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alzheimer disease AD
progressive neurodegenerative disease of brain
60-80% all cases of dementia
cortical degeneration in frontal lobes
atrophy in all areas of cortex
two forms of AD
familial
sporadic
two categories of genes have a direct link to AD development
risk genes
deterministic genes
cause of AD
unknown
AD common risk factors
advanced age over 80
genetic factors- APOE epsilon 4 allele
down syndrome
exposure to aluminum
traumatic brain injury
cardiovascular disease
diabetes
dyslipidemia
early changes AD
memory loss that affects job skills
difficulty performing familiar tasks
difficulty learning and retaining new information
inability to concentrate
deterioration in personal hygiene and appearance
AD signs as disease progresses
degenerative disorder of frontal lobe
difficulty with abstract thinking and activities that require judgment
progressive difficulty in communicating
severe deterioration of memory, language and motor function
repetitive actions
restlessness, wandering
irritability, depression, mood swings, paranoia, hostility, combativeness
nocturnal awakenings
disorientation
preclinical ad
before memory loss and confusion about time and place develop
mild cognitive impairment MCI due to AD
mild changes in memory and thinking ability
small personality changes and forgetfulness
decrease in ability to plan and organize
dementia due to AD
thinking impairment
memory impairment
behavioral changes that impair ability to function in daily life occur
severe impairment in cognitive function and inability to perform self-care activities
treating AD
no cure
cholinesterase inhibitors
memantine
monoclonal antibody type agents mAbs
cholinesterase inhibitorys AD
donepezil, rivastigmine, galantamine
prevent breakdown of acetylcholine and keep its levels high
memantine
uncompetitive low-to-moderate affinity N-methyl-D-aspartate receptor antagonist
regulates activity of glutamate which is involved in info processing storing and retrieval
monoclonal antibody type agents mAbs
aducanumab
lecanemab
immuse response againts beta-amyloid proteins
common signs of dementia
amnesia
anomia forgetting names of people and objects
apathy
apraxia- inability to perform simple actions
agnosia- inability to recognize familiar objects and their purpose
tests for AD
PET scan
CT scan
MRI
EEG
CSF
cerebral blood flow studies
blood biomarkers
PET scan AD
positron-emission tomography scan measures metabolic activity of cerebral cortex and may help confirm early diagnosis
CT scan AD
computed tomography scan may show more brain atrophy than what occurs in normal aging
MRI
magnetic resonance imaging evals condition of brain and rules out intracranial lesions as source of dementia
EEG
evaluates brain electrical activity and may show brain wave slowing late in disease
helps to differentiate tumors, abscesses, and other intracranial lesions that might cause symptoms
CSF analysis AD
shows beta-amyloid and tau proteins
helps determine whether signs and symptoms stem from a chronic neurologic infection
cerebral blood flow studies may detect abnormalities in
blood flow to brain
potential diagnostic tools under investigation include blood biomarkers that show
level of beta-amyloid and tau protein accumulation and biomarkers that show injured or actually degenerating nerve cells
amyotrophic lateral sclerosis
aka Lou Gehrig disease
progressive neurodegenerative disease that affects motor nerve cells of brain and spinal cord
motor neurons eventually die and voluntary muscle movement is impacted
two types of als
sporadic
familial
familial als
disease is inherited
als causes
gene mutation
chemical imbalance from higher levels of glutamate
accumulation of abnormal forms of proteins which destroy nerve cells
autoimmune disorders
precipitating factors for acute deterioration in als
trauma
viral infection
physical exhaustion
als signs and symptoms
muscle weakness
difficulty walking, clumsiness, muscle twitching, muscle spasms
impaired speech
difficulty chewing and swallowing
difficulty breathing
