jdlevenson's version from 2015-06-21 02:12


Question Answer
Most common motor neuron diseaseALS. Both UMN and LMN. Middle aged people and progressive. High mortality within 5 years (near 100%).
How do people with ALS dieRespiratory complications.
ALS, where on spinal cordAnterior horn (LMN) AND lateral corticospinal tracts (UMN). Also loss of motor nuceli in CN 5, 9, 10, 12.
Babinski response will be dorsal in infants up to what age? Why?Normal for infants up to 12 months of age to have a positive Babinski response due to incomplete myelination of corticospinal tracts. Once myelination is complete, upper motor neurons suppress the pathologic/ dorsiflexion response.
Normal pressure hydrocephalus, order of sxsGait -> urinary -> dementia. Why? Distortio of periventricular white matter. Bladder control is also controlled by descending cortical fibers and eventually loss of cortical inhibition on sacral micturition center causes incontinence. No sensation when bladder full and no control over bladder function.
Micturition controlled by(1) Sacral mict center – s2-4, bladder contraction (2) pontine mict center- external urethral sphincter relaxation with bladder contraction and (3) cerebral cortex, that inhibits sacral mict center
Normal pressure hydrocephalus, reversible or irreversibleReversible.
Norma l pressure occurs inElderly.
Normal pressure hydrocephalusEnlarged ventricles despite ICP being normal.
Ependymal layer histologySimple ciliated columnar epithelium with tight junctions; sit on top of outgrowth of pia matter capillaries that are fenestrated (unlike others); in 4 locations, 1 in each ventricle.
Communicating hydroceph from dysfunction or obliteration of subarachnoid villi is usually a sequela ofMeningeal infection (including TB) or subarachnoid/ intraventricular hemorrhage.
Non-communicating hydroceph usually rom obstruction likeArnold-Chiari or Dandy-Walker or Aqueductal stenosis
Arnold-Chiari malformations are due to impaired development of posterior fossa. Arnold-Chiari I vs II ?I is relatively benign whereas II is severe and evident in new born. II often presents with lumbosacral meningomyelcele and paralysis below defect as well as hydrocephalus, and compression of medulla (difficulty swallowing, dysphonia, stridor, apnea)
Hydrocephalus complications and whyStretching of periventricular pyramidal tracts leads to hypertonicity and hyperreflexia as well as visual disturbances and learning disabilities
Increased protein in CSF with normal cell countGuillain-Barre; albumin-cytologic dissociation
Segmental demyelination + endoneural inflammatory infiltrate (lymphocytes and macrophages)Guillain-Barre nerves
Guillain-Barre may be fatal ifSupport is not given for respiratory muscle paralysis. Also it may ascend as far as CN7.
Pseudotumor cerebriElevated ICP and young women who are overweight.
When do you see elevated CSF hydrocephalusChoroid plexus papilloma
How to confirm hydrocephalus ex vacuo?CSF pressure is not increased.
MS and axons, when do axons degenerateOnly with chronic plaques
Definitive dx of MSMRI needed.
MS histology of a plaqueDemyelination with relative preservation of axon; accumulation of lipid-laden macrophages; astrocytosis and infilitration by lymphocytes and mononuclear eclls.
Muscle fiber inflammation and necrosisPolymyositis and dermatomyositis
MS symptoms worsen withHeat exposure.
Amaurosis fugax vs optic neuritisA. fugax is transient mononuclear blindness from TIA whereas optic neuritis is from MS with visual disturbances and painful eye movement and central scotoma maybe too.
Elevated 14-3-3 protein in CSFCJD
Decreased melatonin in CSFAD
Low 5-hydroxyindole-acetic acid in CSFImpulsive destructive behaviors such as aggression, suicide, and violence.


