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STEP2 > Neurology > Flashcards

Neurology Flashcards

1
Q

What are the four major risk factors for stroke?

A
  • hypertension
  • hyperlipidemia
  • diabetes
  • smoking
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2
Q

Describe the symptoms of an ACA stroke.

A

patients have personality or cognitive defects, leg more than arm weakness, and urinary incontinence

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3
Q

Describe the symptoms of a PCA stroke.

A

patients have a contralateral homonymous hemianopsia with macular sparing, contralateral sensory loss of the limbs, ipsilateral sensory loss of the face, and 9th and 10th cranial nerve palsy

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4
Q

Describe anti-platelet management for those who suffer an ischemic stroke.

A
  • start aspirin within 24 hours of stroke onset

- if patient was already on aspirin at the time of the stroke, add dipyridamole or switch to clopidogrel

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5
Q

The etiologic workup for stroke should include what?

A
  • echocardiogram looking for damaged valves, thrombi, atrial enlargement, or a PFO for paradoxical emboli
  • ECG, tele, and holter
  • carotid duplex ultrasound
  • metabolic labs including lipid profile and HbA1c
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6
Q

What secondary prevention should be added for all patients who suffer a stroke?

A
  • aspirin, aspirin + dipyridamole, or clopidogrel
  • a statin with goal LDL less than 70
  • diabetic control with HbA1c less than 7.0
  • blood pressure control
  • smoking cessation
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7
Q

If a PFO is discovered during the course of a stroke workup, what is the proper management?

A

repair the PFO if all three of the following are true: patient is less than 60, bubble study demonstrates a right-to-left shunt, and imaging shows an embolic-appearing cryptogenic ischemic stroke

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8
Q

Describe the risk factors, presentation, diagnosis, and treatment of pseudo tumor cerebri.

A
  • risk factors include obesity, vitamin A toxicity, tetracycline use, and oral contraceptives
  • presents with signs and symptoms of increased intracranial pressure as well as a 6th nerve palsy
  • diagnosis requires CT/MRI to rule out mass lesion and an LP demonstrating only increased opening pressure
  • treat with weight loss and acetazolamide; add steroids and serial LPs until a VP shunt can be placed if not well controlled
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9
Q

Describe the presentation, diagnosis, and treatment of giant cell temporal arteritis.

A
  • presents with headache, visual disturbance, jaw claudication, and systemic symptoms of muscle pain, fatigue, and weakness
  • an elevated ESR is expected but diagnosis should be made with temporal artery biopsy
  • begin steroids before results of biopsy are back to prevent vision loss
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10
Q

What medications are available for migraine abortion and prophylaxis?

A
  • for abortive therapy, begin with NSAIDs, then triptans and ergotamines, and then IV anti-emetics like prochlorperazine
  • begin prophylaxis with propranolol, valproate, topiramate, or TCAs if patients have more than 3 headaches a month
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11
Q

What medications are available for cluster headache abortion and prophylaxis.

A
  • for abortive therapy, use 100% oxygen

- for prophylaxis, begin verapamil or lithium at the start of each cluster

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12
Q

What two medications are used to treat trigeminal neuralgia?

A

oxcarbazepine and carbamazepine

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13
Q

What is the indication for zoster vaccination? What is the treatment for zoster and post-herpetic neuralgia?

A
  • the zoster vaccination is indicated for all individuals over age 60
  • if zoster is still acquired, treatment with anti-virals shortens the course and reduces the risk of post-herpetic neuralgia
  • post-herpetic neuralgia can be treated with a combination of lidocaine, capsaicin, TCAs, gabapentin, pregabalin, carbamazepine, and phenytoin
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14
Q

Describe possible etiologies for seizure and the diagnostic workup that must follow a first time seizure.

A

the following must be ruled out with lab testing and CT/MRI before an EEG should be performed:

  • electrolyte imbalances: hypernatremia, hyponatremia, hypocalcemia, and hypomagnesemia
  • metabolic imbalances: uremia, hepatic failure, and hypoglycemia
  • drugs: alcohol or barbiturate withdrawal, cocaine intoxication
  • CNS infection or lesion
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15
Q

How is status epilepticus treated?

