QuestionAnswered step-by-step1.Question 1Use the following case to answer questions 1-4Case 7A 56-year-old woman was referred to a neurology practice specializing in movement disorders following a nine-year history of bradykinesia (slowness) and rigidity.In more recent years, she developed resting tremor in her hands and difficulties walking.She has been treated with levodopa (Sinemet), which helped for a few years, but then she developed severe ON-OFF fluctuations?lternating between incapacitating dyskinesias (involuntary, repetitive body movements) and total body freezing.Her sensory functions were intact, but bodily movements were increasingly difficult to govern.On the basis of the symptoms and signs described above, what is the most likely medical diagnosis?1 pointmeningitisencephalitisamyotrophic lateral sclerosisHuntington’s diseaseParkinson’s diseaseAlzheimer’s disease2.Question 2Given the benefit of levodopa, at least for a few years, where in the nervous system of this patient is there likely to be histopathological degeneration of neuronal cell bodies?1 pointsubthalamic nucleusventral pallidumstriatumputamensubstantia nigra pars compactasubstantia nigra pars reticulatanucleus accumbensglobus pallidus3.Question 3How does this histopathology (if left untreated) affect the activity of neurons in the basal ganglia?1 pointactivity decreases in the striatal neurons that contribute to the indirect pathwayactivity diminishes in the subthalamic nucleusactivity increases in the internal segment of the globus pallidusactivity diminishes in the internal segment of the globus pallidusactivity increases in the striatal neurons that contribute to the direct pathway4.Question 4In the course of medical care, this patient was evaluated for neurosurgical placement of a deep brain stimulator for relief of her movement disorder.This procedure entailed MRI-based surgical planning using a stereotaxic system, intraoperative neurophysiological recording to identify target structures, and then final positioning of the bipolar electrode for deep brain stimulation.After a brief recovery period, the patient was then subject to a second minor surgical procedure that connected the device to a subcutaneous controller and power supply.The controller was then programmed and therapeutic stimulation parameters were determined empirically.Her bradykinesia and rigidity were greatly improved and there was a marked reduction of her ON-OFF fluctuations and dyskinesias.For this woman and many like her, deep brain stimulation for movement disorders targets the subthalamic nucleus.Although the mechanisms of therapeutic action remain uncertain, one rationale for targeting the subthalamic nucleus with deep brain stimulation is provided by which of the following statements?1 pointDeep brain stimulation of the subthalamic nucleus normalizes the balance of activity in the direct and indirect pathway, leading to more appropriate and functional disinhibition of the motor thalamus.Deep brain stimulation of the subthalamic nucleus is designed to increase the discharge rate of subthalamic neurons, which in turn disinhibits the motor thalamus.Deep brain stimulation of the subthalamic nucleus increases the steady-state output of the internal segment of the globus pallidus, which facilitates the initiation of movement.Deep brain stimulation of the subthalamic nucleus is safer than the alternative targets, since subthalamic nucleus neurons are GABAergic and stimulating them cannot induce excitotoxicity.5.Question 5Use the following case to answer questions 5-12Case 8A 50-year-old man went to bed feeling very dizzy, with complaints of an occipital headache.The next day, neurological examination revealed the following:The right eyelid was closed. The right globe was deviated laterally and could not be moved upward or inward. The right pupil was dilated and did not react to light directly or consensually, or during accommodation. Light shown into the right eye caused contraction of the left pupil.There was marked hemiparesis on the left, with moderately increased muscle tone and deep reflexes on the left. An extensor plantar response (positive Babinski sign) was elicited on the left.On the left side of the body, a constant rhythmical tremor at rest was noted that was worse on movement. Movements of the left limbs were ataxic.There was hemianesthesia to all sensory modalities over the left face and the left side of the body and limbs.If not described above, then all other aspects of the neurological exam and the integrity of all other body structures were found to be within normal limits.Beginning with the first cluster of signs listed above, which extra-ocular muscles are affected in this patient? (Select all that apply.)1 pointleft inferior rectusright lateral rectusright medial rectusleft medial rectusright inferior rectusleft lateral rectusright superior rectusleft superior rectus6.Question 6Damage to which pathways/structures provides for the BEST explanation of the pupillary signs in this case?1 pointdamage to the right optic