Neuro Flashcards
Most common adult brain tumors and key histologic characteristics of each
“MGM Studios”
- Metastasis
- Glioblastoma - GFAP+, pseudopallisading
- Meningioma - Psammoma bodies, assoc NF2
- Schwannomas - around CNVIII, S100, assoc NF2
Oligodendroglioma - fried egg, frontal lobe “O-leggo-my-eggo”
Most common childhood brain tumors and key histology characteristics of each
“Prepubescent Minds Eaten by Cancer”
- Pilocytic astrocytoma - GFAP+, Rosenthal fibers (red coils), in posterior fossa
- Medulloblastoma: Homer-Wright Rosettes (Homer is married to Marge, they have KIDS… so it’s the M one), cerebellar, compresses 4th ventricle –> noncommunicating hydrocephalus
- Ependymoma: perivascular pseudo rosettes, compress 4th ventricle –> noncommunicating hydrocephalus
- Craniopharyngioma: rathe’s, supratentorial, compresses optic chiasm –> bitemporal hemianopsia
Signs of subfalcine herniation
compresses ACA –> lower body
Signs of uncal herniation
Compress CN III
- parasympathetics lost to pupil –> mydriasis
- lose motor –> down and out
Contralateral homonymous hemianopsia - PCA compression
Ipsilateral paresis as contralateral side compressed
Direct hemorrhages in paramedian arteries
UMN lesion sx
problem above anterior horn of spinal cord
spastic paralysis
hyperreflexia
babinski reflex present
LMN lesion sx
problem w/ nerves from anterior horn
flaccid paralysis
atrophy of muscles
muscle fasciculations
hyporeflexia - loss reflex arc
Polio
fecal-oral virus - replicate in oropharynx before going to GI
-can recover virus in throat and stool for confirmation
Damage anterior horn –> LMN sx
other nonspecific sx: fever, HA, malaise, N, abd pain, sore throat
Asymmetric limbs d/t atrophy
CSF:
lymphocytic pleocytosis
slight increased protein
no change in glucose
Brown-Sequard Sn
Complete hemisection of spinal cord
ipsilateral UMN, tactile, vibration, proprioception, LMN - flaccid paralysis below lesion
contralateral pain/temp 2-3 segments below lesion
at lesion - ipsilateral pain and temp loss for 2-3 segments
Syringomyelia
cavitary lesion of spinal cord that fills with fluid - syrinx
MC in cervical spinal cord - expands longitudinally
assoc w/ Chiari I malformation, spinal cord trauma
Syrinx compresses crossing fibers of spinothalamic tract, damages anterior white commissure
–> b/l loss of pain/temp in upper extremities
If extends laterally –> damage of motor neurons of anterior horn –> weakness and atrophy of hands
Spinal muscular atrophy (Werdnig-Hoffman)
AR
death of neurons in anterior horn of spinal cord
causes infantile flaccid paralysis –> death before 1 yo
Amyotrophic lateral sclerosis
Anterior horn and LCST damage
LMN Sx - anterior horn
UMN Sx - LSCT
rapidly progressive weakness muscle atrophy fasciculations spasticity dysarthria dysphagia dyspnea
cause: defective superoxidase dismutase I
Tx: Riluzole - decreases presynaptic glutamate release that can be neurotoxic
Tabes Dorsalis
Tertiary syphilis obliterates dorsal column
+ Romberg sign - fall down as need 2/3 to maintain balance: vestibular, proprioceptive (destroyed), vision (eyes closed)
Argyll Robinson pupil - accommodate but not reactive
Absent DTR
Sensory ataxia at night - wide based gait to avoid falling
Anterior spinal occlusion
Lesion everything but dorsal columns and lissaur tracts
lose pain and temp
lose b/l motor command UMN and LMN
Below lesion:
complete motor paralysis
loss pain/temp
areflexia
Causes: aortic aneurysms, aortic dissections, direct trauma to aorta, atherosclerosis (severe)
Multiple sclerosis
random and asymmetric lesions in white matter along entire CNS
Dz of oligodendroglia –> demyelination
Autoimmune - women 20-30s
Charcot’s triad: scanning speech, intention tremor, nystagmus
INO if MLF involved - stare at side of lesion (no adduction), nystagmus in abducting eye
CSF: very high protein - Ig light chains - oligoclonal brands on electrophoresis
