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297 Cards in this Set
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localize this lesion ot a part of the NS: distal/symmetric sensory loss /weakness or in specific nerve distribution
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PNS-topographically localized
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localize this lesion ot a part of the NS: proximal, symmetrical weakness
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myopathy
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localize this lesion ot a part of the NS: fatiguable weakness in all areas
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NMJ
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localize this lesion ot a part of the NS: all modalities lost in a specific area
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plexopathy
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localize this lesion ot a part of the NS: horner's
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plexopathy
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localize this lesion ot a part of the NS:segmental pain w/ all modalities lost in a distribution
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radiculopathy
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localize this lesion ot a part of the NS:LMN weakness and reflex loss
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anterior horn
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localize this lesion ot a part of the NS: assymetric and diffuse sensory and reflex loss
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DRG
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localize this lesion ot a part of the NS: UMN below level of lesion, LMN above, sensory level, neurogenic bladder
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spinal cord (myelopathy)
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localize this lesion ot a part of the NS: CN deficits, impiared respiration, crossed or bilateral motor/sensory deficits, impaired conciousness if RAS involvment
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brainstem
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localize this lesion ot a part of the NS: trunkal tremor, ataxia,
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cerbellar vermis
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localize this lesion ot a part of the NS: limb tremor, ataxia
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cerebellar hemisphere
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localize this lesion ot a part of the NS: nystagmus
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cerbellum
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localize this lesion ot a part of the NS: hemisensory loss, disturbed LOC, hemiataxia
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thalamus
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localize this lesion ot a part of the NS: bradykinesia, athetosis, chorea, muscle rigidity
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basal ganglia
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localize this lesion ot a part of the NS: UMN, hemianopia, seizures, aphasia or neglect
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cerebral cortex
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localize this lesion ot a part of the NS:headache, LOC, CN deficits
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Subarachnoid space or meninges
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define a secondary symptom
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a mass effect- i.e. edema, herniation, obstruction of CSF
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Localize visual lesion: poor constriction of both pupils from light in one eye, decreased central vision in 1 eye, poor color vision, dipoplia
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optic nerve (II) Localize
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Localize visual lesion: ipsilateral eye down and out, ipsilateral ptosis, dilated/non reactive pupil, mydriasis
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occulomotor nerve (III) Localize
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Localize visual lesion: Ipsilateral eye high and excylcotorted
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trochlear nerve (IV) Localize
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Localize visual lesion: ipsilateral eye estropia (turn in); look away from lesion
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Abducens nerve (VI) localize
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Localize visual lesion: can't look away from lesion
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FEF Localize
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Localize visual lesion: can't look towards lession (loss of horizontal saccades)
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PPRF
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Localize visual lesion: weakness of adduction of one and and abduction of the other
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MLF (INO) Localize
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Localize visual lesion: loss of temporal vision on both sides
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optic chiasm Localize
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Localize visual lesion: APD (diminished pupil constriction) + loss of temporal vision in both eyes
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optic tract Localize
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Localize visual lesion: contralateral superior deficit
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optic radiations-temporal lobe Localize
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Localize visual lesion: contralateral inferior deficit
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optic radiations- parietal lobe Localize
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Localize visual lesion: homonymous loss of vision w/ macular sparing
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striate lesion Localize
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Localize motor lesion to part of brain: contralateral weakness, increased tone, spaticity/seizures
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motor cortex and corticospinal tract
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Localize motor lesion to part of brain: bilateral apraxia, paratonia, cognitive deficits, seizure
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anterior frontal lobe
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Localize motor lesion to part of brain: bilateral apraxia, cortical sensory deficits, seizure
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posterior parietal cortex
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Localize motor lesion to part of brain: contralateral weakness/tremor + spasticity + sensory deficits
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thalamus
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Localize motor lesion to part of brain: contralatera parkonsonism w/ out weakness
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basal ganglia (-subthalamic nucleus)
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Localize motor lesion to part of brain: chorea + hypotonia
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subthalamic nucleus
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Localize motor lesion to part of brain: ipsilateral tremor, ataxia, dysemetria w/ out weakness + titubation + wide based gait
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cerebellum
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signs of lower motor neuron lesion
