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114 Cards in this Set

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gray matter vs white matter
gray: aggregations of neuronal cell bodies; rims the surfaces of the cerebral hemispheres forming the cerebral cortex
white: neuronal axons that are coated with myelin
internal capsule
white-matter structure where myelinated fibers converge from all parts of the cerebral cortex and descend into the brainstem
reticular activating system
in the diencephalon and upper brainstem; consciousness depends on this
spinal cord termination
L1/L2
where are lumbar punctures performed
L3/L4 or L4/L5
corticospinal (pyramidal) tract
mediate voluntary movement and integrate skilled, complicated, or delicate movements by stimulating selected muscular actions and inhibiting others
- carry impulses that inhibit muscle tone
- originate in motor cortex
- travel down into lower medulla where they decussate at pyramids
- cross in medulla and go downward
** tracts that synapse in the brainstem with motor nuclei of cranial nerves= corticobulbar
bradykinesia
damage to basal ganglia
- slowness or lack of spontaneous and automatic movements
pain and temperature
pass into the posterior horn of the spinal cord and synapse with secondary neurons
crude touch fibers
pass into posterior horn and synapse with secondary neurons
-secondary neurons cross to opposite side and pass upward in spinothalamic tract into the thalamus
position and vibration fibers
pass directly into posterior columns of the cord and travrel up to medulla with fibers of fine touch
-synapse in medulla with secondary neurons
- fibers from secondary neurons cross to opposite side at medullary level and continue on to thalamus
thalamic level
quality of sensation is perceived but fine distinctions are not made
loss of position and vibration sense with preservation of other sensations- where is the lesion?
posterior columnstransection of the spinal cord
loss of all sensations from waist down, with paralysis and hyperactive reflexes in the legs- lesion where?
transection of spinal cord
reflex
involuntary sterotypical response that involves at least one afferent and one efferent across a single synapse
all componenets of a reflex arc
sensory nerve fibers
spinal cord synapse
motor nerve fibers
neuromuscular junction
muscle fibers
ankle reflex
S1
knee reflex
L2-4
brachioradialis reflex
C5-6
biceps reflex
C5-6
triceps reflex
C6-7
abdominal reflex (upper)
T8-10
abdominal reflex (lower)
T10-12
plantar reflex
L5-S1
anal reflex
S2-4
different presentation of myopathy vs polyneuropathy
b/l proximal weakness in myopathy
b/l distal wekaness in polyneuropathy
presentation of paresthesias around the mouth and in hands Ddx?
hyperventilation
dysesthesias
distorted sensation in response to a stimulus (light touch or pinprick as burning or tingling sensation)
vasovagal syncompe
emotional stress and warning symptoms (flushing, warmth, nausea); slow onset, slow offset
cardiac syncope
arrhythmias, sudden onset/offset
presentation of tonic-clonic motor activity, bladder or bowel incontinence, and postictal state
generalized seizure; may bite tongue
stroke
sudden neurologic deficit caused by CV ischemia (80-85%) or hemorrhage (15-20%)
hemorrhagic strokes- two types
intracerebral (10-15%) or subarachnoid (5%)
TIA
sudden focal neurologic deficit- lasting less than 24 hours- more recent: less than 1 hour without underlying structural defects
predictive value of TIAs
15% of patients progress to stroke w/i first 3 months
when is risk of stroke highest
first 30 days after TIA
middle cerebral artery occlusion symptoms
visual field cuts and contralateral hemiparesis and sensory deficits
MCA occlusion in L hemisphere
aphasia
MCA occlusion in R hemisphere
hemineglect
most common cause of hemorrhagic stroke from subarachnoid hemorrhage
rupture of saccular aneurysms in circle of Wilils
ideal level of HgA1C in diabetics to control risk for stroke
< 7.4% so onset of neuropathy drops by 50-60%
loss of sense of smell indicates
sinus congestion, head trauma, smoking, aging, use of cocaine, parkinsons
disc pallor vs disc bulging
pallor: optic atrophy
bulging: papilledema
prechiasmal, anterior defects (visual)
glaucoma, retinal emboli, optic neuritis
bitemporal hemianopsias
defects at optic chiasm- pituitary
homonymous hemianopsias or quadrantanopsia
postchiasmal lesions- parietal lobe- acuity normal
monocular diplopia
local problems with glasses or lenses, cataracts, astigmatism, ptosis
binocular diplopia
CN III, IV, VI, neuropathy (40%), MG, trauama, thyroid ophthalmopathy, INO (muscle disease)
nystagmus (define and when you see it)
involuntary jerking movement of the eyes with quick and slow components
- cerebellar disease (increases with retinal fixation), vestibular disorders (decreases with retinal fixation)
how is nystagmus named
for the direction of the fast component
unilateral weakness in CN V pontine lesions
b/l weakness in cerebral hemispheric disease because of b/l cortical innervation
ipsilateral face but contralateral body sensory loss localizes lesion to?