MRI: lesions in brain and spinal cord
Tx: high dose steroids x 7 days
Beta-interferon
natalizumab
sx treatments
Parkinson Disease
Lewy Body inside cells of substantial nigra pars compacta - interfere w/ functioning –> loss of dopaminergic neurons = can’t make dopamine
hypokinesia, bradykinesia, akinesia
postural instability - can’t make small fine tuning movements
festinating gate - trouble initiating/stopping walking - fall forward
Pill rolling tremor
cogwheel rigidity
mask like facies - expression less
MPTP exposure
manufacturing meperidine (synthetic demerol) produces MPTP in the process
Metabolized to MPP in body which destroys dopaminergic cells in substantial nigra causing parkinsonism features
Tx: selegiline - blocks formation of MPP
Levodopa
L-dopa precursor of dopamine that crosses BBB
Converted to dopamine by dopa carboxylase
First line for PD
Side effects:
Peripheral conversion –> HTN, arrhythmias (give carbidopa to avoid)
Hallucinations, delusions, psychosis
tolerance - “wearing off” phenomenon
Carbidopa
given w/ levodopa to inhibit peripheral conversion of l-dopa to dopamine
more L-DOPA into CNS
Reduces side effects and increases bioavailability
“Other” PD drugs
“BALSA”
Bromocriptine (ergot –> HTN), non ergots (also used in restless leg sn): pramipexole, ropinirole
Amantadine: increase dopamine release, decrease dopamine reuptake
Levodopa-carbidopa
Selegiline, rasagiline - inhibit dopamine breakdown via MAO-B
Antimuscarinics: benztropine - increase ACh to tx rigidity and tremor
Draw basal ganglia regulation of movement pathways
page 84
Result of lesions of substantial nigra pars compacta
hypokinesis - parkinson dz
Result of lesion of sub thalamic nucleus
ex lacunar stroke
hemiballismus - too much movement
Non pharm treatment of PD
create lesion of sub thalamic nucleus
-removes inhibition –> movement
deep brain stimulation exhausts nucleus, not as permanent as surgical lesions
Hemiballismus
wild flailing motion of u/l arm or leg
lesion of sub thalamic nucleus on contralateral side of movement
chorea
brief purposeless, non repetitive jerks of individual muscles
“dancing”
Myoclonus
brief, sudden muscle contractions
Athetosis
slow, writhing, snake-like movements of hands and fingers
Akathisia
compulsion to move, chose to move
Huntington Disease
aka Huntington’s chorea
excessive movement disorder
AD trinucleotide repeat disorder
"C's" CAG trinucleotide repeat Chr cuatro (4) Cuarenta (40 yo) Chorea Cognitive decline - dementia, depression, psychosis Caudate atrophy on MRI (and putamen)
Excessive excitation by glutamate on NMDA receptors (neurotoxic)
Increased dopamine
Decreased GABA and ACh
Tx: block dopamine
-tetrabenzine
Neuroleptics - olanzapine, haloperidol
Guillian Barre syndrome
Autoimmune inflammatory demyelination of peripheral nerves at schwann cells
Associated with preceding infection: Campylobacter jejuni, GI illness - 20% diarrheal in last month
- Respiratory tract infection
- Stress
Ascending muscle weakness - sensory intact
-legs to hands to trunk
-50% facial weakness/paralysis - b/l
-10-30% respiratory m. weakness needing vent support
Sx over days
Recovery phase - weeks to months
Dx: decreased nerve conduction studies
CSF: increased protein w/ normal cell count
Tx: supportive, plasmapheresis, IVIG
Charcot-Marie-Tooth disease
hereditary motor and sensory neuropathy
Progressive loss of muscle tissue and touch sensation across various parts of body
mutations –> defects in neuronal proteins
Progressive multifocal leukoencephalopathy
demyelination of CNS d/t destruction of oligodendrocytes
assoc w/ JC virus - classic AIDS dz
Acute disseminated post-infectious encephalomyelitis
inflammation and demyelination after viral infection or vaccine
-chicken pox, measles
Metachromatic leukodystrophy
AR lysosomal storage dz
def of arylsulfatase A –> buildup of sulfatide –> destruction of myelin