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weakness, atrophy, hypotonia, hyporeflexia
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signs of UMN lesion
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hyperreflexia, spaticity, extensory plantar response
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role of anterior frontal lobe pre-motor cortex
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prepare for movement
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role of posterior frontal lobe supplementary motor area
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program complex movement
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role of posterior parietal cortex
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sensory feedback to motor areas
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role of thalamus
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integration of input from cerebellum and basal ganglia
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role of basal ganglia
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coordination of complex movements, supression of unwanted movemebts, initiation and maintenance fo movements
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role of primary motor cortex/prefrontal cortex
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supress reflex arc
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role of cerebellum
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correction of overshoot
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Localizing sensory lesion - absent reflexes, stocking glove pattern
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peripheral nerve-Localizing sensory lesion
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Localizing sensory lesion- bladder dysfunction, mostly UMN findings, LMN findings in one spot, central pain syndrome/alodynia, sensory level
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spinal cord-Localizing sensory lesion
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localizing sensory lesion- cape distribution of pain/temp loss
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syringomyelia
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Localizing sensory lesion- ipsilateral fine touch, vibration lost; contralatera pain/temp lost;
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brown sequard- hemisection of cord: Localizing sensory lesion
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Localizing sensory lesion - loss of all modalities in face, arm and leg; Central pain syndrome/allodynia
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thalamus
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Localizing sensory lesion - loss of 2 point discrimination, grapheshtesia, sterognosis, seizures
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cortex-Localizing sensory lesion
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Localizing motor lesion - decreased sensation, decreased strength, hyperreflexia, corssed signs (CN and sensorimotor tracts), decerebrate (extension) response, imapired-lonciousness, eye movements, respiration
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brainstem-localizing motor lesion
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localizing sensory lesions-brainstem need to learn
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need to learn!
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Tx of migraine headache
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triptan-%HT (1b/1d receptor agonist)
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prophylatic tx of migraine headache
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Anticonvulsant/antidepressant, beta blocker, ca channel agonist, serotonin antagonist
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describe migrine headache
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unilateral, pulsating w/ photophobia
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describe cluster headache
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unilateral, orbital/temple, 15 min-3 horus of severe pain
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which headaches or indomethacin responsive
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cough, coital, chronic paroxysmal
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describe chronic paroxysmal headache
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3-45 min of pain in temple, forehead, eye area; multiple attacks/day; can occur at night; autonomic symtpoms present; precipitated by neck/head flexion
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DDx included w/ cough headache?
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tumor or arnold-chiari tonsil malformation
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thunderclap headache is which type of headache
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secondary
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features of thunder clap headache
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sudden, severe pain w/ neck stiffness and impaired LOC. Due to SAH
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describe giant cell arteritis headache
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change in patter w/ pain in temples. Temples are tender/lack pulse. Headache is throbbing. Associated w/ fever, weight loss, jaw claudication.
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which headache can cause blindness (amaurosis fugax) if left untreated?
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giant cell arteritis
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describe trigeminal neuralgia
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V2/V3 (jaw/check) areas have unilateral electric shock pain
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ddx of bilateral tirgeminal neuralgia
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MS
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describe meningitis headache
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ddiffuse w/ stiff beck and kernig's sign (back pain)
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mechanism of triptains
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highly selective serotonin agonist aht work at 1b-d receptor on intracranial blood vessels and/or trigeminal sensory nerve endings
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Describe weakness, sensory loss, reflexes, and EMG of Muscular Dz
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proximal weakness, normal sensor, decreased reflexes in areas of weakness, small amplitude brief EMG w/ occasional fibrilation
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Describe weakness, sensory loss, reflexes, and EMG of Axonal dz
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distal weakness; stocking glove sensory loss; distal reflex loss; EMG w/ large amplitude, large duration, and fibrilations
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Describe weakness, sensory loss, reflexes, and EMG of myelin dz
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general limb weakness, mild distal sensory loss, general reflexes lost; EMG w/ slow conduction blocks and focal reductions in amplitude w/ more proximal stimulation
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Describe weakness, sensory loss, reflexes, and EMG of NMJ
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general weakness including face that is variable w/ fatiuge, all else is normal; EMG has decremental responses w/ repetitive stimulation
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Describe weakness, sensory loss, reflexes, and EMG of motor neuron cell body