nervedamage to descending sympathetic fibers on the rightdamage to parasympathetic fibers coursing with the right oculomotor nervedamage to parasympathetic fibers coursing with the left oculomotor nervedamage to descending sympathetic fibers on the leftdamage to the posterior commissuredamage to the left optic nerve7.Question 7Which nerve appears to be damaged in this man, and is the damage located within the brainstem or along the extramedullary (outside of the CNS) course of the nerve?1 pointlong ciliary nerve (sympathetic fibers) within the left orbital fissure in the base of the skullleft and right CNs II (optic nerve), within the optic chiasmright CN III (right oculomotor nerve), within the right cavernous sinus in the base of the skullright CN III (right oculomotor nerve), within the midbrainleft CN III (left oculomotor nerve), within the midbrainright CN VII (right facial nerve), within the right stylomastoid foramen in the base of the skulllong ciliary nerve (sympathetic fibers) within the right orbital fissure in the base of the skullleft CN III (left oculomotor nerve), within the left cavernous sinus in the base of the skullleft CN VII (left facial nerve), within the left stylomastoid foramen in the base of the skull8.Question 8Damage to which motor pathway (at the specified level or side) most likely accounts for the weakness as well as changes in muscle tone, reflexes and extensor plantar response?1 pointcorticospinal fibers within the base of the left side of the pons (basis pontis)corticospinal pathway at the level of its decussationreticulospinal fibers on the leftcorticospinal fibers within the base of the left cerebral peduncle (basis pedunculi)lateral vestibulospinal pathway on the leftlateral vestibulospinal pathway on the rightreticulospinal fibers on the rightcorticospinal fibers within the base of the right cerebral peduncle (basis pedunculi)corticospinal fibers within the base of the right side of the pons (basis pontis)9.Question 9Damage to which neural structure(s) most likely accounts for the constant rhythmical tremor on the left side of the body at rest?1 pointsubstantia nigra, pars reticulata on the leftsubthalamic nucleus on the rightsubthalamic nucleus on the leftsubstantia nigra, pars reticulata on the rightglobus pallidus, internal segment on the leftsubstantia nigra, pars compacta on the rightglobus pallidus, internal segment on the rightsubstantia nigra, pars compacta on the left10.Question 10Damage to which neural structure(s) most likely accounts for the uncoordinated (ataxic) behavior of the left limbs during movement in this patient?1 pointventral lateral and ventral anterior nuclei of the thalamus (i.e., the motor thalamus)dentate-thalamic tract (projections from the cerebellar dentate nucleus to the contralateral motor thalamus) on the right side of the brainstem rostral to the decussation of the superior cerebellar pedunclesdentate nucleus in the right cerebellar hemispheredentate-thalamic tract (projections from the cerebellar dentate nucleus to the contralateral motor thalamus) within the decussation of the superior cerebellar peduncles in the rostral ponsdentate nucleus in the left cerebellar hemispheresuperior cerebellar peduncle on the rightsuperior cerebellar peduncle on the left11.Question 11Based on your analysis of the case, where is the most likely site of the lesion?1 pointcaudal midbrain (level of inferior colliculus), paramedian tegmental areacaudal pons, right lateral tegmental arearight central cortex, involving the precentral and postcentral gyriright rostral midbrain (level of superior colliculus) involving the cerebral peduncle and extensive portions of the tegmentum, with the midline being the medial margin of the damagerostral pons, paramedian tegmental arealeft central cortex, involving the precentral and postcentral gyricaudal pons, left lateral tegmental arealeft rostral midbrain (level of superior colliculus) involving the cerebral peduncle and extensive portions of the tegmentum, with the midline being the medial margin of the damage12.Question 12The localized and relatively rapid onset of symptoms in this gentleman suggests a pathological process involving the blood supply or drainage of the affected region.Which vessel is likely affected in this case?1 pointpenetrating lateral branches of the left posterior inferior cerebellar arteryright middle cerebral arterypenetrating medial branches of the right posterior cerebral arterypenetrating lateral branches of the right anterior inferior cerebellar arterypenetrating lateral branches of the right posterior inferior cerebellar arterypenetrating medial branches of the left posterior cerebral arteryleft middle cerebral arterypenetrating medial branches from the pontine segment of the basilar arterypenetrating lateral branches of the right vertebral arterypenetrating lateral branches of the left vertebral arterypenetrating lateral branches of the left anterior inferior cerebellar arteryScienceBiologyCHEM-UA 015Share Question
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