Neurology Flashcards

1
Q

What is the significance of doll’s eyes?

A

Doll’s eyes, when the eyes keep “looking” in the original direction when the head is turned, signify that the brainstem is working normally.

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2
Q

Which pupil finding can be seen with uncal herniation?

A

In uncal herniation there is one dilated and nonreactive pupil.

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3
Q

What is the presentation of locked-in syndrome?

A

In locked-in syndrome a patient is awake and aware of the surrounding environment but may only have the ability to control eye movements.

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4
Q

What is the definition of persistent vegetative state?

A

A persistent vegetative state is a comatose state lasting more than 4 weeks.

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5
Q

What is akinetic mutism vs. catatonia?

A

Patients with akinetic mutism are profoundly apathetic, although they register most of what is happening around them. Patients with catatonia are unresponsive although they have preserved oculocephalic reflexes (ie. doll’s eyes).

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6
Q

How is brain death diagnosed? Is an EEG required?

A

EEG is not required for diagnosis of brain death. Brain death requires knowledge of a preceding catastrophic event (clinical or imaging) responsible for the current state and exclusion of all possible metabolic confounders. Temperature should be normal and SBP >100 (with pressors if needed). Absence of brainstem function can then be documented with loss of spontaneous eye movements, midposition of eyes, loss of oculocephalic reflexes, dilated or midpoint fixed pupils, paralysis of bulbar musculature, absence of motor or autonomic responses to noxious stimuli, and absence of spontaneous respiratory movements.

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7
Q

Name some environmental triggers for seizures in susceptible people.

A

Triggers for seizures in susceptible people include alcohol, cocaine, intense emotions, strobe lighting, loud music, stress, menses, and lack of sleep.

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8
Q

What are some differences between generalized and focal seizures?

A

Focal seizures involve 1 side of the body and are not associated with impaired consciousness. Generalized seizures have altered consciousness and usually movement of both sides of the body.

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9
Q

Which test should you order if you suspect recurrent psychogenic nonepileptic seizures (PNES)?

A

An EEG with video monitoring should be ordered in a patient with suspected PNES.

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10
Q

What is the treatment of status epilepticus?

A

The treatment of status epilepticus involves correcting hypoglycemia if present with IV thiamine followed by IV dextrose. Then give a benzodiazepine followed by a loading dose of phenytoin.

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11
Q

Which drug is used to treat absence seizures?

A

Ethosuximide is used only to treat absence seizures.

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12
Q

Which AEDs decrease the effectiveness of oral contraceptives?

A

The effectiveness of OCPs is reduced by phenytoin, phenobarbital, carbamezpine, lamotrigine, oxcarbazepine, and topiramate.

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13
Q

Which AED serum concentration is reduced by estrogens?

A

Estrogen can reduce the drug concentration of lamotrigine.

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14
Q

Which AED reduces the serum concentration of progestins?

A

Lamotrigine can reduce the concentration of progestins.

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15
Q

What is the definition of dementia?

A

Dementia is a chronic cognitive decline with or without behavioral impairment that is progressive, interferes with normal daily function, and is not due to delirium or underlying psychiatric disorder.

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16
Q

Which 5 domains may be impaired in patients with dementia?

A

The 5 cognitive domains that may be affected in dementia are memory, executive, perception, language, and behavior.

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17
Q

What is the definition of mild cognitive impairment?

A

MCI is diagnosed when only 1 domain of cognitive is in decline but does not significantly impact daily functioning.

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18
Q

What is the clinical triad of normal pressure hydrocephalus?

A

The triad of normal pressure hydrocephalus is gait apraxia, dementia, and urinary incontinence.

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19
Q

How is Alzheimer disease diagnosed?

A

Alzheimer disease is diagnosed in a patient with insidious, progressive illness with marked impairments in > 2 cognitive domains. Do not diagnose AD in patients with history of significant cerebrovascular disease, clinical features of frontotemporal dementia or dementia with Lewy bodies, has evidence of another psychiatric or neurologic illness, or takes medication that can cause cognitive impairment.

