Neurology Quiz | Neuroq quiz | Practice MCQ #mcq.ImBooz

• (A) Monophasic
• (B) Rapidly lethal
• (C) Associated with brainstem and spinal cord disease
• (D) Associated with magnetic resonance imaging (MRI) lesions, which may resolve

Check AnswerSolution[A]:-Acute disseminated encephalomyelitis is a demyelinating disease of the brain, brainstem, and spinal cord that is indistinguishable from MS on MRI. It is, however, monophasic, meaning that it occurs acutely on a single occasion and not in a recurrent fashion like MS. It usually develops within days or weeks of a viral illness or an immunization. Childhood exanthems are especially likely to precipitate ADEM, as are smallpox and rabies immunizations. As in MS, the lesions associated with ADEM usually produce perivenous demyelination with sparing of the nerve axons.

• (A) The disk is laterally herniated at C7.
• (B) The disk is causing radicular pain.
• (C) The cauda equina is being crushed.
• (D) A thoracic disk is involved.

Check AnswerSolution[C]:-Surgery may eventually be necessary with any intervertebral disk herniation, but with acute, massive cauda equina injury, surgery must be performed before the deficits are irreversible. Signs of cauda equina compression include loss of bladder and bowel control and paraparesis or paraplegia. An acutely evolving focal motor deficit in the legs, such as a footdrop, associated with sphincter dysfunction is justification for emergency laminectomy and disk resection. Pre-operative studies should be obtained to be sure that the responsible lesion is disk herniation, because metastatic cancers, such as prostate and breast carcinoma, may imitate acute disk herniations. Establishing the identity of the lesion is important because many tumors are better managed with high-dose corticosteroids and radiation therapy than with surgery. Osteomyelitis of the vertebral body may also produce cauda equina compression; a decompressive laminectomy is usually indicated with focal infections of this sort to maximize the recovery achieved with antibiotic therapy.

• (A) Inhaled 100% oxygen
• (B) Sublingual nitroglycerin
• (C) Oral methysergide
• (D) Oral propranolol

Check AnswerSolution[A]:-Oxygen may terminate a cluster headache within minutes. Some physicians recommend inhaling 4 L/minute of 100% oxygen by mask as soon as signs of an impending headache develop. This has prompted many sufferers of cluster headaches to keep a cylinder of compressed oxygen at home during the season when they are most likely to develop such headaches. Cluster headaches usually occur at night when the patient is asleep, and so practical access to the oxygen tank is possible. Methysergide is effective in preventing cluster headaches for many persons, but it does rarely cause the worrisome adverse effect of fibrosis. Retroperitoneal, pulmonary, and endocardial fibroses are potential adverse effects of methysergide. Sublingual nitroglycerin may in fact trigger a headache and is not recommended for patients with migraine or cluster headaches. Propranolol is a ?-adrenergic-blocking agent that is useful in the prophylaxis of some vascular headaches, but it is of no value in aborting a cluster headache. Dihydroergotamine suppositories may abort some vascular headaches, but they do not have as obvious an effect in cluster as in classic or common migraine syndromes.

• (A) Dehydration
• (B) Hypomagnesemia
• (C) Wernicke encephalopathy
• (D) Hypoglycemia

Check AnswerSolution[C]:-Wernicke encephalopathy is a potentially fatal consequence of thiamine deficiency, a problem for which this woman was at risk by virtue of being an alcoholic. When she came to the emergency room, intravenous fluids were started that probably contained glucose. The stress of a large glucose load will abruptly deplete the central nervous system (CNS) of the little thiamine it has available and will precipitate the sort of deterioration evident in this woman. Features characteristic of a Wernicke encephalopathy include deteriorating level of consciousness, autonomic disturbances, ocular motor problems, and gait difficulty. Autonomic disturbances may include lethal hypotension or profound hypothermia. Hemorrhagic necrosis in periventricular gray matter will be evident in this woman’s brain if she dies. The mamillary bodies are especially likely to be extensively damaged.

• (A) Suxamethonium
• (B) Nitrous oxide
• (C) Succinylcholine
• (D) Dantrolene

Check AnswerSolution[D]:-Malignant hyperthermia is characterized by acute severe fever, tachypnea, tachycardia, and rigidity, and high mortality rate if left untreated. It is typically precipitated by volatile anesthetics, especially halothane, or muscle relaxants such as succinylcholine. Patients may become severely acidotic and develop rhabdomyolysis. Pathology shows diffuse segmental muscle necrosis. It appears to be a metabolic myopathy in which there is abnormal release of calcium from the sarcoplasmic reticulum and ineffectual uptake afterward. Genetic defects in the ryanodine receptor, involved in calcium flux in the sarcoplasmic reticulum, are responsible for about 10% of cases, although as yet unidentified abnormalities of this or related proteins probably play a role in most cases. It is inherited in an autosomal dominant fashion. Certain other myopathies, including Duchenne muscular dystrophy and central core myopathy, are associated with this condition as well. Treatment consists of discontinuation of anesthesia, administration of dantrolene, which prevents release of calcium from the sarcoplasmic reticulum, and supportive measures

