Parkinson's disease is a chronic degenerative disorder of the _________ that produces _______ problems



What is the cause of PD?


Primary or idiopathic PD thought to have ______ and ______ factors



T/F: exposure to specific viruses and toxins can damage cells and activate PD
True False


Characteristics of secondary PD (not true PD)




vascular disease

exposure to toxins

antipsychotic medications

over-dose of narcotics

repeated chronic head trauma

Risk factors of PD (4)




exposure to environmental toxins

Incidence/prevalence of PD

increases with age

men are more likely to develop PD

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

result from decreased NE

Early signs/symptoms (5) of PD


muscle weakness

muscle aching

decreased flexibility

less spontaneous change in facial expression

Clinical features (5) of PD

pill rolling

increased muscle rigidity

difficulty initiating movements


loss of automatic movements

Tremors (affect where first?)

affect hands, arms, leg first

then progress to jaw tongue forehead eyelids

PD posture

stooped, leaning forward, head and neck flexed

non-motor functions


voice low

chewing/swallowing issues

masked face


memory loss

co-morbidities (4) of PD


UTI/ respiratory infections


disturbed sleep, fatigue

Tests of PD

currently no diagnostic tests but can use MRI, EEG, CAT

Stages of PD (5)



3-balance problems develop, ambulate w/o assistance

4-assistance needed during ambulation

5-w/c bound

Sub-types of PD

juvenile-extremely rare

early onset-rare

prognosis of PD

no cure

case by case basis

treatments of PD

meds (levidopa, dopamine agonists, anti-cholinergics, MAO-Binhibs, NMDA, glutamate)

deep brain stimulation-brain pacemaker


causes of Alzheimers

exact cause is unknown

genetic, environmental, lifestyle factors can contribute

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


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

more women then men

more education = less chance for AD

7 stages of AD

1-none2-very mild cognitive decline3-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/ ADLs6-severe cognitive decline-decline in memory, may have personality changes7-very severe cognitive decline-

amyloid plaques

beta-amyloid proteins

found in extracellular CNS

stimulates production of free radicals

neurofibrillary tangles

tau proteins

lead to cell death

NT's affected

decrease in Ach in baslis nucleus of meynert

decrease in serotonin in median raphe

decrease in 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)

forgetting where you placed an object

lost on familiar trips

personality changes/social impairments

loss of interests

middle signs of AD

forgetting details about current events/past events

change in sleep patterns

reading/writing impairments


increased difficulty with ADLs

severe AD

cant understand language

cant recognize family members

cant perform ADLs

subtypes of AD

early onset-progresses rapidly appears before 60hereditary link
late onset-more commondevelops after 60may be hereditary

co-morbidities of AD



muscle contractures

broken bones

loss of social instabilities

treatments of AD

Ach esterase


Vitamin E



background of MS

demyelination of brain, spinal cord, cranial nerves

characterized by remissions, exacerbations

etiology of MS

unknown cause but may appear as autoimmune

has genetic, immunlogic and environmental components

viral infections

climate can impact a person

incidence/prevalence of MS

more common in white people

more common in women

occurs between 20-40

Relapsing-remitting MS

most common form

characterized by exacerbations and remissions followed by partial or complete recovery

85% of people being with this one

Primary progressive MS

progression of disability from onset without plateaus of remissions but can have periods of stabilization

does not experience acute attacks

10-15% people with MS have this

Secondary progressive MS

begins as relapsing remitting followed by progression of disability that may include occasional relapses , minor remissions and plateaus

of the 85% that start out as RRMS more than 50% will develop SPMS within 10 years, 90% within 25 yrs

progressive-relapsing MS

least common

shows progression of disability from onset but with clear acute relapses with w/o full recovery

5% of people have this

Pathophys of MS


loss of myelin sheath causing loss of saltatory conduction

affects all types of nerve fibers: sensory and autonomic

earliest lesions occur as inflammation of myelin sheath lost in white matter of brain and spinal cord

plaques are what and where are they found?

seen in lateral ventricles of brain, brain stem and optic nerve

larger areas of inflammation and demyelination

Testing for MS


neuro exam

visual/auditory/somatosensory testing


lumbar puncture

Clinical features of MS

blurred vision is common 1st sign due to plaques on corticospinal tract

diplopia, nystagmus, vertigo,

numbness, tingling, tightness


progressive weakness, paralysis in UE

motor symptoms of MS

paraperesis or paraplegia more common than UE weakness

spasticity more common in legs than arms

amyotrophy can occur

coordination symptoms of MS

gait imbalance

slurred speech

co-morbidities of MS


complications of immobility

respiratory infections

bed sores


Treatments of MS

no specific treatment at this time

medications (corticosteroids,beta interferons, copaxone, tysabri,novantrone)

plasma exchange


Goals of MS (4)

improve speed of recovery from attacks

reducing number of attacks and lesions

slow progression of disease

find relief from other complications

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

10% genetic

Incidence of ALS

40-60 yrs old



smoking, family history

males more likely to have it than females

whites more common

course of ALS

no 2 people go through the same course of ALS

death usually occurs within 3-5 years

ALS is a _________ disease


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


Wallerian Degeneration =?

process by which motor axons die

death in anterior horn of cell body

degeneration of associated motor axons

Schwann cells break down myelin

axon breaks into pieces

macrophages clean up axon

Upper motor neurons

degeneration of corticospinal upper motor neurons

loss of these leads to:spastic paralysishyperreflexiastiffness

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 paralysisdecreased muscle tonedecrease reflexesmuscle weaknessmuscle 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

2-sensory neurons

3-cognitive function

4-bowel and bladder function

diagnostic tests for ALS

determined by ruling out all other tests

family history, lab tests, CT/MRI, EMG, blood tests, gene testing

early stage clinical features of ALS

painless, weakness and difficulty breathing

soft/spastic muscles


atrophy of muscles

localized or sporadic symptoms

muscle imbalance

weak grip

middle stage features of ALS

symptoms worsen

muscle paralysis


joint pain/deformity

difficulty swallowing

final stage clinical features of ALS

paralysis of voluntary muscles

severe breathing insufficiency

susceptible to lung infections

speech failure

problems eating/speaking due to dysphagia

death after 3-5 years

Sporadic ALS

most common form

accounts for 90-95% reported cases

Familial ALS

gene related

connected to defective gene on chromosome 21

Guamanian ALS

extremely high incidence in Guam



weight loss





pressure sores

lung failure