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177 Cards in this Set
- Front
- Back
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 |
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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 |
mediate voluntary movement and integrate skilled, complicated, or delicate movements by stimulating selected muscular actions and inhibiting others |
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bradykinesia |
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 |
pass directly into posterior columns of the cord and travrel up to medulla with fibers of fine touch |
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thalamic level |
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? |
posterior columnstransection of the spinal cord |
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all componenets of a reflex arc
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sensory nerve 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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what presents with lesions in sensory cortex |
astereognosis, inability to recognize numbers (graphesthesia), increase distance between two recognizable points, impairs ability to localize points accurately
-only one stimulus will be recognized--sensation on opposite side of the damaged cortex is gone |
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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 (seen in MD) / 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 |
*arousal centers poisoned or critical substrates depleted* |
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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 |
staggering, unsteady, wide based |
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sensory ataxia
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- gait unsteady, wide based |
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this suggests progressive subacute onset of distal lower extremity weakness |
guillan barre syndrome |
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what indicates an abrupt onset of motor and sesory deficitis |
TIA or stroke |
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ataxia, diplipa, and dysarthria indicate |
vertebrobasilar TIA or stroke also consider posterior fossa tumor and vertebrobasial or hemicranial migraine |
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this suggests chronic more graduate, onset of weakness in lower extremities |
metastatic cord lesions and lumbar disc disease |
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central focal or asymmetric weakness suggest |
ischemic, thrombotic, or mass lesions |
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peripher focal or asymmetric weakness sugest |
nerve injury to the NMJ, to myopathies or intrinsic muscle diseases |
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proximal limb weakness usually symmetric and without sensory loss suggests |
myopthaties from alcohol, drugs like glucocorticoids, and inflammatory muscle disorders (myosities and dermatomyositis) |
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proximal typically asymmetric weakness that gets worse with effort and associated with bulbar symptoms lke diplipa, ptosis, and dysarthria, and dysphagia suggest.. |
myasthenia graves |
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sensory changes that arise from local nerve compression or entrapment in hand numbness suggests a problem with.. |
medial, ulnar, or radial nerve |
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sensory changes in nerve root compression suggest.. |
issues with dermatomal sensory loss from vertebral bone spurs or herniated discs or central lesions from stroke or MS |
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diabetic with burning pain suggests.. |
sensory neuropathies |
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behavioral risk factors for ischemic stroke |
1. hypertension 2. dislipedemia 3. weight 4. exercise 5. smoking 6. alcohol use |
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top contributing factors for stroke |
1. AA 2. HTN 3. diabetes 4. left ventricular hypertrophy 5. income and insurance gaps |
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what are stroke warning signs |
numbness/weakness; confusion/trouble speaking; trouble seeing and walking; dizziness; balance problems; severe headache |
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early predictions of stroke |
ABCD2 a=age >60 b=BP >140/90 c=clinical features--focal weakness or impaired speech d=duration--up to >60min d=diabetes |
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common causes of acute symptomatic seizures |
1. head trauma 2. alcohol 3. cocaine 4. w/drawal from alcohol, benzos, and barbs 5. metabolic issues like low gluc, low Ca, low Na 6. stroke 7. meningitis 8. encephalitis
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what suggests parkinsons disease |
-low frequency unilateral resting tremor -rigidity -bradykinesia (slow movement) |
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this is high-frequency, bilateral, upper extremity tremor, with both limb movement, and sustained posture, w/ possible head, voice, and leg tremors present |
essential tremors |
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what are disease specific risk factors for stroke |
1. atrial fib -CHADS2 --c=CHF --h=HTN --a=age >75 --d=diabetes --s=prior stroke or TIA
2.carotid artery disease |
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categories for ischemic stroke |
-large artery atherosclerotic infarction -cardiac embolism -small vessel lacunar disease -dissection -hypercoagulable states -paradocial embolism through foramen ovale |
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most comon diabetes peripheral neuropathy |
distal symmetric sensorimotor polyneuropathy (burning electrical pain in lower extremities at night) |
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five categories for a comprehensive or screening neuro exam |
1. mental status, speech, language 2. CN 3. motor-coordination, gait, and strength 4. sensory-light, temp, touch, vibrations, discrimination 5. reflexes-DTR and plantar responses |
