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

• (A) Posterior cord of the brachial plexus
• (B) Medial cord of the brachial plexus
• (C) Lateral cord of the brachial plexus
• (D) T1 spinal root

Check AnswerSolution[A]:-The radial nerve supplies the extensors of the wrist and derives from the posterior cord of the brachial plexus. The brachial plexus arises from C5, C6, C7, C8, and T1. These spinal roots form the trunks of the brachial plexus. C5 and C6 form the upper trunk; C7, the middle trunk; and C8 and T1, the lower trunk. The trunks in turn divide into anterior and posterior divisions, which associate into cords: The anterior division of the upper and middle trunks gives rise to the lateral cord, the posterior divisions of all the trunks give rise to the posterior cord, and the anterior division of the lower trunk gives rise to the medial cord.

• (A) Node dissections in the axilla
• (B) Birth trauma
• (C) Aneurysm of the subclavian artery
• (D) Pancoast tumor

Check AnswerSolution[B]:-The upper brachial plexus includes the fifth and sixth cervical spinal roots. Damage to these roots occurs during a difficult birth if the head and the shoulder are forced widely apart. This could result in stretching or even avulsion of these cervical spinal roots from the spinal cord. Node dissection in the axilla or a Pan-coast tumor at the apex of the lung may produce brachial plexus injury, but it is the lower plexus that is vulnerable. Dislocation of the head of the humerus or aneurysm of the subclavian artery will typically injure the cords of the brachial plexus, the final elements of the plexus from which the principal nerves of the arm arise.

• (A) Cerebellar cortex
• (B) Inferior olivary nuclei
• (C) Anterior horns of the spinal cord
• (D) Spinocerebellar tracts

Check AnswerSolution[D]:-Degeneration occurs primarily in the spinal cord rather than the cerebellum or brainstem in patients with Friedreich disease. Both the dorsal and ventral spinocerebellar tracts are involved. The other spinal cord structures exhibiting degeneration include the posterior columns and the lateral corticospinal tracts.

• (A) Inappropriate antidiuretic hormone
• (B) Diabetes mellitus
• (C) Panhypopituitarism
• (D) Progressive adrenal insufficiency

Check AnswerSolution[B]:-More than 10% of patients with Friedreich disease develop diabetes mellitus. A more life-threatening complication of this degenerative disease is the disturbance of the cardiac conduction system that often develops. Visual problems occur with the hyperglycemia of uncontrolled diabetes mellitus, but even Friedreich patients without diabetes develop optic atrophy late in the course of the degenerative disease.

• (A) Campylobacter jejuni
• (B) HIV
• (C) Chlamydia psittaci
• (D) Mycoplasma pneumoniae

Check AnswerSolution[A]:-Serologic studies have shown that C jejuni is the most common infection preceding Guillain-Barr� syndrome. Other, less common infections include viral illnesses such as CMV, HIV, and Epstein-Barr virus; Lyme disease; and M pneumoniae infection. Guillain-Barr� syndrome has also been associated with surgical procedures, exposure to thrombolytic agents, lymphoma, and certain vaccines.

• (A) Chromosome 21
• (B) Chromosome 9
• (C) Chromosome 6
• (D) The Y chromosome

Check AnswerSolution[B]:-Spinocerebellar atrophy does occur linked to chromosome 6, but this is distinct from Friedreich ataxia. The site of the mutation responsible for Friedreich ataxia has been identified on chromosome 9, and the gene product, the protein frataxin, has been identified. Friedreich disease is inherited as an autosomal recessive defect.

• (A) Neonatal period
• (B) Juvenile period
• (C) Early adulthood
• (D) Middle age

Check AnswerSolution[B]:-Congenital abnormalities are rarely evident with Friedreich disease, but kyphoscoliosis, pes cavus, and other musculoskeletal abnormalities may become evident quite early in childhood. Gait difficulty usually develops during childhood in persons with Friedreich disease. Visual loss, syncope, vertigo, and dysarthria may develop during the course of this degenerative disease, but the appearance of these other problems may be decades after that of the gait ataxia. Visual loss may develop with optic atrophy or retinitis pigmentosa. Strictly cerebellar or spinocerebellar tract signs include limb ataxia, nystagmus, dysarthria, and gait difficulty. Systemic problems often found in persons with Friedreich disease include diabetes mellitus and cardiac conduction defects.