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general,assymetric weakness that involves arms first; selective- motor or sensory; selective reflex loss; EMG w/ paraspinous denervation and fasiculations
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Component of the Nervous system: Myasthenia gravis
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NMJ
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Component of the Nervous system: Duschenees Muscular Dystrophy
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muscle
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Component of the Nervous system: ALS
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neuron cell body
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Component of the Nervous system: guillian-berre
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myelin
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eaton-lamber myasthenic syndrome
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NMJ
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anterior cord syndrome
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loss of bilateral pain/temp; bilateral paralysis
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posterior cord syndrome
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loss of bilateral touch; +/- bilateral paralysis
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central cord syndrome
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arm> leg weakness; sensory loss varies
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Motor, Sensory, and reflex abnormalities associated with: C5
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deltoid weakness, shoulder sensory loss
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Motor, Sensory, and reflex abnormalities associated with: C6
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bicep weakness, thumb sensory loss, loss of bicep reflex
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Motor, Sensory, and reflex abnormalities associated with: C7
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tricep weakness; 2/3 finger sensory loss; loss of tricep weakness
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Motor, Sensory, and reflex abnormalities associated with: C8
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interossei weakness; 4/5 finger sensory loss; Horne's syndrome
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Motor, Sensory, and reflex abnormalities associated with: L5
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foot drop, diffuclty walking on heels, dorsiflexion; pain and numbness of leg and toes; loss of internal hamstring reflex
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Motor, Sensory, and reflex abnormalities associated with: s1
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loss of plantar flexion, difficulty walking on toes, pain and numbess of leg and calf; lost ankle jerk reflex
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C7/C8 disk herniation compresses which nerve root
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C8
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indications for surgery in radiculopathy
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failure of medical management, progressive neurologic deficit, myelopathy, bowel/bladder infection
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describe myelopathy
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compression of spinal cord w/ dnilateral distal sensory loss not in nerve root distribution and brisk reflexes
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tx for acute releif of migraine
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sumatriptan injection, DHE injection, O2 inhalation, corticosteroids, beta blocker
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effect of hyperventilation of CBF
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decrease
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COPD on CBF
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increase (increase PCO2)
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effect of anemia on CBF
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increase (increase PCO2)
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effect of polycythemia on CBF
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decrease
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effect of inc BP on CBF?
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inc or keep the same by inc MAP
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effect of dec in BP on CBF?
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inc
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what happens when CPP drops below 60?
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inc O2 extraction fraction
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risk factors for ischemic stroke
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age, male when les than 85, black/hispanic, HTN-most modifiable risk factor, cardiac dz, smoking, DM, hyperlipidemia
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risk factors for ischemic stroke in kids
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cardiac dz, heme disorder, vasculopathy, infection
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common causes of iscchemic HT
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atherosclerois, cardiac emboli ( afib,, acute MI), Ocs, migraine, sickle cell, coke
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prognosis of ischemic stroke
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better- 90% survive initially, 10% risk of recurrent stroke in first year, 50% 5 year mortality; , 1/3 won't return to independent fxn
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risk factors for intracerebral hemorrhage
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over 60, non-white
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common causes of intracerebral hemorrhage?
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HTN (rupture of small arteries), amyloid (rupture of small arterioles causing cortical bleed); anticoagulants, neoplasms, drugs, aneuyrsm/avm
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prognosis of intracerebral hemorrhage?
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bad- 50% mortality in 30 days; 1/2 independent at 6 months; most don't get better
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predict for bad outcome of ICH?
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large size, low GCs, older age
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causes for neurological deterioration in ischemic stroke?
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edema, hemorrhagic transformation; stroke recurresence, seizure, pulmonary/cardiac dz, metabolic-renal, hepatic failure, SIADH; fever; sepsis; drugs
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what is the most worrisome cause of neurological deterioration in ischemic stroke?
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edema- everyone gets it b/c dead cells swell
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when is edema in ischemic stroke even more worrisome?
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large; at a young age- no brain atrophy
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when does hemmorrhagic transformation happen in an ischemic stroke?sx
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5 days; often asymptomatic
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what are predictors for hemorrhagic transformation in an ischemic stroke?
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large lesion, cardioembolic source, hyperglycemia, trhombolytic tx
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time course of cerebral edema in ischemic stroke?
