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ABPN-VNE - American Board of Psychiatry and Neurology - Vascular Neurology Exam - Dump Information

Vendor : Certification-Board
Exam Code : ABPN-VNE
Exam Name : American Board of Psychiatry and Neurology - Vascular Neurology Exam
Questions and Answers : 512 Q & A
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ABPN-VNE Questions and Answers

ABPN-VNE

Question: 502


Recovery of motor function following stroke with severe hemiparesis:


  1. May improve signifi cantly between 6 and 24 months.

  2. Cannot be predicted at 1 month.

  3. Is essentially complete at 6 months.

  4. Is independent of patient age.


Answer: C


Explanation:

Although improvement over years is recognized, functional recovery generally remains constant after 6 months. Th e level of 6- month recovery can be reliably predicted at 1 month to within 86%. Recovery is better in younger patients.


Question: 503


Th e Extremity Constraint-Induced Th erapy Evaluation (EXCITE) trial:


  1. Used constraint-induced movement therapy (CIMT) on patients in the

  2. Constrained the nonparetic leg to maximize function in the paretic leg.

  3. Found benefi t with CIMT that persisted for at least a year.

  4. Used CIMT for 6 months to show any benefi t.

  5. Found no statistically signifi cant diff erence between the two therapies


Answer: C


Explanation:

Th e Extremity Constraint-Induced Th erapy Evaluation (EXCITE) trial was a randomized multicenter trial comparing usual rehabilitation therapy with constraint-induced movement therapy (CIMT). Th e patients wore a restraining mitt on the nonparetic hand for 3 to 9 months after an ischemic stroke. Th erapy was continued for 2 weeks and showed persistent, statistically signi?

cant bene? ts.


Question: 504


Th e Barthel scale:


  1. Measures acute neurologic dysfunction.

  2. Measures activities of daily living.

  3. Is a predictor of functional independence when the score is below 20.

  4. Must be administered by a physician.

  5. Requires face-to-face contact with the patient to administer.

Answer: B


Explanation:

Th e Barthel score measures walking, dressing, feeding, grooming, and bowel and bladder control. Th e maximum score is 100. A score of above 60 represents relative independence, with a score of 100 being the best level of function. It does not measure acute neurologic dysfunction. It is relatively simple to administer, not requiring specialized medical training, and can be determined by telephone with a reliable patient or a caretaker. It is frequently used in clinical trials as an outcome measure.


Question: 505


Which of the following may be an eff ective adjunct to speech and languagetherapy in post-stroke aphasia?


  1. Transcranial magnetic stimulation.

  2. Piracetam (Nootropil, Myocalm).

  3. Donepezil (Aricept).

  4. Bromocriptine (Parlodel).

  5. All of the above.


Answer: E


Explanation:

Th e supplementation of those neurotransmitters required for synaptic plasticity is an attractive idea for the pharmacotherapy of aphasia, and there have been some reports of utility for all of the agents listed However, clinical trial results are not particularly encouraging. Although some studies using transcranial magnetic stimulation have shown bene? t, di? culties with treatment blinding hamper interpretation of the data. Piracetam, a ?-aminobutyric acid (GABA) derivative, has shown some weak bene? t but the drug is not readily available in the United States. Donepezil, a centrally acting reversible acetyl cholinesterase inhibitor, may be of bene? t but there have been no randomized trials in aphasic stroke patients. Th e dopamine D2 receptor agonist, bromocriptine, has been evaluated with con? icting results.


Question: 506


Match the disorder of speech and language with its best defi nition. Useeach answer only once.


  1. A. Aphasia Impairment of speech intelligibility.

  2. B. Dysarthria Disturbance of semantics, phonology or syntax.

  3. C. Apraxia Impaired speech planning and programming.

  4. D. Aphonia Inability to speak.

  5. E. Abulia Decreased speech and movement.


Answer: A 2, B 1, C 3, D 4, E 5.


Explanation:

Cerebrovascular disease can cause multiple speech disorders. Aphasia and apraxia of speech are caused by dominant hemispheric lesions. Dysarthria can be due to multiple di? erent upper or lower motor neuron lesions. Bilateral subcortical infarcts can cause aphonia. Abulia, a decrease in spontaneous speech and movement, is associated with lesions of the cingulate gyrus or the supplementary motor area.

Question: 507


Which statement best describes recovery after rehabilitation following cerebellarinfarction?