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20
Q

Which class of drugs is the 1st line treatment for Alzheimer disease?

A

Cholinesterase inhibitors are 1st line therapy for Alzheimer disease.

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21
Q

Which drug is used with a cholinesterase inhibitor for the treatment of advanced Alzheimer disease?

A

Memantine (Namenda) can be added to a cholinesterase inhibitor in advanced AD.

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22
Q

What is the potential complication from the use of atypical antipsychotics in elderly patients with dementia?

A

Atypical antipsychotics are associated with increased mortality in AD.

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23
Q

Compare and contrast the features of NPH, AD, and vascular dementia.

A

NPH presents with a triad of dementia, gait ataxia, and urinary incontinence. AD is predominantly a progressive decline in cognitive function. Vascular dementia often follows a stepwise deterioration.

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24
Q

How does the clinical presentation of frontotemporal dementia differ from that of Alzheimer disease?

A

Frontotemporal dementia differs from AD in that it has a more rapid onset and more prominent behavioral and personality changes, often with disinhibition or language deficits.

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25
Q

Is CJD insidious or rapid?

A

CJD causes a rapidly progressive dementia

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26
Q

How do you diagnose CJD?

A

Gold standard for diagnosis of CJD is brain biopsy. However, T1/T2 MRI with diffusion-weight images, EEG (periodic sharp waves and complexes), and 14-3-3 protein in an otherwise bland CSF can help with diagnosis.

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27
Q

Compare and contrast dementia with Lewy bodies and progressive supranuclear palsy with Parkinson disease dementia.

A

Parkinson disease dementia primarily affects executive functions and attention in its early stages. When dementia precedes or develops within one year of motor symptoms in PD, consider dementia with Lewy bodies. Progressive supranuclear palsy presents with dementia, gaze palsy, and falls.

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28
Q

What is the problem with using antipsychotic drugs to treat patients with Parkinson disease?

A

Antipsychotic drugs have an increased risk of death in patients with PD.

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29
Q

What are the clinical features of Huntington disease?

A

Huntington disease causes dementia, chorea, and psychiatric disturbances, including personality changes, depression and psychosis.

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30
Q

Name some features that distinguish depression from dementia.

A

Patients with dementia often have frontal release signs (grasp, root, suck, and palmomental reflex) which are not seen in depression. Also, immediate recall is poor in depression due to poor attention but are preserved in early dementia.

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31
Q

What are the 2 hallmarks of delirium?

A

The clinical hallmarks of delirium are decreased attention span and varying states of confusion.

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32
Q

What are two ocular presentations of multiple sclerosis?

A

Two ocular presentations of MS are optic neuritis and internuclear ophthalmoplegia. In INO the patient has difficulty with horizontal eye movements but normal convergence.

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33
Q

Which findings in CSF are helpful for the diagnosis of MS?

A

Oligoclonal bands are IgG directed at myelin. There presence in CSF is helpful in diagnosis of MS.

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34
Q

What is the treatment for an acute exacerbation of MS?

A

Treatment for acute exacerbation of MS is steroids.

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35
Q

Natalizumab can cause what neurologic disease?

A

Natalizumab has been associated with PML.

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36
Q

What is the cause of central pontine myelinolysis? Which clinical findings are seen in this condition?

A

Central pontine myelinolysis is seen with overly rapid correction of hyponatremia. It can present with quadriparesis, mutism, pseudobulbar palsy, chewing or swallowing dysfunction, or locked-in syndrome.

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37
Q

What are the 4 motor features of parkinsonism?

A

The 4 motor features of PD are: 1) resting tremor, 2) rigidity and flexed posture, 3) retarded movement, and 4) loss of postural reflexes.

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38
Q

Name some drugs commonly used to treat Parkinson disease.

