Neuro Injuries/Random Review Slides Flashcards
pure sensory stroke of thalamus
- lacunae in VPL, VPM
- –loss of all sensation in body/face
- infarct due to small vessel disease
- associated with HTN, DM
typified by:
- microatheroma
- lipohyalinosis
microatheroma
- deposit or degenerative accumulation of lipid-containing plaques on the innermost layer of the wall of an artery
- typical of a pure sensory stroke of thalamus
lipohyalinosis
- degenerative changes in small blood vessels
- accumulation of glassy/waxy looking lipid in vessel wall
-typical of pure sensory stroke of thalamus
thalamic hemorrhage
- spontaneous intracerebral hemorrhage
- associated with HTN
- involvement of adjacent internal capsule (dominates, adds hemiparesis)
- also sensory involvement
common sx of thalamic hemorrhage
- numbness, sensory deficits on CONTRAlateral side
- sometimes developing into thalamic pain
- hemiparesis
Thalamic coma
- bilateral involvement of reticular activating system
- embolus at top of basilar a., before bifurcation
damage to prefrontal cortex is associated with which disorders?
(frontal lobe, social judgement etc.)
- schizophrenia
- antisocial PD
- ADHD
*phineas gage
unilateral lesion to parietal lobe?
- causes contralateral neglect
- pt fails to pay attention to contralateral side
- R lesion: only draw numbers on L side of clock
primary sensory cortex lesion
cause loss of sensation in corresponding area
prosopagnosia
- “face blindness”
- disruption of circuits in fusiform gyrus (higher order cortical center)
-poss via bilateral temporal lobe injury
(facial recognition center: underside of temporal and occipital lobes on both sides of the cortex)
Kluver-Bucy syndrome
- behavioral syndrome
- due to bilateral removal of medial temporal lobes in monkeys
- fearless/placid
- hypersexuality
- excessive sniffing/oral examination
SHOWED IMPORTANCE OF INTACT LIMBIC STRUCTURES AND CONNECTIONS TO APPROPRIATE BEHAVIORAL PATTERNS
(note: amygdala was also taken)
HM research patient
- seizures
- experimental surgery to take out MEDIAL TEMPORAL structures, amygdala, hippocampus (and surrounding cortex) bilaterally
After
- few seizures
- unable to form NEW long-term memories
- profound retrograde amnesia
hippocampus has been implicated in:
- MEMORY function
- Alzheimer’s disease
- SCHIZOPHRENIA
- hippocampal sclerosis and EPILEPSY
- AUTISM
- DEPRESSION
- modulating endocrine functions (via input to hypothalamus)
- modulation of aggressive behaviors
amygdala is implicated in:
- temporal lobe epilepsy
- schizophrenia
- Alzheimer’s
- autism
- anxiety states/PTSD
- affective disorders
- panic disorders
- emotional memory
missing amygdala
- has no fear
- cannot recognize fear
- cannot draw fear
Broca’s aphasia
motor aphasia
- unable to form words
- “broke”, labored speech
- inferior frontal lobe
Wernicke’s aphasia
sensory aphasia, fluent aphasia
- can talk freely, but makes no sense (“were”-“nick”)
- no comprehension of what you say or what they are saying
- “what?”