Question Answer
Park -> Dementia vs Dementia -> ParkFormer is PD and latter is LD; both have lewy bodies.
2nd most common cause of dementia after ADVascular dementia from multiple infarcts. A/w HTN, systemic atherosclerosis.
How does AD lead to troubleSenile amyloid deposits are just those that damage brain parenchyma but Amyloid angiopathy* -> damanges media and adventitia of cerebral vessels causing thickening of BM, fragmentation of IEL and stenosis of the lumen (But also recall both may be present in healthy individuals)
Stressor + confusion + declining cognitive function in older personPseudodementia from depression
Social disinhibiton + speech abnormalities + emotional flatteningPick’s disease/ FTD.
FTD vs AD, ageFTD 50s and 60s and AD 60s and 70s and older.
FTD vs AD, histologyFTD –neuronal loss in FTD lobes with Pick bodies (cytoplasmic inclusions of microtubule associated protein tau) vs AD – neurofibrillary tangles and amyloid plaques
FTD vs AD presentationFTD – behavior changes (apathy, social disinhibition) and altered speech patterns from frontal and prefrontal cortex vs AD – impairments involving recent memory
Alzheimers dxClinical and -> Gradual progressive cognitive decline + apraxia (ADL) or aphasia (language) or agnosia (recognizing objectS) or disturbed excecutve functioning.
AD, where atrophies mostTempoparietal lobes and hippocampus; especially hippocampus
AD, biochemical abnormalityDecreased levels of Ach in the nucleus basalis of meynert (memory and cognition; base of forebrain) and the hippocampus (new memories); decreased choline acetyltransferase activity in these cerebral structures.
AD, clinical, macroscopic, microscopic and biochemicalProgressive memory loss; Mild to moderate generalized brain atrophy; neurofibrillary tangles, senile plaques and amyloid angiopathy; decreased Ach in hippocampus and nucleus basalis of meynert
For MPTP associated PD, which drug is bestMAO-B inhibitors such as selegiline.
Mesolimbic-mesocortical pathway for dopamine, function? Disease?Function – regulates behavior; Disease – Schizophrenia. This is where neuroleptics act.
Nigrostriatal pathway for dopamine, function? Disease?Function – coordination of voluntary movements; Disease – Parkinsonism
Tuberoinfundibular pathway for dopamine, function? Disease?Function –controls prolactin secretion; Disease – Hyperprolactinemia


Question Answer
Jaw pain in the middle of a mealTemporal arteritis. Lumen can’t open. Also may have tongue pain during meal from claudication there.
Scalp tenderness and headacheTemporal arteritis.
Temporal arteritis patients also often haveMorning stiffness and muscle pain from polymyalgia rheumatica (50% of patients). Neck, torso, shoulder, and pelvic girdle pain specifically.
If suspect Temporal arteritis, what 3 thingsStart treatment with steroids, check ESR (which is almost always elevated) and take biopsy of temporal artery
Temporal arteritis affects what part of artery and isSegmental* and granulomatous (hence giant cell*) and affects media*
Recurrent episodes of sleeping or napping multiple times within same day (occurring at least 3x weekly for 3 months) + at least 1 of the following (Cataplexy (conscious, sudden, bilateral muscle tone loss precipitated by laughter or joking/ spontaneous abnormal facial movements without emotional triggers) and or Hypocretin 1 deficiency in CSF and or rapid eye movement latency <15 minutes)Narcolepsy. Also may see sleep paralysis and hallucinations upon waking.
Most common cause of excessive daytime sleepinessObstructive sleep apnea -> poor oropharyngeal tone -> daytime sleepiness, morning headaches, and depression.
Irresistible and refreshing sleep?Narcolepsy.
Treatment for narcolepsy?Modafinil, a non-amphetamine stimulant that is well tolerated since it is effective and drug abuse is rare as well as scheduled daytime naps.
Risk factors for osa that are not obesityTonsillar hypotrophy and hypothyroidism.
Chronic OSA leads toPulm HTN and RVF.
Question Answer
Central sleep apnea occurs whenPatient’s central drive to initiate breaths is absent.


Question Answer
Conversion disorder definitionSymptoms must be neurologic; cannot be produced intentionally; no neurologic explanation for patient’s symptoms exist; cannot be limited to pain and or sexual dysfunction
Conversion disorder profileYoung women post emotional stressor/ significant life event
Somatization disorder definitionNumerous physical complaints over years for which no physical explanation can be found; must have stared
Body dysmorphic disorderPatient who believes body is pathologically flawed when it is not
MalingeringSecondary gain, particularly financial
Factitious disorderPurposeful faking of symptoms in order to receive medical attention; feigned physical psychological or both
Munchausen’s syndrome Describe chronic factitious disorder with physical symptoms**
Acute stress disorder vs PTSDAcute stress disorder (<4 weeks) vs PTSD (>4 weeks) otherwise identical symptoms –recurrent nightmares and flashbacks, potential memory loss, exaggerated startle response