Clinical Neurology Flashcards
A common sign of multiple sclerosis
A. Convergence nystagmus
B. Dissociated nystagmus (internuclear ophthalmoplegia)
C. Downbeat nystagmus
D. Impairment of optokinetic nystagmus
E. Ocular bobbing
F. Seesaw nystagmus
G. Spasmus mutans
A. Convergence nystagmus
B. Dissociated nystagmus (internuclear ophthalmoplegia)
C. Downbeat nystagmus
D. Impairment of optokinetic nystagmus
E. Ocular bobbing
F. Seesaw nystagmus
G. Spasmus mutans
Convergence nystagmus (A) is a “rhythmic oscillation in w hich a slow abduction
of the eyes with respect to each other is followed by a quick movement
of adduction,” and may be accompanied by other signs of Parinaud’s phenomenon,
suggesting a lesion of the pineal region or midbrain tegmentum.
Dissociated nystagmus (B) is horizontal nystagmus that occurs only in the
abducting eye—this is a sign of internuclear ophthalmoplegia and is associated
with multiple sclerosis. Downbeat nystagmus (C) has been associated
with lesions of the cervicomedullary junction including Chiari malformation,
syrinx, and basilar invaginat ion. Impairment of optokinetic nystagmus (D)
is associated with lesions to the parietal lobe—“the slow pursuit phase of the
OKN may be lost . . . when a moving st imulus . . . is rotated toward the side of
the lesion.” Ocular bobbing (E) involves a “spontaneous fast downward jerk
of the eyes followed by a slow upward drift to midposition,” and has been associated
with large destruct ive lesions of the pons. Seesaw nystagmus (F) is
a “torsional-vertical oscillation in which the intorting eye moves up and the
opposite (extort ing) eye moves down, then both move in the reverse direction.”
Seesaw nystagmus (F) has been associated w ith chiasmatic bitemporal
hemianopsia due to lesions of the parasellar region. Spasmus mutans (G) is
a pendular nystagmus of infancy that is typically idiopathic and self-limited.1
Most often associated with large destructive lesions of the pons
A. Convergence nystagmus
B. Dissociated nystagmus (internuclear ophthalmoplegia)
C. Downbeat nystagmus
D. Impairment of optokinetic nystagmus
E. Ocular bobbing
F. Seesaw nystagmus
G. Spasmus mutans
A. Convergence nystagmus
B. Dissociated nystagmus (internuclear ophthalmoplegia)
C. Downbeat nystagmus
D. Impairment of optokinetic nystagmus
E. Ocular bobbing
F. Seesaw nystagmus
G. Spasmus mutans
Convergence nystagmus (A) is a “rhythmic oscillation in w hich a slow abduction
of the eyes with respect to each other is followed by a quick movement
of adduction,” and may be accompanied by other signs of Parinaud’s phenomenon,
suggesting a lesion of the pineal region or midbrain tegmentum.
Dissociated nystagmus (B) is horizontal nystagmus that occurs only in the
abducting eye—this is a sign of internuclear ophthalmoplegia and is associated
with multiple sclerosis. Downbeat nystagmus (C) has been associated
with lesions of the cervicomedullary junction including Chiari malformation,
syrinx, and basilar invaginat ion. Impairment of optokinetic nystagmus (D)
is associated with lesions to the parietal lobe—“the slow pursuit phase of the
OKN may be lost . . . when a moving st imulus . . . is rotated toward the side of
the lesion.” Ocular bobbing (E) involves a “spontaneous fast downward jerk
of the eyes followed by a slow upward drift to midposition,” and has been associated
with large destruct ive lesions of the pons. Seesaw nystagmus (F) is
a “torsional-vertical oscillation in which the intorting eye moves up and the
opposite (extort ing) eye moves down, then both move in the reverse direction.”
Seesaw nystagmus (F) has been associated w ith chiasmatic bitemporal
hemianopsia due to lesions of the parasellar region. Spasmus mutans (G) is
a pendular nystagmus of infancy that is typically idiopathic and self-limited.1
Seen exclusively in infants
A. Convergence nystagmus
B. Dissociated nystagmus (internuclear ophthalmoplegia)
C. Downbeat nystagmus
D. Impairment of optokinetic nystagmus
E. Ocular bobbing
F. Seesaw nystagmus
G. Spasmus mutans
A. Convergence nystagmus
B. Dissociated nystagmus (internuclear ophthalmoplegia)
C. Downbeat nystagmus
D. Impairment of optokinetic nystagmus
E. Ocular bobbing
F. Seesaw nystagmus
G. Spasmus mutans
Convergence nystagmus (A) is a “rhythmic oscillation in w hich a slow abduction
of the eyes with respect to each other is followed by a quick movement
of adduction,” and may be accompanied by other signs of Parinaud’s phenomenon,
suggesting a lesion of the pineal region or midbrain tegmentum.
