neuro rotation

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  1. what are two types of Arnold Ciari?
    • Type I and II.
    • Type I is often asymptomatic and only has downward displacement of pons and cerebellar vermis
    • Type II also has the downward displacemet of pons and vermis, but also may be associated with spinal minigomyelocele.
  2. what are the classic findings in UMN lesions?
    • spasticity, weakness, clasp knife like movements, Burbinski sign, hyperreflexia.
    • Recall that fasciculation is a finding of LMN.
  3. Where is the lesion for Fredreich ataxia located on the spinal cord?
    It is located on the spinocerebellar tract.

    nerves from lower extremities enter through DRG go to Clark's nucleus and then travel up the spinocerebellar tract and to the cerebellum through the inferior peduncles.

    nerves from upper extremities enter through DRG and synapse at external cuneate nucleus and also enter to the cerebellum through the inferior peduncle.
  4. what are some of the manifestations of Tabes Dorsalis?
    • Late stage syphilis
    • paresthenias, pain, polyuria, positive Romberg sign, sensory ataxia, Argyll Robertson pupils, and suppressed reflexes.

    • This is common at the lumbar region.
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  5. What is Argyl Robertson pupil?
    They accomodate (object getting close) but not react to light (pupillary reflex)

    A late shyphilis finding.
  6. What is the area that ALS acts on and how
    • It is mostly at the cervical enlargement. affects both the cortical spinal tract and the anterior horn cells at that level. Therefore:
    • Spastic paralysis of the lower extremitirs and flaccid paralysis of the upper extermities.
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  7. subacute combined degeneration?
    • This is due to B12 deficiency.
    • Can lead to degeneration of the dorsal collumn, spinocerebellar tract, and corticospinal tracts.

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  8. What is syringomyelia?
    this is a central cavitation that mainly occurs at the level of the cervical spinal cord. Can lead to bilateral loss of pain and temperature, and eventually can also lead to flaccid pralysis at the lesion gets bigger.

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  9. What are some of the diagnostic differences between PD and ET?
    In essential tremor there is often associated head tremor involvement, it is often bilateral, associated with purposeful movement, and the latency period is immediate.

    In parkinson disease the tremors are unilateral, associated with stooped posture, shuffling gair, memory loss, resting tremors which abates with movement, and longer latency period.
  10. how is essential tremor treated?
    With propanolol, or primidone (50 to 700 mg/QD) other options include diazepam and alprazolam if tremors are worsened with tension or anxiety.

    Botox can also be used for treating some of the tremors that may include the head and voice.
  11. molecular or genetic basis of huntington disease?
    CAG repeats on a gene called huntingtin with repeats greater than 40 nearly always being associated with clinical HD.

    this phenomenon is called anticipation.
  12. what is athetosis?
    twisting and writhing movements often associated with chorea
  13. what are some of the findings in physical exam in a pt with HD?
    • slowing of the saccadic eye movements is an early sign.
    • Increased reflexes with disinhibition of premitive reflexes
    • problems with executive functions
    • depression
    • behavioral disinhibition

    If this disease starts at an early age, it is more severe Westphal variant, which may have of parkinsonism with bradykinesia and rigidity, distonia, myoclonus and sezures.
  14. What are the management steps of a pt with HD?
    • 1. Using dopamine blocking agents often help with the Chorea. However these drugs (i.e. Haloperidol) may cause tardive dyskinesia. Particularly as the HD progresses and leads to bradykinesia by itself, these drugs can exacerbate it.
    • - once dz progresses to bradykinesia Levodopa can actually be helpful
    • 2. SSRI for the depression component
    • 3. Aspiration is a common risk which can be limited by palcing a PEG line
    • 4. precautions for falling risk factor
    • 5. Genetic counseling of the pt's relatives is very important.
  15. how many different types of dystonia are there?
    15 different types of primary dystonia

    The secondary dystonias are usually due to drugs while the primary ones are due to non-discernible causes.
  16. what is the most common type of early onset dystonia?
    CAG deletion in DYT1 (torsin A) gene which starts in a limb. This is brain protein of unknown function with highest concentration in the substantia nigra.

    Often misdiagnosed as psychogenic disorders.

    PET scan may be useful in diagnosis.
  17. what are some of the things that would make you suspect secondary dystonia vs primary dystonia?
    • hx of trauma
    • dystonia at rest
    • hemidystonia
    • early onset of speech abnormality
    • presence of other abnormalities other than dystonia on the the neurological exam.
    • abnormal brain imaging
    • abnormal labratory tests
  18. management of dystonia?
    symptomatic treatment with essentialy DA replacement. Including Levodopa, muscarinic cholinergic receptor blockers, benzodiazepines, baclofen.

    also DBS of the GPi (internal segment of the globus pallidus).
  19. what is a drug that can cause dystonic reaction in an otherwise healthy individual?
    Haloperidol and other blockers of DA2 receptors.
  20. how to distinguish between a lesion of the abducents nucleus vs abducents nerve?
    in right abducents nucleus lesion neither of the eyes can look to the right while in right abducents nerve one the rgith eye cannot look to the right.

    Also note that due to the close proximity of the facial nerve to the abducents nucleus, often there is ipsilateral bells palsy present with abducents nucleus lesions.
  21. anterior spinal artery lesion will result in what physical findings?
    Contralateral spastic weakness, contralateral loss of touch, vibration, proprioception and ipsilateral CN XII lesion with deviation of toung toward the lesion.