  1. Patients with cerebellar infarcts in general have poor functional recovery.

  2. Patients with cerebellar hemorrhage have better functional outcome than

  3. Patients with infarcts in the territory of the posterior inferior cerebellar

  4. Functional Independence Measure (FIM) scores generally do not reach a


Answer: C


Explanation:

Patients with posterior inferior cerebellar artery (PICA) infarcts (Wallenberg syndrome) generally have better recovery than patients with superior cerebellar artery (SCA) infarcts. Patients with cerebellar infarcts in general have good recovery, with FIM scores compatible with independence at the time of discharge and continued improvement after discharge. Patients with ischemic cerebellar infarcts have shorter inpatient stays and better outcome following rehabilitation than do patients with cerebellar hemorrhages. Cerebellar edema from either hemorrhage or infarction, with herniation and hydrocephalus that is not surgically treated, can signi? cantly worsen outcome.


Question: 508


Which statement best describes post-stroke depression?


  1. Th e defi nition of post-stroke depression is a worsening of the Hamilton

  2. Approximately 25% of potential patients are excluded from trials of poststroke

  3. Antidepressants should be used with caution following stroke, because

  4. should be changed after 6 weeks if no improvement is noteAntidepressants


Answer: D


Explanation:

Trials of depression after stroke have failed to yield clear treatment recommendations for several reasons. Th e use of appropriate diagnostic criteria, including depression scales, has not been systematically applied to post-stroke depression patients. A full 50% of stroke patients have been excluded from trials because of communication problems. Th e duration of treatment has been inadequate, with the average total duration of treatment being only 6 weeks. Th ere has also been inadequate duration of follow-up to determine relative outcomes following treatment. Th e American College of Physicians suggests that antidepressants should be continued for 4 months or more beyond improvement and that treatment should be switched if no clinical improvement is seen by 6 weeks. Several antidepressive agents may have neuroprotective e? ects, but clinical e? cacy for the prevention of depression after stroke or for improved stroke recovery has not been proven.


Question: 509


Which statement about brain plasticity is true?


  1. Stimulation of N-methyl-d-aspartate (NMDA) receptors may be detrimental.

  2. ã-Aminobutyric acid (GABAA) receptor antagonists may increase plasticity

  3. Serotonin has no impact on plasticity.

  4. Mechanisms involved in plasticity are consistent throughout brain cortical

Explanation:

?-Aminobutyric acid (GABAA) antagonism stimulates long-term potentiation (LTP). Glutamate is an important excitatory neurotransmitter that has multiple mechanisms related to acute brain injury and recovery. Animal studies have shown N-methyl- d-aspartate (NMDA) receptor antagonists to be neuroprotective in acute cerebral ischemia, but translational studies to humans have been disappointing. Glutamate is an excitatory neurochemical that excites NMDA receptors and enhances brain plasticity. Th e inhibition of glutamate following stroke is a complex topic, because glutamate may enhance acute neuronal damage but may be necessary for recovery and plasticity. Serotonin may enhance plasticity, and trials of this category of antidepressant are

underway as a treatment to ameliorate post-stroke depression while enhancing recovery. Th e mechanisms for brain plasticity are highly variable among di? erent cortical regions of the brain.


Question: 510


Which statement best describes brain plasticity?


  1. Animal studies have demonstrated improved performance in animals exposed

  2. Animal studies suggest motor activity (e.g., wheel running, etc.) is more

  3. Learning and repetition will increase the number of dendritic spines in

  4. Transient alterations of cortical representation areas may be common in


Answer: D


Explanation:

Transient alterations of cortical representation areas have been demonstrated with learning tasks in human volunteers. Animal studies have demonstrated that an enriched environment is useful to stroke recovery, even when introduced as late as 15 days following stroke. Social interaction appears more important than motor activities. Repetitive activities do result in an enlarged area of cortical representation for that activity.


Question: 511 Stem cells:


  1. Are found in the brains of adult rodents but not adult humans.

  2. Are found in adult human brains but are not capable of diff erentiating.

  3. Are found in adult human brains and can diff erentiate into glial cells but

  4. Are found in adult human brains and can diff erentiate into neurons.


Answer: D


Explanation:

Stem cells in adult brains were ? rst identi? ed in rodents but have now been found in human brains. Di? erentiation into neurons has been observed in the dentate gyrus. Th e clinical implications of manipulation of endogenous stem cells is a subject of speculation at present.


Question: 512

  1. B. trend toward worsened outcome that does not reach statistical signifi -

  2. A trend toward worsened outcome that does not reach statistical signifi -

  3. Increased incidence of claustrophobia in treated versus sham patients.

  4. Th e occurance of signifi cant barotrauma in approximately half of treated


Answer: B


Explanation:

Although statistical signi? cance was not reached, the trend suggests that hyperbaric oxygen treatment does not help patients with acute stroke and may result in clinical worsening. Claustrophobia was the same in treated and sham patients as all entered the hyperbaric chamber. Only a single treated patient had symptoms of barotrauma. Trials of hyperbaric oxygen to improve chronic, established neurologic de? cits due to ischemia are underway.


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