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189 Cards in this Set
- Front
- Back
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Where are the D1 receptors located?
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cerebral cortex, basal ganglia
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Where are D2 receptors located?
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striatum (caudate and putamen)
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Where are D3 & D4 receptors located?
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limbic system
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Where are D5 receptors located?
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hypothalamus and hippocampus
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What is the difference between schizophreniform disorder and schizophrenia?
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Schizophreniform symptoms that impact functioning last at least 1 month but less than 6 months. Schizophrenia symptoms impact functioning last more than 6 months (2 out of 5 positive/negative symptoms only need to last 1 month)
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What is the prognosis for schizophreniform disorder?
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33% will recover within 6 months
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What is the best studied SSRI in pregnancy?
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Fluoxetine
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Which SSRIs have the best profile in regard to sexual side effects?
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fluoxetine and fluvoxamine
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Which SSRI has the longest half life?
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fluoxetine
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What is considered the most potent SSRI?
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paroxetine
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What are the clinical characteristics of serotonin syndrome?
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altered mental status
agitation tremor hypotension fever ataxia diarrhea hyperreflexia myoclonus |
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What is the MOA of buproprion?
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DNRI
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What dose of Buproprion can lead to seizures?
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more than 450 mg per day
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What arethe MOA of duloxetine?
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SNRI
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What is the MOA of Mirtazpine?
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enhances release of NE, inhitibits 5HT2 and 5HT3 receptors, alpha 2 adrenergic agaonist
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What is the MOA of Nefazodone?
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5HT2 antagonist/reuptake inhibitor
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What is the MOA of trazodone?
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5HT2 receptor antagonist/weak inhibtor of 5HT reuptake
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What are the SE of clozapine?
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sedation, wieght gain, orthostatic hypotension, hypersalivation, eosinophilia, hypertriglyceridemia, hyperglycemia, agrnaulocytosis, seizures
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What is MOA of lithium?
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inhibits inositol-1-phosphatase decreases cellular responses to neurotransmitters
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What are 3 MOA of VPA?
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1) Na channel blocker
2) T-type calcium channel blocker 3) GABA transaminase |
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What is the MOA for GABApentin?
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increase GABA synthesis
reduce levels of glutamate |
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What is the MOA of Topiramate? (3)
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na channel blocker
carbonic anhydrase inhibitor weakly enhances post-synaptic GABA (adjunct for bipolar disorder) |
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What illegal drugs do not lead to withdrawal symptoms?
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cannabis, hallucinogens, inhalants, or phencyclidine
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What SSRIs have short half lives leading to concern for serotonin discontinuation syndrome?
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paroxetine and fluvoxamine
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Which subtype of schizophrenia has the best prognosis?
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paranoid subtype
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What is Fregoli syndrome?
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id a familiar person in various other people without physical resemblance, believe they are pscyhchologically identacal
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What clang?
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thoughts proceed from one to another by sound of words, such as rhyming
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What is the difference between schizoaffective disorder and schizophrenia?
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schizoaffective disorder prominent mood symptoms with psychosis and at least 2 weeks of psychosis without mood symptoms
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What is the prognosis for brief psychotic disorder?
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50-80% completely recover
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What is the differential for medical & neurologic causes of psychotic disorder due to a general medical condition?
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Vascular: stroke left hemisphere
Infection: CJD, HIV, syphillis, TB Trauma: Autoimmune: Lupus Metabolic: Thyrotoxicosis, hypothyroidism, Diabetes, B12 deficiency, Pellagra Iatrogenic: Neoplastic: Cancer, Pareneoplastic Neurodegen: Dementia, Wilson's Disease, Huntington's disease, Temporal Lobe Epilepsy, MS, Parkinson's disease |
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What is the rate of recurrence of postpartum depression?
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30-50%
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What is the incidence of post-partum depression?
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1:500 to 1:1000 births
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How many patients have chronic depression?
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20% OF mdd PATIENTS
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What percentage of patients commit suicide with MDD?
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10-15%
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What are the criteria for dysthymic disorder?