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  22. findings in a lateral medullary syndrome and what artery is involved?
    PICA, this is also called Wallenberg syndrome

    Ipsilateral pain and temperature loss on the face, and ipsilateral horners.

    Contralateral loss of pain & temp from the limbs and trunk.

    In addition since CN X is also lateral, can have hoarsness, pharynx weakness, uvula diviation.

    • Moreover, since infirior cerebellar peduncles can be involved pt may have ataxia.
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  23. how to distinguish between medial pons vs medial medulla lesion?
    In the medial pons there is abducents deficiet since they exit medially whereas in medial medulla there is hypoglossal with tounge involvement.

    They both will have the similar contralateral spastic weakness and contralateral loss of touch, vibration and proprioception.
  24. How to distinguish lateral pontine syndrome from lateral medullary syndrome?
    In lateral pontine syndrome there is a loss of CN VII and VIII while in lateral medullary there was a CN X deficiet.

    They both have ipsilateral loss of pain and temp on the face with ipsilateral horner and contralateral loss of pain and temp in the limbs and trunk.

    AICA is the culprit artery.
  25. what is the first diagnostic step in a pt with parkinson's disease?
    MRI to r/o other ddx.

    Treat with DA agonists or MAO-B inhibitors. No medication slows the progression of the dz. mcc are idiopathic.

    pts have tremor at rest, rigidity, hypokinesia, and postural instability, other things include difficulty arising from a chair, turning in bed, masked facies, shiffling gait, stooped, anosmia is almost universal. Executiv dysfuction can be seen. ~50% of pts develope dementia.
  26. what are some of the ddx to consider with PD?
    MSA (multiple system atrophy) type P and C. MSA-P resembles PD except that tremors are smaller and it tends to be asymetric. In MSA-C there is cerebellar syndrome. Both have impotence and prominent autonimic insufficiency including orthostatic hypotension.

    Dementia with Lowy bodies which has prominant cognitive dysfunction, which can have hallucinations, dementia, delusions, and fluctuations in consciousness.

    Corticobasalganglionic degeneration which is typically unilateral coarse tremore, rigidity, increased reflexes as well as limb apraxia/limb dystonia/aline limb phenomenon.
  27. what the treatment options for PD?
    PT, speech therapy are important.

    • Pharmacologically:
    • Levodopa (crosses BBB vs DA which does not). Carbidopa is utilized to inhibit the pripheral breakdown of Levodopa in the gut. Tolcapone is also used to inhibit COMT which can also breakdown Levodopa pripherally.

    bromocriptine, pramipexole, ropinirole are DA2 agonist which can cross the BBB and directly stimulate the DA receptors.

    MAO-B inhibitors such as Selegiline & Rasagline and improve sx in monotherapy or be added to pt on levodopa therapy.

    Anticholinergics such as trihexyphenidyl or diphenhydramine (Benadryl) are used for tremors as well.

    Amantadine which blocks NMDA receptors has been shown to attenuate resting tremor and alleviate levodopa induced dyskinesias.
  28. whats a good way of testing if a pt has PD?
    Diagnostic trial of Levodopa at least 600mg/daily
  29. Mention a few non genetic causes of ataxia
    PCD (paraneoplastic cerebellar disease) associated with specific tumor type antineuronal antibodies that are relative frequent cause of late-onset ataxia

    hypothyroidism can present with ataxia as well.
  30. what is the definitive dx test for spinal cerebellar ataxia?
    DNA testing

    • Also to note SCA age of onset is around 20-30 yrs.
    • MRI or CT of the brain can detect atrophy of the cerebellum and variety of other subcortical structures.
  31. most common type of SCA?
    • SCA-3.
    • common manifestations include pure cerebellar ataxia, familial parkinsonism, hereditary spastic paraplegia, restless legs syndrome, impaired temperature discrimination in all limbs and even trunk and face.

    There is no treatment for SCA
  32. a high T2 weighted "hot cross bun" signal in the brainstem is seen with _____?
    MSA (multiple system atrophy)
  33. what are the drugs that can cause tardive dyskinesia?
    DA receptor antagonists. (ex. metoclopramide)

    Risk factors include, old age, female gender, conexistent brain damage.

    TD are treated by initially stoping the culprit drug. BDZ and baclofen has been shown to be helpful. Botulinum toxin injection can also be useful.

    arching of the back and neck are classic findings of TD. Remember that anticholinergics often make the TD worse.
  34. Presentation of someone with epidural bleed?
    LOC after the injury, lucid interval (~30% will have this) then downward course of sx which can include vomiting, HA, seizures.

    Posterior fossa epidural hematoma are particularly dangerous in that they can deteriorate very rapidly.