• (A) Hyperthyroidism
• (B) Diabetes mellitus
• (C) Cerebral aneurysm
• (D) Orbital pseudotumor

Check AnswerSolution[B]:-The third cranial nerve (the oculomotor nerve) controls several movements of the globe, including upward and medial movements, through its control of the medial rectus, superior rectus, and inferior oblique muscles. Its inactivity leads to displacement of the eye down and out. Fourth-nerve palsy leads to weakness of the superior oblique muscle, with resultant difficulty looking down and medially; patients often complain of trouble walking down stairs. Sixth-nerve palsy produces weakness of the lateral rectus muscle, causing horizontal diplopia. Fractures of the orbit can entrap individual muscles, but there is no history of this here. Thyroid ophthalmopathy, or Graves disease, can produce diplopia, but there is usually proptosis or lid retraction. The inferior and medial recti are most frequently affected. Because this is caused by infiltration of the muscles, there is usually limitation of passive movement of the eyes (ie, forced ductions). Diabetes is a common cause of third-nerve palsy (approximately 10% of cases). Usually, when diabetes is the cause, there is sparing of the pupillomotor parasympathetic fibers, which travel on the outside of the nerve. Diabetes causes third-nerve palsy via nerve infarction, which affects the interior of the nerve but spares the external fibers. Compressive lesions, however, can injure the surface fibers, thereby causing pupillary dilation due to unopposed sympathetic activity.

• (A) Conjunctivitis
• (B) Congenital
• (C) Pupillary sphincter injury
• (D) Carotid artery dissection

Check AnswerSolution[B]:-Sympathetic innervation of the iris is required for the change in the color of the iris to occur after birth and infancy. Congenital Horner syndrome, which may be inherited as an autosomal dominant trait, is characterized by failure of one eye to develop normal iris color (heterochromia iridis). Any injury to the eye after this early developmental period would not be expected to leave a difference in eye color from one side to the other.

• (A) Minimal
• (B) Mild
• (C) Moderate
• (D) Severe

Check AnswerSolution[D]:-The GCS was introduced in 1974 by Teasdale and Jennett. It has three parts: best motor response (1-6 points), best verbal response (1-5 points), and eye opening (1-4 points). The total score ranges from 3 to 15 (normal). The presence of coma is defined as GCS of 8 or less, which represents a patient who does not follow commands, speak, or open the eyes. Head injuries may be defined on the basis of the GCS: mild injury (GCS 14-15), moderate injury (GCS 9-13), and severe injury (GCS ? 8). Although patients with mild head injuries may receive a score of 15, the maximum on the GCS, they may still have more subtle cognitive difficulties that are not reflected by this easy-to-use and simple scale.

• (A) Subdural hemorrhage
• (B) Basilar skull fracture
• (C) Parenchymal hematoma
• (D) Ocular injury

Check AnswerSolution[B]:-The presence of periorbital ecchymosis (raccoon eyes), ecchymosis over the mastoid region (Battle sign), hemotympanum (blood behind the eardrum), or CSF rhinorrhea or otorrhea should be considered evidence of a basilar skull fracture.

• (A) Diffuse axonal injury
• (B) Uncontrolled hypertension
• (C) Amyloid angiopathy
• (D) Coagulopathy

Check AnswerSolution[A]:-Diffuse axonal injury is the most common cause of coma in the head-injured patient without an intracranial mass lesion. It is characterized pathologically by diffusely spread axonal swellings affecting the white matter, corpus callosum, and upper brainstem. These foci are usually hemorrhagic. The etiology is thought to be due to shearing forces on axons in certain susceptible regions of the brain, notably those that are particularly vulnerable to rotational forces, such as the subcortical white matter, corpus callosum, and upper brainstem. Uncontrolled hypertension may occur in patients with hypertension, but would be unlikely to produce this pattern of injury. Amyloid angiopathy causes multiple hemorrhages, but affects elderly patients. The decreased cerebral perfusion pressure associated with brain swelling and increased intracranial pressure could cause ischemic infarction, but this would not be expected to give this appearance on MRI. Coagulopathies also occur in up to 20% of patients.

• (A) Corticosteroids
• (B) Hyperthermia
• (C) Prophylactic hyperventilation
• (D) Hypothermi

Check AnswerSolution[D]:-Hypothermia has been shown to reduce cerebral injury from ischemia both in experimental models and in clinical studies of patients with traumatic brain injury. Hypothermia decreases cerebral metabolism, reduces acidosis, attenuates changes in the blood-brain barrier, and inhibits the release of excitatory neurotransmitters that can be harmful. Hypothermia may be achieved by packing the body in ice or using intravenous cooling systems. Corticosteroids, prophylactic hyperventilation, and prophylactic anticonvulsants have not been shown to be of benefit in the long-term prognosis of severely head-injured patients. Hyperthermia is detrimental to such patients.