brainstem
acoustic neuroma presentation
absent blinking and sensorineural hearing loss
conductive vs. sensorineural hearing loss
conductive: impaired air thorugh ear transmission
sensorineural: damage to chochlear branch of CN VIII
Rinne vs Weber test
Rinne: air and bone conduction- normal air > bone- conductive- bone longer than air in affected ear- sensorineural- air longer than bone but less than 2:1 ratio
Weber: lateralization- normal NONE- conductive- lateralization of deaf ear
sensorineural- lateralization to better ear
causes of conductive hearing loss
cerumen, otosclerosis, otitis media
b/l lesion of vagus nerve
failure of palate to rise
u/l lesion of vagus
one side doesnt rise and with uvula is pulled toward normal side
tongue atrophy and fasciculations
amyotrophic lateral sclerosis, polio
unilateral cortical lesion
protruded tongue deviates transiently in a direction away from the side of cortical lesion, toward side of weakness
pseudohypertrophy and when seen
increased bulk with diminished strength: DMD
sign of atrophy in the hands
flattening of thenar and hypothena eminences and furrowing b/w metacarpals; median and ulnar nerve damage, respectively
weakness of extension
peripheral nerve disease such as radial nerve damage and in CNS disease producing hemiplegia- stroke/MS
weak grip (C7-T1)
cervical radiculopathy, de Wuervain's tenosynovitis, CTS, arthritis, epicondylitis
weak finger abduction
ulnar nerve disorders
weak opposition of the thumb
medial nerve
flexion of hip tests
L2-L4; iliopsoas
signs of cerebellar disease
ataxia, nystagmus, dysarthria, hypotonia
dysdiadochokinesis
when one movement cannot be followed quickly by its opposite; movements are irregular, slow, clumsy- cerebellar disease
dysmetria
finger initially overshoots but eventually reaches it
differentiation of ataxia from dorsal column disease vs cerebellar disease
cerebellar: difficulty standing with feet together whether eyes are open or closed
-those with dorsal column problems compensate by eyes then demonstrate (+) romberg sign
pronator drift
sensitive and specific for corticospinal tract lesion originating in contralateral hemisphere
stereognosis, number identification, two-point discrimination impaired in?
posterior column disease
astereognosis
inability to recognize objects placed in hand
-suggest lesion in sensory cortex
lesions in sensory cortex
astereognosis, inability to recognize numbers (graphesthesia), increase distance between two recognizable points, impairs ability to localize points accurately
neck stiffness and resistance to flexion in what perfect of pts with acute bacterial meningitis vs subarachnoid hemorrhage
90%- meningitis
20-85%- subarachnoid hemorrhage
Brudzinski's Sign
flex the neck; watch the hips and knees- positive when hips and knees flex
Kernig's Sign
flex the leg at both hip and knee then straighten- pain and increased resistance to extending the knee- (+) Kernig's sign- b/l indicates meningeal irritation
positive straight leg test?
