PathophysExam2


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


CNS

movement


What is the cause of PD?


unknown


Primary or idiopathic PD thought to have ______ and ______ factors


genetic

environmental


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


True


Characteristics of secondary PD (not true PD)

(7)


encephalitis/meningitis

stroke

vascular disease

exposure to toxins

antipsychotic medications

over-dose of narcotics

repeated chronic head trauma


Risk factors of PD (4)


age

gender

genetic

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


fatigue

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

bradykinesia

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


dysarthria

voice low

chewing/swallowing issues

masked face

pain

memory loss


co-morbidities (4) of PD


dementia

UTI/ respiratory infections

depression/anxiety

disturbed sleep, fatigue


Tests of PD


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


Stages of PD (5)


1-unilateral

2-bilateral

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

PT/OT


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


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

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

aphasia

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


depression

dysphagia

muscle contractures

broken bones

loss of social instabilities


treatments of AD


Ach esterase

Memantine

Vitamin E

TENS

PT/OT/SLP


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


autoimmune

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


history

neuro exam

visual/auditory/somatosensory testing

MRI

lumbar puncture


Clinical features of MS


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

diplopia, nystagmus, vertigo,

numbness, tingling, tightness

pain

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


depression

complications of immobility

respiratory infections

bed sores

contractures


Treatments of MS


no specific treatment at this time

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

plasma exchange

PT/OT/


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

environment

genetics

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


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

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

twitches

atrophy of muscles

localized or sporadic symptoms

muscle imbalance

weak grip


middle stage features of ALS


symptoms worsen

muscle paralysis

contractures

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


co-morbidities


anxiety

weight loss

fatigue

aspiration

pneumonia

depression

pressure sores

lung failure