• (A) Cytomegalovirus (CMV)
• (B) Treponema pallidum
• (C) Chlamydia pneumoniae
• (D) Clostridium botulinum

Check AnswerSolution[D]:-The rapid onset of bulbar paresis is consistent with acute inflammatory demyelinating polyneuropathy (AIDP, or Guillain-Barr� syndrome), botulism, tick paralysis, and several other conditions. The normal conduction velocities argue against demyelinating neuropathy, which may be associated with C jejuni. Cytomegalovirus and T pallidum may cause several different neurological syndromes, but acute bulbar paresis is not among them. C pneumoniae is under investigation as a cause of atherosclerosis, strokes, and MS, but it does not cause acute motor weakness.

• (A) Dexamethasone
• (B) Amphotericin B
• (C) Gamma globulin
• (D) Acyclovir

Check AnswerSolution[D]:-The presentation suggests a viral encephalitis. Herpes simplex is the most common cause of viral encephalitis. The diagnosis of herpes encephalitis is more controversial than the treatment. A few authorities believe brain biopsy should be performed whenever the diagnosis is suspected, but the availability of polymerase chain reaction for herpes simplex virus in the CSF and MRI have made diagnosis easier. A high index of suspicion must be maintained, and treatment must be initiated quickly. Acyclovir must be given intravenously for at least 14-to-21 days.

• (A) Antibodies to the acetylcholine receptor
• (B) Impaired formation of acetylcholine-laden vesicles
• (C) Depolarizing blockade of the potassium channel
• (D) Antibodies to the calcium receptor

Check AnswerSolution[B]:-Botulinum toxin, a 150-kDa polypeptide chain, is cleaved into two chains: a 100-kDa chain required for neuronal binding and a 50-kDa chain that destroys important proteins required for neurotransmitter packaging. The toxin reduces the amount of acetylcholine available for release when a motor neuron is depolarized. Eight serotypes of botulism toxin are now recognized: A, B, C1, C2, D, E, F, and G. Although the toxins cleave different proteins, they interfere with the same step in vesicle formation

• (A) Oral prednisone
• (B) Intravenous methylprednisolone
• (C) Cyclophosphamide
• (D) Plasma exchange

Check AnswerSolution[B]:-Clinical trials have shown that intravenous methylprednisolone for an attack of optic neuritis is associated with a better outcome than oral prednisone. Intravenous methylprednisolone is thus recommended by most experts as appropriate therapy for acute exacerbations of MS involving more than sensory manifestations alone.

• (A) 0
• (B) 0.05
• (C) 0.25
• (D) 0.75

Check AnswerSolution[D]:-The risk of developing MS after optic neuritis was 74% in women and 34% in men after 15 years of follow-up in one study. Other studies have found similarly high rates. The longer the follow-up period, and the more rigorously signs of MS are sought, the more likely it is that MS will be found. Most patients develop MS within 5 years of the initial attack of optic neuritis. MRI scanning of the brain at the time of optic neuritis is, in fact, abnormal in between 50% and 72% of patients, suggesting the presence of subclinical MS.

• (A) Aspirin
• (B) Acetaminophen
• (C) Ibuprofen
• (D) Carbamazepine

Check AnswerSolution[D]:-This man has exhibited two different episodes separated in time and space, a clinical pattern that must raise the possibility of MS in a man this age. The pattern of pain is suggestive of trigeminal neuralgia (tic douloureux), a facial pain syndrome that often develops in persons with MS. Alternatives to carbamazepine in the palliation of trigeminal neuralgia include phenytoin and baclofen.

• (A) Oxybutynin
• (B) Phenytoin
• (C) Carbamazepine
• (D) Baclofen

Check AnswerSolution[A]:-Bladder dysfunction with MS is usually a consequence of corticospinal tract disease. This lesion of the upper motor neuron produces a spastic bladder. Tricyclic antidepressants such as imipramine exert an anticholinergic effect and thereby inhibit premature emptying of the bladder have been used. Oxybutynin also works through anticholinergic mechanisms. Cholinergic drugs, such as methacholine, are useful if the patient has a flaccid bladder, but that is much less frequently the problem with MS.

• (A) Imipramine
• (B) Phenytoin
• (C) Baclofen
• (D) Carbamazepine

Check AnswerSolution[C]:-Baclofen affects spasticity through an unknown mechanism and may cause considerable sedation. Sedation is less a concern if spasticity is interfering with the patient’s ability to sleep. The drug is usually given orally at a dose of 10 mg three or four times daily, but most patients must start at a much lower dose and gradually build up tolerance. Baclofen has been given intrathecally with an implanted pump injector, but this highly invasive therapy is appropriate only in patients with extreme spasticity. Candidates for intrathecal treatment are functionally paraplegic and may recover considerable mobility with elimination of the spasticity. Tizanidine is a centrally active ?2-adrenergic agonist that appears to relieve spasticity without affecting strength

• (A) An intraventricular drain to monitor intracranial pressure
• (B) Lorazepam for intravenous administration
• (C) Carbamazepine by nasogastric tube
• (D) Phenytoin by nasogastric tube