Neuro PANCe

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Neuro PANCe
2012-08-09 12:56:39

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  1. M/C type of stroke
    ischemic stroke (80%)
  2. What is the breakdown of the different types of ischemic stroke?
    2/3 are thrombotic, 1/3 embolic
  3. Where do emboli come from that cause strokes?
    heart, aortic arch, or large cerebral arteries
  4. What is the workup for a stroke?
    CBC, ESR, platelet count, PT/PTT, cholesterol and lipids, and blood glucose level; CT scan; EKG
  5. When can thrombolytics for strokes be given?
    They are most effective within 3 hours, but can be attempted up to 12 hours
  6. Contraindications to thrombolytics
    • Suspicion of current bleed
    • Recent intracranial surgery
    • Serious head trauma or previous stroke
    • Hx of heed bleed
    • Bleeding problem
    • Uncontrolled HTN (>185/110)
    • Seizure at stroke onset
    • internal bleeding
    • brain tumor
    • AVM or aneursym
    • Heparin use within 48 hours
    • Plt count <100,000
  7. When do you initiate antiplt vs anticoagulant therapy?
    Anti plt is for ischemic stroke and TIA, anti coag is for cardiac embolus
  8. When are endarterectomies performed?
    >70-90% stenosis of the common or internal carotid artery
  9. How do you manage hemorrhagic stroke?
    • conservative and supportive measures
    • management of HTN and anti-edema therapy (mannitol and corticosteroids)
  10. Pts with TIA related to carotids demostrate what type of sx?
    contralateral hand-arm weakness with sensory loss, ipsilateral visual sx or aphasia, or amaurosis fugax
  11. Those with vertebrovascular TIA experience what types of sx?
    diplopia, ataxia, vertigo, dysarthria, CN palsies, lower extremity weakness, dimness or blurring of vision, perioral numbness, or drop attacks
  12. What is the definitive study for TIA?
  13. When do you initiate prophylactic antiplatelet therapy in a TIA? What type of meds are used?
    When it is not cardiogenic; ASA, ticlopidine, clopidogrel, sulfinpyrazone, or dipyridamole
  14. How do you tx a cardiogenic TIA?
    anticoagulation, initially with IV heparin for those who are admitted to the hospital, and warfarin for long term therapy
  15. What is the m/c nontraumatic cause of a subarachnoid hemorrhage?
    ruptured berry aneurysm
  16. What age range is m/c affected by subarachnoid hemorrhages?
    50-60 yo
  17. When are AVMs m/c dx?
    b/w 20-40 yo
  18. S/sx of SAH
    • "Worst HA of my life," N/V, AMS
    • HA remains constant for days
    • BP rises
    • meningeal signs
  19. What does CSF analysis show in SAH?
    increased opening pressures and grossly bloody fluid
  20. How do you tx SAH?
    • provention of elevated arterial or ICP that might lead to rerupture of the vessel
    • strict bed rest, mild sedation, or administration of stool softeners to prevent straining
  21. At what ages do idiopathic seizures generally begin?
    5-20 yo
  22. What is the def of a generalized seizures vs partial seizure?
    sudden loss of consciousness vs no loss of consciousness
  23. jacksonian march
    phenomenon with seizures whereisolated tonic activity of a limb speads to entire side of body
  24. What is the difference between complex partial and simple partial seizures?
    complex partial has an impairment of consciousness (ie, aura)
  25. What do EEGs show in generalized absence seizures?
    generalized spikes and associated slow waves
  26. What does an EEG show in simple partial seizures?
    focal rhythmic d/c at the onset of the seizure, but occsionally, no ictal activity will be seen
  27. What does an EEG show in complex partial seizures?
    interictal spikes or spikes associated with slow waves in the temporal or frontotemporal areas
  28. How do you manage?
    Correct any underly hypoglycemia, hyponatremia, or drug intoxication
  29. What meds are used for generalized nonconvulsive seizures?
    valproic acid or ethosuximide
  30. Why is status epilepticus an emergency?
    possibiliy of permanent brain damage secondary to hyperthermia, circulatory collapse, or excitotoxic neuronal damage
  31. How do you manage status epilepticus?
    Diazepam or lorazepam is administered IV until seizure stops, a loading dose of phenytoin or fosphenytoin is also given
  32. What is the definition of MS?
    inflammation associated with multiple foci of demyelination in the CNS white matter
  33. What is the proposed cause of MS?
    CNS IG production and alteration of T lymphocytes; a viral infection may act as a precipitant
  34. What are sx of MS?
    focal weakness, numbness or tingling, optic neuritis, diplopia, focal neuralgias, balance problems, or urinary sx
  35. what does CSF show in MS?