A

Drugs that are commonly used to treat PD are levodopa + carbidopa, non-ergotamine dopamine receptor agonists (ropinirole, pramipexole, and rotigotine), amantadine, anticholinergics, and MAO-B inhibitors (selegiline and rasagiline).

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39
Q

What is the potential side effect of anticholinergic drugs when used to treat Parkinson’s? Ropinirole has which side effects?

A

Anticholinergics can cause altered mental status. The dopamine receptor agonists like ropinirole can cause impulse control disorders like hypersexuality, compulsive shopping, and pathological gambling.

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40
Q

Selegiline can cause serotonin syndrome when combined with which other drugs?

A

Selegiline combined with tricyclics or SSRIs can trigger serotonin syndrome.

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41
Q

What is the clinical presentation of serotonin syndrome?

A

Serotonin syndrome presents with cognitive impairment, autonomic effects (hyperthermia, tachycardia, shivering, and sweating), and somatic effects such as hyperreflexia, clonus, twitching, and tremors.

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42
Q

What is the potential complications of an L-dopa dose reduction in a patient with Parkinson psychosis?
P

A

atients with PD psychosis are at risk for neuroleptic malignant-like syndrome with dose reduction of L-dopa.

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43
Q

What is the classic eye finding of progressive supranuclear palsy?

A

Patients with progressive supranuclear palsy develop vertical ophthalmoplegia within 2 years of diagnosis which progresses to complete ophthalmoplegia in all directions.

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44
Q

What is the clinical presentation of essential tremor? What improves it?

A

Essential tremor is a fine action tremor. It tends to decrease with alcohol intake.

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45
Q

What causes tardive dyskinesia? How is it treated?

A

Tardive dyskinesia is caused by long-term antipsychotic use. Mild TD can be treated with benzodiazepines. More severe cases can be treated with botulinum toxin.

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46
Q

What is the clinical presentation of neuroleptic malignant syndrome?

A

Neuroleptic malignant syndrome presents with hyperthermia, rigidity, diaphoresis, autonomic instability, and altered mentation. Labs often show leukocytosis, electrolytes disturbances, and elevated CK.

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47
Q

Which comorbidities are associated with Tourette syndrome?

A

Tourette syndrome is associated with the comorbid conditions of ADHD, OCD, learning disorders, and conduct disorders.

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48
Q

Which antihypertensive drug is used to treat tics in Tourette syndrome?

A

Clonidine is 1st line treatment of Tourette syndrome.

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49
Q

What is the classic triad of symptoms observed in patients with brain abscess?

A

The classic triad of brain abscess is fever, headache, and focal neurologic symptoms.

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50
Q

How does treatment of a varicella infection differ from the treatment of herpes simplex?

A

Varicella zoster infection requires higher doses of antiviral medicines than herpes simplex.

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51
Q

What is the diagnostic test for West Nile virus encephalitis?

A

Diagnosis of West Nile virus requires demonstration of antibody in spinal fluid.

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52
Q

Aside from patients with AIDS, PML can occur in which patients? What are the symptoms of PML?

A

In addition to AIDS patients, PML is seen in patients on immunosuppressive therapy and who are receiving natalizumab.

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53
Q

What is the treatment for CNS toxoplasmosis?

A

CNS toxoplasmosis is treated with sulfadiazine, pyrimethamine, and leucovorin.

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54
Q

What is the clinical presentation of neurocysticercosis?

A

Neurocysticercosis presents when the cysts rupture causing cerebral edema, usually with seizures as the 1st symptom.

55
Q

Characterize the CSF of a patient with cryptococcal meningitis.

A

The CSF in a patient with cryptococcal meningitis generally has a very high opening pressure and positive cryptococcal antigen.

56
Q

How useful is the CSF/serum cryptococcal antigen (sensitivity/specificity) in diagnosing meningitis?

A

The sensitivity/specificity of CSF cryptococcal antigen in HIV-infected patient is >95%. In non-HIV-infected patients it is still 93-98% sensitive.