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loss of smell can occur in.. |
sinus conditions, head trauma, smoking, aging, cocaine use, and PD |
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large pupil reacts poorly to light or aniscoria worsens in light and large pupil has abnormal pupillary constriction..this is seen in.. |
CN 3 palsy |
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if pt awake and if ptosis and opthalmoplegia also present with anisocoria then consider... |
intracranial aneurysm |
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if pt in coma, with ptosis and opthalmoplegia also present with anisocoria then consider... |
transtentorial herniation |
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binocular diplopia suggests... |
CN3, 4, and 6 neuropathies (40% of patients) and eye muscle diseases (MG, trauma, thyroid opthalmopathy, and internuclear opthalmoplegia) |
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involuntary jerking movements of the eyes with quick and slow components |
nystagmus |
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how is nystagmus named |
for the direction of the quick component (horizontal, vertical, mixed, or rotary) |
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nystagmus presents in what kind of diseases |
Cerebellar disease, like gait ataxia and dysarthria and vestibular disorders and internuclear opthalmoplegia |
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CN 5 carries which blinking reflex |
sensory limb |
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CN 7 carries which blinking reflex |
motor response |
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what portion of face does a peripheral injury (CN7) affect and an example |
Bells palsy -both upper and lower face |
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what portion of face does a central lesion affect |
mainly lower b/c upper face will receive upper motor neurons from opposite side of face |
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loss of taste, hyperacusis, and increased or decreased tearing is seen in... |
bells palsy |
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hypertrophy |
increased muscle bulk with proportionate strength |
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lesion to corticospinal tract causes and what is a common cause |
-spascity (hypertonia=increased muscle tone) --common cause: stroke |
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basal ganglia |
-controls muscle tone and controlled body movements (walking) |
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lesion to basal ganglia would result in and a common cause |
-rigidity (increased resistance, esp during ROM) --common cause=parkinsons |
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lead pipe rigidity |
-increased resistance that persists throughout the movement arc and independ of rate of movement |
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cogwheel rigidity |
with flexion and extension of the wrist or forearm, a superimposed ratchetlike jerkiness |
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paresis |
impaired strength (weakness) |
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paralysis or plegia |
absence of strength |
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hemiparesis |
weakness to one half of the body |
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paraplegia |
paralysis of the legs |
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quadriplegia |
paralysis of all four limbs |
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what is a grade 0 on the muscle strength scale |
no muscular contractions detected |
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what is a grade 5 on the muscle strength scale |
normal muscle strength |
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inability to heel walk is a sensitive test for... |
corticospinal tract damage |
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disease example of loss of vibration sense in posterior column disease |
tertiary syph and vit B 12 deficiency |
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disease examples of loss of position sense in posterior column disease |
MS, tabes dorsalis, vit B 12 deficiency, and peripheral neuropathy from DM
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reflex |
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 |
sensory nerve fibers |
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CNS lesion along descending corticospinal tract is.. |
hyperactive reflexes (hyperflexia) |
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other associated upper motor neuron findings of hyperactive reflexes are... |
weakness, spasticity, or a positive Babinski |
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hypothyroidism is seen and felt where.. |
ankle reflexes |
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what does sustained clonus indicate |
CNS disease |
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abdominal reflexes are absent in.... |
CNS and PNS disorders |
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loss of S2-4 anal reflex suggests.. |
cauda equina lesion |
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subarachnoid space inflammation will cause resistance in.... |
-nuchal flexion (neck); brudzinski (femoral n.); and kernigs signs (sciatic n.) |
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sciatica is 5x more likely when... |
-confirm ipsilateral calf wasting -weak ankle dorsiflexion
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how does lethargic pt look |
-drowsy, opens eyes and responds, falls back to sleep |
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how does obtunded pt look |
-opens eyes, responds slowly, somewhat confused -alertness and interest in environment decreased |
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how does a stuporous pt look |
-painful stimuli needed -verbal response slow or absent -unresponsive when stimuli ceases -minimum awareness of self or environment |
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how does comatose pt look |
-unarousable and eyes closed |