Neurology Flashcards
Metastases to brain by incidence
Lung (80% and multiple lesions) > Breast (single lesion) > melanoma (multiple lesion) > colon (single lesion)
prostate is exceedingly rare
**If single lesion, standard of care is to resect
Amaurosis fugax
painless loss of vision in eye from emboli. “curtain coming over eye”
Impending risk of TIA/Stroke. Most emboli from carotid bifurcation -> test with duplex US of neck
strabismus
improper alignment of eyes
disorder of EOM or of CN III/IV/VI
Febrile Seizure age range
6mo-6years
Does the use of antipyretics reduce the incidence of febrile seizures?
No it does not (more specifically it doesn’t reduce the recurrence rate of febrile seizures in those known to have them).
Normal cup to disk ratio?
pathologic?
.3 is avg, up to .5 physiologic
> .5 ratio = pathologic
often indicative of glaucoma
dysarthria
motor speech disorder
aphasia
difficulty with language (production or understanding)
multiple OILY cysts in sella turcica, bitemporal hemianopsia,
craniopharyngeoma from rathke’s pouch
more common in children, but bimodal distribution with increased incidence again in 50’s-60’s
meningismus triad
headache, photophobia, nuchal rigidity
perivascular cuffing
accumulation of lymphocytes densely around vessel, an indicator of inflammation.
Bulbar symptoms
refers to medullary CN’s 9,10,11,12
- dysphagia (difficulty swallowing)
- dysarthria
- spasticity of tongue or weakness
- ect
-in ALS, often starts with bulbar and progresses to involve other CN’s
ddx; ALS, Myasthenia Gravis, botulism, infarct, guillan-barre…
Area postrema
A circumventricular region of brain (no BBB)
A spot on the posterior medulla that receives sensory input and largely controls vomiting through autonomic processes.
- ICP can stimulate the area postrema
- samples blood for toxins/noxious substances
how to find mastoiditis?
May see fluid accumulation in mastoid air cells on CT and MRI
1st unprovoked seizure
-workup
- MRI/CT
- consider EEG
If unsure
- tox screen
- metabolite screen
#
triad of brain abscess
Fever, focal neurologic defects, headache (nighttime/morning = mass effect headache)
- seizure initial presentation in 25%
- temporal/parietal
- frontal/ethmoid sinusitis -> frontal
- dental infection -> frontal
- bacteremia -> multifocal gray/white junction
indolent
disease with slow progression
or a slow healing (indolent ulcer, indolent
neuroimaging findings
Autism OCD Panic Disorder PTSD Schizophrenia
Autism: increased total brain volume
OCD: orbitofrontal cortex and striatum
Panic Disorder: Decreased amygdala volume
PTSD: decreased hippocampal volume
Schizophrenia: increased cerebral ventricle volume (esp. lateral)
*Routine imaging not done for known psychiatric disorders, other than to rule out other organic causes
**amygdala: emotional learning, memory modulation (esp tied to emotions), olfactory memory. They are medial nuclei in basalar temporal lobe.
dysmetria
dysmetria = “wrong length”
lack of coordination of range in movement (typified by undershoot or overshoot)
manage alzheimer’s
1st: acetylcholinesterase inhibitors: donepezil (Aricept), rivastigmine (Exelon), galantamine (Razadyne)
# Vitamin E # memantine (NMDA receptor antagonist). USED IN MODERATE TO SEVERE DEMENTIA
Multiple System’s Atrophy
Shy-Drager Syndrome + olivopontocerebellar atrophy + striatonigral degeneration
Degenerative Disease with
1) Parkinsonism
2) Autonomic dysfunction (orthostatic hypotension, abnormal sweating/bowel/saliva, impotence…)
3) Widespread neurologic signs (cerebellar, UMN, LMN)
# bulbar symptoms also occur and can be fatal #anti-parkinson drugs are not effective
- *cognitive function relatively well preserved
- ** alpha synuclein present
parkinson’s tx
EARLY
Dopamine Agonists: Bromocriptine ergot replaced by nonergot’s: pramipexole, ropinirole, rotigotine
MAO-B inhibitors: selegiline/rasagiline; prevent dopamine breakdown centrally and provide symptomatic (possible disease modifying) as monotherapy.
COMT inhibitors: entacapone and tolcapone:
pramipexole
Dopamine Agonist used in parkinsonism and RLS
*less prone to promote dyskinesia than levodopa
ropinirole
Dopamine Agonist used in parkinsonism
*less prone to promote dyskinesia than levodopa
rotigotine
Dopamine Agonist used in parkinsonism
*less prone to promote dyskinesia than levodopa
Selegiline
MAO-B inhibitor centrally acting for parkinsons. prevent dopamine metabolism. may have some disease modifying effects
**MAO-Ai’s are in the gut and associated with htn and tyramines. MAO-Bi’s are not assoc with this at standard doses.
***Selegeline may has some MAO-Ai at higher doses
rasagiline
MAO-B inhibitor centrally acting for parkinsons. prevent dopamine metabolism. may have some disease modifying effects
**MAO-Ai’s are in the gut and associated with htn crisis and tyramines. MAO-bi’s are not assoc with this at standard doses.
entacopone
tolcapone
COMT inhibitors: in presence of carbidopa (decarboxylase inhibitor), COMT becomes major metabolizer of dopamine… so these inhibit that and increased levodopa
**action primarily in periphery
Stalevo
combo tablet
levodopa, carbidopa, entacapone
semiology of mesial temporal seizures
A SYNDROME
Most common focal epilepsy syndrome. Often arises from near/within hippocampus. associated with hippocampal sclerosis on MRI. often impaired consciousness
aura: rising epigastric sensation, deja vu, fear, jamais ju
(being in a situation you have before but not really recognizing it)
automatisms (usually same side as seizure): stereotyped lip smacking, picking with hands.
vs dystonic posturing is often contralateral to lesion
**Often refractory to anticonvulsants but responds well to surgical intervention
focal seizure vs stroke lesion eyes
look away from the light (frontal lobe seizure)
look toward the lesion (stroke)
**UNLESS Thalamic lesion; look away from lesion
frontal lobe seizure semiology
+- impaired consciousness
eyes look away from lesion (not head)
hemiclonic: isolate muscle movement -> may jacksonian march
how much of dementia does multi-infarct dementia account for?
15-20%
what happens to the sella turcica in 70% of people with idiopathic intracranial hypertension (IIH/pseudotumor cerebri)?
The sella turcica becomes flattened -> empty sella on MRI
**ventricles are often shrunk
bilateral acoustic neuromas and cataracts
neurofibromatosis type 2
multiple areas of T2 weighted periventricular hyperintensities
(not time/space)
multiple infarct dementia
anterior (ventral) ventral cord syndrome s/s and cause
this is your anterior spinal artery occlusion with distal paresis/UMN signs/loss pain/temp
hyperextension injury in setting of pre-existing degenerative changes (spondylosis) of cervical spine
central cord syndrome (CCS)
involves bilateral paresis of arms (more medial) and decussating fibers of spinothalamic tract (pain/temp) in a dermatome or three
*syringomyelia can also cause this
**cervical spondylosis causes may cause progressive narrowing of central canal, but may be asymptomatic before trauma