57
Q

Name some triggers of migraine headaches.

A

Triggers for migraines include certain foods, alcohol, menstruation, exposure to glare or other strong sensory stimuli, and rapid changes in barometric pressure.

58
Q

What is the main difference between a complicated migraine and a migraine with aura?

A

An aura lasting longer than 60 minutes is indicative of complicated migraine or concern for stroke.

59
Q

Which migraine patients should not receive a triptan drug?

A

Triptans are contraindicated in complicated or basilar migraines, coronary heart disease or Prinzmetal angina, history of stroke, uncontrolled hypertension, and pregnancy.

60
Q

Which migraine prophylactic drug causes kidney stones?

A

Topiramate is associated with kidney stones.

61
Q

Are cluster headaches more common in men or women?

A

Cluster headaches are 5 times more common in men than women.

62
Q

What are the clinical features of a cluster headache?

A

Cluster headaches cause unilateral, peri- or retroorbital, severe pain characterized as an “ice pick” or “hot poker”. It may be associated with vasomotor phenomena.

63
Q

How do you treat a cluster headache?

A

The primary treatment of cluster headache is oxygen. Subcutaneous or intranasal triptans are also used.

64
Q

Which agent is first line to prevent cluster headaches?

A

Verapamil is the drug of choice for preventing cluster headaches.

65
Q

What is the most common variety of headache?

A

Tension headache is the most common variety of headache.

66
Q

Name a risk factor that is associated with idiopathic intracranial hypertension?

A

Obesity is strongly associated with idiopathic intracranial hypertension.

67
Q

What is the clinical presentation of idiopathic intracranial hypertension?

A

The cardinal symptom of idiopathic intracranial hypertension is a morning headache that is worse with coughing or straining. There is almost always peripheral visual field loss though patients may not notice this. Pulse-synchronous tinnitus may be present.

68
Q

Which viral infection increases risk of stroke?

A

Varicella zoster infection increases the risk of stroke.

69
Q

In addition to exercise, smoking cessation, and control of diet, blood pressure, and lipids, which other interventions should be offered to certain patient groups in order to prevent stroke?

A

Carotid endarterectomy should be considered on patients with >70% stenosis of the carotid artery if surgical morbidity and mortality is <3%. Screen high risk patients for aneurysms, including patients with 2 or more 1st degree relatives with history of SAH/aneurysm and patients with ADPKD with 1 or more relatives with history of SAH/aneurysm.

70
Q

Which imaging study would you do for a patient with a suspected subarachnoid hemorrhage?

A

Non-contrast head CT is the test of choice for suspected SAH.

71
Q

Which imaging studies are recommended for evaluation of vasculature in patients with TIA or stroke?

A

CTA or MRA should be done for evaluation of the vasculature in patients with TIA or stroke. CTA is better than MRA at identifying intracranial lesions.

72
Q

How does a patient with an ACA stroke typically present?

A

A patient with ACA stroke typically presents with leg weakness opposite to the side of the stroke.

73
Q

How does a patient with an MCA stroke typically present?

A

A patient with MCA stroke presents with arm/leg weakness that is opposite the side of the stroke. There is also a language deficit if the dominant hemisphere is involved.

74
Q

How does a patient with a PCA stroke typically present?

A

A patient with PCA stroke commonly presents with visual field defects plus color anomia plus paresthesias without motor signs.

75
Q

How do you distinguish a central vs peripheral 7th nerve palsy on physical exam?

A

Distinguish a central vs. peripheral 7th nerve palsy based on ability to move the eyebrow. This is intact in central 7th nerve palsy and absence in peripheral 7th nerve palsy.

76
Q

What is the clinical presentation of lateral medullary syndrome? What type of stroke causes it?

A

Lateral medullary syndrome (Wallenberg syndrome) presents with ipsilateral cerebellar signs, nausea, vomiting, nystagmus, ipsilateral Horner syndrome, ipsilateral palate and vocal cord weakness, and “crossed” sensory loss (ipsilateral face and contralateral body). It is caused by vertebrobasilar stroke.

