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162 Cards in this Set
- Front
- Back
What are the 3 features of alpha activity that are important to notate? 1
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1) symmetry (up to 50% variance of 20 microvolts usually the right is higher side)
2) location- usually posterior dominant, anterior dominant can be seen in alpha coma 3) reactivity- attenuates with eye closure; paradoxical alpha is when atteuates with eye opening (just waking without visual fixation or sedation) |
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What is the usual frequency of alpha waves?
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8 to 13 hz
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What is the usual frequency of beta waves?
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>13 hertz
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What is the usual etiology of frontal predominant or diffuse beta?
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medications such as barbiturates or benzodiazepines
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What is the usual etiology theta frequency?
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drowsiness
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What is the usual etiology of temporal alpha?
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can be normal variant in elderly
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What is jamais vu?
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a familiar situation which is not recognized
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What are three ways to characterize automatisms?
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de novo- complex motor activity begins after sz onset
reactive automatisms- activity is a reaction to ext. stimulus perseverative automatisms- continuation of motor activity initiated before seizure onset |
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What does the term uncinate fits refer to?
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olfactory halllucinations arising from the temporal lobe
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Where can bicycling, pedaling movements or sexual gesturing during aseizure localize to?
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frontal lobe
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What is the most common extratemporal partial epilepsy?
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frontal lobe seizures
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What are some examples of occipital seizures?
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elementary visual hallucinations, bright lights, flashes of light, geometric objectives and versive eye movements
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What are the characteristic of benign neonatal seizures?
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clonic or myoclonic seizures/apneic events during first few weeks after birth, stop by 6 weeks, normal development; 10-15% later have epilepsy; treatment not necessary (can give 1 month phenobarb)
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What is the etiology of benign familial neonatal convulsions?
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autosomal dominant inheritance, mutation of KCNQ2 or 3 genes
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What is early myoclonic enphalopaty?
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focal myoclonus that migrates to different body parts, occurs in early infancy, other seizure types; many etiologies (cryptogenic, HONK, inherited, developmental malformation)
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What is the etiology of AD partial epilepsy with auditory features?
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Leucine-rich, glioma inactivated 1 gene
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What is a caveat about the EEG in myoclonus?
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may not have EEG correlate on EEG and be normal initially
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What is the prognosis with early myoclonic encephalopathy?
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more than 50% die
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What is Ohtahara syndorome?
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early infantile epileptic encephalopathy with suppression bursts
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What is the difference between Ohtahara syndrome and early myoclonic encephalopathy?
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Ohtahara syndrome has burst-suppression on EEG, no myolocnic seizures, can treat with vigabatrin, same prognosis
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What is the etiology of pyridoxine dependent seizures in infancy?
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possibly decreased glutamic acid decarboxylase activity
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What is the difference between pyridoxine dependent and deficient seizures?
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pyridoxine dependent requires larger doses of B6, life long B6 and occurs early than pyridoxine deficient (caused by breastfeeding malnourished mothers)
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What is the difference between benign myclonus of infancy and myoclonic encephalopathy?
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developmentally normal, clusters for weeks then less freuqent by 3 months and stops by 2 years
normal eeg |
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What is the triad in West's syndrome?
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infantile spasms
hypsarrhythmia developmental arrest |
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What is the triad for Aicardi's syndrome?
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infantile spasms
agenesis of the corpus collosum and retinal malformations X linked dominant |
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What is benign myclonic epilepsy of infancy?
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EEG with spike & wave or polyspike and wave
excellent dvelopmental outcome with treatment with VPA 1/3 have family history |
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What is Dravet syndrome?
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severe myoclonic epilepsy in infancy, begins within 1 year afterbirth, no previous brain abnormality except diffuse atropy, partial seizures later, 1/4 have family hx of sz, dev delay, EEG general, focal or multifocal abnL
idiopathic generalized epilepsy |
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What are the features of benign epilepsy with central temporal spikes?
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onset 4-12 resolve by mid-teens
motor, simple sensory, tonic-clonic movements, speech arrests can have secondary generalization more sz with speech half of releatives have EEG changes but only 12% would have sz not necessary to treat idiopathic focal epilepsy |
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What is Panayiotopoulos syndrome?