Dissociated nystagmus (B) is horizontal nystagmus that occurs only in the
abducting eye—this is a sign of internuclear ophthalmoplegia and is associated
with multiple sclerosis. Downbeat nystagmus (C) has been associated
with lesions of the cervicomedullary junction including Chiari malformation,
syrinx, and basilar invaginat ion. Impairment of optokinetic nystagmus (D)
is associated with lesions to the parietal lobe—“the slow pursuit phase of the
OKN may be lost . . . when a moving st imulus . . . is rotated toward the side of
the lesion.” Ocular bobbing (E) involves a “spontaneous fast downward jerk
of the eyes followed by a slow upward drift to midposition,” and has been associated
with large destruct ive lesions of the pons. Seesaw nystagmus (F) is
a “torsional-vertical oscillation in which the intorting eye moves up and the
opposite (extort ing) eye moves down, then both move in the reverse direction.”
Seesaw nystagmus (F) has been associated w ith chiasmatic bitemporal
hemianopsia due to lesions of the parasellar region. Spasmus mutans (G) is
a pendular nystagmus of infancy that is typically idiopathic and self-limited.1
Associated with lesions of the cervicomedullary junction
A. Convergence nystagmus
B. Dissociated nystagmus (internuclear ophthalmoplegia)
C. Downbeat nystagmus
D. Impairment of optokinetic nystagmus
E. Ocular bobbing
F. Seesaw nystagmus
G. Spasmus mutans
A. Convergence nystagmus
B. Dissociated nystagmus (internuclear ophthalmoplegia)
C. Downbeat nystagmus
D. Impairment of optokinetic nystagmus
E. Ocular bobbing
F. Seesaw nystagmus
G. Spasmus mutans
Convergence nystagmus (A) is a “rhythmic oscillation in w hich a slow abduction
of the eyes with respect to each other is followed by a quick movement
of adduction,” and may be accompanied by other signs of Parinaud’s phenomenon,
suggesting a lesion of the pineal region or midbrain tegmentum.
Dissociated nystagmus (B) is horizontal nystagmus that occurs only in the
abducting eye—this is a sign of internuclear ophthalmoplegia and is associated
with multiple sclerosis. Downbeat nystagmus (C) has been associated
with lesions of the cervicomedullary junction including Chiari malformation,
syrinx, and basilar invaginat ion. Impairment of optokinetic nystagmus (D)
is associated with lesions to the parietal lobe—“the slow pursuit phase of the
OKN may be lost . . . when a moving st imulus . . . is rotated toward the side of
the lesion.” Ocular bobbing (E) involves a “spontaneous fast downward jerk
of the eyes followed by a slow upward drift to midposition,” and has been associated
with large destruct ive lesions of the pons. Seesaw nystagmus (F) is
a “torsional-vertical oscillation in which the intorting eye moves up and the
opposite (extort ing) eye moves down, then both move in the reverse direction.”
Seesaw nystagmus (F) has been associated w ith chiasmatic bitemporal
hemianopsia due to lesions of the parasellar region. Spasmus mutans (G) is
a pendular nystagmus of infancy that is typically idiopathic and self-limited.1
Associated with lesions of the parasellar region
A. Convergence nystagmus
B. Dissociated nystagmus (internuclear ophthalmoplegia)
C. Downbeat nystagmus
D. Impairment of optokinetic nystagmus
E. Ocular bobbing
F. Seesaw nystagmus
G. Spasmus mutans
A. Convergence nystagmus
B. Dissociated nystagmus (internuclear ophthalmoplegia)
C. Downbeat nystagmus
D. Impairment of optokinetic nystagmus
E. Ocular bobbing
F. Seesaw nystagmus
G. Spasmus mutans
Convergence nystagmus (A) is a “rhythmic oscillation in w hich a slow abduction
of the eyes with respect to each other is followed by a quick movement
of adduction,” and may be accompanied by other signs of Parinaud’s phenomenon,
suggesting a lesion of the pineal region or midbrain tegmentum.
Dissociated nystagmus (B) is horizontal nystagmus that occurs only in the
abducting eye—this is a sign of internuclear ophthalmoplegia and is associated
with multiple sclerosis. Downbeat nystagmus (C) has been associated
with lesions of the cervicomedullary junction including Chiari malformation,
syrinx, and basilar invaginat ion. Impairment of optokinetic nystagmus (D)
is associated with lesions to the parietal lobe—“the slow pursuit phase of the
OKN may be lost . . . when a moving st imulus . . . is rotated toward the side of
the lesion.” Ocular bobbing (E) involves a “spontaneous fast downward jerk
of the eyes followed by a slow upward drift to midposition,” and has been associated
with large destruct ive lesions of the pons. Seesaw nystagmus (F) is
a “torsional-vertical oscillation in which the intorting eye moves up and the
opposite (extort ing) eye moves down, then both move in the reverse direction.”
Seesaw nystagmus (F) has been associated w ith chiasmatic bitemporal
hemianopsia due to lesions of the parasellar region. Spasmus mutans (G) is
a pendular nystagmus of infancy that is typically idiopathic and self-limited.1
Associated with lesions of the parietal lobe
A. Convergence nystagmus
B. Dissociated nystagmus (internuclear ophthalmoplegia)
C. Downbeat nystagmus
D. Impairment of optokinetic nystagmus
E. Ocular bobbing
F. Seesaw nystagmus
G. Spasmus mutans
A. Convergence nystagmus
B. Dissociated nystagmus (internuclear ophthalmoplegia)
C. Downbeat nystagmus
D. Impairment of optokinetic nystagmus
E. Ocular bobbing
F. Seesaw nystagmus
G. Spasmus mutans
Convergence nystagmus (A) is a “rhythmic oscillation in w hich a slow abduction
of the eyes with respect to each other is followed by a quick movement
of adduction,” and may be accompanied by other signs of Parinaud’s phenomenon,
suggesting a lesion of the pineal region or midbrain tegmentum.