pain radiating into ipsilateral leg indicating lumbosacral radiculopathy, sciatic neuropathy, or both
sensitivity and specificity of straight leg raise for disc herniation vs crossed straight-leg raise
95% and 25%
40% and 90%
asterixis
sudden, brief, nonrhythmic flexion of hands and fingers- liver disease, uremia, hypercapnia
winging of scapula
weakness of serratus anterior/ long thoracic nerve
*Five clinical signs that stronly predict death in coma
absent corneal response, absent pupillary response, absent withdrawal response to pain, no motor response; at 72 hours-no motor response
DONTS when assessing comatose patient
1.) don't dilate the pupils! (most important clue to underlying cause of coma [structural vs. metabolic])
2.) don't flex the neck if there is any question of trauma to the head or neck
-immobilize C-spine and get an x-ray first
structural hemispheric lesions (eye direction)
look at the lesion in the affected hemisphere
comatose pt with lack of doll's eye movements
-ability to move both eyes to one side is lost--> lesion of midbrain or pons
hemiplegia of sudden cerebral accidents
flaccid at first causing limp hand drops to form a right angle with the wrist
movement of flaccid leg in acute hemiplegia
falls fast into extension with external rotation at hip
mechanism of acute ischemic stroke
-ischemic brain injury begins with a central core of very low perfusion and often irreversible cell death
-core surrounded by ischemic penumbra of cells that could be salvaged
most irreversible damage occurs when
3-6 hrs after onset of symptoms
NAME THAT STROKE! contralateral leg weakness
ACA
NAME THAT STROKE! contralateral face, arm>leg weakness, sensory loss, field cut, aphasia (L lesion), neglect/apraxia (R lesion)
anterior circulation of MCA
NAME THAT STROKE! contralateral motor or sensory deficit without cortical signs
subcortical circulation- leticulostriate deep penetrating branches of MCA
four common syndromes of lacunar infarcts
1.) pure motor hemiparesis
2.) pure sensory hemianesthesia
3.) ataxic hemiparesis
4.) clumsy hand-dysarthria syndrome
NAME THAT STROKE! contralateral field cut
posterior ciruclation- PCA
NAME THAT STROKE! cortical blindness but preserved pupillary light reaction
b/l PCA infarction
NAME THAT STROKE! dysphagia, dysarthria, tongue/palate deviation and/or ataxia with crossed sensory/motor deficits (ipsilateral face/contralateral body)
posterior circulation- brainstem, vertebral, basilar artery branches
NAME THAT STROKE! oculomotor deficits and/or ataxia with crossed sensory/motor deficits
posterior circulation- basilar artery
decerebrate rigidity (abnormal extensor response)
-jaws clenched, neck extended, arms adducted and stiffly extended at elbows, forearms protonated, wrists/fingers flexed
- legs extended at the knees, feet plantar flexed
- may occur spontaneously
**lesion in diencephalon, midbrain, or pons
**also from severe metabolic disorders- hypoxia or hypoglycemia
hemiplegia (early)
-flaccid (later spastic)
- paralyzed arm and leg slack- fall loosely
- leg may lie externally rotated
- if lower face paralyzed, cheek puffs out with exhalation
- both eyes away from paralyzed side
decorticate rigidity (abnormal flexor response)
- upper arms flexed tight to the sides with elbows, wrists, fingers flexed
- legs extended and internally rotated
- feet are plantar flexed
- lesion of corticospinal tracts w/i or near cerebral hemispheres
bilaterally small pupils
1.) damage to sympathetic pathways in hypothalamus
2.) metabolic encephalopathy
- light rxns normal
pinpoint pupils (<1 mm)
1.) hemorrhage in pons
2.) morphine, heroin, narcotics
midposition fixed pupils
midposition of slightly dilated (4-6mm)- damage in midbrain
b/l fixed and dilated pupils
severe anoxia and its sympathomimetic effects
- atropinelike agents, phenothiazines, TCAs
b/l large reactive pupils
cocaine, amphetamine, LSD, sympathomimetics
one large pupil (fixed and dilated)
herniation of the temporal lobe (compression of CN III and midbrain)
features of toxic-metabolic coma
*arousal centers poisoned or critical substrates depleted*
- regular respiration: normal or fast; irregular: Cheyne-Stokes
-pupils: equal, reactive- may be unreactive if fixed and dilated from anticholinergics/hypothermia
- level of consciousness changes after pupils change
causes of toxic-metabolic coma
uremia, hyperglycemia, alcohol, drugs, liver failure, hypothyroidism, hypoglycemia, anoxia, ischemia, meningitis, encephalitis, hyperthermia, hypothermia
features of structural coma
*lesion destroys or compresses brainstem arousal areas*
- irregular respiration (Cheyne-Stokes or ataxic)
- pupils: unequal or unreactive- midbrain compression if midposition and fixed
- if dilated and fixed- compression of CN III
- level of consciousness changes before pupils change
causes of structural coma
epidural, subdural, intracerebral hemorrhage, cerebral infarct or embolus, tumor, abscess, brainstem infarct, tumor, hemorrhage, cerebellar infarct, hemorrhage, tumor or abscess
steppage gait
- foot drop
- cannot walk on heels
- tibialis anterior and toe extensors are weak
parkinsonian gait
- basal-ganglia defects
- posture is stopped (flexion of head, arms, hips, knees(
- fenestrating
- poor postural control (retropulsion)
cerebellar ataxic gait
staggering, unsteady, wide based
- cannot stand with feet together regardless of eyes
sensory ataxia
- gait unsteady, wide based
- pts throw feet forward and outward and bring them down, first on heels then toes