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also called early onset benign childhood occipital epilepsy
children 3-6 autonomic sz, status epilepticus, ictal vomiting good response to anticonvulsants frequent or nealry continuous rhythmic occipital speaks |
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What is Gastaut type late onset childhood occipital epilepsy?
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children 4-8
visual seizures: hallucinations, blidness, followed by headache, onset with photic stimulation |
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What is the significance of epilepsy with myoclonic absences?
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children age 7
**half have dev delay no eye twitching unlike other absence seizures 1/2 continue to have seizures as adults** |
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What is myoclonic-astatic epilepsy of childhood?
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onset 2-5 with multiple generalized sz types: tonic-clonic, clonic, atonic, myoclonic (NO TONIC unlike LG)
EEG faster than LG 2-3 HZ spike and wave |
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What are the characteristics of Lennox Gastaut syndrome?
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1. mental retardation (severe, progressive due to subclin sz)
2. slow spike & wave 1.5-2.5 HZ (spikes are slow 150 ms) 3. multiple generalized sz types onset 2-8 boys >girls cryptogenic or symptomatic |
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What is Landau Kelfferner syndrome?
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acquired epileptic aphasia, word deafness
onset 3-8 |
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What is the treatment for Lennox gastaut syndrome?
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VPA, felbamate (drop attacks), lamotrigine
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What is the treatment for Landau Kleffner syndrome?
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VPA, Lamotrigine, steroids?
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What are the features of childhood absence epilepsy?
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onset 6 years old (up to 10)
staring spells (can have automatisms, ictal jerks of eye) 1/3 have GTC 90% outgrow by childhood caused by thalamic activity of T type calcium channels |
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What are the differences between juvenile absence epilepsy and childhood absence epilepsy?
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age of onset juvenile is 10-16
more likely to have GTC less likely to outgrow sz |
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What features of absence epilepsy are considered atypical?
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prolonged (more than a few seconds)
assoc with other sz types or MR spike and wave <2.5 HZ (absence can be 2.5 HZ to 4 HZ) |
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What is the differential diagnosis for progressive myoclonic epilepsy?
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lysosomal
Lafora body disease Unverricht-Lundborg syndrome (baltic myoclonus) NCL Sialidoses mitochondrial MERRF |
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What are the features of GEFS plus?
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febrile sz + atypicla feature (sz without fevere, after age 6 or other seizure type)
AD (sodium channel or GABA) |
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What are the clinical features of Rasmussen's encephalitis?
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intractable progressive focal seizures
progressive hemiparesis cog deterioration antibodies to GluR3 (glutamate receptor 3) |
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What is the difference between phenytoin and fosphenytoin?
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Fosphenytoin is the intravenous prodrug of phenytoin, converted to phenytoin by erythrocytes (takes 8 to 16 minutes), water soluble solution (less purple glove syndrome), can give more 150 mg of phenytoin equivalents per minute
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What are the 4 MOA of phenobarbital?
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GABAa
sodium channel blocker T-type calcium channel blocker glutamate blocker |
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What are the 3 MOA of VPA?
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sodium channel blocker
gaba a agonist gaba trasnaminase inhibition t-type calcium channel blocker |
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What arethe side effects of Ethosuximide?
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drowsiness, dizziness, headaches, GI upset, n/v/d, rash,
monitor lfts and cbc |
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What are the side effects of felbamate?
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potentially fatal hepatotsicity and high rates of aplastic anemia, only in severe refractory cases of Lennox-Gastaut as last resort
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How does Felbamate interact with other meds?
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inhibits breakdown of pht, phb, vpa, cbz
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what is the MOA of tiagabine?
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GABA reuptake inhibitor
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What are hte SE of Tiagabine?
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somnolence, dizziness, cognitive, ataxia, tremor
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What is the MOA of Gabapentin?
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increases post-synptic GABA
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What are hte MOA of Lamotrigine?
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inhibits sodium channels and inhibits glutamate release
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What are the RFs for Stevens Johnson with LMG?
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rapid titration
use of VPA use in children |
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What is the MOA of Levetiracetam?