Dissociated nystagmus (B) is horizontal nystagmus that occurs only in the
abducting eye—this is a sign of internuclear ophthalmoplegia and is associated
with multiple sclerosis. Downbeat nystagmus (C) has been associated
with lesions of the cervicomedullary junction including Chiari malformation,
syrinx, and basilar invaginat ion. Impairment of optokinetic nystagmus (D)
is associated with lesions to the parietal lobe—“the slow pursuit phase of the
OKN may be lost . . . when a moving st imulus . . . is rotated toward the side of
the lesion.” Ocular bobbing (E) involves a “spontaneous fast downward jerk
of the eyes followed by a slow upward drift to midposition,” and has been associated
with large destruct ive lesions of the pons. Seesaw nystagmus (F) is
a “torsional-vertical oscillation in which the intorting eye moves up and the
opposite (extort ing) eye moves down, then both move in the reverse direction.”
Seesaw nystagmus (F) has been associated w ith chiasmatic bitemporal
hemianopsia due to lesions of the parasellar region. Spasmus mutans (G) is
a pendular nystagmus of infancy that is typically idiopathic and self-limited.1
Associated with lesions of the pineal region
A. Convergence nystagmus
B. Dissociated nystagmus (internuclear ophthalmoplegia)
C. Downbeat nystagmus
D. Impairment of optokinetic nystagmus
E. Ocular bobbing
F. Seesaw nystagmus
G. Spasmus mutans
A. Convergence nystagmus
B. Dissociated nystagmus (internuclear ophthalmoplegia)
C. Downbeat nystagmus
D. Impairment of optokinetic nystagmus
E. Ocular bobbing
F. Seesaw nystagmus
G. Spasmus mutans
Convergence nystagmus (A) is a “rhythmic oscillation in w hich a slow abduction
of the eyes with respect to each other is followed by a quick movement
of adduction,” and may be accompanied by other signs of Parinaud’s phenomenon,
suggesting a lesion of the pineal region or midbrain tegmentum.
Dissociated nystagmus (B) is horizontal nystagmus that occurs only in the
abducting eye—this is a sign of internuclear ophthalmoplegia and is associated
with multiple sclerosis. Downbeat nystagmus (C) has been associated
with lesions of the cervicomedullary junction including Chiari malformation,
syrinx, and basilar invaginat ion. Impairment of optokinetic nystagmus (D)
is associated with lesions to the parietal lobe—“the slow pursuit phase of the
OKN may be lost . . . when a moving st imulus . . . is rotated toward the side of
the lesion.” Ocular bobbing (E) involves a “spontaneous fast downward jerk
of the eyes followed by a slow upward drift to midposition,” and has been associated
with large destruct ive lesions of the pons. Seesaw nystagmus (F) is
a “torsional-vertical oscillation in which the intorting eye moves up and the
opposite (extort ing) eye moves down, then both move in the reverse direction.”
Seesaw nystagmus (F) has been associated w ith chiasmatic bitemporal
hemianopsia due to lesions of the parasellar region. Spasmus mutans (G) is
a pendular nystagmus of infancy that is typically idiopathic and self-limited.1
Which of the following is false of seizure foci?
A. Epileptic foci are slower in binding and removing acetylcholine than normal
cortex.
B. Firing of neurons in the focus is re ected by periodic spike discharges in the
electroencephalogram (EEG).
C. If unchecked, cortical excitation may spread to the subcortical nuclei.
D. Neurons surrounding the focus are initially hyperpolarized and are
GABAergic.
E. The change in seizure discharge from the tonic phase to the clonic phase
results from inhibition from the neurons surrounding the focus.
A. Epileptic foci are slower in binding and removing acetylcholine than normal
cortex.
B. Firing of neurons in the focus is re ected by periodic spike discharges in the
electroencephalogram (EEG).
C. If unchecked, cortical excitation may spread to the subcortical nuclei.
D. Neurons surrounding the focus are initially hyperpolarized and are
GABAergic.
E. The change in seizure discharge from the tonic phase to the clonic phase
results from inhibition from the neurons surrounding the focus.