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ACHE2S (at loeast 2 of following)
appetite concentration hopelessness energy esteem 2 years sleep |
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What are the critieria for bipolar 1 disorder?
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manic episode for at least 1 week
>4 of the following Distractibility Insomnia Grandiosity Flight of ideas Activities increased pressured Speech Thoughtlessness |
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What is the difference between bipolar ii disorder and bipolar 1 disorder?
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bipolar 2 has at least 1 MDD and 1 hypomanic without any previous manicc episodes
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What is the difference between cyclothymic d/o and bipolar ii d/o?
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@ least 2 years hypomania and depressive sx but do not meet MDD
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What are the physical symptoms associated with panic attacks?
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at least 4 of following
Palpitations, paresthesias, pounding heart Anxiety Nausea Increased perspiration, increased dread/doom, Chest pain, choking, chills, lack of control Sweating, shortness of breath, shaking/trembling |
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What is cynophobia?
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fear of dogs
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What are the criteria for abuse?
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failure at social obligations due to drug use, legal problems, use in hazardous situations, social problems
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What is the differential diagnosis for delirium or encephalopathy?
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Vascular- vasculitis, CNS angiitis, left hemispheric stroke,, brainstem infarct, venous infarct (straight sinus/vein of galen), hypertensive encephalopathy, SAH
Infxn: bacterial: mening fungal viral encephalitis: SSPE, WNV, SLE prion disease Trauma: EDH, SDH Toxins: mercury, lead, arsenic Autoimmune: SLE, APLA, WG, Churg-Strauss, Neuro-Behcet's Metabolic: Acid/Base: Hypoxia Electrolytes: Hypona, Hyperna, Uremic Encephalopathy, Hypoglycemia/Hyperglycemia Endocrine: Cushings, Hypo or hyperthyroid AIP Nutrtitional: B12 deficiency, Wernicke's Inflammatory/Iatrogenic: Sarcoid Drugs of abuse: PCP, Cocaine, Amphetamines Neoplastic: Neoplastic, Paraneoplastic, Carcinomatous mening degen: Epilepsy |
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What is the data for donepezil and amnestic MCI?
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less likely to convert to AD in 1st 12 months, rate of conversion is 15% per year, the effect is gone after 3 years
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What is the current AAN recommendation regarding APOE typing for patients with AD?
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It should not be used currently for diagnosis or management because some carriers will never develop AD (used in studies currently)
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What is the difference between Capgras syndrome and Fregoli's syndrome?
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Capgras syndrome is when a family member is thought to be an impostor, Fregoli syndrome is when an unfamiliar person is id'ed as a family member
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What is the relationship between extrapyramidal symptoms and AD?
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the extrapyramidal symptoms may present in late AD
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What is something to consider in patients on cholinesterase inhibitors prior to general anesthesia?
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These medications should be discontinued
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What are the major side effects of donepezil? (4)
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nausea vomiting diarrhea vivid dreams (watch out for bradycardia)
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When should a patient take donepezil?
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in morning on early stomach
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What is the dosing for Aricept?
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5 mg daily for 1 month then 10 mg daily thereafter
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What is the dosing for Galantamine?
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4 mg twice daily for 1 month, 8 mg twice daily then 12 mg twice daily (if tolerated)
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What is the dosing for rivastigmine?
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twice daily 1.5 mg twice daily then escalate monthly by 3 mg up to 6 mg twice daily if tolerated
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What is the difference between galantamine, rivastigmine and donepezil?
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they all have the same side effect profile but frequency increases in this order
donepezil < galantamine < rivastigmine |
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What are the side effects of memantine with dementia?
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confusion, headaches, dizziness
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When should memantine be used for treatment?
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in patients with moderate to severe dementia
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What is the dosing for memantine?
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5 mg once daily then increase by 5 mg every week upto 10 mg twice daily
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What is initial therapy for apathy?
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acetylcholinesterase inhibitors should be considered first
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What is the effect of memantine on behavior?
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some improvement in irritability and agitation
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What percentage of patients with FTD have sporadic disease?
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only 20% inherited
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What is tau?
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microtubule binding protein
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What chromosome is linked to FTD-MND?