• (A) No abnormalities
• (B) Elevated protein level
• (C) Elevated white blood cell (WBC) count
• (D) NONE

Check AnswerSolution[B]:-This patient’s clinical course is consistent with a diagnosis of acute inflammatory demyelinating polyneuropathy, also known as Guillain-Barr� syndrome. CSF is typically under normal pressure in this syndrome and contains no cells in up to 90% of patients. In 10% of patients, 10-to-50 WBCs, mostly lymphocytes, may appear. Protein levels are generally elevated, sometimes to extremely high levels, reflecting the degree of inflammatory activity taking place at the level of the spinal roots.

• (A) Dorsal root ganglia
• (B) Spinocerebellar tracts
• (C) Anterior horn cells
• (D) Clarke column

Check AnswerSolution[A]:-Degenerative changes in the peripheral nerves of patients with Friedreich disease have several bases. Loss of cells in the dorsal root ganglia makes a major contribution to this phenomenon. Additional sites of degeneration that affect the sensory system include the substantia gelatinosa (Lissauer tract) of the posterior horn and the dorsal roots themselves. The peripheral neuropathy is responsible for the hyporeflexia that is invariably found in the legs of affected persons.

• (A) Corticosteroids
• (B) Cyclophosphamide
• (C) Plasma exchange
• (D) Albumin infusions

Check AnswerSolution[C]:-Treatment of Guillain-Barre syndrome is complicated and is best accomplished in an experienced center. Specific therapies include plasma exchange and intravenous immunoglobulin, which appear to be equivalent in several studies. When instituted early (within 2 weeks of symptom onset), these modalities can reduce the period of hospitalization, the length of time on mechanical ventilation, and the time to begin walking again. Corticosteroids do not appear to be of benefit. The role of other immunosuppressants, such as cyclophosph-amide, has not been evaluated. 3,4-Diaminopyridine is used in the treatment of Lambert-Eaton myasthenic syndrome.

• (A) Corticosteroids
• (B) Cyclophosphamide
• (C) Plasma exchange
• (D) Parsonage-Turner syndrome (brachial plexopathy)

Check AnswerSolution[D]:-Parsonage-Turner syndrome refers to an acute brachial plexopathy. It may also be called brachial neuritis or neuralgic amyotrophy. Usually it begins with acute onset of pain in the neck, shoulder, or upper arm. This is followed 3-to-10 days later by the rapid evolution of weakness affecting the proximal muscles of the arm; rarely, the hand or the respiratory muscles may also be affected. Sensory loss also occurs. Some cases are bilateral. Usually, systemic signs are absent, though mild pleocytosis may occur. The cause is unknown, but the occurrence of the syndrome after vaccination or viral infection has led to the notion that it is an immunological or autoimmune response of some sort. Familial cases also occur with an autosomal dominant pattern.

• (A) Diabetes mellitus
• (B) Temporal arteritis
• (C) Riley-Day disease (familial dysautonomia)
• (D) Systemic lupus erythematosus

Check AnswerSolution[C]:-Familial dysautonomia, or Riley-Day disease, is an autosomal recessive disorder that affects primarily Jewish children. It is characterized by a small-fiber neuropathy affecting both myelinated and unmyelinated small fibers, thereby causing an impairment of pain and temperature sensation. Sympathetic and parasympathetic ganglia are also affected, causing the autonomic features. The autonomic manifestations may include loss of tears on crying, corneal ulceration, absence of pupillary reactivity, poor temperature regulation, excessive perspiration, abnormalities of blood pressure control, dysphagia, recurrent vomiting, and gastric and intestinal dilation. There is absence of the papillae of the tongue. There is no effective treatment other than symptomatic.