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starts to develop in horus; peak 2-4 days
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causes for neurolgic deterioration of ICH?
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hematoma enlargement (within 3 hours)
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importance time course of hematoma enlargement in ICH?
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edema tells if there will be deterioration; most common cause of deterioration; removing doesn't help unless compressing brainstem
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indications for decompressive hemicraniectomy in acute ischemic stroke
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w/ in 48 hours; massive hemispheric infarct of MCA; to decrease swelling/herniation; pt has to be willing to accept results
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tx for secondary stroke prevention ingeneral w/ ischemic stroke?
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tpa in 3 hours; antiplatelt therapy in 48 hours- ASA, clopidogrel, or ticlopidine; antihypertention therapy; statins
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tx for secondary stroke prevention w/ carotid stenois
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carotid endartectomy
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tx to prevent stroke w/ a fib?
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warfarin and vitamin k
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what does glasgow coma scale predict? What are its 3 components?
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eye opening, motor, and speech
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mechanisms of compensationf or increased ICP?
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1. decrease CSF and blood 2. molding of brain to a mass 3. herniation 4. vessel tone
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clinical picture of epidural hematoma-who, cause
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4x more men; skull fractures that rupture MMA
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presentation of epidural hematoma?
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LOC--> lucid interval--> deterioration w/ coma, contralatera hemiparesis, ipsilateral pupil dilation
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CT of epidural hematoma?
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convex and contstricted (by suture lines)
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tx of epidural hematoma?
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evacuation of clot
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clinical picture of subdural hematoma- who, cause
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40yr old men, MVA-laceration of briding cein to mcv--> accupulation due to rupture of parenchyma
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which type of hematoma is more lethal?
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subdural
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what increases risk of subdural hematoma
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anticoagulants
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what do subdural hematoms look like on CT?
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cresecent and crossing (suture lines)
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presenting features of subdural hematoma
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unresponsive pupils, decerebrate, hemiplegia
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what size arteries are aneurysms usually on?
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large
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presentation of SAH?
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suden onset of worst HA of life that lastfor at least a few days. Sometimes vomiting, meningmus, dec LOC/seizure, focal neurolgic signs (CN II,III,VI)
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how to distinguish SAH from thunderclap HA?
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meningmus, depressed LOC, and seizure
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diagnose SAH
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1. CT w/ out contrast in 24 hours + lumbar puncture after 12 hrs if CT is negative
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how to diagnose cuase of SAH?
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1. gold standard is 4 vessel cerebral catheter angiogram 2. MRI Flair/T2 if after 72 hours 3. can also use CT angiogram immediately after CT for diagnoses
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Common causes of SAH
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1. trauma 2. Spontaneous- aneurysm*, preimesencephalic (no cause), coccaine, malformation (AVM is worse)
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order of aneurysms for sAH?
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ACA, ICA, MCA
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common complications of SAH?
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vasospasms, hydrocephalus, rebeelding (high risk) also: hypnatremium, DVT, seizure, psych, cognitive dysfxn
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what causes vasospasm as complication of SAH?
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delayed narrowing of large cerebral arteries + distal autoregulartry dysfxn, cortical spreading depression, microthrombi
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how to prevent vasospasm as a complication of SAH? How to tx if it happens?
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nimodipine x 3 weeks; hypertension/hypervolemia/endovascular therapy
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how to treat hydrocephalus as a complication of sAH?
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ventriculostomy if early, shunt if late
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What is a very common risk of untreated SAH? Why is it important? How to prevent
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re-bleeding; more likely to kill you than first bleed; prevent by treating aneurysm w/ clip if possible, if not coil
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how many seizures are reqd for diagnosis of epilepsy?
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2
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difference between simple and complex partial seizure
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you can remember a simple one
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types of generalized seizures?
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absence, tonic, clonic, atonic
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what type of seizure often has poly spike and wave, w/ predomincance over bifrontal regions?
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generalized
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which type of seizure is likely to be preceeded bya n aura?
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partial
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best medicine for generalzed clonic tonic seizures?
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valproate* +"ates", mides, lamotrigine, levetracetam
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side fx for valproate?
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fetal malformations, metabolic
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Side fx for CBZ (2nd choice for generalized clonic tonic seizures)?