The change from the tonic to the clonic phase results from diencephalic
inhibition of the ring cortex, not from inhibit ion of the neurons surrounding
the focus as described in (E). The other statements are true: Epileptic foci
are slower in binding and removing acetylcholine than normal cortex (A);
ring of neurons in the focus is re ected by periodic spike discharges in the
electroencephalogram (B); if unchecked, cortical excitation may spread to
the subcort ical nuclei (C); and neurons surrounding the focus are initially
hyperpolarized and are GABAergic (D).1
An abnormal optokinetic response is more likely to be obtained by rotating the
optokinetic nystagmus drum
A. Away from an occipital lobe lesion
B. Away from a parietal lobe lesion
C. Toward an occipital lobe lesion
D. Toward a parietal lobe lesion
E. Toward a temporal lobe lesion
A. Away from an occipital lobe lesion
B. Away from a parietal lobe lesion
C. Toward an occipital lobe lesion
D. Toward a parietal lobe lesion
E. Toward a temporal lobe lesion
An abnormal optokinetic response (loss of the slow pursuit phase) is more
likely to be obtained by rotating the optokinetic nystagmus drum toward a
parietal lobe lesion (D).1
4 to 7 Hz
A. Alpha
B. Beta
C. Delta
D. Theta
E. 3-per-second spike and wave
A. Alpha
B. Beta
C. Delta
D. Theta
E. 3-per-second spike and wave
Normally may be present over the temporal lobes of the elderly
A. Alpha
B. Beta
C. Delta
D. Theta
E. 3-per-second spike and wave
A. Alpha
B. Beta
C. Delta
D. Theta
E. 3-per-second spike and wave
Recorded from the frontal lobes symmetrically
A. Alpha
B. Beta
C. Delta
D. Theta
E. 3-per-second spike and wave
A. Alpha
B. Beta
C. Delta
D. Theta
E. 3-per-second spike and wave
Associated with absence seizures
A. Alpha
B. Beta
C. Delta
D. Theta
E. 3-per-second spike and wave
A. Alpha
B. Beta
C. Delta
D. Theta
E. 3-per-second spike and wave
Attenuated or abolished with eye opening or mental activity
A. Alpha
B. Beta
C. Delta
D. Theta
E. 3-per-second spike and wave
A. Alpha
B. Beta
C. Delta
D. Theta
E. 3-per-second spike and wave
Alpha waves (A) are 8–12 Hz waves that are present in the occipital and parietal
region and are at tenuated or abolished with eye opening or mental
activity. Beta waves (B) are of faster frequency (. 12 Hz) and lower amplitude
than a waves and are recorded from the frontal areas symmetrically.
Theta waves (D) are 4–7 Hz, and m ay be present over the temporal regions—
especially in the elderly. Delta waves (C) are 1–3 Hz and are not present in
the normal waking adult. A 3-per-second spike and wave (E) EEG pat tern is
associated with absence seizures.1
Which of the following drugs is least e ective in the treatment of trigeminal
neuralgia?
A. Baclofen
B. Carbamazepine
C. Clonazepam
D. Phenytoin
E. Ketorolac tromethamine (Toradol)
A. Baclofen
B. Carbamazepine
C. Clonazepam
D. Phenytoin
E. Ketorolac tromethamine (Toradol)
Of the options listed, ketorolac (Toradol [E]), a nonsteroidal ant i-in ammatory
drug (NSAID), is the least e ect ive in relieving the pain of trigeminal
neuralgia. Anticonvulsants such as carbamazepine (B), clonazepam (C), and
phenytoin (D) are often useful. Baclofen (A) is m ost helpful as an adjunct to
one of the ant iconvulsant drugs.1
Which of the following is true of papilledema?
A. Absence of venous pulsations is a reliable indicator of papilledema.
B. Pupillary light re exes remain normal.
C. The congested capillaries derive from the central retinal vein.
D. Unilateral edema of the optic disk is never seen.
E. Visual acuity usually decreases.
A. Absence of venous pulsations is a reliable indicator of papilledema.
B. Pupillary light re exes remain normal.
C. The congested capillaries derive from the central retinal vein.
D. Unilateral edema of the optic disk is never seen.
E. Visual acuity usually decreases.
Venous pulsations are absent in 10 to 15% of normal individuals (A is
incorrect). The congested capillaries are derived from the short ciliary arteries
(C is incorrect). Unilateral edema can occur with optic nerve tumors
(D is incorrect). Visual acuity is usually normal in papilledema (E is incorrect).
Pupillary light re exes typically remain normal in papilledema (B).1
Which of the following can occur in glossopharyngeal neuralgia?
I. Pain in the throat
II. Syncope
III. Pain in the ear
IV. Bradycardia
A. I, II, III
B. I, III
C. II, IV
D. IV
E. All of the above
Glossopharyngeal neuralgia is less common than t rigeminal neuralgia and
is characterized by pain in the throat (I) that is often exacerbated by swallowing,
talking, or yawning. Pain may also radiate to the ear (III). Abnormal
a erent inputs to cardioregulatory centers may trigger syncope (II) or
bradycardia (IV), which are not associated with trigeminal neuralgia or hemifacial
spasm.1
Features of trisomy 13 (Patau’s syndrome) include
I. Microcephaly
II. Hypertonia
III. Cleft lip and palate
IV. Dextrocardia
A. I, II, III
B. I, III
C. II, IV
D. IV
E. All of the above
Trisomy 13, or Patau’s syndrome, is characterized by microcephaly (I),
hypertonia (II), cleft lip and palate (III), and dextrocardia (IV). Other features
of this dysgenetic syndrome include corneal opacities, polydactyly, impaired
hearing, and severe mental retardat ion. Death usually occurs in early childhood.
Trisomy 18, Edwards’ syndrome, is characterized by low-set ears,
micrognathia, mental retardation, and rocker-bot tom feet.1
Which of the following is not a feature of Parinaud’s syndrome?
A. Dissociated light–near response
B. Lid retraction
C. Nystagmus retractorius
D. Paralysis of upgaze
E. Third nerve palsy
A. Dissociated light–near response
B. Lid retraction
C. Nystagmus retractorius
D. Paralysis of upgaze
E. Third nerve palsy
Parinaud’s syndrome (dorsal midbrain syndrome) is a constellat ion of symptoms
that include paralysis of upgaze (D), mydriasis and lid retraction (B),
nystagmus retractorius (C), and a dissociated light-near response (A).