• (A) Corticosteroids
• (B) Cyclophosphamide
• (C) Plasma exchange
• (D) Chronic inflammatory demyelinating polyneuropathy (CIDP)

Check AnswerSolution[D]:-CIDP is similar to Guillain-Barre syndrome, but it takes a slowly progressive or remitting course rather than one of acute onset and rapid resolution. It is a polyradiculoneuropathy, implying that it affects the proximal portions of the nerves where they exit the spinal cord at the root level. This is the reason for the increase in protein, indicating an inflammatory disorder affecting nerve roots and causing demyelination. Because nerve roots are affected, this chronic neuropathy is not limited at onset to the distal feet, as a diabetic or other degenerative neuropathy might be. Patients therefore experience paresis and sensory loss proximally as well as distally.

• (A) Cerebellar cortex
• (B) Inferior olivary nuclei
• (C) Panhypopituitarism
• (D) Acute intermittent porphyria

Check AnswerSolution[D]:-Porphyric polyneuropathy is associated with acute intermittent porphyria, which is a disorder of heme biosynthesis in the liver resulting from increased production and excretion of porphobilinogen and ?-aminolevulinic acid. The skin is not abnormal in this disorder. Instead, it is characterized by recurrent attacks of abdominal pain, gastroparesis and constipation (due to autonomic neuropathy), psychosis, axonal motor neuropathy, and autonomic instability. Seizures and syndrome of inappropriate antidiuretic hormone may also occur. Attacks may be fatal if respiratory paralysis or cardiac arrest occurs. Attacks may be provoked by porphyrinogenic drugs, such as barbiturates, phenytoin, sulfonamide antibiotics, and estrogens. These should be avoided in such patients. Treatment is best accomplished with use of intravenous hematin when supportive measures are not adequate or the case is severe.

• (A) Cerebellar cortex
• (B) Inferior olivary nuclei
• (C) Panhypopituitarism
• (D) Nitrous oxide poisoning

Check AnswerSolution[D]:-Peripheral neuropathy from exposure to anesthetic agents is an occupational hazard faced by many health care providers. Megaloblastic anemia may develop along with peripheral neuropathy in nitrous oxide-induced neuropathy. This hazard is greatly increased if the health care worker uses the anesthetic agent as a recreational drug, which is a relatively common practice with nitrous oxide. Substance abuse involving agents intended for only occasional or short-term use, such as anesthetic agents, opiates, and opioids, must be rigorously explored with health professionals who develop inexplicable neurological syndromes. Long-term abuse of nitrous oxide may lead to numbness, paresthesias, limb spasticity, and ataxia, signs pointing to central, rather than peripheral, nervous system damage. The syndrome is difficult to distinguish from vitamin B12 deficiency and appears to result from interference with the vitamin B12-dependent conversion of homocysteine to methionine.

• (A) Neonatal period
• (B) Juvenile period
• (C) Early adulthood
• (D) Sarcoidosis

Check AnswerSolution[D]:-Early in its evolution, sarcoid may be misconstrued as MS, especially if all the obvious deficits can be traced to the central nervous system (CNS). Optic atrophy and facial nerve palsies are common in sarcoid that gravitates to the nervous system. Peripheral neuropathy does not occur as a feature of MS, a strictly CNS disease, but it is still possible to have peripheral neuropathy along with MS, especially if the patient has been treated with a neurotoxic agent, such as cyclophosphamide.

• (A) Cerebellar cortex
• (B) Inferior olivary nuclei
• (C) Panhypopituitarism
• (D) Thiamine deficiency

Check AnswerSolution[D]:-Thiamine deficiency commonly produces a painful sensory neuropathy in persons with alcoholism and poor nutrition. This man’s history of esophageal varices and acknowledged alcohol abuse makes it highly likely that he has alcoholism-associated thiamine deficiency. Other vitamin deficiencies, including pyridoxine deficiency, are undoubtedly present, but thiamine deficiency is the most likely to evoke a painful neuropathy earliest. Dysesthesias and hyper-pathia associated with this neuropathy may be so severe as to make it impossible for the patient to walk or tolerate any type of garment on the feet.