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rash; induces its own metabolism so requires lower does to start
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best medicines for partial sizures?
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CBZ, PHT, all new drugs approved
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pharmacokinetics of phenytoin?
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at high does, moves from linear to 0 order pharmacokinetics, so it can become toxic
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list old AEDs (worse drug interactiosn)
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valproate, carbamazepine, phenobarbitol, phenytoin, primidone
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what can worsen myoclonic seizures associated w/ juvenile myoclonic epilepsy?
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carbamazepine
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what AED is not metabolized by the liver?
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gabapentin
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what AED is known to have cognitive side fx?
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topiramate
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when is epilepsy surgey an option
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medically refractory (fail 3 meds); noneloquent/less necessary part of brain; very localized abnormality; often used in mesial temporal lobe epilepsy
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dysomnia vs. parasomnia
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dysomnia- poor quality of sleep; parasomnia- usual sleep related behavior
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who is more likely to have RLS?
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women
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what is underlying the pathophysiology of restless legs?
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DA receptors and irone metabolsim
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exacerbating factorrs of RLS?
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methylxantines, Lithium, dopamine antagonist, andidepressants, iron deficiency
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Treatment of RLS syndrome?
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dopamindergic agents (topiderol), benzos (quanipen), opioids, and antiepileptics (gabapentin)
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cliniical features of narcolepsy?
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equal in males and females, cataplexy,automatic behaviors, REM-sleep phenomena- sleep paralysis, hypnagogic hallucinations
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what sx is required for diagnosis of epilepsy?
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excessive sleepiness for atleast 3 months
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Treatment of slepiness w/ narcolepsy?
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modafinil, amphetamines/methylphenidate, xyrem, adjunctive stimulants- buproprion, fluoxetine
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treatment of Cataplexy for narcolepsy?
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xyrme, amphetamines/methylphenidate; tricyclica antidepresants, MAOIs, SSROs, venlafaxine, atomoxetine
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clinical feature of periodic limb movement disorder?
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may not know fallen asslpe, often extend big toe or dorsiflex ankle, often asymptomatic,increases w/ age
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Tx of periodic limb movement disorder
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dopaminergic agents, benzodiazapines, oopioids, antiepileptic drugs
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who gest delayed sleep phase syndrome? How to diagnose?
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adolescents (part environment, part intrinsic); sleep diary/actigraphy
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tx of delayed sleep phase syndrome?
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mroning light, evening melatonin/ramelteon
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what can cause an irregular sleep wake pattern?
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environment, agent, degenerative brain disorder, destroyed suprachiasmatic nucelus
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long term hypotics for chronic insomnia?
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benzo, ramelteon (melatonin agonist)
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how long should you intend to use a hypotonic?
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< 3 weeks
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why should antihistamines be used as a sleep med? Benzo?
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antihistamines- daytime sedation; ethanol- rebound excitation/sleep fragmentation
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first sign of uncal herniation?
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ipsilateral dilating pupil--> contralateral hemiperesis
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sign of kernohan's notch?
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ipsilateral hemiparesis
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2 ways to cause a coma?
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dysfunction of RAS 2. bilateral cerebral hemispheres
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lesions that can cause dysfxn of RAS--> coma
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infratentorial destructive/mass lesion 2. compression by supratentorial process 3. late metabolic disorder
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lesions that can damage bilateral cerebral hemispheres--> coma
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metabolic 2. diffuse brain disease 3. supratentorial mass lesions
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best way to differentiate structural from metabolic coma?
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pupillary light refelx is resistant to metabolic insult EXCEPT in hypoxia or very late metabolic coma
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pupils in diencephalon coma
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small reactive
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pupils in midbrain coma?
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normal/large; fixed
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pupils in pons lesion coma?
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pinpoint; reactive
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pupils in CN3/uncal herniation lesion?
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ipsilateral dilating pupil
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dysconjugate idicates coma due to what?
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structural cause
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Doll's/Calorics in metabolic coma?
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Dolls- brisk/positive until late stages; caloric normal- deviate towards side of water
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Doll's/Calorics in MLF (pontine/medial mibbrain)
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Doll's-negative (ipsilateral eye can't adduct), Calorics-negative: both dysconjugate
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Doll's/Calorics in PPRF coma (mid to lower pontine)
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no response
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what is present in persistent vegatiative state?