77
Q

Which tests are recommended in the initial evaluation of ischemic stroke?

A

Initial evaluation of ischemic stroke includes NECT, chemistries, CBC, coags, ECG and telemetry monitoring.

78
Q

If imaging for SAH is negative and suspicion is high, what is the next diagnostic test and what does it look for?

A

If suspicion is high for SAH but CT is negative perform a lumbar puncture to examine for xanthochromia (pink or yellow supernatant).

79
Q

What is the timeframe for prescription of tPA in patients with ischemic stroke?

A

The absolute timeframe for tPA administration in ischemic stroke is 4.5 hours.

80
Q

Which patients with a stroke between 3 and 4.5 hours are excluded from tPA?

A

The exclusion criteria for tPA in the 3-4.5 hour timeframe are age > 80, severe stroke (NIHSS > 25), on anticoagulation regardless of INR, and history of both diabetes and prior ischemic stroke.

81
Q

What are the recommendations for lowering BP in patients with ischemic stroke who do not receive tPA?

A

If no tPA is given withhold medicines for BP < 220/120. If BP > 220/120 treat to reduce by ~15%. If tPA is to be given BP must be < 185/110.

82
Q

Why should you keep a patient with ischemic stroke in the posterior fossa under close observation?

A

A patient with ischemic stroke of the posterior fossa needs close observation because of risk of herniation, either up or down.

83
Q

What are the recommended antiplatelet regimens post-ischemic stroke?

A

Patients with history of ischemic stroke should be treated with aspirin 50-325 mg daily, ASA + dipyridamole, or clopidogrel.

84
Q

What are the most common causes of an intracerebral hemorrhage?

A

The two most common causes of intracranial hemorrhage are hypertension and amyloid angiopathy.

85
Q

Which further evaluation is indicated in cocaine users who present with a cerebral bleed even if hypertensive?

A

Cocaine users with a cerebral bleed still need CTA or MRA to rule out AVM or aneurysms.

86
Q

What are the recommendations for treatment of BP in a patient with an intracerebral hemorrhage?

A

Patients with intracranial hemorrhage need to have their SBP lowered to below 140.

87
Q

What is the most common cause of SAH?

A

The most common cause of SAH is an aneurysm of the circle of Willis.

88
Q

What causes mycotic aneurysms?

A

Mycotic aneurysms are caused by septic emboli most commonly from infected heart valves.

89
Q

Which patient groups are prone to subdural hematomas?

A

Elderly patients with falls, alcoholism, and MVAs are at highest risk for SDH.

90
Q

Describe the differences between subdural and epidural hematomas.

A

SDH evolves slowly whereas epidural hematoma progresses rapidly. In epidural hematoma there may be a short period of lucency before rapid obtundation.

91
Q

Describe the findings in subacute combined degeneration due to B12 deficiency.

A

Subacute combined degeneration due to B12 deficiency presents with gradual weakness with paresthesias and loss of proprioception with development of ataxia.

92
Q

Which other mineral deficiency can present like the subacute combined degeneration due to vitamin B12 deficiency?

A

Copper deficiency can present like the subacute combined degeneration due to B12 deficiency.

93
Q

What are the risks for an epidural abscess? What is the most common cause?

A

The risk factors for epidural abscess are immunodeficiency states and bahviors that lead to transient bacteremia.

94
Q

What causes Pott disease?

A

Pott disease is tuberculous osteomyelitis of the spine.

95
Q

Describe the clinical presentations of neurosyphilis.

A

Neurosyphilis causes PARESIS. Personality changes, Affect changes, Reflexes, Eyes (Argyll-Robertson pupil), Sensorium, Intellect, and Speech.

96
Q

What is the clinical presentation of transverse myelitis?