choking
excessive drooling
depression
inappropriate laughing
crying spells
treating als
no cure
drug therapy
stem cell
tests to diagnose als
electromyography
muscle biopsy
csf analysis
neurologic examination
bell palsy
aka acute peripheral facial paresis
facial nerve disorder
inflammation of cranial nerve VII on one side of face in absence of stroke or other disease
cause of bell palsy
unknown
risk factors bell palsy
being in third trimester of pregnancy
early postpartum
older adults
people w diabetes or hypothyroidism
persons with tick bite
etiology of bell palsy
unknown
suggestion of acute demyelination of nerves s
strongest supported cause of als
reactivation of herpes simplex virus isoform HSV1
reactivation of herpes zoster virus HZV
has been linked to lyme disease
signs and symptoms als
rapid onset of facial weakness on one side
pain around and behind ear
recent viral illness or tick bite
numbness of face, tongue, and ear
ringing in ear
headache
hearing deficit in ear on affected side
drooping of mouth
inability to close eyelid on affected side
tests for als
MRI
CT
blood tests
bell palsy is considered
benign
most recover 3 weeks to 6 months
epilepsy
aka seizure disorder
neurologic disorder where brain activity is abnormal causing seizures
epilepsy is diagnosed if a patient has
two unprovoked seizures occurring more than 24 hours apart
a single unprovoked seizure if recurrence risk is high
diagnosis of an epilepsy syndrome
seizures
paroxysmal events associated with abnormal electrical discharges of neurons in brain
discharge may trigger a convulsive movement, an interruption of sensation, an alteration in consciousness, or combination of these
epilepsy causes
no known cause
seizures are caused by abnormal brain activity
in about 50% cases
epilepsy has no known causes
possible causes of epilepsy
genetic influences
perinatal injuries
metabolic abnormalities
brain conditions
infections
traumatic brain injury
ingestion of toxins
status epilepticus
continuous seizure state that must be interrupted by emergency measures
4 phases of emergency treatment for status epilepticus
stabilization phase
initial therapy phase
second therapy phase
third therapy phase
types of seizures
partial seizures
Jacksonian seizure
sensory seizure
complex partial seizure
secondarily generalized seizure
generalized seizures
absence seizure
myoclonic seizure
generalized tonic-clonic seizure
akinetic seizure
treating epilepsy
drug therapy
surgery
tests for epilepsy
EEG
CT scan
MRI
serum glucose studies
calcium studies
skull xrays
lumbar puncture
brain scan
guillain-barre syndrome
GBS aka acute inflammatory demyelinating polyneuropathy AIDP
rapidly progressing acute autoimmune process occurring every few days to weeks following a viral or bacterial infection
GBS 3 phases
acute phase- first definitive symptom develops and ends 1-3 weeks later when no further deterioration is noted
plateau phase lasts several days to 2 weeks
recovery phase- remyelination and axonal process regrowth, can last 4 months to 3 years
cause of GBS
unknown
thought to be cell-mediated, immunologic attack on peripheral nerves in response to a virus or other cause of cell injury
signs and symptoms of GBS
tingling and numbness
muscle weakness
immobility
paralysis
muscle stiffness and pain
sensory loss
loss of position sense
diminished or absent deep tendon reflexes
tests to diagnose GBS
csf analysis
electromyography
electrophysiologic testing
treating gbs
endotracheal intubation
tracheotomy
most recover spontaneously
meningitis
brain and spinal cord meninges become inflamed
blood flow to brain is reduced
origin of meningeal inflammation may be
bacterial
viral
protozoal
fungal
most common causes of meningitis
bacerial
viral
risk factors for meningitis
malnourishment
immunosuppression
cns trauma
signs and symptoms of viral meningitis
drowsiness
confusion
stupor
slight neck or spine stiffness
headache
nausea
vomiting
signs and symptoms of meningitis
headache
stiff neck and back
malaise
photophobia
chills
fever
vomiting
twitching
seizures
confusion or delirium
