chapter 45 Flashcards
seizure disorder
transient neurological event of paroxysmal. abnormal or excessive electrical discharges
manifestions of seizure disorder
disturbances of
- skeletal motor function
- sensation
- autonomic visceral function
- behavior
- consciousness
epilepsy or seizure disorder
recurrent seizures
seizure disorder acquired by
cerebral injury pathologic process -lesion, tumor -blood clots -infection
seizures are classified by
s/s and EEG features
manifestations determined by area of brain involved, area of origin, and areas to which seizure spreads
generalized seizure
whole brain affected metabolic or toxin induced thalamus and reticular activating system: LOC includes - absence (petite mal) - atypical absence - myoclonic - atonic (drop attack) - tonic-clonic (grand mal)
absence (petite mal) seizure
- children
- sometimes identified in children with poor academics
- brief: 2-10 seconds
- staring spells
- unaware of surrounding
atypical absence seizure
accompanied by myoclonic jerks and automatisms
- lip smacking, repetitive seemingly voluntary movement.
myoclonic seizure
extremely brief
single jerk or multiple jerks of one or more muscle groups
atonic seizure
sudden complete loss of muscle tone
-falls
tonic-clonic (grand mal) seizure
sudden LOC muscle rigidity (tonic phase) - lasts 10-15 seconds clonic activity - voilent rhythmic contractions - 1-2 minutes - apnic
status epilepticus
continuing seizures without period of recover between
irreversible brain damage, possible death from hypoxia, dysrhythmia, lactic acidosis
partial seizures
activity in one brain hemisphere
- simple partial
- complex partial
- partial seizures secondarily generalized
simple partial seizure
no change in LOC s/s: motor, sensory, autonomic, or combined - motor: may be limited to one body part - sensory: tingling or numbness ---auditory sounds ---olfactory ---visual manifestation -autonomic: pupil dilation ---sweating, flushing ---respiratory changes
complex partial seizure
different combos of cognitive, affective, and psychomotor
- loss or altered LOC
- can be aggressive
- postictal stage
partial seizures secondarily generalized
begin as simple partial and progress to involve both hemispheres
Dx seizures
Pt history
neuro exam
EEG
seizure tx
maintain airway
protect from injury
identify location focus
anticonvulsants
dementia
syndrome associated with many pathologic processes
progressive deterioration and decrease of memory and other cognitive changes
personality and behavior changes
causes/types of dementia
alcoholism tumor hydrocephalus parkinsons lewy body huntingtons Multiple sclerosis pick disease
hallmark structural changes of dementia
intracellular neurofibrillary tangels and extracellular amyloid plaques.
neuroinflammation
vascular dementia
single cerebrovascular insult multiple lucunar infarcts microvascular pathology - risk: --stroke --HTN --diabetes
manifestations of dementia
- gradual onset with chronic decline in cognitive function
- memory loss, especially ST memory
- thinking ability decline
- decrease function at work/social settings
- anxiety, agitation
- difficulty with judgement, problem-solving, communication
Dx of dementia
Hx and physical
CT, MRI
mental status
Tx of dementia
2 drug classes acetylcholinesterase inhibitors - mild to moderate alzheimers -stabilize cognitive function -slow progression N-methyl-D-asparate (NMDA) receptor antagonist - moderate to severe alzheimers -blocks stimulation by glutamate -slows progression
vascular dementia tx
reduce risk of cerebral damage
control BP, blood sugar, and lipids
Parkinson’s
mobility disorder idiopathic or acquired - infection - intoxication - trauma degeneration of pigmented dopaminergic neurons found in substantia nigra and elsewhere in brain
parkinsons s/s
early signs - loss of flexibility - aching - fatigue initally worse on one side of body tremor-generallly at rest, unilaterally affecting distal extremity bradykinesia regidity loss of facial expression later stage - small handwriting, evidence of tremor -low volume speech, monotonous, mumble -bradykinesia effects swallowing, and level of mobility -drooling, aspiration risk -falls -dementia
tx parkinsons
no cures slow progression - increase dopamine in CNS --dopamine does not cross BBB ---levodopa and carbidopa combined will cross BBB and then convert to dopamine
cerebral palsy
diverse group of crippling syndromes that appear in childhood and involve permanent, non-progressive damage to brain.