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sleep-wake cycles, autonomic fxns, spontaneous smiling/crying
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what is absent in persistent vegatative state?
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awareness, purposef ful movement, concious experience of pain, sustained visual tracking (but may tun towards large sound)
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required for diagnosis of persistent vegatative state?
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>1 month, known cause, nothing reversible
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what causes persistant vegatative state?
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profound damage to subcortical whtie mater/thalamic relay nuclei
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what haps to be absent to call someone brain dead?
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apnea (PCO2>60), brain function, brainstem relfexes-pupils, OCR/VOR, corneal, gag, cough
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what can be present on brain dead people?
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spinal reflexes- BP, babinskin, knee jerk; slight respiratory movements; PUPILS MUST be midposition or dilated and fixed
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Triple Repeat Dz
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Fragile X, Hintington, Spinocerebellar ataxia
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clinical presentation of fragile X
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retardation, autism, ADHD, impiared motor skills, carniofacial ab, macroorchidism, joint abnormalities
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what sex is most affected by fragile X?
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males
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pathology of fragile X
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200-800 CCG repeats on X chromosome
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fragile X premutation?
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55-200 CCG repeates w/ adult onset ataxia/tremor/parkinsonism and some congnitive issues
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pathology of huntington's dz?
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CAG expansions
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juvenile Huntington's dz?
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55 + repeats giving parkinsonian dz- slow movements/dystonia/tremor (not chorea)
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pathology of spinocerebellar ataxia?
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glutamine repeats
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whend does huntingtons normally present in adults?
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40s
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what triplet repeat dz has anticipation phenomena?
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huntington
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sings of LMN/ peripheral NS floppy baby?
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coexistent weakness, reduced/absent reflexes, fasiculatios, contractures, no CNS features
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signs of UMN/cenetral NS floppy baby?
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hypotonia is more profound than weakness, increased/normal reflexes, seizures, lethargy/decreased alertness, no PNS features
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Broca's aphasia?
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expressive aphasia, ton-ton guy
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speech, comprehension, repetition, writing, reading, other signs in broca's aphasia
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nonfluent, normal comprhension, repeat single words, impaired writing,normal reading, right arm/face weakness
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speech, comprehension, repetition, writing, reading, other signs in Wernicke's aphasia?
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fluent speech, no comprehension, repeat only high frequency words, reading/writing impaired, other- visual field cut, sensory deficits on right side of body
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global aphasia?
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everything impaired, non-fluent; +/- right hemiplegia
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location of flobal aphasia?
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left perisylvian or separate frontal and temoroparietal damage
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conduct aphasia?
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lesion of connection betweeb Broca's and wernickes. Repetition is impaired . Speech has difficlt word finding/many phonemic paraphasias. May have cortical sesnory loss/weakness
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transcortical motor aphasia?
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broca's w/ normal repetition (repetition is normal, but output impaired). Difficulty initiating speech
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transcortical sensory aphashia?
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like wernicke's but normal repetiotn (repetition is normal but comprhension is imparied).
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mixed transcortical aphasia
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entire extrasylvian region; can ONLY repeat. Echolalia (parrot)
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which of 2 apahsia's recovers better?
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wernicke's
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bad prognostic signs for recovery of aphasia
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bad area, stroke, ischemia, over 12 yo
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meds for aphasia?
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donepizil: inhibits Ach
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typical neglect?
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left side neglect, right side lesion
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perceptual deficits in unilateral spatial neglect?
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extinction (can't detect 1 of 2 stimuli on opposite sides fo body), search imagery
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where is typial lesion of unilateral spatial neglect?
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right brain- parietal cortex, frontal lobe, basal ganglia, thalamus (if right side damaged, more sevre neglect)
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which part of unilateral nelect is lateral? Nonlateral?
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viligance is lateral (right hemisphere); spatial attention is bilateral (dorsal)
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nt w/ positive effect on neural plasticity?
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inc NorA, inc 5HT
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Nt w/ negative effect on neural plasticity?
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inc GABA, dec NorA, dec DA
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cardinal manifestations of parkinson's dz
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resting remor, bradykinesa/akineasia, postural instability,rigidity
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describe parkinson's tremor
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resting, 3-6 hz, assymetric, begins in limb
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describe parkinson's bradykinesia?
