Parkinson's disease is a chronic degenerative disorder of the _________ that produces _______ problems
CNS
What is the cause of PD?
unknown
Primary or idiopathic PD thought to have ______ and ______ factors
genetic
T/F: exposure to specific viruses and toxins can damage cells and activate PDTrue False
True
Characteristics of secondary PD (not true PD)
encephalitis/meningitis
Risk factors of PD (4)
age
Incidence/prevalence of PD
increases with age
PD is the disruption of which motor system?
extrapyramidal motor system
Pathophys of PD
substania nigra in basal ganglia contain dopamine, dopamine is an inhibitory NT that controls movement, cells that have decreased dopamine become overly excited
Overly excited neurons cause what?
movement and postural abnormalities
Lewy bodies are what?
clumps of proteins found in the brain of most PD patients
Early signs/symptoms (5) of PD
fatigue
Clinical features (5) of PD
pill rolling
Tremors (affect where first?)
affect hands, arms, leg first
PD posture
stooped, leaning forward, head and neck flexed
non-motor functions
dysarthria
co-morbidities (4) of PD
dementia
Tests of PD
currently no diagnostic tests but can use MRI, EEG, CAT
Stages of PD (5)
1-unilateral
Sub-types of PD
juvenile-extremely rare
prognosis of PD
no cure
treatments of PD
meds (levidopa, dopamine agonists, anti-cholinergics, MAO-Binhibs, NMDA, glutamate)
causes of Alzheimers
exact cause is unknown
mutations on which chromosomes contribute to Alzheimers?
1, 14, 21, 19
T/F: People with Down syndrome have an increased chance in developing Alzheimers?True False
True
which lifestyle factors can contribute to Alzheimers?
obesity, smoking, diabetes, stress
Environmental factors which can cause Alzheimers?
viruses, metals (zinc, aluminum)
Prevalence of Alzheimers
1 in 8 people over 65 has AD
7 stages of AD
1-none 2-very mild cognitive decline 3-mild cognitive decline (friends family become aware of decline) 4-moderate cognitive decline-(detectable by medical interview) 5-moderately severe cognitive decline-noticeable gaps in memory/thinking, need assistance w/ ADLs 6-severe cognitive decline-decline in memory, may have personality changes 7-very severe cognitive decline-
amyloid plaques
beta-amyloid proteins
neurofibrillary tangles
tau proteins
NT's affected
decrease in Ach in baslis nucleus of meynert serotonin in median raphe NE in locus cerulues
Tests of AD
only true test is by an autopsy
Early signs of AD
language problems (foregetting names of common things)
middle signs of AD
forgetting details about current events/past events
severe AD
cant understand language
subtypes of AD
early onset -progresses rapidly appears before 60 hereditary link late onset -more common develops after 60 may be hereditary
co-morbidities of AD
depression
treatments of AD
Ach esterase
background of MS
demyelination of brain, spinal cord, cranial nerves
etiology of MS
unknown cause but may appear as autoimmune
incidence/prevalence of MS
more common in white people
Relapsing-remitting MS
most common form
Primary progressive MS
progression of disability from onset without plateaus of remissions but can have periods of stabilization
Secondary progressive MS
begins as relapsing remitting followed by progression of disability that may include occasional relapses , minor remissions and plateaus
progressive-relapsing MS
least common
Pathophys of MS
autoimmune
plaques are what and where are they found?
seen in lateral ventricles of brain, brain stem and optic nerve
Testing for MS
history
Clinical features of MS
blurred vision is common 1st sign due to plaques on corticospinal tract
motor symptoms of MS
paraperesis or paraplegia more common than UE weakness
coordination symptoms of MS
gait imbalance
co-morbidities of MS
depression
Treatments of MS
no specific treatment at this time
Goals of MS (4)
improve speed of recovery from attacks
What happens to nerve axons of patients with MS during remission?
limited remyelination
definition of ALS is....?
progressive neurodegenerative disease that attacks nerve cells in the brain and spinal cord resulting in muscle weakness and atrophy
amyotrophic =?
muscle wasting
sclerosis =?
hardening of the lateral corticospinal tract
cause of ALS
90% is unknown
Incidence of ALS
40-60 yrs old
course of ALS
no 2 people go through the same course of ALS
ALS is a _________ disease
neurodegenerative
ALS degenerates both _________ and ________motor neurons
upper and lower
as motor neurons degenerate the anterior and lateral columns of the spinal cord are replaced by fibrous ______ causing hardening of these areas
astrocytes
Wallerian Degeneration =?
process by which motor axons die
Upper motor neurons
degeneration of corticospinal upper motor neurons
loss of these leads to: spastic paralysis hyperreflexia stiffness
lower motor neurons
degeneration of lower motor neurons that reside in anterior horn of spinal cord and in brainstem
loss of these leads to: flaccid paralysis decreased muscle tone decrease reflexes muscle weakness muscle atrophy
progressive bulbar palsy
bulbar involvment (facial muscles)
progressive muscle atrophy
pure lower motor neuron degeneration
primary lateral sclerosis
pure upper motor neuron degeneration
ALS do not affect (4)
1-cranial nerves
diagnostic tests for ALS
determined by ruling out all other tests
early stage clinical features of ALS
painless, weakness and difficulty breathing
middle stage features of ALS
symptoms worsen
final stage clinical features of ALS
paralysis of voluntary muscles
Sporadic ALS
most common form
Familial ALS
gene related
Guamanian ALS
extremely high incidence in Guam
co-morbidities
anxiety
