Neurology Flashcards

0
Q

Define agnosia

A

Agnosia is the inability to recognize previously familiar sensory input, and is a modality bound deficit. For example it results in a loss of the ability to recognize objects.

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1
Q

Define apraxia

A

Apraxia is a transmission disturbance on the output side, which interferes with skilled movements. For example if a patient is asked to stick out his Tongue, he understands the request but he is unable to perform the task when asked. He may then perform it after a time delay.

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2
Q

Define u

A

Astereognosis is the ability to recognize objects by palpation in one hand but not the othe

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3
Q

What does the combination of a headache and oculomotor nerve palsy suggest?

A

An aneurysm of the posterior communicating artery.

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4
Q

What clinical features suggest a subarachnoid hemorrhage?

A

A sudden onset severe headache. It occurs with exertion on about 20% of patients. Meningismus is present in more than 50%. Seizures occur in 17%.

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5
Q

What is the treatment for benign essential tremor?

A

The first line therapy is a beta blocker such as propranolol. An alternative is primidone.

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6
Q

What antidepressants are most likely to be helpful for neuropathic pain?

A

A trycyclic antidepressant or an SNRI. SNRIs include duloxetine which is approved for diabetic neuropathy, and milnacipam, which is as effective as amitriptyline in rodent studies.

Trazodone does not have analgesic properties. The data are unclear regarding bupropion. And the data is conflicting for SSRIs.

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7
Q

What are the first line treatments for postherpetic neuralgia?

A

Tricyclic antidepressants or preGabalin
are first-line treatments.

Topical lidocaine may be considered first-line in the elderly with postherpetic neuralgia, especially if there are concerns regarding the CNS side effects of oral medications.

Strong opioids and capsaicin cream are recommended as second line choices for postherpetic neuralgia. Capsaicin patches are promising, but the long-term effects of repeated applications are not clear.

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8
Q

What are the types of aphasia and how are they manifested?

A

Broca’s aphasia is an expressive aphasia. Patients are unable to produce fluent, understandable language. Comprehension is intact. Wernicke’s aphasia is a receptive aphasia. Patients are able to speak fluently; however, the content is often incorrect. Comprehension is poor. Global aphasia is a combination of both Brokas and Wernicke’s.

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9
Q

With reference to the number of hours after the event has occurred, what is the accuracy of a CT scan without contrast in picking up a subarachnoid hemorrhage?

A

CT without contrast is 100% accurate in cases within 12 hours of the bleed. It drops to 93% within 24 hours and remains at up to 50% to seven days.

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10
Q

In what situations is thrombolysis contraindicated for an acute stroke?

A

It is contraindicated if it is more than three hours past the onset of the neurological deficit. It is also contraindicated in patients with blood glucose of less than 50 or more than 400, with a resolving transient ischemic attack, and with hemorrhage visible on CT.

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11
Q

What are the common toxicities shared by all antiepileptic drugs?

A

Suicide risk is twice that compared with placebo. There are neurotoxicities which include ataxia, dizziness, somnolence, fatigue and headache. Rash is common and may vary from simple maculopapular rashes to Stevens-Johnson syndrome. Liver enzyme induction or inhibition is common.

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12
Q

Which antiepileptic drugs are most likely to interfere with the action of oral contraceptive medication?

A

Carbamazepine, phenytoin, phenobarbital/primidone, topiramate, and oxcarbazepine.

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13
Q

What supplements should a pregnant woman on antiepileptic take?

A

Women taking carbamazepine or valproic acid should take 4 mg of full like acid per day beginning prior to conception. Women on phenobarbital, carbamazepine, phenytoin, topiramate and oxcarbazepine should supplement with vitamin K 10 to 20 mg per day in the last month of pregnancy.

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14
Q

Women may breast-feed on which antiepileptic drugs?

A

All except Lamotrigine (Lamictal)

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15
Q

When and how should levels of antiepileptic drugs be monitored in pregnancy?

A

Both total and free drug levels should be checked at six weeks, 10 weeks, then once a trimester, then first or second postpartum week.

16
Q

What are the diagnostic criteria for migraine without aura?

A

A headache lasting 4 to 72 hours with two of the following: unilateral, throbbing, moderate to severe, worsened by usual physical activity. In addition there must be at least one of the following: photophobia, phonophobia, nausea and vomiting. There should be no evidence of any other underlying disease.

17
Q

What are the diagnostic criteria for migraine with aura?

A

The same as for migraine without aura but in addition the following must be present: transient neurological symptoms which start gradually over 5 to 20 minutes, last less than 60 minutes, and are followed by a headache that starts within 60 minutes. The types of aura include: visual with flickering lights spots or lines, sensory with pins and needles or numbness, or dysphasic speech. These symptoms are fully reversible. At least two attacks of headache with aura must occur.

18
Q

What are the red flags that indicate that a patient with a possible migraine needs neuroimaging?

A

Rapidly increasing headache frequency, history of lack of coordination or localized neurological signs during the headache (not preceding it), and headaches that awaken the patient from sleep.

19
Q

Triptans should be avoided in what patients?

A

Patients with familial hemiplegic migraine, with basilar migraine, with ischemic stroke, with ischemic heart disease Prinzmetal’s angina or uncontrolled hypertension, and pregnancy.

20
Q

What types of migraines should get prophylactic treatment rather than treatment of the acute symptoms?

A

Hemiplegic migraines, basilar migraines, and migraines with a prolonged aura.

21
Q

What drugs have been used for the preventative treatment of migraine?

A

Antihypertensives including beta blockers, calcium channel blockers, ACE/ARB’s. Antidepressants including amitriptyline and venlafaxine Anticonvulsants including valproate, gabapentin, and topiramate.

22
Q

What are the clinical features of femoral neuropathy and who is likely to get it?