    EDH are half as common as subdural hematoma, male predominant, occur between the ages of 2 and 60. EDH can be acute caused arterial tear or subacute of even chronic. ~60% are in the termporoparietal regions caused by damage to middle meningeal artery and 10% in frontal and 10% occipital.
  35. What are some physcial findings to watch out for in brain injury, and some lab studies to order?
    • - cushing response (high ICP -> bracycardia, HTN, kusmall breathing)
    • - dilated, sluggish or fixed pupils.
    • - decerebrate positioning
    • - hemiplegia contralateral to the injury site
    • - focal neurological finding

    • LABS:
    • - CBC, with platelets to asses for furhter risk of bleeding and infection
    • - PT and PTT since coagulopathies are common with exposing brain which is associated with DIC
    • - Chem panel, BUN, electrolytes to asses other complicating factors
    • - toxicology
    • - type and hold appropriate amount of blood

    • IMAGING:
    • unenhanced head CT is the imaging of choice
    • Will see smoothly marginated, rarely crosses the suture lines because the dura is toughly adherant.
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  36. what is the GCS?
    the score varies between 3 and 15 has components for E (eye-opening)+M(motor)+V(verbal).

    • E:
    • 1. none
    • 2. to pain
    • 3. to voice
    • 4. spontaneous

    • V:
    • 1. none
    • 2. no word-only sounds
    • 3. words, but not coherent
    • 4. disoriented conversation
    • 5. normal conversation

    • M:
    • 1. none
    • 2. decerebrate
    • 3. decorticate posture
    • 4. withdraws to pain
    • 5. localized to pain
    • 6. normal
  37. causes of SAH
    • rupture of an aneurysm
    • AVM
    • neoplasm
    • angioma
    • cortical thrombosis
    • mycotic aneurysm tear
    • spread of blood or dissection from an intraparencymal hemorrhage or trauma
  38. characteristic of delirium?
    • acute mental status change
    • abnormal atention
    • and a fluctuating couse
    • about 40% of pt in ICU have delirium

    • Delirium must be differentiated from dementia in which pt has attention and the condition is a chronic (>6 months) progression of sx. Also fluctuations are less common.
  39. how can attention be tested?
    by asking to spell a word backward
  40. what are some drugs used in treatment of delirium?
    • Lorazepam
    • Halopridol
    • risperidone
  41. what are the different types of concussion?
    • Grade 1-3.
    • In grades 1 & 2 there is no LOC while in grade 3 there is.
    • In grade one all symptoms resolve within 15 minutres while in grade 2 it takes longer.

    Grade 1 & 2 can be sent home from the ER with no need for hospitalization.
  42. New Orleans Criteria for performing CT for concussion?
    • do a head CT if:
    • 1. emesis
    • 2. age >60
    • 3. persistant HA
    • 4. drug or EtOH intoxication
    • 5. eivdence of soft tissue and bony involvement above the clavicle
    • 6. persistant anterograde amnesia
    • 7. seizures
  43. What is the postconcussion syndrome
    90% of pt following a concussion will have HA and dizziness for at least a month.

    in 30%-80% of cases pt get PCS (post concussion syndrome), which occurs within 4 weeks after the injury and pt will complain of irritability, insomnia, depression, subjective intellectual dysfunction, fatigue, anxiety and excessive noise sensitity.

    usually symptoms will resolve within 3 months, although about 25% will still have sx up to 6 months. Psychiatric consultation may render helpful in these cases.
  44. what is rough return to play guidlines following a concussion?
    • First concussion of the season:
    • grade 1: can return to the same game
    • grade 2: return to game after a week
    • grade 3: go to the ER for CT and evaluation, return to game between 1-2 weeks depending on the length of the LOC

    • For second concussion of the season:
    • grade 1: 1 weeks before gaming
    • grade 2: 2 weeks before gaming
    • grade 3: one month of being symptom free
  45. How is management of ischemic stoke differe from that of hemorrhagic stroke?
    TPA is helpful in ischemic stroke while it is contraindicated in hemorrhagic. In hemorrhaginc sx treatment is what can be done, including, hyperventilation, monitoring ICP, osmotic therapy and neurosurgical consult for possible decompression.

    In the case of the ischemic stroke blood pressure should not be reduced in the first few days unless it is extremely high. Iatrogenic hypotension can exacerbate focal cerebral ischemia.
  46. what are some of the diagnostic work up of stroke?
    • Carotid US, CT, MRI, EKG, cerebral arteriogram
    • folate, B12, fasting lipid, homocystein, RPR, HIV, ESR, toxicology screen, HA1C
  47. lacunar strokes?
    These are associated with HTN or DM which leads to pure motor or pure sensory stroke which acts on the penetrating arteries in the brain.

    This is considered small vessel stroke.
  48. what are the risk factors for stroke?
    • same as those for CAD which include
    • Old age, HTN, smoking, DM, hyperlipidemia, heart disease, hyperhomocysteinemia, and family history.
  49. what arteries are involved in the aphasia, agnosia, apraxia, diplopia, vertigo, crossed neurological findings, homonymous hemianopia?
    • Crotid (anterior lesion)
    • Aphasia: inability to comprehend language
    • Agnosia: inability to recognize persons
    • Apraxia: inability to execute learned purposeful movements

    Diplopia, hemianopia, vertigo all mean posterior (vertebrobasilar) circulation lesions.
  50. How can you distinguish between hemorrhagic and ishemic stroke on clinical grounds?

    HA, extremely high BP, depressed levels of consciousness are suggestive of hemorrhagic
  51. What are some of the contraindication to tPA use? and how soon does it have to be used?
    used within the first 3 hours of the onset of sx of stroke

    active bleeding, recent stroke, hx of intracerebral hemorrhage. If contraindicated, then use ASA unless also contraindicated.