A
  1. benzodiazepine
  2. fosphenytoin
  3. phenobarbital
  4. intubation and general anesthesia
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16
Q

How are simple and complex partial seizures differentiated?

A

complex are those with any alteration of consciousness while consciousness is retained throughout a simple partial seizure

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17
Q

Under what circumstances would you start an anti-epileptic medication for a first time seizure?

A

if that individual had:

  • status epilepticus or focal signs on presentation
  • a family history of seizures
  • abnormal EEG or lesion on CT
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18
Q

Which anti-epileptics having the following characteristics:

  • best for pregnancy
  • highest risk of hyponatremia
  • predictable SJS response
A
  • for pregnancy: lamotrigine or levetiracetam
  • carbamazepine is most likely to cause hyponatremia
  • carbamazepine and phenytoin have predictable SJS reactions in those with the HLA-B1502 genotype
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19
Q

When should anti-epileptic medications be stopped?

A

all patients should be treated until seizure-free for at least 2 years; at that time, a sleep deprivation EEG should be performed and if no seizure activity occurs, the medication can be discontinued

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20
Q

Most subarachnoid hemorrhages are the result of a rupture of which vessels?

A

usually a vessel located in the anterior division of the circle of Willis

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21
Q

Describe the presentation and diagnosis of SAH.

A
  • typically presents with sudden onset of severe headache and meningismus (photophobia, stiff neck, and fever)
  • best initial test is CT without contrast
  • most accurate test is LP
  • angiography is used to identify the precise location of the lesion for coiling/clipping
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22
Q

How can CSF analysis help you distinguish SAH from meningitis?

A
  • both will have elevated white blood cell count

- however, in those with SAH, the ratio of WBCs to RBCs will be normal (1 per 500-1000 RBCs)

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23
Q

How should SAH be managed?

A
  • get a CT without contrast, follow with an LP if the CT is unrevealing
  • perform an angiography to guide intervention, either coiling or clipping
  • start nimodipine to prevent vasospasm and subsequent ischemia
  • start phenytoin to prevent seizure
  • watch for complications: rebleed, vasospasm, seizure, hydrocephalus, SIADH
  • if hydrocephalus develops, place a VP shunt
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24
Q

Describe the presentation, diagnosis, and treatment of cerebral vein thrombosis.

A
  • presents with headache and focal signs, much like SAH
  • CT and LP are normal
  • diagnosis requires an MRV
  • treat with LMWH bridge to warfarin
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25
Q

How should spinal trauma or compression be treated?

A

start with glucocorticoids, imaging, and then decompressive surgery

26
Q

Describe the etiology, presentation, diagnosis, and treatment of syringomyelia.

A
  • it is most often congenital (associated with Chiari I malformations) or acquired from trauma or tumor
  • presents with a cape-like distribution of loss of pain and temperature sensation, diminished reflexes, and atrophy
  • diagnosis is made with an MRI
  • treat with surgical removal of tumor or drainage of the fluid from the cavity
27
Q

Describe the presentation, diagnosis, and empiric treatment for brain abscesses.

A
  • it typically presents with fever, headache, nausea, vomiting, and seizures or focal deficits
  • best initial test is CT or MRI showing a ring-enhancing lesion
  • most accurate test is biopsy as this is the only way to differentiate it from a tumor and characterize the organism responsible
  • treat empirically with penicillin, metronidazole, and ceftriaxone
28
Q

What are the features of tuberous sclerosis?

A
  • the cutaneous hallmarks are hypopigmented Ash leaf patches and leathery plaques known as Shagreen patches
  • neurologic manifestations include seizures, psychomotor retardation, slowly progressive mental deterioration
  • cardiac rhabdomyomas and retinal lesions are also seen
29
Q

What are the features of Sturge-Weber syndrome?

A
  • the hallmark is a port wine stain on the face
  • other symptoms include homonymous hemianopsia, hemiparesis, and mental subnormality
  • plain radiographs of the skull reveal calcification of intracranial angiomas
  • treatment focuses on seizure control
30
Q

What are the features of NF1 and NF2?

A
  • both present with neurofibromas, cafe-au-lait spots, and axillary or inguinal freckles
  • NF1 presents with optic gliomas and Lisch nodules on the iris
  • NF2 presents with bilateral acoustic neuromas
31
Q

Describe an essential tremor and the appropriate treatment.