    sterile inflammation with mild lymphocytosis or slight protein elevation, elevated IG index, oligoclonal bands, and increased myelin basic protein
  36. How do you manage MS?
    • High dose steroids
    • Interferon B to decrease frequency of relapse
    • daily sub-q injections of glatiramer acetate to decrease frequency of relapses
    • Amantadine and pemoline for fatigue
    • Baclofen and diazepam for spasticity
  37. Pathology of alzheimers
    intracellular neurofibrillary tangles and extracellular neuritic plaques
  38. What are the four ACH inhibitors?
    tacrine, donezepil, galantamine, or rivastigmine
  39. Sx of vascular dementia
    • forgetfulness in the absence of depression and inattentiveness
    • sx occur in STEPWISE fashion
    • Social graces may be well maintained
    • Progression leads to loss of computational ability, problems with word finding and concentration, difficulty with routine daily activities, and complete disorientation and social withdrawal
  40. What is the pathophys of tension HA?
    abnl neuronal sensitivity, muscle contraction, stress or minor trauma to head and neck
  41. M/c type of HA
  42. How do you manage tension HA?
    ASA, APAP, or NSAIDs; local heat and relaxants
  43. Sx of migraine HA
    U/L pain with throbbing or pulsing discomfort
  44. Pathophys of migraines
    intracranial vasopasm followed by extracranial vasodilation; dysfunction of the trigeminovascular system, resulting in the perivascular release of substance P
  45. classic migraine
    migraine with an aura
  46. common migraine
    migraine without aura
  47. Migraine management
    • ASA, APAP, NSAIDs, or isometheptene
    • Triptans or ergotamines
    • Prophylaxis: Beta blockers, TCAs, CCBs, NSAIDs, valproic acid, or topiramate
    • botox in pts with severe, intractable, migraines
  48. Pathophys of benign essential tremor
    idiopathic, inherited in autosomal dominant manner
  49. Management of essential tremor
    propanolol at low doses; may try primidone if propanolol fails
  50. pathophys of Parkinson's disease
    degeneration of cells in the substantia nigra, causing a deficiency of the neurotransmitter dopamine, and an imbalance of dopamine and acetylcholine
  51. Why is levodopa used in parkinsons?
    It is the precursor to dopamine
  52. What is the main direction of parkinson's tx?
    to restor balance between dopamine and acetylcholine by blocking the effect of acetylcholine with anticholinergic drugs, adminstering levodopa (precursor of dopamine) or a combo of both
  53. What is amantadine?
    an anticholinergic, good for parkinson's sx, specifically tremor, but not rigidity
  54. What is carbidopa?
    A drug used in Parkinson's that lowers doses of carbidopa and reduces side effects
  55. How do you tx parkinson's pts when they become refractory to levodopa therapy?
    dopamine agonists (like bromocriptine)
  56. selegiline
    MAO-B inhibitor, inhibits breakdown of dopamine, may arrest progression of the disease
  57. genetics of huntington's disease
    autosomal dominant disorder
  58. gene resposible for huntington's disease
    short arm of chromosome 4
  59. earliest signs of huntington's
    mere restlessness or fidgetiness
  60. What can RLS be secondary to?
    peripheral neuropathy, uremia, pregnancy, IDA
  61. When do sx of RLS occur?
    during periods of prolonged inactivity
  62. drug sof choice for RLS
    dopamine agonists or ropinirole
  63. epidemiology of Bell's palsy
    pregnant women and people with diabetes
  64. How do you manage Bell's Palsy?
    PO course of prednisone with or without acyclovir
  65. M/c type of diabetic peripheral neuropathy
    mixed (motor, sensory, and autonomic)
  66. what is guillan-barre syndrome?
    an idiopathic polyneuropathy often following minor infections, immunizations, or surgical procedures, but in many cases, no cause is identified
  67. pathogen associated with guillan-barre syndrome
    campylobacter jejuni, usually with infection of lungs or GI tract
  68. Clinical features of guillan-barre syndrome
    • symmetrical extremity weakness that begins distally and ascends; promximal muscles affected more than distal muscles; decreased or absent DTRs
    • pain
    • autonomic dysfunction (tachycardia, cardiac irregularities, labile blood pressure, disturbed sweating, impaired plum function, spincter disturbances, or paralytic ileus)
  69. Dx workup of guillan-barre syndrome
    • EMG
    • CSF (elevated protein, nl cell counts)
  70. tx of guillan-barre syndrome
    • hospitalized with close monitoring of respiratory status
    • plasmapheresis
    • IVIG
    • PT/OT/ST
  71. Epidemiology of myasthenia gravis
    m/c in young women and older men
  72. pathophys of myasthenia gravis
    Abs directed against the ACH receptor on the muscle surface cause an increased rate of receptor destruction, leading to weakness
  73. Clinical features of myaesthenia gravis
    • muslce weakness and fatiguability which improve with rest
    • Ptosis, diplopia, difficulty in chewing or swallowing, respiratory difficulties, limb weakness
    • sx fluctuate in intensity throughout the day, and there is a tendency to have longer-term spontaneous relapses and remissions that may last for weeks
