UWORLD Flashcards
contralateral somatosensory and motor deficit, predominantly in lower extremity
abulia (lack of will)
dyspraxia (clumsiness)
urinary incontinence
ACA stroke
contralateral somatosensory and motor deficit in FACE, ARM, AND LEG)
homonymous hemianopia
aphasia (dominant hemisphere)
hemineglect (non dominant hemisphere)
conjigate eye deviation toward side of infarct
MCA stroke
unilateral motor impairment
no sensory/cortical deficit
no visual field abnormalities
lacunar infarct (posterior limb of internal capsule)
headache worse at night
n/v
mental status changes
focal neurologic deficit/vision changes
intracranial HTN
symmetric proximal limb muscle weakness (standing up, combing hair, putting stuff in cabinets)
reduced/absent DTRs
autonomic dysfunction
lung mass
lambert eaton
treatment for agitation from delirium in ELDERLY and young
elderly - haloperidol (less adverse effects/addiction vs lorazepam)
young - lorazepam
what kind of gait is associated with Parkinsonism
NARROW BASED
shuffling
hypokinetic gait
MVA; CT shows minute punctate hemorrhages with blurring of gre-white interface
diffuse axonal injury
can lead to persistent vegetative state; major cause morbidity from TBI
loss of pain/temp ipsilateral face and contralateral body, ipsilateral bulbar muscle weakness, vestibulocerebellar impairment, horner’s syndrome…motor function face and body spared
wallenberg syndrome (LATERAL MEDULLARY INFARCT usu due to occlusion of PICA or vertebral artery)
patient with giant cell arteritis develops PAINLESS proximal muscle weakness (lower extremity); normal CK and ESR
glucocorticoid induced myopathy
different from polymyalgia rheumatica which is painful and has no muscle weakness
asymmetris resting tremor assocaited with rigidiy; gets better with activity
dx and treatment for tremor
parkinsonian tremor
anticholinergics like TRIHEXYPHENIDYL
patient hx of HTN presents with sudden onset hemisensory loss, hemiparesis, homonymous hemianopsia, gaze palsy
basal ganglia bleed
prolonged seizures increases risk of what brain structural abnormality
cortical laminar necrosis (hallmark of prolonged seizures; due to excitotoxicity)
leads to persistent neurologic deficits and recurrent seizures
NMS is due to blockade of which neurotransmitter in what pathway
dopamine (d2 receptor blocking)
in nigrostriatal pathway
seizures, diaphoresis, tremulousness, tachycardia, HTN afterone day in hospital…dx and treatment
alcohol withdrawal
lorazepam
acute confusion, hyperthermia (greater than 105F), tachhy cardia, persistent bleeding (i.e. epistaxis) after direct work under sunlight
heat stroke
risk of benzos in elderly
increased risk of cognitive impairment, paradoxical agitation, and falls
initial work up for first time seizure in adult
electrolytes glucose Ca/Mg CBC renal and LFTs
URINE TOXICOLOGY SCREEEEEEEEEEN
pathogenesis NPH
transient increase in ICP which causes ventricular enlargement, which will then normalize. Increase in ventricular size due to diminished CSF absorption at arachnoid villi or obstructive hydrocephalus
what kind of gait is typically seen in NPH
slow BROAD BASED shuffling gait
how do parkinsonian tremors worsen?
distractibility (mental tasks)
goes away with movement and re-emerges when ovement is stopped
how is physiologic tremor worsened
worsened - anxiety, caffeine, hyperthyroidism, drugs
symptoms of cerebellar dysfunction
gait instability truncal ataxa difficulty with rapid altermating movements hypotonia INTENTION TREMOR