A
  • presents as a bilateral tremor, predominately in the hands, which is present at rest and with intention, worsens with caffeine, and improves with alcohol
  • treat with propanolol and add primidone if needed
32
Q

Describe the pathophysiology and presentation of Parkinson disease.

A
  • it is due to the loss of dopaminergic neurons in the substantia nigra
  • presents with tremor, cogwheel rigidity, akinesia, and postural instability
33
Q

What is Shy-Drager syndrome?

A
  • also known as multi-system atrophy, it is a combination of parkinsonism and autonomic dysfunction
  • it doesn’t respond well to dopaminergic agents and treatment focuses on blood pressure maintenance
34
Q

Describe each of the following drugs:

  • amantadine
  • entacapone
  • tolcapone
  • selegiline
  • pramipexole
  • ropinirole
A
  • amantadine: promotes production and release of endogenous dopamine in the substantia nigra
  • entacapone: a COMT inhibitor that increases the effectiveness of L-dopa
  • tolcapone: a COMT inhibitor with greater central action and CNS effectiveness
  • selegiline: an MAO-B inhibitor that increases the effectiveness of L-dopa
  • pramipexole: a direct dopamine agonist useful as monotherapy for parkinsonism
  • ropinirole: another direct dopamine agonist
35
Q

How should psychosis be treated in those with Parkinson disease?

A

should try to reduce dopamine agonist medications; however, when this is not possible, use a low-potency antipsychotic or pimavanserin

36
Q

What is pimavanserin?

A

an antipsychotic helpful particularly for those with Parkinson disease because it is a serotonin antagonist and has no effect on dopamine activity

37
Q

Describe the pathophysiology, presentation, diagnosis, and treatment for Huntington disease.

A
  • it is due to a CAG trinucleotide repeat on chromosome four that demonstrates paternal anticipation and leads to loss of GABAergic neurons
  • presents with choreiform movement disorder, dementia, and behavioral changes between 30-50 years of age
  • the diagnosis is made with genetic testing
  • there is no specific treatment and so motor and cognitive disturbances are treated symptomatically
38
Q

What is the treatment for Tourette disorder?

A
  • inherent in management is ADHD treatment with methylphenidate as first line
  • fluphenazine, clonazepam, and alpha2-agonists help with control of the tics
39
Q

What is the best initial and most accurate test for MS? What other testing is helpful?

A
  • MRI is both the best initial test and most accurate

- although LP shows oligoclonal bands, this is non-specific

40
Q

How is MS treated?

A
  • steroids and plasmapheresis are used for acute exacerbations
  • interferon and glatiramer are the preferred maintenance therapies
41
Q

If a patient with MS on suppressive medication develops worsening neurologic deficits and new white matter lesions, what is the most likely offending agent?

A

Natalizumab, a alpha-4 integrin inhibitor, which is associated with the development of progressive multifocal leukoencephalopathy in patients using if MS suppression

42
Q

What is Natalizumab?

A

an MS maintenance therapy which works as an alpha-4 integrin inhibitor but has been associated with progressive multifocal leukoencephalopathy and thus may be responsible for worsening neurologic deficits and new white matter lesions in these patients

43
Q

Describe the presentation, diagnosis, and treatment of ALS.

A
  • it presents with a combination of upper and motor neuron loss, sparing sensory systems and sphincters
  • in particular, a weak cough and dysphagia are indicative of a poor prognosis
  • diagnosis is with EMG
  • there are two specific treatments including riluzole, a glutamate antagonist, and edaravone, an antioxidant
  • supportive treatment includes baclofen for spasticity and CPAP with eventual tracheostomy for respiratory support
44
Q

Describe the presentation, associations, and treatment of pseudobublar affect.

A
  • it is a form of emotional incontinence characterized by intermittent episodes of inappropriate laughter or crying
  • is is seen in those with ALS, MS, and stroke
  • treat with dextromethorphan and quinidine
45
Q

Describe the presentation and diagnosis of Charcot-Marie-Tooth disease.