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Chromosome 9
ubiquitin immunoreactive, tau negative inclusion bodies in motor neurons |
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What is Sneddon's syndrome? (6)
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1. small vessel strokes
2. extensive white matter disease 3. livedo reticularis 4. antiphospholipid antibodies 5. seizures 6. miscarriages recurrent |
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What are the features of Lindenberg-Spatz disease or Buerger's disease?
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rare cause of vascular dementia determined by biopsy showing "thromboangiitis obliterans" without media wall thickening/eo deposits (CADASIL) or inflammation/amyloid/granulomatous depositis (amyloidosis, granulomatous disease, vasculitis) and obliteration/occlusion of the vessels (unlike Binswanger's which has thickening of layers without obliteration/occlusion)
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What is the difference between Buerger's disease and Lindenberg-Spatz?
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Buerger's does not occur in women, non-smoker, non-hypertensive
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What variants are associated with Creutzfeldt Jakob disease? (4)
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1. Heidenhain variant (rapidly progressive cortical blindness-occipital lobes)
2. amyotrophic variant- prominent early LMN signs 3. Brownell-Oppenheimer variant- early prominent progressive ataxia 4. Stern-Garcia- x-pyr variant |
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What is the etiology of fatal familial insomnia?
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mutation of PRNP D178N in addition to MET residue at codon 129, affects mediodorsal thalamic nuclei little spongiform change
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what are the clinical features of fatal familial insomnia?
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intractable insomnia
subacute onset, rapidly progressive dysautonomia (hypertension, tachycardia, hyperhidrosis) ataxia, myoclonus, pyr signs, x-pyr features, tremor |
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what percentage of patients with Whipple's disease have the pathognomonic oculomasticatory myorhythmia?
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20% of patients
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What are the characteristic affected structures in Marchiafava-Gibnami Disease?
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central corpus callosum, optic chiasm, cbl peduncles, pons, commisure and deep white matter
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What heavy metal has been associated with "dialysis dementia"?
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aluminum
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What is the usual age of onset and ethnicity in patients with adult polyglucosan body disease?
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5th and 7th decades
Ashkenazi Jewish patients |
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What are the usual clinical features of adult polyglucosan body disease?
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peripheral neuropathy, dementia, neurogenic bladder, UMN signs
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What is seen in pathology for adult polyglucosan body disease?
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accumulation of cytoplasmic PAS + polyglucosan bodies in CNS & PNS
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What are some caveats to watch out for interpreation of nerve biopsy with polyglucosan bodies?
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nonspecific and can bee seen in normal subjects, axonal neuropathies and ALS patients (must combine with clinical features)
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What is the etiology of transient global amnesia?
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5 in 100000 in Minnesota
24% will have recurrent episodes, none at greater risk for subsequent strokes |
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What is the risk of recurrence (another child with autism) after 1 child with autism?
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5%
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What is developmental dyslexia?
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diagnosis delayed until 3 rd grade, unexpected difficulty reading despite normal intelligence
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What is the definition of MR?
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below-average intelligence, 2 SD below mean IQ <70
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What is the risk of recurrence (another child with autism) after 1 child with autism?
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5%
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What is developmental dyslexia?
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diagnosis delayed until 3 rd grade, unexpected difficulty reading despite normal intelligence
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What is mild MR?
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55-70
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What is moderate MR?
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40-55
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What is the definition of MR?
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below-average intelligence, 2 SD below mean IQ <70
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What is mild MR?
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55-70
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What is moderate MR?
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40-55
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What is severe MR?
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25-40
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What is profound MR?
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<25
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When do patients with Trisomy 21 usually develop AD?
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late 30s early 40s
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What is the etiology of Down's patients developing AD?
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amyloid precursor protein is on chromosome 21
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What are Brushfield's spots?
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small white spots in the iris
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What is associated with trisomy 18?
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rocker bottom feet, dev dissbility, global psychomotor retardation, cardiac malformations, hearing loss, cleft lip
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What is the etiology of cri du chat syndrome?
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chrosome 5 deletion
"meowing" cry round face, microcephaly, hypertelorism, low set ears, micrognathia |
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What is Fragile X syndrome?