• (A) Glucose
• (B) Magnesium sulfate
• (C) Pyridoxine
• (D) Thiamine

Check AnswerSolution[D]:-Without rapid replacement of thiamine stores, the patient with acute Wernicke encephalopathy may die. Usually 50-to-100 mg of thiamine is given intravenously immediately. This is followed over the course of a few days with supplementary thiamine injections of 50-to-100 mg. Without thiamine, the patient will develop periaqueductal and mamillary body lesions, which will be clinically apparent as autonomic failure. With chronic thiamine deficiency, neuronal loss occurs in alcoholic persons at least partly because of this relative vitamin deficiency. Purkinje and other cells in the cerebellar vermis will be lost to so dramatic an extent that gross atrophy of the superior cerebellar vermis will be evident.

• (A) Abnormal visual evoked responses (VERs)
• (B) Abnormal brainstem auditory evoked potentials
• (C) Posttetanic potentiation of the compound muscle action potential
• (D) Conduction block

Check AnswerSolution[C]:-Botulism is a disorder of the neuromuscular junction (NMJ). The characteristic findings are decremental response of the muscles to repetitive stimulation of the nerve at a low frequency (2-5 Hz) and incremental response to repetitive stimulation at high frequency (20-50 Hz). Other disorders of the NMJ, such as myasthenia gravis and Lambert-Eaton myasthenic syndrome (LEMS), also manifest with decremental response to repetitive stimulation at low frequencies due to depletion of acetylcholine in the synaptic cleft. Higher rates of stimulation lead to increased calcium in the presynaptic terminal, which allows more acetylcholine to be released in presynaptic disorders such as botulism and LEMS, thereby increasing the response of muscle. However, in myasthenia gravis, which is characterized by loss of acetylcholine receptors postsynaptically, there is no increase in response at higher rates of stimulation, because there is already a maximal amount of acetylcholine present in the synaptic cleft. Abnormal visual evoked and brainstem auditory evoked potentials would be seen in disorders affecting central pathways, such as MS. Conduction block occurs in demyelinating disorders affecting the nerves. Fibrillation potentials are present in denervation and certain myopathic conditions; they may occur in botulism, as well as in patients treated with botulinum toxin for therapeutic purposes, but this is not diagnostic of clinical botulism.

• (A) All febrile seizures justify spinal taps.
• (B) Most febrile seizures are due to bacterial infections.
• (C) Febrile seizures cause increased intracranial pressure that must be relieved by withdrawing cerebrospinal fluid (CSF).
• (D) Children this age may have meningitis with no manifestations other than fever and seizures.

Check AnswerSolution[D]:-Between birth and 1 year of age, what appears to be a simple febrile seizure may actually be a seizure provoked by a bacterial meningitis. The agents most likely to be responsible in a 6-month-old child are Haemophilus influenzae, Streptococcus pneumoniae, and Neisseria meningitidis. Since the introduction of vaccination against H influenzae, however, the incidence of meningitis due to this organism has been drastically reduced. Below 3 months of age, group B streptococci, Escherichia coli, and Listeria monocytogene must also be considered. All require rapid diagnosis and early treatment if the child is to survive. Even though the child may not have substantial neck stiffness, the CSF will typically reveal glucose content less than two-thirds the serum level, elevated white blood cell count, and increased protein content. The responsible organism may be isolated and cultured, but treatment of the meningitis should begin before the organism is identified. A delay of hours in treatment may be lethal. Intravenous antibiotics should be started as soon as there is convincing evidence that febrile seizures are secondary to a bacterial meningitis. The drug chosen should be the one most effective against the most probable organism. The child’s age, exposure, and symptomatology must all be considered in deciding what organism is most likely responsible for the infection.