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inhibits burst firings of neurons withoutaffecting normal neuronal activity, not exactly known
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What are the side effects of LEV?
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mild cognitive-drowsiness, dizziness, ataxia
psychiatric-agitation, emotional lability, behavioral |
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What are the MOA of Topiramate?
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sodium channel inhibition
gaba a agonist NMDA blocker carbonic anhydrase inhibitor |
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What are the side effects of TOP?
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kidney stones, paresthesias, angle closure glaucoma, weight loss, word findingdifficulty, weight loss
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What are the interactions of TOP with OCP?
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can decrease effectiveness of OCP
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What is the difference between VPA and DVP?
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VPA should be given TID
DVP can be given BID |
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What is autoinduction in CBZ?
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after being on CBZ for a few days to weeks can lead to autoinduction and half-life changes from 30 hrs to 10-20 hrs
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What is a caveat regarding CBZ interpretation levels?
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CBZ epoxide metabolites can accumulate although the levels may look low (autoinduction, use with VPA)
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What is the relationship between OXC use and OCPs?
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OXC can decrease the effectiveness of OCPs
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What should be monitored in LMG?
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nothing
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What is MOA of BZDZ?
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GABAa channels, increase chloride channel opening FREQ
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What are the SE of BZDZ?
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cardiovascular collapse, somnolence, resp depression, , withdrawal, hepatotoxic, neutropenia/pancytopenia/thrombocytopenia
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What is MOA of Ethosux?
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T-type calcium channels
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Wat are the SE of ethosux?
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rash, leukopenia, Stevens-Johnson, pancytopenia, agranulocytosis, aplastic anemia
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What should be monitoried with ethosux?
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LFTs and CBC
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What is the MOA of Tiagabine?
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GABA transporter inhibitor
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What are the SE of tiagabine?
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poor responder rate
GI upset, cognitive, dizziness, ataxia, tremor, requires frequent dosing |
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What is the MOA of Gabapentin?
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increases post-synaptic Gaba
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What is the MOA of Lamotrigine?
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inhibits sodium channels and glutamate release
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How is LMG affected by OCPs?
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OCPs can actually change the half life of LMG
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What are the 3 MOA of ZNS?
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GABAa agonist
inhibits sodium channels inhibits T-type calcium channels |
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What is the most feared SE of Vigabatrin?
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retina toxicity causing field cus
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How does Vigabatrin work?
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GABA transaminase
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What are the SE of Pregabalin?
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drowsiness, ataxia, dizziness, weight gain, euophoria
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What is propofol infusion syndrome triad?
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severe hypotension
lipidemia metabolic acidosis |
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Why does estrogen have a proconvulsant effect?
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It downregulates GABAa receptor synthesis
acts as NMDA agonist |
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What is the localization of an early unforced head turn?
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the ipsilateral temporal lobe
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What is the abnormality in PARK1 gene?
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mutation in alpha synuclein
early onset parkisonism and dystonia autosomal dominant inheritance |
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What is the abnormality in PARK2 gene?
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early onset parkinsonism and dystonia
autosomal recessive may be responsible for up to 1/2 cases of PD most common hereditary cause* |
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What are the side effects of Sinemet?
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nausea (make sure at least 100-150 mg/day of carbidopa)
dyskinesias hallucinations orthostatic hypotension psychosis |
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What are the side effects of dopamine agonists?
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non-ergot derivatives: pramipexole & ropinorole
nausea less dyskinesias than levodopa sleep attacks & sedation peripheral edema more likely than levodopa to cause hallucinations, psychosis, orthostatic hypotension |
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What are the side effects of ergot derivative dopamine agonists?
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pulmonary, retroperitoneal vavlcular fibrosis?
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What are the side effects of COMT inhibitors?
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Tolcapone- fatal hepatoxicity
Entocapone nausea, GI upset urine discoloration can predispose to dyskinesias |
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What are the side effects of anticholinergic agents?
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dry mouth, urinary retention, constipation, confusion; can be helpful in tremor (trihexyphenidyl)
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What are the side effects of MAO inhibitors?