fretfulness
bulging of fontanels
refusal to eat
signs of meningitis
Brudzinski sign
Kernig sign
tests to diagnose meningitis
lumbar puncture
CT scan
MRI
EEG
chest xrays
sinus and skull xrays
WBC count
CT scan
blood cultures
treating meningitis
prevention and vaccinations
MCV4 vaccine
MPSV4 vaccine
serogroup B meningococcal vaccines
antibiotics
bed rest
hypothermia
fluid therapy
migraine
episodic neurologic disorder characterized by a headache lasting 4 to 72 hours
people who menstruate may experience migraines
more frequently before and during menstruation or report a decrease during pregnancy and menopause
migraine phases
premonitory phase'/prodome
migraine aura
headache phase
recovery phase/postdrome
diagnosis of migraines
made from medical history and physical exams
EEG and imaging
management of migraines
avoiding triggers
use pharmacologic management
using transcutaneous electrical stimulation devices providing trigeminal nerve stimulation
multiple sclerosis
MS
results from progressive demyelination of white matter of brain and spinal cord leading to widespread neurologic dysfunction
causes of MS
unknown
autoimmune disorder in which antibodies destroy myelin sheaths around sensory and motor neurons
trigger for development of antibodies is unknown
genes may be a part
signs and symptoms of MS depend on four factors
extent of myelin destruction
site of myelin destruction
extent of remyelination
adequacy of subsequent restored synaptic transmission
treating MS
no cure
drugs
bed rest
massage
prevention of fatigue and rpessure ulcers
tests to diagnose MS
MRI
CSF analysis
evoked potential tests
myasthenia gravis
autoimmune disease which produces sporadic progressive weakness and abnormal fatigue of voluntary skeletal muscles
causes of myasthenia gravis
unknown
commonly accompanies autoimmune disorders and disorders of thymus
signs and symptoms of myasthenia gravis
extreme muscle weakness
fatigue
ptosis
diplopia
difficulty chewing and swallowing
sleepy masklike expression
drooping jaw
bobbing head
arm or hand muscle weakness
two crises of myasthenia gravis
myasthenic crisis
cholinergic crisis
test used to differentiate two types of crises
edrophonium test
treating myasthenia gravis
anticholinesterase drugs
plasmapheresis
thymectomy
endotracheal intubation and mechanical ventilation
tests to diagnose myasthenia gravis
edrophonium test
electromyography
nerve conduction studies
chest xray or CT scan
parkinson disease PD
progressive muscle rigidity
loss of muscle movement
involuntary tremors
causes of pd
unknown
genetic and environmental factors
signs of pd
muscle rigidity
akinesia
pill-roll tremor
high-pitched monotone voice
drooling
dysarthria
dysphagia
fatigue
muscle cramps
oily skin
increased perspiration
insomnia
mood changes
treating pd
drugs
physical therapy
stereotactic neurosurgery
pd
urinalysis
CT scan
MRI
stroke
cerebrovascular accident cva or cerebral infarct
sudden impairment of cerebral circulation in one or more of blood vesels supplying brain
stroke can be due to either of two processes
ischemic stroke
hemorrhagic stroke
transient ischemic attack tia
caused by a temporary interruption of blood flow
patient recovers circulation and has no neurological deficit
factors that increase risk of stroke
history of TIA
atherosclerosis
hypertension
arrhythmias esp atrial fibrillation
carotid artery stenosis
rheumatic heart disease
diabetes mellitus
orthostatic hypotension
cardiac enlargement
high serum triglyceride levels
lack of exercise
hormonal contraceptive use
drug misuse
smoking
family history of cerebrovascular disease
sickle cell disease
top 3 causes of stroke
thrombosis
embolism
hemorrhage
most common artery affected by either ischemic or hemorrhagic stroke
middle cerebral artery
tests to diagnose stroke
CT scan
cerebral angiography
digital subtraction angiography
PET scan
single-photon emission computed tomography
MRI
magnetic resonance angiography
transcranial Doppler studies
cerebral blood flow studies
ophthalmoscopy
EEG
treating stroke
physical rehabilitation
dietary and drug regimens
surgery