Third nerve palsy (E) is not associated w ith Parinaud’s syndrome.1
Which of the following is true of tuberculous meningitis?
A. Headache is usually absent.
B. If untreated, the clinical course is self-limited.
C. The in ammatory exudate is con ned to the subarachnoid space.
D. The in ammatory exudate is found mainly at the convexities.
E. The protein content of the cerebrospinal uid (CSF) is almost always
elevated
A. Headache is usually absent.
B. If untreated, the clinical course is self-limited.
C. The in ammatory exudate is con ned to the subarachnoid space.
D. The in ammatory exudate is found mainly at the convexities.
E. The protein content of the cerebrospinal uid (CSF) is almost always
elevated
Headache occurs in more than half of cases (A is incorrect). Confusion, coma,
and death usually result if the patient is unt reated (B is incorrect). The inammatory
exudate occurs mainly in the basal meninges and frequently invades
the underlying brain by spreading via pial vessels (C is incorrect). The
CSF protein is always elevated to 100 to 200 mg/dL or higher (E).1
Which of the following CSF ndings is least suggest ive of acute multiple sclerosis?
A. An IgG index greater than 1.7
B. Increased myelin basic protein
C. Increased protein to 200 mg/dL
D. Presence of oligoclonal bands
E. Slight to moderate monocytic pleocytosis
A. An IgG index greater than 1.7
B. Increased myelin basic protein
C. Increased protein to 200 mg/dL
D. Presence of oligoclonal bands
E. Slight to moderate monocytic pleocytosis
The CSF protein is slightly increased in 40% of pat ients with multiple
sclerosis (MS). A concent rat ion of . 100 mg/dL is rare (C). If the ratio of
CSF IgG/serum IgG to CSF albumin/serum albumin is more than 1.7, the
diagnosis of MS is probable (A). This ratio is known as the IgG index. Testing
for oligoclonal bands (D) in CSF is the most widely used test for MS. Increased
CSF myelin basic protein (B) can be present in acute MS exacerbations
and is therefore consistent with a diagnosis of MS; however, increased
MBP may be present in any process where myelin is destroyed. A slight to
moderate monocytic pleocytosis (E) is present in approximately one-third
of MS patients.1
- Each of the following is true of myasthenia gravis except
A. A decrementing response to peripheral nerve stimulation is typical.
B. Aminoglycoside antibiotics may worsen the symptoms.
C. Females are more frequently a ected in the , 40 age group.
D. Females predominate in the subset of patients with a thymoma.
E. Ten to 15% of patients have no antibodies to the acetylcholine receptor.
A. A decrementing response to peripheral nerve stimulation is typical.
B. Aminoglycoside antibiotics may worsen the symptoms.
C. Females are more frequently a ected in the , 40 age group.
D. Females predominate in the subset of patients with a thymoma.
E. Ten to 15% of patients have no antibodies to the acetylcholine receptor.
The majorit y of patients with myasthenia gravis harboring a thymoma are
older (50–60 years) and male (D is false). The disease is two to three times
more common in women than men in patients , 40 years of age (C is true).
A decrease in muscle action potential with nerve st imulation at 3 Hz (a decrement
ing response) is seen (A is true). Certain aminoglycoside ant ibiot ics
can impair transmit ter release by inhibit ing calcium ion uxes at the neuromuscular
junction (B is true). Ten to 15% of patients have no ant ibodies to the
acetylcholine receptor (E is true)
- A defect in mitochondrial DNA is found in each of the following disorders except
A. Kearns-Sayre syndrome
B. Leber’s hereditary optic atrophy
C. Leigh’s subacute necrotizing encephalopathy
D. Mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke
(MELAS)
E. Menkes’ syndrome
A. Kearns-Sayre syndrome
B. Leber’s hereditary optic atrophy
C. Leigh’s subacute necrotizing encephalopathy
D. Mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke
(MELAS)
E. Menkes’ syndrome
Menkes’ (kinky hair) syndrome (E) is a rare sex-linked recessive disease characterized
by severe copper de ciency due to failure of intest inal absorption of
copper. The other disorders (Kearns-Sayre syndrome [A], Leber’s hereditary
optic atrophy [B], Leigh’s subacute necrotizing encephalopathy [C], and
mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke
[MELAS; D]) have point m utations or deletions of m itochondrial DNA as part
of their pathogenesis.1
Symptoms of spontaneous carotid artery dissection include
I. Dysgeusia
II. Eye pain
III. Tongue weakness
IV. Horner’s syndrome
A. I, II, III
B. I, III
C. II, IV
D. IV
E. All of the above
Symptoms of spontaneous carot id arter y dissection may include eye pain (II)
or unilateral headache as well as the presence of a Horner’s syndrome (IV)
that is due to the disruption of sympathet ic nerves running along the carot id
artery. Signs of ischemia in the territory of the a ected internal carotid artery
may be present. Small branches o of the carot id artery may supply the cranial
nerves extracranially; ischemia to these branches may lead to cranial nerve
dysfunction such as dysgeusia (impaired taste, I) or tongue weakness (III).1
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
A. I, II, III
B. I, III
C. II, IV
D. IV
E. All of the above
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
Genes responsible for cavernous malformations have been mapped to
chromosomes
A. 1 and 3
B. 3 and 5
C. 3 and 7
D. 4 and 5
E. 5 and 7
A. 1 and 3
B. 3 and 5
C. 3 and 7
D. 4 and 5
E. 5 and 7
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
Each of the following is characteristic of a diabetic third nerve palsy except
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
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
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