A

Weakness of the quadriceps with sparing of hip Iliopsoas weakness is fairly common, though not always present. Sensory loss of the anterior thigh and most of the medial thigh is typical. The sensory loss extends down the medial shin to the region of the arch of the foot. The knee-jerk is typically decreased or absent.

It may be caused by trauma such as pelvic or hip fracture. It may be iatrogenic and is a recognized complication of childbirth and procedures such as hip replacement, abdominal and pelvic surgery or laparoscopy, and inguinal lymph node biopsy. It is occasionally seen in patients with diabetes.

23
Q

What are appropriate prophylactic medications for migraine headaches in children under 12?

A

Propranolol and amitriptyline. Carbamazepine might be used but it has significant side effects and requires monitoring. Sumatriptan is not approved for children under 12.

24
Q

What is the common the presentation of pseudotumor cerebri?

A

Usually presents in an obese woman of childbearing age. Headache is the most common presenting presenting symptom. Many but not all patients note that the headache pain is of unusual severity. Associated nausea and vomiting are not infrequent. Headache may worsen with posture changes and improve with NSAIDs. Retro bulbar pain and pain with eye movement or globe compression are somewhat more specific features for IIH. Neck stiffness is also commonly reported. Transient visual obscurations occur in about two thirds of patients that last seconds at a time and may be bilateral or unilateral. Photopsias or brief sparkles or flashes of light may also occur and can be provoked by positional changes and Valsalva. Pulsatile tinnitus is common and somewhat specific for the diagnosis. Diplopia may occur and is usually horizontal.

The most common signs on physical examination aren’t papilledema, visual field loss, and sixth nerve palsy.

25
Q

That is Friedreichs ataxia?

A

It is an autosomal recessive progressive spinocerebellar disorder. It is generally diagnosed in childhood–patients generally present in childhood with difficulty walking. The disease progresses to involve the arms and trunk. Eventually speech is affected and scoliosis develops. Depressed knee and ankle tendon reflexes are seen on physical exam. MRI may show spinal cord and cerebellar atrophy. EKG maybe significant for ventricular hypertrophy. There is no effective treatment. Patients generally die by the age of 35.

26
Q

What is Broca’s aphasia?

A

Broca’s aphasia is an expressive aphasia. Patients are unable to produce fluent, understandable language. Comprehension is intact.

27
Q

What is Wernicke’s aphasia?

A

Wernicke’s is a receptive aphasia. Patients are able to speak fluently; however, the content is often incorrect. Comprehension is poor.

28
Q

What is Wernicke Korsakoff syndrome?

A

It I s seen in alcoholics as a result of vitamin B1 or thiamine deficiency. It is a combination of Wernicke encephalopathy and Korsakoff syndrome. Wernicke encephalopathy is a common acute neurological disorder manifested by a clinical triad of encephalopathy, oculomotor dysfunction, and gait ataxia. Korsakoff syndrome is a late, neuropsychiatric manifestation of Wernicke encephalopathy in which there is a striking disorder of selective anterograde and retrograde amnesia.

29
Q

Describe the presentation and management of Guillain-Barré syndrome.

A

It is an autoimmune disorder characterized by progressive ascending muscle weakness beginning in the lower extremities. It is often triggered by an infection, frequently Campylobacter. It can also be triggered by Hodgkin’s disease, mononucleosis, and HIV. Patients present with a history of weakness and tingling sensations in their lower extremities. As the disease progresses, patients may develop shortness of breath, difficulty with bowel and bladder control, and eventually facial weakness and difficulty swallowing. Physical exam is significant for the absence of DTRs in the lower extremities. CSF shows an elevated protein count and normal cell count. EMG is significant for slowed conduction velocity. The disease typically peaks in two to three weeks, but can have a much more rapid course and progress to respiratory failure in hours. Treatment includes plasmapheresis and IVIG. The mortality rate is 5%.

30
Q

Describe the presentation and management of ALS.

A

ALS is a progressive neurodegenerative disease that is generally fatal in 3 to 5 years. It causes degeneration of both upper and lower motor neurons. The cause is unknown and most cases are sporadic. Symptoms can initially be subtle. Patients may have weakness or clumsiness. Patients eventually develop difficulty speaking, swallowing, and breathing. The cause of death is usually respiratory failure. The diagnosis is made clinically based on the presence of both upper and lower motor neuron dysfunction. EMG can be used to confirm the diagnosis. Riluzole is the only drug available for treating ALS and there is some evidence that it may slow the progression of the disease. Otherwise treatment is supportive care with physical and occupational therapy, nutritional and psychosocial support.

31
Q

What are the signs and symptoms of hyperkalemia?

A

Symptoms include weakness, muscle paralysis, and cardiac arrhythmias. Findings include peaked T waves, flattened P waves and prolonged QRS complex on EKG, with ventricular fibrillation in severe cases.

32
Q

What conditions and drugs may cause hyperkalemia?

A

Conditions: excessive potassium intake or excessive potassium release from cells as in trauma, burns or tumor lysis syndrome. It may also result from massive hemolysis. Insufficient elimination from renal insufficiency is also a cause. It is seen when there is metabolic acidosis and in uncontrolled diabetes.

Medications: ACE inhibitors, ARB’s, potassium sparing diuretics, NSAIDs, and heparin, and oral drospirenone/ ethinyl estradiol (Yaz Yasmin)

33
Q

What are the causes of hypokalemia? How does it present?

A

Hypokalemia may result from inadequate intake, metabolic alkalosis, excessive G.I. losses, and excess renal excretion. Patients are usually asymptomatic until potassium is below 3.0. They may present with weakness and cardiac arrhythmias. EKG findings include flattened T waves, U waves, ST depression,and a prolonged QT interval.