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mutation in the FMR1 gene caused by trinucleotide repeat expansion >200 with MR in all males and half of females
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What is FXTAS?
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permutation caused by 50-200 triplet repeats associated with normal intelligence, ataxia and tremor
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What is Rett's syndrome?
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X linked dominant d/o, MECP gene mutation
1. hypotonia/truncal ataxia 2. nl dev. until 7-18 mos. then regression 3. stereotypy of hand movement 4. loss of speech/communication 5. seizures 6. sudden death/prolonged QT interval 7. microcephaly/deterioration in growth 8. hyperventilation/apnea |
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What is Williams syndrome?
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1. difficult visuospatial skills
2. supravalvular ao stenosis 3. short stature 4. infantile hypercalcemia 5. elfin like facies, micrognathia |
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What is Prader Willi syndrome?
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imprinting, deletion of paternal 15q11-q13 chromosomal region
1. small hands & feet 2. hypopigmentation 3. short stature 4. hypogonadotrophic hypogonadism 5. hyperphagia, morbid obesity 6. mild to moderate MR |
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What is Angelman syndrome?
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maternal deletion of 15q11-q13
1. severe MR 2. ataxia, hyperactive, hypotonic "happy puppet" 3. happy disposition 4. absence of inteliggible spech 5. seizures prior to age 2 |
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What is the breathing pattern in a comatose patienht with a cortical lesion?
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cheyne-stokes
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What is the breathing pattern in a patient with diencephalon lesions?
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cheyne stokes
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What is the breathing pattern in a patient with a midbrain lesion?
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tachypnea/hyperventilation
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What is the breathing pattern in a patient with pontine lesion?
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apneustic or cluster
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What is the breathing pattern in a patient with lesion caudal to the pons?
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ataxic
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Differentiate between decorticate and decerebrate posturing?
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decorticalte, flexor elbow and flexor wrist, feet pointed downard
decerebrate posturing extended elbows, wrists flexed out and toes plantar-flexed |
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Differentiate between decorticate and decerebrate posturing?
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decorticalte, flexor elbow and flexor wrist, feet pointed downard
decerebrate posturing extended elbows, wrists flexed out and toes plantar-flexed |
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What are the position of the eyes in cortical lesions?
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can have a dilated eye or be normal
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What is the position of eyes in diencephalon lesions?
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small reactive
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What are the eyes characterized by in midbrain lesions?
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midposition fixed
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What are eyes characterized by in pontine lesions?
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pinpoint pupils
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What are eyes characterized by in lesions caudal to pons?
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large and dilated, unreactive
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Will oculocephalic maneuvers overcome gaze preference caused by frontal eye field lesions?
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yes (will not be overcome if pontine lesions look away from stroke)
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What is the etiology of periodic alternating gaze?
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bilateral cerebral hemisphere dysfunction
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What is the etiology of ocular bobbing?
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localize to pons
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What are 2 most consistent predictors of outcome for ICH?
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volume more than 60 Ml and GCS less than 8
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What is Terson's syndrome?
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vitreal hemorrhage and SAH
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what is the sensitivity of CT scan within 24 hours after bleed?
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92%
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What is the sensitivity of CT scan within 1 week after bleed?
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50%
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What is definition of giant aneurysm?
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>25 ,, om doa,eter
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What percentage of patients with SAH develop hydrocephalus?
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20-25%
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What is the usual timing of vasospasm?
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day 4- 14
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What are EKG findings associated with SAH?
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U waves, arrhythmia, myocardial stunning
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What percentage of patients have multiple aneurysms?
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20-30%
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What 5 etiologies may predispose to aneurysms?
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1. Neurofibromatosis
2. Pseudoxanthoma elasticum 3. Marfan's 4. ehler's Danlos 5. coarctation of aorta |
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What percentage of aneurysms are mycotic?
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3% of all IC aneurysms
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What is the definition of a fusiform aneurysm?
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Dilation of an artery more than 1.5 times normal size without a definable neck
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What is the 20/30/40 rule for impending neuromuscular failure?