- Transverse white lines in the ngernails
A. Arsenic poisoning
B. Lead poisoning
C. Manganese poisoning
D. Mercury poisoning
E. Phosphorus poisoning
A. Arsenic poisoning
B. Lead poisoning
C. Manganese poisoning
D. Mercury poisoning
E. Phosphorus poisoning
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
- Black lines at the gingival margins
A. Arsenic poisoning
B. Lead poisoning
C. Manganese poisoning
D. Mercury poisoning
E. Phosphorus poisoning
A. Arsenic poisoning
B. Lead poisoning
C. Manganese poisoning
D. Mercury poisoning
E. Phosphorus poisoning
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
- Later symptoms resemble those of Parkinson’s disease
A. Arsenic poisoning
B. Lead poisoning
C. Manganese poisoning
D. Mercury poisoning
E. Phosphorus poisoning
A. Arsenic poisoning
B. Lead poisoning
C. Manganese poisoning
D. Mercury poisoning
E. Phosphorus poisoning
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
- Treated with atropine
A. Arsenic poisoning
B. Lead poisoning
C. Manganese poisoning
D. Mercury poisoning
E. Phosphorus poisoning
A. Arsenic poisoning
B. Lead poisoning
C. Manganese poisoning
D. Mercury poisoning
E. Phosphorus poisoning
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
- Penicillamine is the treatment of choice in the chronic form
A. Arsenic poisoning
B. Lead poisoning
C. Manganese poisoning
D. Mercury poisoning
E. Phosphorus poisoning
A. Arsenic poisoning
B. Lead poisoning
C. Manganese poisoning
D. Mercury poisoning
E. Phosphorus poisoning
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
- Characterized by mood changes, tremors, and a cerebellar syndrome
A. Arsenic poisoning
B. Lead poisoning
C. Manganese poisoning
D. Mercury poisoning
E. Phosphorus poisoning
A. Arsenic poisoning
B. Lead poisoning
C. Manganese poisoning
D. Mercury poisoning
E. Phosphorus poisoning
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
- Treated with ethylenediaminetetraacetic acid (EDTA) and dimercaprol (BAL)
A. Arsenic poisoning
B. Lead poisoning
C. Manganese poisoning
D. Mercury poisoning
E. Phosphorus poisoning
A. Arsenic poisoning
B. Lead poisoning
C. Manganese poisoning
D. Mercury poisoning
E. Phosphorus poisoning
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
- Increased excretion of urinary coproporphyrin
A. Arsenic poisoning
B. Lead poisoning
C. Manganese poisoning
D. Mercury poisoning
E. Phosphorus poisoning
A. Arsenic poisoning
B. Lead poisoning
C. Manganese poisoning
D. Mercury poisoning
E. Phosphorus poisoning
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
- Diagnosis can be made by the examination of hair samples
A. Arsenic poisoning
B. Lead poisoning
C. Manganese poisoning
D. Mercury poisoning
E. Phosphorus poisoning
A. Arsenic poisoning
B. Lead poisoning
C. Manganese poisoning
D. Mercury poisoning
E. Phosphorus poisoning
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
- Which of the following is not a characterist ic of Adie’s syndrome?
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
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
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
Characteristics of infantile seizures include
I. Lip smacking
II. Hypsarrhythmia
III. Generalized tonic-clonic activit y
IV. Myoclonic head jerks
A. I, II, III
B. I, III
C. II, IV
D. IV
E. All of the above
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
Muscles of the trunk and lower extremities are more frequently involved than
the extraocular muscles
A. Myasthenia gravis
B. Eaton-Lambert myasthenic syndrome
C. Both
D. Neither
A. Myasthenia gravis
B. Eaton-Lambert myasthenic syndrome
C. Both
D. Neither
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
Poor response to anticholinesterase drugs
A. Myasthenia gravis
B. Eaton-Lambert myasthenic syndrome
C. Both
D. Neither
A. Myasthenia gravis
B. Eaton-Lambert myasthenic syndrome
C. Both
D. Neither
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
An incrementing response (marked increase in the amplitude of the action
potential with fast rates of nerve st imulation) is typical
A. Myasthenia gravis
B. Eaton-Lambert myasthenic syndrome
C. Both
D. Neither
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
A. Myasthenia gravis
B. Eaton-Lambert myasthenic syndrome
C. Both
D. Neither
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
Associated with antibodies to the presynaptic voltage-dependent calcium channel
A. Myasthenia gravis
B. Eaton-Lambert myasthenic syndrome
C. Both
D. Neither
A. Myasthenia gravis
B. Eaton-Lambert myasthenic syndrome
C. Both
D. Neither
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
The dorsal scapular nerve innervates the
I. Supraspinatus
II. Rhomboids
III. Subscapularis
IV. Levator scapulae
A. I, II, III
B. I, III
C. II, IV
D. IV
E. All of the above
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
Teres major
A. Axillary nerve
B. Dorsal scapular nerve
C. Subscapular nerve
D. Suprascapular nerve
E. None of the above
A. Axillary nerve
B. Dorsal scapular nerve
C. Subscapular nerve
D. Suprascapular nerve
E. None of the above
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
Teres minor
A. Axillary nerve
B. Dorsal scapular nerve
C. Subscapular nerve
D. Suprascapular nerve
E. None of the above
A. Axillary nerve
B. Dorsal scapular nerve
C. Subscapular nerve
D. Suprascapular nerve
E. None of the above
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
Subscapularis
A. Axillary nerve
B. Dorsal scapular nerve
C. Subscapular nerve
D. Suprascapular nerve
E. None of the above
A. Axillary nerve
B. Dorsal scapular nerve
C. Subscapular nerve
D. Suprascapular nerve
E. None of the above
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
Levator scapulae
A. Axillary nerve
B. Dorsal scapular nerve
C. Subscapular nerve
D. Suprascapular nerve
E. None of the above