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assymetric, lower amplitude w/ repetition
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describe parkinson's rigidity
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uniformly increased resistance to passive range of motion; worse w/ reinforcement (i.e. opening hand)
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describe parkinson's posturablity
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fall back or forward, often on shoulder when preturbed. Most affected side of body is flexed. Sometime have freezing
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what makes parkinson's features worse? What makes them go away?
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stress/fatigue; sleep
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additiona not cardinal manifestations of parkinson's
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heat intolerance,convergence problems, soft, monotone speech, swallowing problems, drooling, ortostasis constipation, sexual dysfxn, anxiety/depression/ sleep problems/dementia
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how is parkinson's dementia different than AD?
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parkinson's has no tau
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etiology of parkinson's dz?
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white men, average 60 yo (some in 20s), welders, manganese workers, and pesticides, NE and midwest
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pathology of parkinsons
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1. syn nucleonopathy (apha-syn) 2. DA neuron loss in midbrain, substantia nigra, striatium--> lewy bodies w/ alpha-syn intranuclear cytoplasmic inclusions
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tx of parkinson's dz
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L-dopa + carbidopa (which blocks decarboxylase in the periphery); +/- MAOb or COMT inhibiton to stop increasing dose over itme (selegine/rasalgine)
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complication of parkinson's tx and tx for that
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dyskinesia ; tx w/ amantadine or deep brain stimulation
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how is essential tremor different than parkinson's
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symmetric, fast, action tremor
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how is multisystem atrophy different than parkinson;s?
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symmetric, fast autonically, no response to meds, wide gait
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how is progressive supranuclear palsy different than parkinsons
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symmetric, fast progression, no response to meds, eye movement probems
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how is cortical basal degernation different than parkinson's
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early assymetric morvement problems-dystonia, apraxia, myoclonus, alien limb syndrome, faster progressing of speech problems/dementia; no response to meds
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describe essential tremor
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3-8 hz but decreases w/ age; hand affected most; relieved by alcohol;
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etiology of essential tremor
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women age 45, but peaks in 2nd and 6th decade (when we are most neurotic, we get a tremor during action-we get it from our mamas) AD inheritance
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tx of essential tremor
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thalamic stimulation (TAPP the thalamus), topiramate, alcohol, primiridone, propanolol
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what is dystonia?
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segmental, generalized, or progressive syndrome of sustained muscle contraction that causes repetitive movements, twisting, or abnormal postures
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how to relieve cervical dystonia?
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touch chin, lean head on wall (cervical=neck)
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what are sone dystonia's responsive to?
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dopa
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most common type cause of larygeal dystonia? What does it sound like?
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adduct- voice gest tigher as cords jam together
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uncommon type of laryngeal dystonia? What does it sound like?
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abductor- harsh K's/Gs, sudden loss of voice, normal e's and wisphering
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Tx for dystonia
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botox, L-dopa (for responsive only), anticholinergics, gaba agonist,surgery/deep brain stimulation of globus pallidus, muscle relaxants
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types of dystonia in different populations?
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children more likely to have generalized; if it starts in face more likely to spread
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clincal manifestations of huntington's diseze?
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chorea, dementia, postural instability, and psychiatric abnormalities. Includes decreased saccades, dsyarthria/dysphasia, parkinsonism, dystonia, bradyphrenia, dementia, irrability, depression, psychosis
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etiology of huntingtons
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mean onset 40, juvenile onset 20
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differen in juvenile huntington's dz
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dystonia and bradykinesa (not chorea)
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genetics of huntington's dz
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>40 CAG expansions in IT15 gene on chromosome 4 polygultamine incorporated in huntington protein
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cut offs for levels of huntingto dz
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27-34 mutable; 36-39 require long life for manifestations
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pathology of huntington's dz
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loss of medium spiny nuerons in striatum; Putamen* and cuadate shrink. Striatal and cortical atrophy
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temporal pattern of dementia
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7-10 year course w/ insidious onset. Early-forgetfulnnes, socially withdrawn. Later- decline in orientation, executive fxn, reasoning, focus
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moderate vs. severe dementia
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moderate- only highly learned material recalled, supervised BADLs, no IADLs; severe- only oriented to self, akinetic mutism, no BADLs
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risk factors for AD
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age, insulin resistance, metabolic syndrome, CVD risk factors, genetics-APOE4, APP, PSEN 1/2
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decreased risk for AD
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APOE2, good diet, moderate alcohol intake, good lifestyle
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genetic disorders associated w/ AD
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down's syndrome (all develop AD);APOE4 (polymorphism), APP, PSEN2 (single gene mutation
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most reatable form of MS?