- superior temporal lobe
transcortical motor aphasia
-looks like Broca’s aphasia, but CAN repeat
- can repeat
- cannot initate own
- adj to Brocas in mid frontal gyrus
transcortical sensory aphasia
-looks like Wernicke’s but CAN repeat
- can repeat
- cannot understand
global aphasia
- no understanding
- no naming
- no repeating
- no expression
usually due to a larger vessel (proximal occlusion)
conduction aphasia
- fluency relatively intact
- comprehension impaired
- arcuate fasciculus
- inability to repeat (connects wernickes to brocas)
DISCONNECTION SYNDROME
split brain syndrome
- corpus callosum affected
- disconnect between both sides of brain
Due to:
- epilepsy surgery
- tumor
- EtOH abuse
Balint Syndrome
BILATERAL PARIETAL LESIONS
- simultanagnosia: inability to perceive visual field as a whole (name objects in kitchen but not situation)
- oculomotor apraxia: difficulty fixating the eyes
- optic ataxia: inability to move hand to a specific object using vision
- fail to apprehend all but 1 of simultaneously presented objects at the same location
- –object based, not location based
- –multicolored dots seen if connected by lines
Gerstmann Syndrome
dominant parietal lobe
- agraphia
- acalculia
- finger agnosia
- right left confusion
non-dominant parietal signs
- denial of deficits (anosagnosia)
- visual, tactile, auditory extinction
- spatial disorganization
- neglect of left space
frontal lobe syndrome signs
- problems with sequences tasks (Stroop test)
- grasp reflexes
- paratonia (Gegenhalten)
- suck and snout reflex
- perseveration (repeat self, locked in idea)
- Luria test (pattern repeat)
- incontinence
Anton syndrome
- bilateral occipital lobe injury (PCA)
- CORTICAL BLINDNESS
- cannot see, but will flinch when confronted
- confabulation: can see but cannot interpret signal so brain makes something up
- headache, psychosis
-unawareness and denial of cortical blindness
Alexia w/o agraphia
posterior cerebral artery stroke involving SPLENIUM
disconnection syndrome
occipital cortex involved
can write but cannot read what they wrote
Agraphia and acalculia
dominant parietal lobe lesion
Gerstmann syndrome
- problems with sequences tasks (Stroop test)
- grasp reflexes
- paratonia (Gegenhalten)
- suck and snout reflex
- perseveration (repeat self, locked in idea)
- Luria test (pattern repeat)
frontal lobe syndrome signs
loss of initiative and drive
w/ loss of taste/smell
subfrontal meningioma (–> pure frontal lobe syndrome and compresses olfactory nerves)
conditions that affect the temporal lobe bilaterally
- herpes encephalitis
- seizures
fluent aphasia
wernicke’s aphasia
lacunar stroke in internal capsule
arm and leg equally affected
small lacuna in the internal capsule can disrupt ___ and ___
CST and CBT
macular (center) sparing –> indication of lesion in
primary visual cortex
frontal lobe behaviors represent a failure of control of ________ impulses
frontal lobe behaviors represent a failure of control of LIMBIC impulses
insensitive to consequences lack of insight irritable euphoric apathy crude humor (witzersucht) slowed motor/mental actions (abulia)
pt has trouble repeating phrase correctly, and does worse w/ more attempts he makes
conduction aphasia
arcuate fasiculus –> connects wernickes to brocas
pt lost ability to form new memories and has trouble recognizing faces, which lobe affected?
temporal lobe
hippocampus, fusiform gyrus
pt has change in personality and shows grasp reflex when finger in hand, which lobe affected?
frontal lobe
capsular lacunes, if situated in region of CST…
contralateral hemiparesis (involving arm, leg, face equally)
“pure motor hemiplegia”
internal capsule lesion
pure motor stroke
leg=arm=face(CBT)
no other signs
all effects CONTRALATERAL to lesion
small vessel disease, lacunes
Corticospinal tract lesion
Spastic paralysis, hyperreflexia, and other upper motor neuron signs are present
CST lesion in spinal cord
There is a spinal cord level and there is weakness or paralysis from that level and below
CST lesion in brainstem
Hemiparesis (C) and cranial nerve signs (I)
Medulla: XII; Pons VI, Midbrain III
in brainstem, corticospinal tract always ventral or dorsal?
ventral
hemiparesis combined with
paralysis of the tongue
medial medulla
paralysis of abducens
medial pons
paralysis of medial rectus
medial midbrain
superior MCA-ACA lesion
paralysis + loss of sensory info on side opposite the lesion
hyperkinesia
–> disease?
Huntington’s
Hemiballismus
damage to contralateral subthalamic nucleus
hemiballismus
degeneration of caudate nucleus
Huntington’s disease
loss of DA neurons in substantia nigra
Parkinson’s
hypokinesia
–> disease?