    Secondary storke prevention includes antiplatelets drugs such as ASA and clopidogrel. For pt with afib then must wardarin. Cntrl of HTN is very important, statins for hyperlipidemia (<100 mg/dL). Carotid endartectomy in a pt with carotid stenosis and hx of TIA.
  52. what is neurogenic pulmonary edema?
    It is a rare menifestation of SAH. The mechanism of which is not entirely known.
  53. Talk about SAH?
    Best dx test? prognosis?
    Often there is a recent moderate HA as a result of sentinel bleed. 60% of the SAH occur during physical activity (i.e. excersise, emotional strain, head trauma, defecation, coitus.

    Common complications include partial seizures, hemiparesis, which can occur because of the vasospasm of blood vessels (most commonly with aneurysmal SAH, 4-14 days after the hemorrhage), extension of the hemorrhage in to the prynchema with edema.

    Hyponatremia is seen often due to SIADH, cerebral salt wasting, and elevated ANP

    communicating hydrocephalus is a common outcome because of the blockage of the subarachnoid granulation.

    Non-contrast head CT can detect bleed with high sensitivity 24hrs after bleed and can detect it as late as a week later. Bleeding in the ventricle is worse prognosis and more related to hydrocephalous. A negative CT shold be confrimed with LP looking for xanthochromia with increased RBC cells.

    Up to 60% of pt die in the first 30 days after SAH. 10% due without any warning.
  54. What are some of the associated etiologies with aneurysm?
    • 1. fibromuscular dysplasia is an associated 25% of aneurysm pts
    • 2. polycystic kidney disease in 3% of cases
    • 3. chronic high blood pressure with diastolic greater than 110mmHg
    • 4. tobacco use
    • 5. EtOH
    • 6. OCP
    • 7. Marfan syndrome
    • 8. infectious (mycotic) aneurysm
    • 9. AVM
    • 10. coccain & amphetamine
  55. What are the differnt grades of SAH?
    • Grade I-V
    • I: alert with mild HA and nuchal rigidity 3-5% mortality
    • II: moderate to severe HA & nuchal rigidity 6-10% mortality
    • III: pt have added confusion
    • IV: stupor and moderate hemiparesis
    • V: comatose with signs of severe increased ICP 50-70% of mortality.
  56. Treatment of SAH?
    • grades I&II can be just observed after dx work up has been done.
    • Emergent angiography is warrented is a ruptured aneurysm is suspected & neurosurgical intervention is required.
    • Endovascular coiling can reduce the risk of rebleed greatly.

    • Clipping must be performed in the first 48hrs or be posponded for 2 weeks to avoid the window of greatest risk for vasospasms.
    • Medical management is triple H therapy which is hypertensive hypervolemic hemodilution to maintain the cerebral perfusion and nimodipine which is a CCB

    symptomatic tx of hyponatremia (SIADH, cerebral salt wasting) neurogenic pulmonary edema, cardiac complications (arrhythmias) seizures and etc.
  57. where is an EVD placed?
    At the Kocher's point which is 11cm posterior to the nasion and 3cm lateral to the saggital suture.
  58. what is the artery that can compress the CN III?
    Posterior communicating artery

    • CN III passess right between superior cerebellar artery and posterior cerebral artery and then runs along the posterior communicating artery.
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  59. an important diagnostic association with carnicervical (carotid) dissection?
    • ipsilateral horner syndrome.
    • This is because the sympathetic fibers travel along the IC artery.
  60. what is moyamoya, how is treated?
    These are idiopathic noninflammatory cerebral vasculopathy charactrized by progressive occlusion of the large arteries at the circle of Willis.

    STA-MCA bypass (superficial temporal artery to middle cerebral artery) and encephaloduroarteriosynangiosis (EDAS)
  61. drugs associated with stroke?
    Cocaine & amphetamines are associated with both ischemic and hemorrhagic stroke.

    Oral contraceptive are at risk for thomboembolic especially if also a smoker.
  62. Horner syndrome in a pt with HA and a recent head or neck injury?
    Carotid dissection

    Note that if the problem is with the ICA then the resultant Horner syndrome will not have anhydrosis on the same side because the sympathetic fibers responsible for sweating track along the ECA (external carotid artery)
  63. Is there an LOC in partial seizures?
    • Not in the simple partial seizures.
    • However in the complex partial seizures they do have an alteration or LOC.
  64. What % of pt who seize for the first time with normal neurological exam and no obvious cause will seize again?
    Only 25% have epilepsy and 75% will not seize again.

    Many neurologist will not treat the fist seizure and wait for a second one to occur before treating since there is not different in prognosis.
  65. What are the aniepileptid drug of choice for simple and complex partial seizures?
    Partial seizures: Carbamazepine, lamotrigine, VPA, gabapentin, phenytoin, topiramate

    • Absence: VPA, ethosuximide, lamotrigine,
    • Tonic-clonic: VPA, lamotrigine, topiramate, carbamazepine, phenytoin.
  66. when does the juvenile myoclonic seizures occur mostly?
    • one of the most common causes of epilepsy syndromes.
    • 7% of of all the cases of epilepsy.
    • Mainly occurs in the early morning hours and soon after awakening. Brought on by sleep deprivation and EtOH ingestion.
  67. Most common type of aura for simple partial seizure?
    • abdominal disomfort.
    • However anything can occur.