A. Axillary nerve
B. Dorsal scapular nerve
C. Subscapular nerve
D. Suprascapular nerve
E. None of the above
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
Supraspinatus
A. Axillary nerve
B. Dorsal scapular nerve
C. Subscapular nerve
D. Suprascapular nerve
E. None of the above
A. Axillary nerve
B. Dorsal scapular nerve
C. Subscapular nerve
D. Suprascapular nerve
E. None of the above
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
Infraspinatus
A. Axillary nerve
B. Dorsal scapular nerve
C. Subscapular nerve
D. Suprascapular nerve
E. None of the above
A. Axillary nerve
B. Dorsal scapular nerve
C. Subscapular nerve
D. Suprascapular nerve
E. None of the above
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
Rhomboids
A. Axillary nerve
B. Dorsal scapular nerve
C. Subscapular nerve
D. Suprascapular nerve
E. None of the above
A. Axillary nerve
B. Dorsal scapular nerve
C. Subscapular nerve
D. Suprascapular nerve
E. None of the above
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
- The motor unit potential in myopathy is of
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
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
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.
Which is true of myotonic dystrophy?
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.
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.
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
Subacute combined degeneration of the spinal cord is caused by a de ciency of
A. Cobalamin
B. Folic acid
C. Nicotinic acid
D. Pyridoxine
E. Thiamine
A. Cobalamin
B. Folic acid
C. Nicotinic acid
D. Pyridoxine
E. Thiamine
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
The marker linked to the Huntington gene is localized to the short arm of
chromosome
A. 4
B. 11
C. 17
D. 22
E. None of the above
A. 4
B. 11
C. 17
D. 22
E. None of the above
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
Alexia without agraphia is most likely to occur with a lesion involving the
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
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
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
Deviation of the eyes to the right is most likely to occur with occlusion of the
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
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
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
Which of the following antiepileptic drugs has the shortest half-life?
A. Carbamazepine
B. Ethosuximide
C. Phenobarbital
D. Phenytoin
E. Valproate
A. Carbamazepine
B. Ethosuximide
C. Phenobarbital
D. Phenytoin
E. Valproate
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
- Weakness and atrophy of the hands
A. Amyotrophic lateral sclerosis
B. Syringomyelia
C. Both
D. Neither
A. Amyotrophic lateral sclerosis
B. Syringomyelia
C. Both
D. Neither
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
Hypo- or are exia
A. Amyotrophic lateral sclerosis
B. Syringomyelia
C. Both
D. Neither
A. Amyotrophic lateral sclerosis
B. Syringomyelia
C. Both
D. Neither
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
Absence of sensory changes
A. Amyotrophic lateral sclerosis
B. Syringomyelia
C. Both
D. Neither
A. Amyotrophic lateral sclerosis
B. Syringomyelia
C. Both
D. Neither
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
Biochemical studies of neurons from a seizure focus have shown all of the
following except
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
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
Increased glycine levels have been found in neurons in seizure foci (D is false).
- The most reliable indicator of an intracellular cobalamin (vitamin B12) de ciency is
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
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
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
Each of the following is true of radiation myelopathy (delayed progressive type)
except
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
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
In radiation myelopathy, sensory changes usually precede the weakness
(D is false). The other responses are characteristics of radiation myelopathy
(delayed progressive type).1
Fasciculation potentials indicate
A. Motor nerve fiber irritability
B. Motor nerve ber destruction
C. Motor unit denervation
D. Muscle atrophy
E. Reinnervation of muscle units
A. Motor nerve fiber irritability
B. Motor nerve ber destruction
C. Motor unit denervation
D. Muscle atrophy
E. Reinnervation of muscle units
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
Di- or triphasic pattern
A. Fasciculation potential
B. Fibrillation potential
C. Both
D. Neither
A. Fasciculation potential
B. Fibrillation potential
C. Both
D. Neither
5 to 15 milliseconds in duration
A. Fasciculation potential
B. Fibrillation potential
C. Both
D. Neither
A. Fasciculation potential
B. Fibrillation potential
C. Both
D. Neither
May take the form of positive sharp waves
A. Fasciculation potential
B. Fibrillation potential
C. Both
D. Neither
A. Fasciculation potential
B. Fibrillation potential
C. Both
D. Neither
Seen in poliomyelitis
A. Fasciculation potential
B. Fibrillation potential
C. Both
D. Neither
A. Fasciculation potential
B. Fibrillation potential
C. Both
D. Neither
Usually develops 24 to 36 hours after the death of an axon
A. Fasciculation potential
B. Fibrillation potential
C. Both
D. Neither
A. Fasciculation potential
B. Fibrillation potential
C. Both
D. Neither
- May be visible through the skin
A. Fasciculation potential
B. Fibrillation potential
C. Both
D. Neither
A. Fasciculation potential
B. Fibrillation potential
C. Both
D. Neither
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
- What characteristics of motor unit potentials are typical soon after reinnervation?