damage to upper motor neurons
-voluntary and involuntary movement
cerebral palsy classified based on
neuro s/s - spasticity - ataxia - dyskinesia or combo
Spastic cerebral palsy s/s
most common
- hypertonia
- prolonged reflexes
- increased deep tendon reflexes
- clonus
- rigidity of limbs
- scoliosis
- contractures
- scissors gait, toe walking
- spastic paralysis
- hemipegia, paraplegia, triplegia, quadriplegia
dyskinetic/athetoid cerebral palsy s/s
difficulty with purposeful movement and fine motor skills
slow, jerky, uncontrolled, abrupt movements
- injury to basal ganglia or extrapyramidal tracts
ataxia cerebral palsy s/s
gait disturbances
instability
hypotonia at birth, stiffness of trunk in infancy
pure ataxia cerebral palsy s/s
maldevelopment of the cerebrum or its pathways
-cognitive impairment
common cerebral palsy s/s
seizures intellectual difficulty visual problems orthopedic disabilities hearing impaired communication disorder respiratory problems bowel/bladder problems
tx of cerebral palsy
goal to increase functionality muscle relaxers selective dorsal rhizotomy botox - reduce pain and increase ROM anticonvulsants orthopedic surgery, casts, braces, traction
selective dorsal rhizotomy
portion of dorsal roots of lumbar spine cut
- decreases spasticity in cerebral palsy
hydrocephalus
abnormal accumulation of CSF in cerebral ventricular system
associated with congenital defect, usually neural tube
-viral infections of neruotoxic agent during pregnany
-occasionally in adults from
lesions, trauma, hemorrhage, infections: meningitis
3 types of hydrocephalus
normal pressure
obstructive/noncommunicating
nonobstructive/communicating
normal pressure hydrocephalus
increased CF volume without change in intracranial pressure because brain tissue has been lost
- abnormal absorption of CSF
- -ventricles distend, compressing brain tissue and vessels
s/s of normal pressure hydrocephalus
gait instability
urinary incontinence
dementia
obstructive/noncommunicating hydrocephalus
most common in children
abnormal cerebral aqueduct or lesion in 4th ventricle
- congenital
obstruction of CSF flow
nonobstructive/communicating hydrocephalus
abnormal capacity to absorb fluid from subarachnoid space
- infection, trauma, tumors
tx of hydrocephalus
surgical correction with shunting
cerebellar disorders myriad causes
abscess hemorrhage tumor trauma viral infection chronic alcoholsim
cerebellar disorder s/s
ataxia hypotonia intention tremors gait disturbances balance disturbance staggering/lurching clumsy
multiple sclerosis
chronic demyelinating disease of CNS
significant disability in young adults
autoimmune: inflammation and scarring of myelin sheaths covering nerves
multiple sclerosis s/s
vary daily can be mild or extreme slow or interrupt conduction of nerve impulses -imparied vision -weakness/numbness -spasticity -gait disturbance -bowel/bladder maybe -tingling -fatigue -imbalance -movement disorders
relapsing-remitting MS
most common form
defined exacerbations with acute decline in neuro function
followed by periods of partial/complete recovery and remissions
primary progressive MS
slow but continuous decline in neuro function
plateaus may occur
severe disability develops
secondary progressive MS
approx. 50% of relapsing-remitting pt develop this form
- begins as relapsing-remitting; followed by steady decline in neuro function with or without occasional relapses, remission, or plateaus
progressive relapsing MS
progressive from outset, but with clear exacerbations with or without recovery.
tx of MS
managing symptoms
minimize damage inflicted by autoimmune attack
spina bifida
defective closure of the bony encasement of spinal cord (neural tube)
-spinal cord and meninges may or may not protrude
further classified by neural involvement
spina bifida occulta
anomaly not visible
spina bifida cystica
external protrusion
spina bifida environmental and genetic factors
vitamin deficiency: folate
anticonvulsants
chromosomal abnormalities
maternal obesity and diabetes
spina bifida occulta s/s
change in skin and body hair - coarse or silky hair along spine midline dimple cutaneous port-wine angioma subcutaneous mass- lipoma or demoid cyst usually no serious neuro problems gait disturbances positional deformity of feet bowel/bladder dysfunction
spina bifida cystica (meninogocele)
saclike cyst filled with CSF protrudes through spinal defect, does not involve spinal cord
spina bifida cystica (myelomeningocele or meningomyelocele)
deformity contains meninges, CSF, and portion of spinal cord
spina bifida cystica s/s
permanent neuro dysfunction motor weakness or paralysis sensory deficit below defect bowel/bladder dysfunction scoliosis hydrocephalus seizures worsen as child grows and cord ascends -pulling at scar tissue and tethering cord.
spina bifida tx
severity of defect and neuro dysfunction
supplement folic acid: prevent
amyotrophic lateral sclerosis (ALS)
- progressive degenerative disease affecting upper and lower motor neurons
- characterized by muscle wasting and atrophy of hands, arms, and legs
- some cases cognitive changes and dementia
- progressive paralysis and death
hallmark of ALS
misfolded protein aggregate inclusions in affected motor neurons and glial cells
ALS s/s
muscle weakness and atrophy muscle twitching, cramping, stiffness hands/upper limbs affected first hyperreflexia in a weak atrophied extremity die of respiratory failure maintain sensory and cognitive function
ALS tx
glutamate inhibitor
-prolongs life
bell palsy
acute idopathic paresis or paralysis of facial nerve with inflammatory reaction at or near stylomastoid foramen or in boney facial canal
-compression, ischemia, demylination
bell palsy risk factors
diabetes
hypothyroidism
pregnancy
bell palsy s/s
rapid over 24-48 hours
unilateral facial weakness with facial droop and diminished eye blink
bell palsy tx
spontaneous recovery approx. 3 weeks
prevention of corneal damage (unable to blink)
- drops, ointment, eye patch
corticosteroids