    In the case of simple partial seizures pts are able to interact with their environment except for what is limited by their actual seizure.
  68. What are two seizure types that can cause LOC?
    • Tonic clonic seizures
    • Complex partial seizures
  69. How can you distinguish between simple and complex partial seizures/
    In the simple form there is no LOC and pts are able to interact with their environment.

    In complex partial seizure there is bilateral spread of the seizure, impaired consciousness, automatisms (lip smacking, chewing, gesturing, ongoing motor tasks)

    If they are restrained they may become aggressive.

    Post inctal confusion. 3/4 of the cases start from temporal lobe.
  70. explain abscence seizure?
    • Petit mal
    • these present with momentary lapse of awareness, however no automatism (lip smacking, repeatitive movement, etc), No aura, no post ictal confusion.

    Often occur in childhood between 4-14 years old and are 70% resolve by the age of 18.
  71. best imaging for mesial temporal sclerosis and best for seeing vascular or tumor?
    T2 FLAIR is great for mesial temporal sclerosis ( as seen often seen in the case complex partial seizures)

    MRI with Gadolinium contrast is great for seeing tumor and vascular abnormalities.
  72. what is the diagnostic EEG finding in absence seizure?
    regular and symmetrical 3 Hz, with possible 2- to 4 Hz spike-and-slow-wave complexes.

    the next step is to do a sleep deprived EEG, and next EEG video monitoring.
  73. what are the safer anticonvulsant meds? and should medication be continued during pregnancy?
    the newer ones including Gabapentin, lamotragine, pregabalin, topiramate, zonisamide.

    most anticonvulsant drugs are category D (unsafe during pregnancy) however, if they must be used to control the seizure then they are used.

    VPA is the most likely one to be associated with congenital birth defects.
  74. what is the most common type of seizure in adult population?
    Complex partial seizure
  75. ddx of syncope/LOC?
    • vasovagal: look for causes
    • Orthostatic hypotension: check orthostatic BP
    • cardiogenic: i.e. sick sinus syndrome, arrhythmias, aortic stenosis
    • neurogenic: tonic-clonic seizure/complex partial seizures can also cause LOC
    • metabolic
    • hypoglycemia
  76. can there be micturation with vasovagal syncope?
    yes if bladder was full prior to syncope. However bowel incontinence is specific to seizure.
  77. evaluation of seizure in a pt with known hx of seizure should be centered around?
    antiepileptic medications

    • often non-complience or durg-drug interaction causing reduced levels of the anti-epileptic med, the blood level of the med should be measured.
    • Sometimes despite nrl blood levels this can occure which sometimes is due to behavioral changes (i.e. staying up all night, skipping meals, drinking EtOH)
  78. what are pseudoseizures?
    These are attacks that resemble seizures but having purely psychological causes.

    This is different from malingering in which case the pt is intentionaly feigning symptoms for sake of gains.
  79. whats a good way to dx a pt with pseudoseizure?
    video EEG

    about 1-3% of pt with pseudoseizures actually have true organic seizures
  80. what % of migraine HA have aura associated with them?
  81. Can meds be started for migraine without any workup? what are some of the work up that is done?
    Yes it can be if the neurological exam is normal and if history is typical for migraine.

    • tests include blood work up, LP, imaging, sedimentation rate.
    • BLOOD: CBC, HIV, tox, vasculitis screen, thryoid fnx, chem
    • SED RATE: temporal arteritis should be suspected in ts older than 60 yrs old which is treated with PO steroid to avoid vision loss.
    • LUMBAR PUNCTURE: If there is any fever, head stiffness LP should be performed. Also if SAH is suspected.
    • IMAGING: MRI is superior to CT, if LP is to be ordered should get the MRI prior to the LP.
  82. what are some causes of headache to keep in mind beside migraine?
    • Postspinal HA
    • Postcoital cephalgia: before and after coitus.
    • Pseudotumor cerebri: hight ICP with no tumor, often relieved with LP
    • Crotid dissection: can have head and neck pain, with Horner's syndrome
    • Acute glaucoma: sudden eye pain with nausea and vomiting
    • Brain tumor: can be bad enough to wake one up from sleep, papilledema is seen
    • Sinusitis: can cause HA
    • SAH: "worse HA in life", nausea, vomiting,
  83. what are the abortive treatment for migraine?
    • 1) triptan: should be take early in the course (prodrome preferably), must not take more than 3 doses in 24hrs, side effects include nausea, vomiting, tingling, and is contraindicated in coronary artery disease and HTN. 5HT-1D receptor agonists
    • 2) ergotamine: Only used if triptans fail.
    • 3) dihydroergotamine (DHE): use IV or IM for intractable HA, intranasal is now also available. Also give metoclopramide for nausea, if pt responds then repeat the DHA+metoclopramide for two more dose separated by 8hrs.
    • 4) Midrin: 3 component drug (APAP, dichloralphenazone - muscle relaxant-, isometheptne mucate - a vasocontrictor) this drug is actually a bridge point between abortive treatment and prophylactic treatment.
  84. what are some drugs used for prophylactic migraine treatment?
    Prophy is used if pt has at least 3 attacks a month,

    commonly used is Topomax (Topiramate), others include beta blocker, gabapentine, midrin, divalproex (Depakote), CCB (verapamil), antidepressant (duloxetine, amitriptyline)

    interestingly menopause improves the migraine sx in 67% of women.
  85. what is the management of chronic daily headache?
    Taper off the analgesis such as APAP and start VPA or topiramate.
  86. Although there is no diagnostic test for AD, there are some test findings that can be helpful, what are they?
    • CSF studies have shown decreased Aβ1-42 and an increased amount of τ protein.
    • Also APO-E variatino of ε4 is a risk factor.
    • Imaging will show cortical atrophy.

