syndrome C. central cord syndrome D. AandB E. none of the above *
C. central cord syndrome
dreaming A. REM sleep B. non-rapid eye movement (NREM) sleep C. both D. neither
C. both
adult somnambulism A. REM sleep B. non-rapid eye movement (NREM) sleep C. both D. neither
B. non-rapid eye movement (NREM) sleep
desynchronization of the EEG A. REM sleep B. non-rapid eye movement (NREM) sleep C. both D. neither
A.REM sleep
K complexes A. REM sleep B. non-rapid eye movement (NREM) sleep C. both D. neither
B. non-rapid eye movement (NREM) sleep
sleep spindles A. REM sleep B. non-rapid eye movement (NREM) sleep C. both D. neither
B. non-rapid eye movement (NREM) sleep
Glucose metabolism in the brain is increased in comparison to the waking state.
A. REM sleep
B. non-rapid eye movement (NREM) sleep
C. both
D. neither
A. REM sleep
For questions 108-113 see V&A pp. 405-407. Although most dreams occur inrapid eye movement (REM) sleep, they can occur in non-REM (NREM) sleep.Adult somnambulism, K complexes, and sleep spindles all occur in NREM sleep (the latter two in stage 2). Glucose metabolism in the brain isincreased in REM and decreased in NREM sleep in comparison to the wakingstate.
myophosphorylase deficiency
A. glycogen storage disease type 11 (acid maltase deficiency)
B. glycogen storage disease type V (McArdle’s disease)
C. both
D. neither
B. glycogen storage disease type V (McArdle’s disease)
Large amounts of glycogen are deposited in various organs.
A. glycogen storage disease type 11 (acid maltase deficiency)
B. glycogen storage disease type V (McArdle’s disease)
C. both
D. neither
A. glycogen storage disease type 11 (acid maltase deficiency)
Three clinical forms are noted.
A. glycogen storage disease type 11 (acid maltase deficiency)
B. glycogen storage disease type V (McArdle’s disease)
C. both
D. neither
A. glycogen storage disease type 11 (acid maltase deficiency)
X-linked recessive inheritance
A. glycogen storage disease type 11 (acid maltase deficiency)
B. glycogen storage disease type V (McArdle’s disease)
C. both
D. neither
D. neither
For questions 114-117 see V&A pp. 1513-1516. Glycogen storage disease type I1results from acid maltase (alpha-1,4-glucosidase) deficiency and has threeforms: childhood (Pompe’s disease), childhood, and adult forms. Glycogenaccumulates in lysosomes throughout the body. Glycogen storage diseasetype V (McArdle’s disease) results from myophosphorylase deficiency.Glycogen cannot be converted to glucose-6-phosphate, and the blood lactatedoes not rise after ischemic exercise. Both types
Wilson's disease is characterized by I. high urinary copper excretion 11. high serum copper 111. low ceruloplasmin levels IV. hyperdensity of the globus pallidus and putamen on CT A. I, 11, 111 B. I, I11 C. 11, IV D. IVE. all of the above
B. high urinary copper excretion, . low ceruloplasmin levels
V&A pp. 1026-1030. Wilson’s disease is characterized by an increased urinarycopper excretion, low serum copper levels, and low ceruloplasminlevels. The computed tomographic (CT) scan sometimes shows hypodenseareas in the lenticular nuclei.
Each of the following is true of central pontine myelinolysis except
A. A marked inflammatory response with destruction of nerve cells in thepons 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.
A. A marked inflammatory response with destruction of nerve cells in thepons is seen.
V&A p. 1193. Microscopically, destruction of the medullated sheaths withrelative sparing of the axis cylinders and preservation of nerve cells in thepons is seen. An inflammatory response is absent.
arachnodactyly A. homocystinuria B. Marfan's syndrome C. both D. neither
C. both
mental retardation A. homocystinuria B. Marfan's syndrome C. both D. neither
A. homocystinuria
brain infarcts A. homocystinuria B. Marfan's syndrome C. both D. neither
A. homocystinuria
For questions 120-122 see V&A p. 1037. Patients with homocystinuria andthose with Marfan’s syndrome have a tall, thin frame and arachnodactyly.Patients with homocystinuria (cystathione synthase deficiency) also showevidence of mental retardation and are prone to strokes.
Dressing apraxia is associated with a lesion in the A. dominant frontal lobe B. dominant parietal lobe C. nondominant frontal lobe D. nondominant parietal lobe E. nondominant temporal lobe
D. nondominant parietal lobe
The axillary nerve innervates the A. coracobrachialis B. rhomboids C. supraspinatus D. teres major E. teres minor
E. teres minor
All of the following are seen in Sturge-Weber syndrome except
A. calcified cortical vessels
B. facial nevus contralateral to seizure activity
C. hemisensory deficit contralateral to facial nevus
D. meningeal venous angiomas
E. tramline calcifications outlining the convolution of the parieto-occipital
cortex
A. calcified cortical vessels
V&A p. 1078. Skull films may reveal “tramline calcification” is present in the
parieto-occipital cortical substance, not the vessels.
The normal sensory nerve conduction velocity in the median and ulnar nerves is approximately A. 10 meters per second (mls) B. 25 m/s C. 50 m/s D. 100 m/s' E. 150 m/s
C. 50 m/s
Each of these statements is true of Charcot-Marie-Tooth disease except
A. Autosomal dominance is the usual mode of inheritance.
B. Distal muscle atrophy is prominent.
C. It can affect the upper extremities.
D. Steroids have no effect on disease progression.
E. The autonomic nervous system is usually involved.
E. he autonomic nervous system is usually involved.
V&A pp. 1417-1419. The autonomic nervous system is usually not involved in
Charcot-Marie-Tooth disease.
Cranial nerves that may be affected by a clival chordoma include I. cranial nerve XI1 11. cranial nerve V 111. cranial nerve X IV. cranial nerve I1 A. I, 11, I11 B. I, 111 C. 11, IV D. IV E. all of the above
E. I. cranial nerve XI1
11. cranial nerve V
111. cranial nerve X
IV. cranial nerve I1
Which of the following CSF findings is least consistent with tuberculous
meningitis?
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%
E. white blood cell count (WBC) of 200 cells/mm3
D. protein of 35 mg%
V&A p. 758. The protein is elevated in tuberculous meningitis; usually 100 to
200 mg/dL.
The syndrome of PICA occlusion results in all of the following except
A. contralateral Horner’s syndrome
B. contralateral loss of pain and temperature over the body
C. ipsilateral ataxia
D. ipsilateral numbness of the limbs
E. ipsilateral paralysis of the palate
A. contralateral Horner’s syndrome
V&A pp. 844-845. lpsilateral Horner’s syndrome is seen in the posteroinferior
cerebellar artery (PICA) occlusion syndrome.