A

The clinical presentation of transverse myelitis is acute and progressive development of paresthesias, bilateral leg weakness, and numbness with a sensory level below the affected level.

97
Q

What is Devic disease? Which auto-antibody is the culprit?

A

Devic disease (neuromyelitis optica) is a variant of myelitis affecting the optic nerves and spinal cord. It involves serum NMO-IgG antibodies, also known as anti-aquaporin antibodies. These are 73% sensitive and 91% specific for Devic disease.

98
Q

What are the symptoms of cervical myelopathy?

A

Cervical myelopathy causes spasticity, hyperreflexia, and gait abnormalities.

99
Q

What is lumbar spinal stenosis? What are the classic exacerbating and relieving body positions and movements?

A

Lumbar spinal stenosis is a congenital narrowing of the spinal canal. It is typically worsened by upright posture and walking downhill and improves with bending forward or walking uphill.

100
Q

From a patient’s history, which clues help you differentiate lumbar spinal stenosis from vascular claudication?

A

Lumbar spinal stenosis causes leg pain with walking that requires sitting down to relieve it. With vascular claudication the pain goes away with stopping walking without a need to sit down.

101
Q

What is the clinical presentation of syringomyelia?

A

Syringomyelia causes painless weakness and wasting in the hands and arms and segmental sensory loss of dissociative type (ie. loos of thermal and painful sensation with sparing of tactile, joint position, and vibratory sensation).

102
Q

What is the clinical presentation of ALS?

A

Patients with ALS typically present with diffuse hyperreflexia and spasticity (UMN) along with fasciculations, weakness, and atrophy (LMN).

103
Q

What conditions can cause UMN and LMN signs in the same patient?

A

Conditions that cause UMN and LMN signs in the same patient include ALS, B12 deficiency, cervical myelopathy, syringomyelia, Friedrich ataxia, and neurosyphilis.

104
Q

Where are the main points of compression for ulnar, median, and peroneal nerves?

A

The ulnar nerve gets compressed at the cubital tunnel of the elbow. The median nerve gets compressed in the carpal tunnel. The peroneal nerve is compresses at the proximal head of the fibula.

105
Q

What frequently causes nocturnal awakening with hand pain? Which nerve?

A

Carpal tunnel syndrome frequently causes nocturnal awakening with hand pain. It is caused by compression of the median nerve.

106
Q

Mononeuritis multiplex is caused by which diseases?

A

Mononeuritis multiplex is caused by vasculitis, diabetes, connective tissue diseases, RA, and Lyme disease.

107
Q

Which infection should you consider in a hiker from Connecticut who presents with new onset of foot drop?

A

Lyme disease should be considered in a hiker who presents with foot drop.

108
Q

Name 3 disease processes that can cause facial palsy.

A

HSV, varicella zoster infection, Lyme disease, and acute HIV can all cause facial palsy.

109
Q

What is the clinical presentation of Bell’s palsy?

A

Bell’s palsy presents with unilateral facial palsy affecting the eyebrow

110
Q

Diabetes can cause which neuropathies?

A

Diabetes most commonly causes a symmetrical, distal, sensory neuropathy. It can also cause cranial neuropathy, lumbosacral plexopathy (diabetic amyotrophy), and autonomic neuropathy.

111
Q

Which CSF findings are characteristic of Guillain-Barre syndrome?

A

Patients with GBS have high protein with normal cell count (“albuminocytologic dissociation”) in the CSF.

112
Q

How does treatment of CIDP differ from the treatment of Guillain-Barre syndrome?

A

Glucocorticoids are not helpful in Guillain-Barre syndrome, but they can hasten recover and prevent relapse in CIDP.

113
Q

Name the drug used to treat diabetes that also can induce B12 deficiency and cause a severe peripheral neuropathy.

A

Metformin can cause B12 deficiency and cause peripheral neuropathy.

114
Q

What are the clinical presentations of myasthenia gravis?