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relapsint-remiting
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gender prevalance in MS
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motstly females except primary progressive type
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tx of relapsing-remiting MS?
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beta-interferons, copaxome, natalzuman; steroids during attacks
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which type of MS has no tx?
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primary progressive
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initial sx of MS lsion?
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limb weakness; optic neuritis/diploplia/poor vision; weird sensory feelings; vertigo, bladder problems--> white matter signs
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white matter signs of MS?
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bilateral INO; hyperreclexia, clonus,spaticity, baiskin; posterior column sensory deficits vibration> proprioception; cerebellar problems-tremor,dysmetria
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location of lesions in <S
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perivascular cuff's (dawson's finger)-corpus callosum, optic nerve, cervical region of spinal cord (CNS dz of white matter)
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exam findints of optic neuritis
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dic pallor, afferent pupil deficit (less constriction); red desaturation; worse w/ heat-Uthoffs; central sarcomas=blind spots
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*** most common cause of bacterial meningitis in neonates
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Group B strep, e. Coli, Listeria monocytogenes
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***most common cause of bacterial meningitis in 1 month-5 years
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Nisseria meningitis, Strep pneumonia, flu b
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***most common cause of bacterial meningitis in >5 years
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Strep pneunomiea, Nisseria meningitis, listeria monocytogenes
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clinical features meningitis in general
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headache, fever, stiff neck, confusion/stupor/seizure
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clinical features bacterial meningitis?
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acute, aggressive, progressive dz
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CSF profile of bacterial meningitis
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elevated pressure, elevated cells, PMN predominant, high protein
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tx of bacterial meningitis
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high dose antibiotics- 3 generation cephalosporin (cetriaxone) + amplicin w/ monocytogenes + IV vanc is nosocomia; fluid restriction due to sIADlowering Na, Steroid if deteriorating
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t/f cultures are important w/ bacterial meningitis?
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TRUE
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most common cause of fungal meningitis?
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cryptoccocal
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clinical features of fungal meningitis?
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insidious, subacute (2-6 week course); usually in immunocrompromised; variably intense sx
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CSF profilfe of fungal meningitis?
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pressure variably elevated, mildly elvated cell count w/ no RBC; protein elevated, glc supressed
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Tx of fungal meningitis?
|
amphotericin b(IV) + flucytosien (oral); lubar puncture to reduce ICP, occational corticosteroid
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viral meningitis CSF profile?
|
normal pressure; cell count slightly elevated w/ very early PMN predominantcs; normal glc and protein (slightly high)
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tx viral meningitis?
|
none; aseptic meningitis. Not ciritcal
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clinical features of proazoa infections?
|
high mortality
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CSF of protazoa infections?
|
amoeba
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treatment of protazoa infection?
|
amphotericin b(IV) + flucytosien (oral); lubar puncture to reduce ICP, occational corticosteroid
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clinical presentation of herpes enchepalitis?
|
most common non-seasonal cause; mental statu change, fevers, seizures-acute and aggressive
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CSF of herpes enchepalitis?
|
increased pressure; slightly elevated cell count, may have red cells; elevated protein; normal or low glc
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tx of herpes encephalitis?
|
acytlovir
|
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clinical features of west nile?
|
focal progressive prain dz symptoms, can be fatal
|
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tx west nile?
|
supportive care
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clinical features of prion dz?
|
devastating neurological deterioration that normally kills pt I 6 months-2 years
|
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tx prion dz?
|
none; aseptic meningitis. Not ciritcal
|
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clinical feature of spinal epidural abcess?
|
back pain that often occurs in kids w/ mild infectious source like acne/staph auerus- don't look at CNS
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tx of herpes zoster?
|
acytlovir
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tx of CMV (HIV complication?
|
ganglicylovir
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Tx of toxoplasmosis (HIV complication from poorly cooked meat)
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