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VC <20 ml/kg, MIP <-30 , MEP M40 could be indications for intubation
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What is the regimen for patients with cord compression secondary to trauma and presenting within 3 hours of symptoms?
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30 mg/kg bolus then 5.4 mg/kg/hour for 24 hours
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What is the dose of steroids to give patients with cord compression secondary to truama presenting 3-8 hours of symptoms?
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30 mg/kg bolus then 5.4 mg/kg/hr X 48 hours
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What is the grading system for periventricular-intraventricular hemorrhage of neonates?
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Grade I: caudate head, subependymal layer
Grade II: extension into lateral ventricle, without ventriculomegaly Grade III: extension in LV, with ventriculomegaly Grade IV: extension into parenchyma |
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What is the prognosis if examination shows complete loss of myotomes/dermatomes below the level 24 hours after presentaiton?
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recovery is unlikely
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What are the 4 segments of the ICA?
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cervical (branch into ICA-ECA at C3-4); petrous (caroticotympanic); cavernous (meningohypophyseal); supraclinoid
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What are the branches of the ICA?
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ophthalmic artery
anterior choroidal artery pcomm aca mca |
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What percentage of people have a complete circle of willis?
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less than 35%
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Where does the vertebral artery enter the vertebral bodies?
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c6 transverse processes
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Where does basilar artery begin & end?
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joining of vertebrals at pontomedullary junction then ascends to the interpeduncular fossa
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What does AICA supply?
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lateral pons
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What does SCA supply?
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part of midbrain and cerebellum
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What supplies the head of caudate?
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recurrent art Huebner & anterior choroidal (anteromedial portion)
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What supplies the lateral GP?
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lateral lenticulostriate arteries
anterior choroidal |
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What supplies the medial gp?
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anterior choroidal artery
pcom |
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What supplies the ALIC?
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lateral and medial lenticulostriates
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What supplies the genu?
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lenticulostriate
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What supplies the PLIC?
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lateral lenticulostriates and anterior choroidal artery
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What supplies the anterior thalamus?
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PCOM anterior thalamoperforating branches
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What supplies the medial thalamus?
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posterior thalamoperforating branches from PCS + basilar + posterior choroidal artery
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What supplies lateral thalamus?
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thalamogeniculate from P2 segment
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What supplies the medial medulla?
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anterior spinal artery
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What supplies the posterior spinal artery?
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posterior 1/3 of spinal cord, including dorsal columns
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What is the watershed area of spinal cord?
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T4-T6 fewer radicular arteries, cervical, intercostal and lumbar arteries contributing to spinal cord
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What is the artery of Adamkiewicz?
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large anterior radicular artery @ level T12, L1 or L2
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What is Osler-Weber-Rendu disease?
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telangiectasia in multiple locations including liver, lung, skin, brain
AD condition |
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How does Osler-Weber-Rendu disease lead to neurologic manifestations?
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pulmonary fistulae leading to cerebral ischemia
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When does the risk of stroke persist until after acute MI?
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1 week highes up to 6 months
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What is the significance of left atrial spontaneous echo contrast?
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local blood stasis unclear significance, Maorecommends further eval with Holter or telemetry
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What is the difference between marantic endocarditis and Libman-Sacks endocarditis?
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They are both under umbrella of nonbacterial thrombotic endocarditis, but marantic endocarditis is generally considered related to malignancy
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What are usual etiologies of non-bacterial thrombotic endocarditis?
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1) HIV
2) SLE 3) Antiphospholipid antibody syndrome 4) malignancy |
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What is the data for PFO and stroke association?
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unclear at this point but generally these factors make PFO + stroke more worrisome: a) dvt b) right to left shunt c) atrial septal aneurysm d) cortical stroke
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Even after device closure and surgery for PFO closure what is the risk for recurrent stroke?
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3 to 4% per year
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What is the prevalence of cardioembolic stroke among all strokes?
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20-25%
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What is the prevalence of extracranial large artery disease among all strokes?
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15-20% of strokes are secondary to large vessel disease
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What are the data for symptomatic ICA stenosis from 70-99%?
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NASCET trial 2 year rate of ipsilateral stroke 26% medically treated 9% surgically treated group
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What are the data for symptomatic ICA stenosis 50-69%?