    the main pathway affected in the cholinergic pathway from the nucleus basalis Meynert.
  87. two main types of dementia?
    Cortical vs subcortical

    Cortical: nrl motor system (posture, tone, gait), disinhibited affect. Maybe be anterior or posterior in nature (i.e. AD).

    Subcortical: PD, HD,

    Dementias with combined cortical and subcortical dysfunction: multi-infarct, prion dz, syphilis, toxic-metabolic etc
  88. Binswanger disease?
    This is a form of dementia with insidious onset (rather than step wise which is often multi-infarct) that is related to HTN.
  89. what are the main medical management available for Alzheimer dementia?
    • These include Donepizil, Rivastigmine which are cholinesterase inhibitors
    • Memantine which is an NMDA receptor antagonist appears to actually slow down the progression of the disease.
  90. what is the main therapy of Lewy body dementia?
    Anticholinesterase medication (rivastigmine, donepezil)

    Must stay away from anti-psychotic as they can worsen sx. For depression can use ECT which has shown to help with the Parkinsonian movement disorders as well.
  91. How to distinguish between AD and DLBD?
    • 1) fluctation in cognitive function (more executive and spatial-spatial impairment rather than the anterograde memory loss of AD)
    • 2) visual hallucinations
    • 3) motor finding resembling that of PD appearing early on.

    • neuroleptic sensitivity
    • REM-sleep disorder
    • unexplained syncope
    • delusions
  92. what are some of clinical manifestations of vitamin B12 deficiency?
    • 1) Neurological: parasthesia, sensory loss, decreased vibration and proprioceptions (dorsal column), distal weakness, ataxia
    • 2) Behavioral: personality changes, psychosis, premature whitening of hair
    • 3) Cardiovascular: tachycardia, congestive heart failure
    • 4) sore, smooth, red tounge
    • 5) megaloblastic anemia
  93. what is the typical finding in optic neuritis?
    change in the visual acuity or visual field out of only one eye, with 90% of pts having pain when moving the eye.

    note that optic neuritis is a general term indicating idiopathic, imflammatory, infectious, demyelinating optic neuropathy.

    strong association with MS (5 year cumulative probability of developing MS is about 30%)

    Treat with IV corticosteriod, however while this hastens the recovery of visual acuity/field it does not change the rate of recurrence nor the possible progression rate to MS. Also treat with INFβ1a if MRI shows demyelination.
  94. what age range do you see MS in? and what are the different types of MS?
    10-60 with most (~70% developing their sx between 21-40 years of age)

    Beningn (about 20% of MS) in which case there is mild attcks with almost full recovery.

    Relapsing/Remitting MS (25% of cases) sx comes and gobut thee is long episodes of stability

    Secondary chronic progressive (40%) worsening sx with eventual platua effect

    primary progressive (15%) keeps getting worse.
  95. What is the charcot's triad?
    What other sx do pt with MS present with?
    Nystagmus, scanning speech, intention tremor

    Often weakness as it can involve with corticospinal tract. Numbness occurs in some 50-70% of the pts. Also cerebelluar ataxia is common. Optic neuritis, trigeminal neuralgia with lancinating pain. Also facial myokymia (a wormlike movement of the muscles that pt feels), electric like sensation that shoots down the spine and into the limbs sometimes (worsen with flexion of the neck)

    increase in body temp (i.e. fever, hot bath, increased physicla exertion) can exacerbate the MS symptoms.
  96. How is MS diagnosed?
    two or more different lesions separated in location and time.

    Hyperintensity areas seen with T2 (mostly with T2 FLAIR) can be seen specially in the corpus callosum perpindicular to the ventricles. NAA can also assist in detecting MS since it is marker for neuronal and axonal function.

    Oligoclonal bands can be seen with CSF analysis with high IgG (not very specific, other inflammatory condition can cause this too). Also increased myelin basic protein can be seen in the CSF.

    Visual evoked response is also helpful.
  97. What is the treatment for MS?
    IV corticosteroid is used for acute attacks. Steroids are not helpful in reducing the frequency of attacks, or the progression of the disease.

    Immunomodulating drugs such as IFNβ-1a and IFNβ-1b have been shown to be helpful on that front. Also antineoplastic drugs (mitoxantrone) have been shown to be helpful. Other immunomodulating drugs such as cyclophophamide, cyclosporine, MTX are also useful is slowing the progresson of the disease.

    Symptomatic tx includes Modafinil (for fatigue), SSRI for for mood stabalization), anticholinergic for bladder dysfunction.
  98. What is ADEM?
    This is acute disseminating encephalomyelitis

    • Often seen post infection (can be post vacination) after 1-3 weeks can present with nausea, vomiting, confusion, can progress to coma. unlike MS, ADEM is monophasic.
    • sometimes can have hemiplegia, and hemiparesis, seizures, myoclonus.

