FINAL NEURO

thrombotic-most often from atherosclerosis (carotid arteries)

embolic-thrombus travels from distant site (atrial fibrillation, DVT, heart valve vegetation or mechanical valave replacement

Caused from intracerebral hemorrhage

high mortatlity due to sudden onset

-long standing HTN=primary cause

-cerebral aneurysms cause it

-arterio/venous malformations cause it

when change of brain tissue, CSF, or blood-

1. edema of brain tissue due to increase in cap. pressure (aka vasogenic edema) or cytotoxic swelling

-(stroke, ischemia, HTN, global ischemia,

2. space occupying processes-tumors, hematomas, abscess

3. accumulation of CSF

headache  vomiting, no nausea  decreased LOC

visual changes    pupillary response declines    changes in resp.  Cheyne-Stokes

Coma

level of consciousness motor testing

-total score=15

(mild neurological dysfunction=12-14

(moderate=9-12)

(severe= less than or equal to 8)

1. Epidural

2. Subdural

3. Subarachnoid

Common cause is skull fracture

Arterial bleeds can expand rapidly & cause acute deteriorization

between dura & arachnoid

venous bleed is common with slower onset--pressing on brain more alot of veins in this area

-acute is within 24 hrs worse prognosis

-subacute is 2-10 days of symptom onset

ex. elderly falls at home and is on anticoagulants

-between subarachnoid & pia mater

-seen as BLOODY CSF

-common with rupture of Cerebral aneurysms or arterio/venous malformations (do lumbar tap and suck off some CSF-look for blood)

-surgery/evacuation of hematoma

-repair skull fracture

-craniectomy

-drainage of CSF

-induce coma (allow brain to rest for a while),

-hypoventilation

-hypothermia

-diuresis

transient event

-sudden explosive discharge of cerebral neurons

-motor or sensory function, sensation, autonomic function, behavior or consciousness

Both hemispheres affected with symmetricalmvmts

ABSENCE-brief staring spell

MYOCLONIC-jerking mvmt of specific muscle groups

ATONIC: drop attacks, loss of muscle tone

TONIC/CLONIC:  loss of consciousness, muscle rigidity (tonic phase) followed by rhythmic contractions (Clonic phase)

Progressive decline of mental processes, esp. memory & cognition

-alzheimers

-vascular type dementia

Patho-:

-intracellular neurofibrillary tangles and presence of extracellular amyloidal plaques

-brain atrophy

-frontal and temporal/parietal portions affected

-gradual onset with progressive decline

-short term memory loss

-decrease ability to function at work & in social situations

-loss of ability to maintain ADLs

(difficulty eating--incontinence

degeneration of dopamine secreting pathway in substantia nigra of the brain

1. RESTING TREMORS (pill rolling)

2. MUSCLE RIGIDITY (trouble moving)

3. BRADYKINESIA (slow mvmt)

no cure

-levadopa/carbidopa (SINIMET)

(precursor to dopamine)

Dopamine agonists-mirapex

-slowly lose efficacy over time

(levadopa changes very quickly-carbidopa helps slow that down to correct rate)

Related to inflammation & scarring of myelin sheath covering nerves

-age of onset (20-50yrs.)

primarily affects optic & oculomotor nerves, corticospinal nerves, & cerebellum

-MOTOR DYSFUNCTION (weakness, spasticity, paralysis, abnormal gait

-SENSORY- shock sensations, decreased sensation to temp

-VISION-blurred vision, blind spots

-CEREBELLAR FUNCTION-tremor, lack of coordination, gait disturbance

-relapsing/remitting  (may go months to yrs without attack)

-steady decline in neurological function

-hyperflexion: associated with most severe deficits

-Hyperextension: most common

-Compression

flaccid paralysis

loss of reflexes

loss of bladder and bowel control

return may be complete or partial- may involve spasticity with hyperreflexia

progressive paralysis over 1-3 wks-maybe longer

progress to resp. failure maybe and autonomic instability & cardiovascular collapse

resolves spontaneously

-decreased cerebral flow, number of neurons, synthesis of metabolism of neurotransmitters, degeneration of myelin sheath and neurofibrillary tangles in hippocampus