  74. How do you dx myasthenia gravis?
    clinical improvement is seen after adminstering anticholinesterase (edrophonium)
  75. Workup of myasthenia gravis
    • CXR to r/o coexisting thymoma
    • EMG
    • Serum assay for elevated levels of Abs (positive in 80-90% of pts)
  76. Tx of myasthenia gravis
    • give cholinesterase inhibitor such as pyridostigmine
    • thymectomy leads to improvement of sx
    • corticosteroids, immunosuppressive agents, IVIG, and plasmapheresis in pts with refractory dz
  77. Lambert-Eaton syndrome
    defective relase of ACH in response to nerve impulse, associated with small cell carcinoma, may surface prior to tumor being dx
  78. How does Lambert-Eaton syndrome differ from myasthenia gravis?
    power increases with sustained contraction
  79. How do you dx Lambert-Eaton syndrome?
    EMG, as muscle response to repeated stimulation is increased significantly
  80. How do you tx Lambert-Eaton syndrome?
    • plasmapheresis and immunosuppressive therapy
    • specific therapy on the tumor
  81. M/C cause of meningitis in infants
    Group B strep
  82. typical s/sx of meningitis
    Fever, HA, vomiting, and a stiff neck are the typical signs and sx
  83. What rash is characteristic of Neisseria meningitidis?
    petechial rash
  84. Workup of meningitis
    • CT performed BEFORE LP to r/o mass
    • Gram stain and culture of CSF
  85. Management of neonatal meningitis
    ampcillin and cefotaxime
  86. Management of infantile meningitis
    Ampicilllin + cefotaxime OR rocephin
  87. Management of meningits b/w 3 mo and 55 years
    Cefotaxime or ceftriaxone plus vanco
  88. Management of  meningitis in adults >55 or immunocompromised
    amp plus vanco plus cefotaxime or ceftriaxone
  89. What should be seen with effective management of meningitis?
    • Repeat LP and CSF analysis; CSF sould be sterile after 24 hours
    • Decrease in pleocytosis and proportion of neutrophils should be seen within three days
  90. M/C cause of viral meningitis
    enteroviruses (coxsackievirus A or B, echoviruses), HSV2, and arthropod-borne viruses
  91. Difference in s/sx b/w viral and bacterial meningitis
    • bacterial is more acute; viral persists for days
    • lots of systemic manifestations (rash, pharyngitis, adenopathy, pleuritis, carditis, jaundice, organomegaly, diarrhea)
  92. difference in CSF b/w bacterial and viral meningitis
    • CSF opening pressure nl in viral, increased in bacterial
    • nl or high nl WBCs in viral
    • protein, glucose, and serum blood counts are nl
  93. Management of viral meningitis
    • None needed, if HSV, give acyclovir
    • tx mild HA with APAP
  94. Tx of increased ICP
    hyperventilation, IV mannitol infusion, and iv furosemide
  95. sx of total cord transection
    • immediate, flaccid paralysis and loss of sensation below the level of the lesion
    • reflex activity is lost for a variable time, urinary and fecal retention
    • with slow return of reflex function, spatic paraplegia or quadriplegia develops, with hyperreflexia and extensor plantar responses
  96. Sx of partial cord injury
    • mild limb weakness or distal sensory disturbance
    • sphincter function impairment may lead to incontinence and urgency
  97. Sx of U/L cord lesion
    ipsilateral motor disturbance with accompanying impairment of propioception and C/L loss of pain and temp below the lesion (aka Brown-Sequard syndrome)
  98. Brown-Sequard syndrome
    ipsilateral motor disturbance with accompanying impairment of propioception and C/L loss of pain and temp below the lesion
  99. sx of central cord lesions
    LMN deficit and loss of pain and temp, with a sparing of posterior column functions
  100. sx of radicular deficit
    occurs at level of injury
  101. managment of cord injuries
    • immobilization, decompressive laminectomy and fusion if there is cord compression