A

Myasthenia gravis causes episodic weakness with repetitive movements. Symptoms tend to be worse at the end of the day. Ptosis is common. Muscle atrophy is rare and reflexes are normal.

115
Q

How is MG diagnosed?

A

Diagnosis of MG is best confirmed by measuring antibodies against acetylcholine receptors (AChR-Abs) and against muscle-specific tyrosine kinase (MuSK-Abs).

116
Q

Which other tests should be done in patients with MG?

A

A CT or MRI of the chest are indicated to rule out thymoma. Thyroid studies should be checked as 30% of MG patients have chronic autoimmune thyroiditis.

117
Q

Which cancers cause Lambert-Eaton myasthenic syndrome?

A

About 60% of patients with LEMS have small cell lung cancer. Other associated cancers include prostate, breast, stomach, rectum, and lymphomas.

118
Q

What happens to deep tendon reflexes in MG and LEMS?

A

Deep tendon reflexes are normal in MG and depressed in LEMS.

119
Q

Where is the muscle weakness that occurs with inclusion body myositis?

A

Inclusion body myositis causes proximal muscle weakness which is slowly progressive and spreads distally.

120
Q

Progressive limb girdle weakness in an adult patient who has a family history of the same is indicative of which diagnosis?

A

Progressive limb girdle weakness in an adult patient with a family history of the same is suggestive of myotonic dystrophy.

121
Q

How do you work up a patient with metatarsal pain?

A

Metatarsal pain may be due to neuroma or metatarsal stress fracture. MRI will make diagnosis.

122
Q

Name the maneuvers frequently employed to treat BPV.

A

Epley and Samont maneuvers are used to treat BPV.

123
Q

What are the clinical features of Meniere disease?

A

The clinical features of Meniere disease are vertigo, tinnitus, and hearing loss.

124
Q

Which TIAs cause vertigo?

o.

A

Vertebrobasilar TIAs cause vertig

125
Q

Which brain lesion is suggested by upbeating jerk nystagmus? Downbeating?

A

Upbeating nystagmus suggests a lesion in the pons but can also be seen in lesions of the medulla and cerebellum (infratentorial). Downbeating nystagmus indicates a lesion in the cervicomedullary junction.

126
Q

A patient with a history of prostate cancer and new onset of urinary incontinence should make you consider which diagnosis?

A

New onset urinary incontinence in a patient with a history of prostate cancer suggests spinal metastasis with cord compression.

127
Q

What is Wernicke encephalopathy? How is it treated?

A

Wernicke encephalopathy is a mild and reversible neurologic dysfunction caused by thiamine deficiency. It presents with global confusion and inattention, disorientation, and memory loss. Abnormal eye movements are typical and include horizontal nystagmus and disordered conjugate gaze. Patients may also have trouble standing or walking due to truncal ataxia. It is treated with IV thiamine.

128
Q

How does the presentation of the typical Wernicke patient differ from that of the typical Korsakoff patient?
.

A

Whereas Wernicke encephalopathy presents with confusion, walking “drunk”, and trouble moving eyes, Korsakoff patients are usually alert and attentive but tell fantastical stories that they do not remember

129
Q

What are the symptoms of lithium toxicity?

A

Lithium toxicity presents with confusion,delirium, dizziness, nystagmus, ataxia, and nephrogenic DI.

130
Q

What effect does the hyponatremic state have on lithium resorption by the kidney?

A

Hyponatremia causes increased lithium resorption from the kidney.

131
Q

What are the causes of acute unilateral blindness in older patients?

A

Acute, unilateral blindness in older patients if usually due to arteritis (5%) or thrombosis (95%) from retinal vein or artery occlusion.

132
Q

What do flashes followed by decreased vision suggest?

A

Retinal detachment causes flashes followed by decreased vision.

133
Q

What 4 symptoms are associated with narcolepsy?

A

The narcolepsy tetrad includes daytime sleepiness, cataplexy, hypnagogic hallucinations, and sleep paralysis.