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serotonin syndrome* (low prevalence rates despite concomitant use in many PD patients ADAGIO, DATATOP)
nausea, GI upset, urine, orthostatic hypotension, confusion |
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What is dopamine dysregulation syndrome?
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punding, hypersexuality, occuring mostly with dopamine agonists
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What are the SE of amantadine?
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can cause livedo reticularis, per Ondo one of worse offenders for confusion/psychosis/hallucinations
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What are some clinical features that may suggest MSA rather than PD?
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early prominent autonomic features (orthostatic hypotension, urinary incontinence- some even do EMG of ext. urthra or anal sphincter to look for long duration, high amplitude units consistent with denervation of Onuf's nucleus)
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What is the histopathologic feature in MSA?
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glial cytoplasmic inclusions
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What is the histopathologic feature in PSP?
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globose neurofibrillary tangles
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Is PSP a synucleinopathy or tauopathy?
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tauopathy like CBGD
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What type of dystonia may be present in MSA?
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antecollis
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What type of dystonia or axial findings in PSP?
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early axial regidity prominent hyperextension on walking
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What findings can be seen on imaging for MSA?
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putaminal hypointensity
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What findings can be found on imaging for PSP?
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mickey mouse midbrain
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What are the characteristic clinical features of CBD?
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alien limb phenomenon
*very asymmetric (dystonia, apraxia, myoclonus, ocular aparaxia, speech apraxia) ideomotor apraxia cortical sensory loss |
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What is the characteristic histopathologic finding of CBGD?
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tau positive intraneuronal inclusions
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What is the differential diagnosis for symmetric basal ganglia calcification?
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Vascular: parinatal anoxia
Infxn: ToRCH, HIV, TB, cysticercosis Trauma/toxins: perinatal anoxia, lead, metotrexate, radiation Autoimmune: none Metabolic: Hypercalcemia, hypoparathyroidism, Amyloid angiopathy, Fahr's disease, Wilson's disease Idiopathic Neoplastic Hereditary: Cockayne syndrome: pigmentary retinal degen, sensorineural hearing loss, dwarfism/short stature, psychomotor retardation, bilateral basal ganglia calcification |
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What are the characteristics of Fahr's disease?
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progressive dementia
parkisonism schizophrenia/psychosis (if presenting age 20-40) bilateral basal ganglia calcification usually sporadic, can be AD chr. 14 |
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Where is the calcification in Fahr's disease?
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could be basal ganglia, dentate nucleus and periventricular region
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What is the presentation of NBIA type 1 or PKAN?
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movement disorders: dystonia, rigidity, gait imbalance,, parkinsonism in adults
progressive dementia psychosis & personality change (other: dysarthria, choreoathetosis, retinits pigmentosa, optic n. degen, sz, pyramidal signs) |
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What is the characteristic imaging finding on MRI for PKAN or NBIA type 1?
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eye of the tiger sign, bilateral low density basal ganglia on CT
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What are the clinical characteristics of Wilson's disease?
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most commonly cranial motor features: (dysarthria, dysphagia, rhisus sardonicus, sialorrhea)
dystonia, parkinsonism, chorea, classic wing beating tremor with change in kinetic liver disease neuropsychiatric symptoms |
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What are the characteristic imaging findings on CT of
Wilson's disease? |
hypodensity of putamen bilaterally
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What are the characteristic findings of Wilson's disease on MRI?
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hyperintensity of dentate nucleus, thalamus and brainstem
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What are the toxic exposures that may lead to PD?
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mangagnese (miners, industrial workers)
MPTP herbicides pesticides well water |
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What are the characteristic imaging findings on T1 for manganese toxicity?
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bilateral T1 hyperintense signal in pallidum
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What are the long-term effects of cyanide toxiciy in patients who survive the acute phase?
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parkinsonism
optic atrophy cerebellar ataxia myelopathy peripheral neuropathy |
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What are the imaging findings in patients with cyanide toxicity?
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bilateral T1 hypointensity in pallidum
bilateral T2 hyperintensity in pallidum |
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What is the differential diagnosis of Parkisonism?