    • high dose corticosteroids within 8 hours of injury will help with recovery
  102. m/c type of brain tumor
  103. m/c spinal tumor
  104. m/c sources of mets to the brain
    lung, breast, kidney, and GI tract Ca
  105. In what stage of sleep do nightmares occur?
  106. In what stage of sleep do sleep terrors occur?
    Stage 3 and 4 delta sleep
  107. In what stage of sleep do sleep walking occur?
    stage 3 or 4 sleep in the first third of the night and with REM sleep later on in the night
  108. In what stage of sleep does nocturnal enuresis occur?
    within 3-4 hours of falling asleep, not associated with any particular changes
  109. How do you manage narcolepsy?
    administration of stiulants including dextroamphetamine and modafinil
  110. How do you manage nocturnal myoclonus?
  111. How do you manage sleep terrors and sleep walking?
  112. What parts of the brain are affected by Alzheimers?
    hippocampus, neocortex, and nucleus basalis
  113. m/c initial sx of alzheimers
    memory impairment for newly acquired information with memory for remote events unimpaired
  114. What is tabes dorsalis?
    late complication of tertiary syphilis, characterized by spirochete invasion of the posterior columns of the spinal cord
  115. Argyll - Robertson pupils
    pupils react poorly to light but well to accomodation
  116. Management of neurosyphilis
    IV aqueous PCN G at 18-24 U/day x10-14d
  117. m/c cause of viral encephalitis
  118. m/c childhood encephalitis
    myxovirus (measles and mumps encephalitis)
  119. Face feels stiff and pulled to one side with flattening of the nasolabial fold
    Bell's palsy
  120. Age of onset of Duchenne's MD
    infancy of early childhood, death usually during adolescence
  121. Age of onset of Becker's MD
    Childhood, adolescence, or early adult; death usually occurs in 5th decade, but some have nl lifespan
  122. Age of onset of Myotonic MD
    early adult onset, slow progression, most pts are confined to a wheelchair or bed within 15-20 years
  123. Pattern of muscular specific features of duchenne's MD
    pelvic-femoral, later on pectoral girdle
  124. Pattern of muscular specific features of Becker's MD
    pelvic-femoral; later on pectoral girdle
  125. Pattern of muscular specific features of myotonic MD
    ocular, facial; sternomastoid; forearm peroneal; cardiac involvement common
  126. Sx of Duchenne's MD
    pseudohypertrophy, respiratory and cardiac involvement; mental retardation
  127. Sx of becker's MD
    Slight cardiac involvement, nl mentation
  128. Sx of Myotonic MD
    Cataracts; testicular atrophy, alopecia
  129. Pathology of MD
    • necrosis of muscle fibers and gradual replacement of fibers with CT and fat; loss of muscle fibers, residual fibers of larger and smaller size than nl in hapzard arrangement;
    • Genetic abnormality (x chromosome) causing dystrophin, a muscle protein, to be absent in Duchenne's dystrophy....results in loss of membrane proteins and initiation of the degeneration of muscle fibers
  130. clinical features of MD
    symmetrical muscle weakness atrophy, contractures, ptosis, dysphagia, mental retardation, myotonia, cataracts, testicular atrophy, alopecia, and cardiac involvement
  131. Workup of MD
    EMG, serum CK (highest in duchenne's), muscle bx, dystrophin analysis, genetic analysis
  132. Management of MD
    • No specific tx
    • Steroids and quinine (for myotonia)
    • Pneumococcoal vaccine and annual influenzae vaccine
    • ACE Is, BBs, and annual echo
    • PT
    • corticosteroids are mainstay > 5 yo
  133. asterixis, and how to do tx
    • flapping of outstretched hands d/t increased ammonia levels
    • tx with lactulose
  134. Which of medication is an  acceptable first-line agent to reduce the frequency and severity of recurrent exacerbations and disease progression in a patient with newly  diagnosed multiple sclerosis?
    Interferon B (corticosteroids are used for acute attacks, but do not alter course of disease)
  135. Tx of Tourrettes
  136. preventative medications for cluster HA
  137. Which medication, if started  within five days of symptoms, has been shown to increase the rate of  full recovery in an acute Bell's palsy patient?
  138. Tramadol should be avoided in seizure disorder because
    it lowers the seizure threshold
  139. central cord syndrome
    • loss of motor function that is more severe in the upper extremities than in the lower extremities, and is more severe in
    • the hands.
    • There is typically hyperesthesia over the shoulders and arms.
  140. Women who suffer from migraine with aura are at increased risk for