A
  • presents with loss of motor and sensory innervation, manifested as distal weakness and sensory loss, waisting of the legs, decreased DTRs, and tremor
  • the most accurate test is EMG
46
Q

Name the five most common causes of peripheral neuropathy.

A
  • diabetes mellitus
  • alcoholism
  • compression/trauma
  • uremia
  • paraproteinemias
47
Q

How can deep and superficial peroneal nerve injuries be differentiated?

A
  • the deep nerve is responsible for ankle dorsiflexion and cutaneous innervation of the first web space
  • the superficial nerve is responsive for ankle eversion and cutaneous innervation of the dorsum of the foot
48
Q

Describe a tibial nerve injury and where the injury is likely to have occurred.

A

it presents as the opposite of a common peroneal injury with poor ankle plantar flexion and sensory loss on the sole of the foot, worse with walking and often due to compression at the lateral malleolus

49
Q

What is complex regional pain syndrome?

A

it is a syndrome of allodynia in the affected limb with vasomotor symptoms, edema, and skin color changes, always preceded by a history of trauma damaging the myelin of peripheral nerves

50
Q

What are four common causes of Bell palsy?

A
  • Lyme disease
  • herpes zoster infection
  • sarcoidosis
  • tumors
51
Q

How can facial weakness from a stroke be differentiated from that of Bell palsy?

A

with Bell palsy there is total facial weakness whereas stroke only causes lower facial weakness

52
Q

Describe the presentation and treatment of Bell palsy.

A
  • presents with complete hemifacial weakness, hyperacusis, and loss of sense on the anterior ⅔ of the tongue
  • treat with prednisone and by tapping shut or covering the eye to avoid corneal ulceration
53
Q

Describe the presentation, diagnosis, and treatment of Guillain-Barre syndrome.

A
  • presents with ascending weakness, loss of DTRs, mild or absent sensory deficits, and autonomic dysfunction, usually with a recent history of infection
  • best initial test is pulmonary function testing
  • most specific test is NCS/EMG but this takes weeks to become abnormal; instead, CSF will demonstrate albuminocytologic dissociation
  • treatment is supportive unless there is respiratory compromise, then use IVIG or plasmapheresis (there is no role for steroids)
54
Q

What is the most important first step when managing Guillain-Barre and what are you looking for?

A
  • the most important first step is pulmonary function testing
  • looking for a decline in forced vital capacity or peak inspiratory pressure, which may signal impending respiratory failure (inspiration is the active part of breathing)
55
Q

Describe the presentation, diagnosis, and treatment of Lambert-Eaton myasthenic syndrome.

A
  • presents with weakness that is more proximal and affects the lower extremities more than upper and improves with use, autonomic dysfunction, and diminished DTRs
  • the best initial test is anti-P/Q-type voltage-gated calcium channel antibody assay
  • the best initial therapy is pyridostigmine for mild disease and IVIG for severe disease
  • will eventually need to do a chest CT looking for SCLC
56
Q

Describe the presentation, diagnosis, and treatment of myasthenia gravis.

A
  • presents with bulbar weakness that worsens with use; reflexes are normal and there is no autonomic dysfunction
  • the best initial test is acetylcholine receptor antibody assay, the most accurate test is EMG, and eventually a CT looking for thymoma or thymic hyperplasia is needed
  • first line treatment is pyridostigmine or neostigmine; for those less than 60, thymectomy is second line; for this greater than 60, prednisone and immune modulators are second line
  • myasthenic crisis is treated with IVIG or plasmapharesis
57
Q

What are four diagnostic tests that should be performed for a new complaint of dementia?

A
  • MRI of the brain
  • TSH
  • B12
  • RPR
58
Q

How is dementia treated?

A

there are no specific treatments, so use acetylcholinesterase inhibitors and memantine (NMDA antagonist)

59
Q

What are the key features of dementia with lewy bodies?

A

dementia within 1 year of parkinsonism onset

60
Q

What are the key features of Creutzfeldt-Jakob disease?

A
  • rapidly progressive dementia
  • myoclonic jerks/startle myoclonus
  • CSF with 14-3-3 protein
  • biopsy for prion proteins is the most accurate test
61
Q

What is the only proven treatment to help prevent falls?

A

exercise and strength training

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