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
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
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
- Which of the following ocular findings is not seen in myasthenia gravis?
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
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
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.
Risk factors for carpal tunnel syndrome include
I. Acromegaly
II. Amyloidosis
III. Hypothyroidism
IV. Pregnancy
A. I, II, III
B. I, III
C. II, IV
D. IV
E. All of the above
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
- Which of the following is true of neurological findings in sarcoidosis?
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.
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.
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
- All of the following are associated with narcolepsy except
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
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
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
Which of the following signs or symptoms occurring in a young person is the
most suggestive of multiple sclerosis?
A. Bilateral internuclear ophthalmoplegia
B. Gait ataxia
C. Lhermitte’s sign
D. Optic neuritis
E. Vertigo
A. Bilateral internuclear ophthalmoplegia
B. Gait ataxia
C. Lhermitte’s sign
D. Optic neuritis
E. Vertigo
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
- The muscles most often involved in thyroid ophthalmopathy are the
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
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
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
- Most cases of “idiopathic” hemifacial spasm are thought to result from
A. Ephaptic transmission
B. Hypersensitivity of facial muscles
C. Hypocalcemia
D. Psychiatric disorders
E. Recurrence of latent viral infection
A. Ephaptic transmission
B. Hypersensitivity of facial muscles
C. Hypocalcemia
D. Psychiatric disorders
E. Recurrence of latent viral infection
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
The diagnosis of neurosarcoidosis is based on
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
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
Although all of the options are seen in act ive neurosarcoidosis, the diagnosis
is made on the basis of answer A.1
- Seen most often in children with neuroblastoma
A. Limbic encephalitis
B. Eaton-Lambert syndrome
C. Moersch-Woltman (stiff -man) syndrome
D. Opsoclonus-myoclonus
E. Sensory neuropathy
A. Limbic encephalitis
B. Eaton-Lambert syndrome
C. Moersch-Woltman (stiff -man) syndrome
D. Opsoclonus-myoclonus
E. Sensory neuropathy
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
- Anti-Hu antibodies
A. Limbic encephalitis
B. Eaton-Lambert syndrome
C. Moersch-Woltman (stiff -man) syndrome
D. Opsoclonus-myoclonus
E. Sensory neuropathy
A. Limbic encephalitis
B. Eaton-Lambert syndrome
C. Moersch-Woltman (stiff -man) syndrome
D. Opsoclonus-myoclonus
E. Sensory neuropathy
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
- Anti-Ri antibodies
A. Limbic encephalitis
B. Eaton-Lambert syndrome
C. Moersch-Woltman (stiff -man) syndrome
D. Opsoclonus-myoclonus
E. Sensory neuropathy
A. Limbic encephalitis
B. Eaton-Lambert syndrome
C. Moersch-Woltman (stiff -man) syndrome
D. Opsoclonus-myoclonus
E. Sensory neuropathy
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
- Autoantibodies to voltage-gated calcium channels
A. Limbic encephalitis
B. Eaton-Lambert syndrome
C. Moersch-Woltman (stiff -man) syndrome
D. Opsoclonus-myoclonus
E. Sensory neuropathy
A. Limbic encephalitis
B. Eaton-Lambert syndrome
C. Moersch-Woltman (stiff -man) syndrome
D. Opsoclonus-myoclonus
E. Sensory neuropathy
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
- Autoantibodies to glutamic acid decarboxylase
A. Limbic encephalitis
B. Eaton-Lambert syndrome
C. Moersch-Woltman (stiff -man) syndrome
D. Opsoclonus-myoclonus
E. Sensory neuropathy
A. Limbic encephalitis
B. Eaton-Lambert syndrome
**C. Moersch-Woltman (stiff -man) syndrome
**D. Opsoclonus-myoclonus
E. Sensory neuropathy
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
Contralateral hemiparesis sparing the face, contralateral loss of position and
vibrat ion sense, ipsilateral paralysis, and atrophy of the tongue
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
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
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
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
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
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
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
Ipsilateral cerebellar ataxia, contralateral loss of pain and temperature in the
body, part ial deafness, and nausea and vomiting
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
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
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
Bilateral motor weakness in all extremities, bilateral cerebellar ataxia, and
diplopia
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
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
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
- The lesion in hemiballismus is localized to the contralateral
A. Brachium conjunctivum
B. Caudate nucleus
C. Dorsomedial nucleus of the thalamus
D. Substantia nigra
E. Subthalamic nucleus
A. Brachium conjunctivum
B. Caudate nucleus
C. Dorsomedial nucleus of the thalamus
D. Substantia nigra
E. Subthalamic nucleus
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