Parkinson’s
cerebellar pathology
- dysmetria (over/undershoot)
- intention tremor
- truncal ataxia
- incoordination (ataxia)
-dysdrochokinesis (difficult rapid alt movements)
nuclei involved in medial brainstem strokes
III
IV
VI
XII
nuclei involved in lateral brainstem strokes
motor V
sensory V
ambiguus (IX, X)
spinal accessory XI
intalaminar nuclei
to cortex
(arousal) reticular activating system
profound anterograde amnesia occurs w/ damage to the
hippocampal formation
entorhinal cortex involved in process
UE tends to be flexed, LE tends to be extended
stroke pt
amaurosis fugax
ipsilateral monocular vision loss
ICA blockage (ophthalmic)
pure motor hemiplegia
internal capsule or ventral pons
Small Vessel (Lacunar) Syndrome
pure hemisensory loss
thalamus
Small Vessel (Lacunar) Syndrome
sensorimotor
thalmocapsular
Small Vessel (Lacunar) Syndrome
clumsy hand-dysarthria and ataxia hemiparesis are types of
Small Vessel (Lacunar) Syndromes
most common region of intracerebral hemorrhages due to HTN
basal ganglia
aneurysm common locations
ACOMM and MCA bifurcations
simple partial seizures
consciousness preserved
complex partial seizures
consciousness altered
generalized seizures are more likely due to
underlying seizure disorder
absence seizures
- staring, lack of awareness
- generalized spike and wave EEG
“petit mal”
myoclonic seizure
diffuse jerking
generalized clonic tonic etc
tonic–> stiff
clonic–> rhythmic jerking
“grand mal”
dysembryonic neuroepithelial tumor (DNET)
neuronal tumor
favors temporal lobe
presents as seizures
meningioma is an ____-axial tumor
meningioma is an EXTRA-axial tumor
slow growing, good prognosis
astrocytoma
pilocytic –> peds, benign
low grade
anaplastic
glioblastoma multiforme –> likes to cross corpus callosum
ependymoma
originates in ventricles
hydrocephalus common
lots of HA if elevated ICP
oligodendroglioma
slow growing
good prog
FRIED EGG
seizures common
pseudopallisading necrosis
histo feature in GLIOBLASTOMA MULTIFORME (astrocytoma)
so agressive, outgrow and obstruct blood supply
which tumor presents w/ bitemporal hemianopia?
SELLA MASSES
sella masses - 2 types?
pituitary adenoma
craniopharyngioma
very cystic tumor, tends to be filled w/ “crank case” oil (black viscous fluid)
craniopharyngioma
type of sella mass
heterotopias
disorder of MIGRATION
extra layer of gray matter, etc.
relapsing-remitting MS
reverts to baseline between attacks
relapsing-progressive
reverts not quite back to baseline between attacks
secondary progressive
eventually, instead of relapsing episodes, just get steady accumulation of disability
primary progressive
progressive course from onset
MS is a ____ matter disorder
MS is a WHITE matter disorder
lesions within corpus callosum, kind of perpendicular to it
seen in MS
Dawson’s fingers
MS dx requires …
demonstration of lesions disseminating in space and time
need hx and new lesions in a different neuro axis in a different time frame
optic neuritis is typical in ___
how is it tested?
optic neuritis is typical in MS
how is it tested? evoked potentials (light checkerboard thing, measure how optic n. is receiving info)
MS pt CSF findings
> 2 oligoclonal bands (MOST IMP)
inc IgG synthesis
not much WBC elevation
lewy body dementia
first hallucinations
also Parkinson’s sx
dementia w/ stepwise progression of cognitive decline
vascular dementia
senile plaques
beta-amyloid
neurofibrillary tangles
tau protein
abnormal genes in familial Alzheimer’s
APP, presenillin 1 (gamma secretase)
AD inheritance
normal pressure hydroceophalus
wet
wacky
wobbly
(impaired CSF absorption –> normal pressure hydroceophalus)
metabolic causes of dementia
thyroid
B12 deficiency
responds to voice, pain but clearly not fully aware of environment
stuporous
subcortical comas show less
subcortical comas show less EYE MOVEMENT
bilateral thalamic injury can lead to coma due to damage of
reticular formation
PVS dx after
1 mo.
1 year in trauma cases
locked-in syndrome
ventral pontine lesion
minimally conscious state
movement?
demonstrates purposeful behavior rather than reflexive
lucid interval
epidural hematoma
biconvex
always acute
subdural hematoma
acute or chronic
glasgow coma scale score indicating serious head injury
8 or less
inducing barbiturate coma can help manage …
elevated ICP
early sign of medial temporal lobe (uncal) herniation
dilated, fixed pupil
abulia
frontal lobe syndrome
slowed response to envio
superior temporal gyrus
heschl’s gyrus
auditory
supramarginal gyrus
language function
angular gyrus
language function
reading
frontal eye fields
cortical control of eye movements
middle frontal gyrus