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Vascular: vascular parkinsonism, post-anoxic
Infxn: bacteria: syphilis, trophyrema whipplei viral: HIV, SSPE, coxsackie virus, polio, western equine, vzv creutzfeldt jakob disease Toxins/Trauma: Dementia pugilistica, MPTP, CO, Methanol, Manganese, pesticide, well water, miners, welders, cyanide Autoimmun: Encephalitis Lethargica or Von Economo's encephalitis Metabolic: Fahr's disease, hypoparathyroidism, central pontine myelinolysis Iatrogenic-tardive dyskinesias Neoplastic paraneoplastic (autoantibodies) Degenerative: - (uam-Dementia-Parkinsonism; FTD-17 Parkinsonism |
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What is the primary generator of tremor in ET?
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the cerebellum/red nucleus
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What is the starting dose & max dose of propranolol for ET?
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40 mg/day up to 320 mg/day maximum
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What is the effectiveness of propranolol for ET?
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60% reduction in tremor
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What is the starting/max dose of primidone?
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50 mg/day up to 750 mg/day
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What is the effectiveness of primidone for ET?
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60% reduction in tremor
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What are the side effects of propranolol?
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AV block, depression, impotence, mask hypoglycemia, worsening asthma or copd
|
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What are the side effects of primidone?
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acute rxn: nausea, dizziness
metabolized to barbiturate cognitive slowing |
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How can one distinguish PD tremor from essential tremor?
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re-emergence of tremor (in PD) and improvement of ET with alcohol
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What is orthostatic tremor?
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occurs in elderly patients > 60
sensation of falling, instability dizziness high-frequency 13 to 18 HZ tremor of legs can move to trunks |
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What is the treatment for orthostatic tremor?
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benzodiazepines, primidone, vpa and GBP
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What are the features of dystonic tremor?
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irregular tremor, focal, kinetic & postural; response to sensory tricks
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What is etiology of Holmes tremor?
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involve nigrostriatal pathway, midbrain and cerebellar output
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What is Guillan Mollaret triangle?
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Dentate nucleus via SCP cross red nucleus, CTT ipsi inferior olive to DN via ICP contra
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What are the clinical characteristics of Holmes tremor?
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low frequency < 5 HZ, high amplitude proximal > distal tremor present at rest & with action, posture, difficult to treat
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What is the etiology palatal tremor?
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generated from guillan mollaret triangle
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What are the features of hereditary geniospasm?
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infants/early childhood, chin tremor without any other abnormalities, benign prognosis
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What type of tremor is characterized by FXTAS?
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premutation with intention tremor in older men with gait instability
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What is titubation?
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low frequency oscillation involving the axial musculature
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What is parakinesia?
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chorea that may seem semipurposeful and may blend into purposeful movements
|
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What is the etiology of DRPLA?
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chroosome 12 unstable trinucleotide CAG repeat expansion
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What are the clinical features of DRPLA?
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progressive myoclonic epilepsy
cognitive decline dystonia, chorea, parkinsonism usually Japan, Af-Am, North Carolina family onset in 30s |
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What are the clinical features of amyotrophic choreoathetosis with acanthocytosis? ?
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chorea *orofacial dyskinesias, tics, dystonia, parkinsonism
cognitive decline neuropsychiatric manifestations McLeod muscle weakness, wwasting seizures acanthocytes on pbs onset 20s-30s |
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What are the clinical features of McLeod's syndrome?
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acanthocytosis
chorea, dystonia, parkinsonism, *orofacial dyskinesias (less prominent that other neuroacanthocytosis) neuropsychiatric manifestations peripheral neuropathy myopathy seizures |
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What is the inheritance of McLeod's syndrome?
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X linked recessive
|
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What are the features of hereditary choreoacanthocytosis?
|
chorea
acanthocytes on pbs dystonia, parkinonism neurpsych manifestations axonal neuropathy |
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What is the method of inheritance of heredtiary choreoacanthocytosis?
|
AR chromosome 9
|
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What are the clinical features of sydenham's chorea?
|
female:male predominance
months after onset of strep A infxn motor and vocal tics, chorea can be hemichorea which generalizes, oculogyric crisis, personality changes |
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What is prognosis of sydenhan's chorea?
