crescent shaped lesion
what is the source?
and the presentation?
rupture of bridging veins
subacute course, hx drowsiness, confusion, speech issues
“the crab of death”
mass effect, bleeding
urinary incontinence, neuro deficits, magnetic gait
Normal pressure hydrocephalus
blood supply to the anterior and superior cortex
anterior cerebral artery
blood supply to the lateral aspects of the cortex
middle cerebral a.
blood supply to the bottom and back aspects of the cortex
posterior cerebral a.
the inside of the brain (subcortex) gets most of its blood from (2)
anterior & posterior cerebral aa.
personality, behavior, decisions
perception, making sense of the world, arithmetic, spelling
memory, understanding, language
contents of the cavernous sinus (3)
all nerves that control EOM
all divisions of CN V except V3
internal carotid a.
issues suggesting a problem in the cavernous sinus? (2)
numbness of the top of the face
subcortical stroke presentation
paralysis of face, arm, and leg
cortical stroke presentation
paralysis of just one area
truncal problems, central ataxia suggests?
central cerebellum lesion
extremity problems, ataxia on finger to nose suggests>
peripheral lesion of the cerebellum
CN localized to the midbrain?
CN localized to the pons
CN localized to the medulla
VIII (and the pons)
CN localized to the spinal cords
site of pyramidal decussation
ipsilateral CN deficits & contralateral body weakness
result from a brainstem lesion
posterior columns of the spinal cord
and where does it cross
lateral spinothalamic tract
crosses at the level it enters
lateral corticospinal tract
Brown Sequard syndrome
loss of pain, temp., light touch on opposite side of lesion
loss of motor function, vibration, position, deep touch of the same side as the cord lesion
central cord syndrome
loss of pain and temp bilaterally
anterior cord syndrome
paralysis, loss of pain and temp
posterior cord syndrome
loss of vibration and proprioception
posterior & lateral cord syndrome
paralysis & loss of vibration/proprioception
cauda equina defining characteristics
more severe pain & weakness
late & less severe bowel & bladder problems
conus medullaris defining characteristics
less severe pain & weakness
early & severe B&B problems
cortex lesion? (4)
hemiparesis/hemisensory involving face & arm mostly
subcortical structures (internal capsule & basal ganglia) lesion? (2)
dense hemiplegia- face, arm, and leg abnormal movements (chorea, ballism, tremor, cogwheeling)
cerebellar lesions (3)
brainstem lesions (2)
spinal cord lesions (4)
motor neuron lesion (2)
no sensory involvement, fasiculations
peripheral neuron lesion (5)
distal weakness sensory involvement stocking-glove distribution (distal > proximal) arflexia hyporeflexia
NMJ lesion (3)
no sensory involvement
muscle lesion (3)
no sensory involvement
biconvex, lens-like lesion
what vessel causes it?
middle meningeal a. (fast blood flow)
lesion of CN II before the optic chiasm
injury to CN II behind the optic chiasm
injury to a portion of nerves behind the optic chiasm
lesion of CN II will affect the pupillary reflex how?
no pupillary response to light
droopy eye indicates?
lesion to CN III
which nerve is the sensory limb of corneal reflex
lack of eyelid closure can indicate
CN VII lesion
lack of weakness in the upper face can indicate?
two CN in the pupillary reflex
II and III
CN in the corneal reflex
CN V1 & VII
vestibulo-ocular reflex CN
VIII, VI, and III
dolls eyes CN?
gag reflex CN
IX and X
how to detect injury to CN XII
tongue will protrude towards lesioned side
achilles tendon DTR
L4 innervates (2)
S1 innervates? (2)
basal ganglia lesion
Romberg tests for?
spastic weakness, hyper-reflexia, and positive Babinski indicate
UMN (brainstem, tracts)
flaccid weakness (decreased tone), hyporeflexia, atropy, fasiculation indicate?
face/arm > leg effect is caused by what vessel
leg > arm/face effect is caused by what vessel
dense unilateral motor or sensory defect
aphasia, apraxia, and agnosia suggest?
unsteady/ataxic gait, spastic weakness, hyporeflexia, absent proprioception & vibration up to the knees, positive romberg,
(what would it be if he had truncal ataxia?)
UMN, spinal cord- posterior column involvement
metabolic- Vitamin deficiency
with truncal ataxia: midline degeneration of the cerebellum due to alcoholism
upper and motor neuron signs can indicate?
degeneration of corticospinal tract as well as lower motor tract
inability to maintain upward gaze for 2 min can indicate