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5 year risk of fatal/nonfatal ipsi stroke was 22% medical and 15.7% surgical group
(poor op prognostic: women, diabetes, contralateral disease, left sided disease, retinal disease, TIA rather than stroke previously) |
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Which patients are considered high risk for CEA?
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age older than 80
cardiac disease pulmonary disease restenosis after CEA contralateral disease previous neck surgery/radiation |
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What is seen on pathology in Takayasu's arteritis?
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granulomatous arteritis affecting large vessels
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What are the clinical symptoms in patients with Takayasu's arteritis?
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elevated ESR
fatigue, weight loss pulseless extremities extremity claudication stroke young, female patients |
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What is the treatment for Takayasu's arteritis?
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immunosuppressants and endovascular surgery are options
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What is the pathology for giant cell arteritis?
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inflammation in media, intimal thickening, fragement IEL, T cell lymphocytes
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When should the biopsy be performed in Temporal arteritis?
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as soon as possible but 2 weeks of steroids should not affect treatment
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What conditions may lead to dissection in a patient?
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a) fibromuscular dysplasia
b) Ehlers-Danlos syndrome type IV c) Marfan's syndrome d) polycystic kidney diseasee) pseudoxanthoma elasticum e) osteogenesis imperfecta |
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What is the etiology of osteogenesis imperfecta?
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AD condition characterized by abnormality in collagen I
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What is Ehler's Danlos type Iv?
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abnormality in collagen- III
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What is the etiology of pseudoxanthoma elasticum?
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AR disease characterized by mutation in ABCC6 gene, MRP 6 protein
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what are the clinical features associated with pseudoxanthoma elasticum?
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raised yellowish bumps on skin
retina looks like an orange skin retinal hemorrhage early atherosclerosis can lead to dissection b |
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Which connective tissue disorder could this finding be associated with?
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Marfan's syndrome
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What are the features of Marfan's syndrome?
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ectopia lentis
long fingers/limbs arachnodactyly pectus deformity predisposed to aneurysm formation |
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What is the etiology of pseudoxanthoma elasticum?
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AR disease of connective tissue progressive dsytrophic minerlization of elastic fibers
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What is Cogan's syndrome?
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interstitial keratitis/scleritis/uveitis
vestibuloauditory dysfunciton systemic symptoms in 10% |
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What is Eale's disease?
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visual loss monocular/binocular, retinal vasculitis, recurrent vitreos hemorrhage and CNS vasculitis
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What is Susac's syndrome?
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microangiopathy affecting arterioles in brain (corpus collosum), retina and cochlea
1) sensorineural hearing loss 2) retinal angiopathy visual field loss 3) encephalopathy, behavioral, affective dysfunction |
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What is Sneddon's syndrome?
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non-inflammatory vasculopathy of medium sized arteries with intimal hyperplasia
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What non-inflammatory vasculopathy could have this skin finding as well as an association with anti-phospholipid syndrome?
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Sneddon's syndrome
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What is the etiology of Kohlmeier-Degos disease?
|
fibrous intimal proliferation accompanied by thrombosis leading to vasculopathy of skin, cerebral circulation and other organs
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What are the symptoms associated with Kohlmeier-Degos disease (or malignant atrophic papulosis)?
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raised papules whith white center (skin infarcts)
GI manifestations: ulcers, bowel dismotility, dilation ischemic stroke/tia |
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What CNS structures are most sensitivie to anoxia?
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purkinje cells, dentate nucleus, globus pallidus, hippocampus CA1 pyramidal cells, cortical layers III and V
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What are the 6 layers of the cerebral cortex?
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I: Molecular layer
II: external granular layer III: ext pyramidal layer IV: internal granular layer V: int pyramidal layer VI:mulforme layer |
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What is the usual etioloogy of transcortical motor aphasia?
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arterial border zones b/t bilateral ACAs and MCAs
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What is the etiology of transcortical sensory aphasia?
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arterial borderzones between bilateral MCAs and PCAs
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What is Sommer's sector of hippocampus?
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CA 1
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