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self limited resolves after 8-9 months
|
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What is the differential diagnosis of chorea?
|
Vascular- strokes <1% (ischemic or hemorrhagic)
infarcts related to infxn: TB moyamoya vasculitis Infectious: bacterial mening aseptic mening TB mening with infarcts Toxoplasmosis post-infxn Sydenham's chorea Trauma/Toxins: Hemorrhagic? Toluene, Manganese CO Autoimmune: SLE, Antiphospholipid, Behcet's, HSP Metabolic: Hyperthyroidism, HONK, pregnancy Iatrogenic: Tardive, Sinemet, lamotrigine, oral contraceptives, LI, methoadone, Cocaine, Amphetamines Neoplastic:Paraneoplastic anti-Hu Degenerative: Huntington's disease, Neuroacanthocytosis, DRPLA, benign familial chorea, senile chorea, |
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What are the histopathologic findings of NBIA type 1?
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excess irone dposits, spheroids, neuronal loss, widespread alpha synuclein
|
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What is eye of the tiger sign on MRI?
|
high signal anteromedially surrounded by low signal
|
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What are Opalski cells?
|
rounds cells with eo cytoplasm an small central nucleus assoc with hepatic encephalopathy
|
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What type of astrocytes are associated with hepatic abnormality?
|
alzheimer type II astrocytes
|
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What is the most common hereidtary dystonia?
|
ad DYT1 rarly onset dystonia, GAG deletion, tosin A
|
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What is DYT 11 or myoclonus-dystonia?
|
epsilon-sarcoglycan gene
chromosome 18 first decade onset sensitive to alcohol, tend to have depression/mood disorder/substance abuse head, arm, upper body affected imprinting |
|
What is DYT5 or DRD?
|
AD chromosome 14
GTP cyclohydrolase 1 sysnthesis of tetrahydrobiopterin diurnal fluctuations marked response to levodopa |
|
What is DYT 10?
|
parosymal kineseogenic dyskinesia
dystonia, chorea lasting a few seconds to 5 minutes precipitated by sudden movements treat with na channel blockers |
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In the context of crime for homicide, the presence of a deadly weapon does what?
|
Creates an inference of an intent to kill.
|
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What is paroxysmal exertional dyskinesia?
|
episodes lasting 5 to 30 minutes, induced by exericse, longer than dyt 10 lasting 5 to 30 minutes
different tx: diamox or bzdz |
|
What is DYT3?
|
X linked dystonia-parkinsonims
40s-50s poor response to tx |
|
What is Niemann Pick disease type C?
|
cholesterol metabolism disorderwith dementia, cataplexy, dysarthria, dystonia, dysphagia, vertical supranuclear gaze palsy and sz; preschool age also with hepatosplenomegaly
|
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How can one distinguish between adductor variety and abductor variety of spasmodic dysphonia?
|
adductor strained
abductor breathy |
|
What are the characteristics clinically of acute dystonic reactions?
|
abrupt onset of dystonic posturing, oculogyric crisis within 2 to 24 hours after first dose of drug, painful, can treat with benztropine or benadryl but stop drug and should resolve spontaneously
|
|
What is the hereditary etiology of hyperekplexia?
|
AD mutation in glycine receptor chromosome 5q
|
|
What is the genetic etiology of sialidosis type I and II?
|
autosomal recessive chromosome 6
|
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Whatis the etiology of GM2 gangliosidoeses?
|
beta hexosamindiase
|
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What is the etiology of Lafora's disease?
|
autosomal recessive, chromosome 6
onset 20s dementia, myoclonus, seizures diagnosis by eccrine sweat gland ducts on biopsy |
|
What is the cause of withdrawal emergent syndrome?
|
abrupt withdrawal of neuroleptics
nonstereotypic choreic hyperkinetic movmeents, parkinsonism |
|
What is painful legs nad moving toes syndrome?
|
peripherla nerve trauma, peripheral neuropathy, radiculopathy, diopathic
pain precedes movement d/o mild and can treat with anticonvulsants (gbp), tca, dopaminergic, sympathetic blockades (usually disappointing results) |