    This is probably a T cell mediated autoimmune disaese acting on the myelin/oligodendrocyte, possibly myelin basic protein (can see hyperintense regions on T2) The neuropatholgy consists of perivenular inflammatory myelinopathy.
  99. Clinical finding in infantile botulism?
    how is it diagnosed? and how is it treated?
    Hypotonia, constipation, hyporeflexia, respiratory problem, cranial never abnormalities, poor feeding, weakness in descending fashion.

    It is diagnosed by fecal cultures and EMG with repetitive nerve stimulation.

    Treatment is with antitoxin (human botulinum immunoglobulin directed toward type A and B)
  100. What is a cmmon clinical picture seen in a pt with HAD (HIV associated dementia)? how is it treated?
    • Initially forgetfullness occurs, poor concentration, personality changes such as social withdrawl, quietness, poor balance, tripping or falling with poor handwriting.
    • As disease progresses then ataxia occurs with myoclonic jerks, bowel and bladder incontinence. No focal neurologic deficits.

    Subcortical dementia

    apraxia, akinetic mutism. Diffuse cerebral atrophy is seen in T2 weighed MRI

    treated with HAART
  101. wha are the different types of CJD?
    • Sporatic CJD (most common ~80%)
    • Hereditary CJD (15%)
    • acquired CJD (onlye about 1% this is through contact with brain)
  102. what is the progression of CJD like?
    • Initially motor problems occur, then personality changes, including impaired memory, judgment, thinking and vision changes.
    • The mental impairment changes as the dz progresses. Can lead to muscle jerks called myoclonus and pt may go blind and even enter coma.
  103. How is neurosyphillis diagnosed? What type of clinical picture is seen? how is it treated?
    Diagnosis: with RPR or VRDL (however these are not very sensitive or specific) therefore if the result is negative however neurosyphillis is still suspected the same tests can be perfoemd on CSF and even a more accurate test FTA-ABS can be performed with is testing specific antibodies to Treponema pallidum.

    Findings: lancinating pain in the legs loss of proprioception and the resultant ataxia, loss of vibration all part of the manifestation of tabes dorsalis. cranial neuropathies including Argyll Robertson pupils (small pupils that are accomodating but not reacting to light). will have normal motor nerve conduction.

    • `
    • : with high dose (2-4 million units of q4hrs for 10-14day of IV aqueous penicillin G.
  104. how do you treat Toxoplasmosis gondii?
    • serum IgG and IgM for titers
    • CSF PCR for T. gondii

    In case of cerebral toxoplasmosis there will multiple (rather than one which would most likely be CNS lymphoma) ring enhancing lesions.
  105. what is the most common cause of focal CNS diease in a pt with AIDS? and how is it treasmisted?

    • 1. By transfer or oocyte from cat feces
    • 2. from ingestion of a cyst from an uncooked meat
    • 3. vertical trasmission
  106. How is toxoplasmosis gondii treated?
    • Pyrimethamine is the main treatment choice. In conjuctin folic acid should also be given since it has selective activity against dihydrofolate reductase which is often given in the form of folinic acid.
    • Sulfadiazine which acts synergistically should also be given. Lastly corticosteroid can be given if there is a lot of edema.
  107. How deos the GCS work?
    • EVM (eye opening + verbal response + Motor`)
    • E: 1 no responce. 2 opens eye with pain 3 opens eye to voice 4 spontaneously
    • V: 1 None 2 no words just sounds, 3 words, but are not coherent, 4 disoriented conversation, 5 normal conversation
    • M: 1 none, 2 decerebrate (below the red nucleus), 3 decorticate posture, 4 withdraws to pain, 5 localize to pain, 6 normal.

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  108. What is Holmes-Adie syndrome?
    This occurs in healthy people and consists of unilateral or in some cases bilateral tonic pupils (unresponsive) impaired, it can also present with impaired corneal sensation, and absent or depressed deep tendon reflexes in the legs.
  109. what are some of the findings in pseudotumor cerebri? What are some of the risk factors? what is the treatment
    may see an empty sella, enlarged optic nerve sheath, small slit-like ventricles. Neuroimaging is typically normal.

    Transient visual obscuration or graying out/dimming of vision (often happening after bending over). Loss of color vision and central visual field. Horizontal diplopia from 6th nerve palsy with a diffuse HA worse in the morning and worse by Valsalva maneuver.

    Risk factors include Obese, fertile age range, female.

