61 terms



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Sudden jerky irregular movements with muscle contractions that are not repetitive or rhythmic but appear to flow from one muscle to the next
Twisting and writhing movements often associated with chorea
Sustained muscle contractions cause twisting and repetitive movements or abnormal postures
tardive dyskinesia
an impairment of voluntary movement caused by use of dopamine antagonists.
smooth, slow and fast eye movements
Westphal variant Huntington
develops in childhood ˜5% of patients, more like parkinsonism with bradykinesia and rigidity
substantia nigra
portion of the midbrain, and a major element of the basal ganglia system. It consists of the pars compacta, pars reticulata, and the pars lateralis.
Lewy body
an eosinophilic, round inclusion found in the cell cytoplasm of substantia nigra, the nucleus basalis of Meynert, locus ceruleus, dorsal raphe, and the dorsal motor nucleus of cranial nerve X.
a presynaptic protein in Lewy bodies
Parkinson disease
difficulty arising from a chair, difficulty turning in bed, micrographia, masked face, stooped, shuffling gait with decreased arm swing; and sialorrhea.
Percentage of Parkinson patients with dementia
pathology in Parkinson disease
loss of pigment in the substantia nigra caused by loss of neurons in this region. The remaining neurons may show Lewy bodies
neurotransmitter problem in Parkinson disease
striatal dopamine (DA) depletion
early onset Parkinson disease
mutation of the parkin gene, which is inherited in an autosomal recessive pattern
Multiple System Atrophy - P
resembles Parkinson disease except that tremor is less prominent, and the disorder tends to be quite symmetric. Prominent autonomic insufficiency. Abnormal MRI.
Multiple System Atrophy - C
also called olivopontocerebellar atrophy, presents as a cerebellar syndrome and autonomic insufficiency. Abnormal MRI.
Dementia with Lewy bodies
prominent cognitive dysfunction as well as parkinsonism. The typical clinical hallmarks include early onset dementia, delusions and hallucinations, fluctuations in consciousness and myoclonus
Corticobasalganglionic degeneration
typically has unilateral, coarse tremor, rigidity, increased reflexes as well as limb apraxia/limb dystonia/alien limb phenomenon. Typically has asymmetric appearance of Parkinson disease.
Progressive supranuclear palsy
supranuclear downgaze palsy (inability to voluntarily look down) and square wave jerks on extraocular motion testing. Typically have an upright rather than flexed posture. Frequent falls can be an early finding. Tremor is not common, and there is a pseudobulbar emotionality.
treatment of Parkinson disease
dopamine agonist
crosses the blood-brain barrier and is converted to dopamine
inhibitors of aromatic amino acid decarboxylase (dichloroisoprenaline [DCI]) - inhibit peripheral breakdown in the gut
COMT (catechol-O-methyltransferase) inhibitors prevent peripheral breakdown of levodopa
COMT (catechol-O-methyltransferase) inhibitors prevent peripheral breakdown of levodopa
dopamine agonist on D2-type receptors
dopamine agonist on D2-type receptors
dopamine agonist on D2-type receptors
MAO-B inhibitor
MAO-B inhibitors
blocks glutamate N-methyl-D-aspartate (NMDA) receptors
mild attenuation of the cardinal symptoms of resting tremor and dystonia
alleviates levodopa-induced dyskinesias
abnormal involuntary choreiform and dystonic movements
problems with longterm levodopa
dyskinesias and motor fluctuations
deep brain stimulation (DBS)
option for Parkinson disease treatment
treatment for tremor
inhibition of the ventrolateral thalamus
cardinal features of Parkinson disease
resting tremor, rigidity, bradykinesia, and postural instability
prochlorperazine (Compazine)
can cause drug-induced Parkinsonism
can cause drug-induced Parkinsonism
sentinel bleed
Intermittent aneurysmal subarachnoid hemorrhage causing lesser headaches that precede the "worst headache" that occurs with rupture of the aneurysm
irritation causes constriction of major cerebral arteries, vasospasm lethargy, and cerebral infarction
vasospasm in aneurysmal bleeds
peaks after 4 to 14 days
Acute communicating hydrocephalus is
a complication that occurs because of obstruction of the subarachnoid granulations in the venous sinuses by the subarachnoid blood
clinical signs of acute communicating hydrocephalus
headache, vomiting, blurry and double vision, somnolence, and syncope
most common aneurysm site
anterior communicating artery
2nd most common aneurysm site
bifurcation of the internal carotid artery with the posterior communicating artery
risk factors for aneurysms
fibromuscular dysplasia, polyscystic kidney disease, chronic severe HTN, liver disease, alcohol, tobacco, vasculitides, Marfan, mycotic infection, oral contraception
Nonaneurysmal causes of subarachnoid hemorrhage
trauma, arteriovenous malformations, and cocaine or amphetamine abuse
Head CT without contrast
most sensitive neuroimaging study for detecting subarachnoid bleeding, appearing as hyperdensity within the cerebral convexities, cisterns, and parenchyma
sensitivity of CT for hemorrhage
greatest 24 hours after the event with 50% still detectable after 1 week
CSF studies are most sensitive
12 hours after onset
treatment of subarachnoid hemorrhage
Emergent conventional angiography
reduces rebleeding in subarachnoid hemorrhage
Endovascular coiling
when to clip subarachnoid hemorrhage to avoid vasospasm
the first 48 hours after onset or delay for 2 weeks
medical management of subarachnoid hemorrhage
TripleH therapy (hypertensive hypervolemic hemodilution) and nimodipine
metabolic complications of subarachnoid hemorrhage
hyponatremia, syndrome of inappropriate antidiuretic hormone secretion [SIADH], cerebral salt wasting
respiratory complication of subarachnoid hemorrhage
neurogenic pulmonary edema
cardiac complication of subarachnoid hemorrhage
treat hydrocephalus
unequal pupil size