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