    Treatment: Large volume LP helps temporarily, Acetozolamide helps to lower the ICP. Optic nerve sheath fenestration. Lumbar peritoneal shunt. Ophthalmologists need to be involved as well to regularly check the visual field.
  110. How do you distinguish between diplopia of the medial rectus vs lateral rectus?
    If the diplopia worsens when looking at near objects it is due to medial rectus, but if it gets worse when looking at far and lateral objects then it is due to lateral rectus.
  111. What is Cholesteatoma?
    This is a benign tumor composed of epithelial debris from the tympanic membrane that becomes trapped in the middle ear.
  112. MCC of isolated facial nerve palsy in children?
  113. Cholesteatoma?
    • epithelial debris that can be properly exfoliated.
    • Usually occurs in pt that have preexisting ear problems, with hearing loss and foul smelling prulent otorrhea.

    complications can lead to sigmoid sinus thrombosis, brain abscess and meningitis.
  114. What are some causes of bilateral facial palsy
    • Lyme disease
    • Guillain-Barre syndrome
  115. How is Ramsay Hunt Syndrome treated?
    • Herpes antivirus is used (IV acyclovir or for PO can use gancyclovir or valacyclovir).
    • Steroid can also be used. However it should be taken into account that it is possible to get a dissemination of the HSV.
  116. How do you treat Tourret's syndrome or Tics?
    • Clonidine
    • Neuroleptic (Haloparidol)
    • BDZ (carbamazapine)
  117. which type of the seizure is the one that can be confused with psychiatric problems?
    • Partial complex.
    • This is particularly the case when the seizure does not evolve to a generalized phase involving tonic-clonic or LOC.

    ex. woman barried his plates in the yard.
  118. what is the definition of status epilecticus?
    Seizure that lasts more than 30 minutes or multiple seizures within 30 minutes without enough time for the pt to regain full consciousness.
  119. What is West syndrome?
    These are generalized seizures that can present infantile spasms.

    has been associated with tuberous sclerosis and ACTH is the only drug for treatment.
  120. Name two drugs are good for absence seizure?
    Ethusuximide and Divalproex sodium (Depakote)
  121. what is the drug of choice to stop seizure in a peregnant in preeclampsia?
    MgSO4 (magnesium sulfate) is good for both preventing and abortive treatment of seizures in pregnancy.

    Infant should be delivered ASAP.
  122. difference between classic and common migraine?
    In classic there is an AURA
  123. What is basilar migraine?
    • This type of migrain is very atypical and differes from classic/common migrain by its severity and characteristic neurological dysfunx.
    • Can lead to transient quadraplegia, may develope into frank psychosis, visual changes may evolve into full blindness.
  124. drugs effective in treating trigeminal neuralgia pain include?
    • Carbamazepine (Tegretol)
    • Phenytoin (Dilantin)
    • Gabapentine (Neurontin)
  125. A few of the causes of symptomatic trigeminal neuralgia?
    • MS
    • Posterior fossa meningioma
    • Basila artery aneurysm
  126. what is the first cranial nerve that becomes affected by sarcoidosis?
    • CN VII
    • other CN include II, III, IV, VI, and VIII
  127. What is the drug of choice to treat L. monocytgens treatment
    Ampicillin + Gentimicin
  128. Ring enhancing lesion in a pt with AIDS, what are the two highest things on your ddx?
    • PCNSL
    • Toxoplasmosi gondii
  129. what are some of the findings in PCD and it is mainly associated with what cancer?
    • Paraneoplastic cerebellar degeneration (PCD)
    • subacute ataxia, dysarthia, and nystagmus.

    seen with small cell carcinoma, ovarian carcinoma, and lymphoma.
  130. How is CIDP and Guillain-Barre syndrome different?
    If the symptoms last more than 8 weeks they are considered CIDP.
  131. What are the clinical finding in CIDP?
    symmetric sensory loss with flaccid weakness with mainly proximal muscles involvement. Reduced or even areflexia. With spontaneous pain that graually developes over weeks.

    associated with a recent hx of infection or vaccination.

    lesions consist of patchy regions of demyelination and edema with variable inflammatory infiltrates of Mo and T cells.

    • Diagnostic test is EMG, NCV, and nerve biopsy.
    • For treatment can use corticosteroid, IVIG, plasma exchange.
  132. what is Miller-Fisher variant?
    This is a subtype of Guilain-Barre syndrome (there are 5 different types) which has a classic triad of ataxia, areflexia, ophthalmoplegia with predominant cranial nerve weakness rather than extermities, and is positive for anti-GQ1b (ganglioside) antibodies.
  133. what is the most common neurologic complication seen in pt with chronic renal failure?
    Pripheral neuropathy
  134. what do pts with cerebellar hemorrhage present with?
    With ataxia, vomiting, occipital headaches, gaze palsy, and facial weakness.
  135. pt with resting tremor and orthostatic?
    Multiple system atrophy
  136. what is an expected electrolyte abnormality seen in a pt with SAH?
    Cerebral salt-wasting syndrome

    • 1) inappropriate secretion of vasopression
    • 2) increased secretion of BNP

    leading to Hyponatremia
  137. what is one of the main complications of VP shunts placement in someone with hydrocephalus?
    • Subdural hematoma.
    • As the pressure in the brain drops the brain can come off of the meninges and pull on and even rupture the bridging arteries.
  138. what is chorea gravidarum?
    • This is a chorea like movement that can occur during pregnancy or can occur with estrogen use. Related to hormonal changes affects on the brain.
    • spontaneously resolves after the hormonal derrangement abates.
  139. what is a drug that is useful to treat the parkinsonism that can develope with Haloperidol?
  140. what is Meig's syndrome?
    • this is a form of focal dystonia characterized by blepharospasm, foreful jaw opening, lip retraction, neck contractions, and tongue thrusting. Mostly seen in women.
    • Botulinum toxin injection has been more effective in treatment than PO meds.
Card Set:
neuro rotation
2011-12-16 03:00:33

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