Final Flashcards

1
Q

are ppl who had TBI more at risk for later cognitive decline?

A

yes

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2
Q

Sequele Post TBI

A
Prolonged Post Concussion Syndrome 
chronic, traumatic encephalopathy-
Child abuse: blow to the head
Clown shot out of a cannon 
Personality changes--due to frontal lode 
Boxer's get PD induced by trauma maybe
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3
Q

Deceleration injury

A

body moves and rapidly stops
hit FRONTAL LOBE then OCCIPITAL LOBE
multiple site injury: coup contracoup
brain hits front of skull and bounce back and hits back of skull
if there are rotational forces get multiple sites of injury

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4
Q

Whiplash

A

hit from behind
first hit OCCIPITAL LOBE then hit FRONTAL LOBE
(rule out cervical spine involvement)

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5
Q

Boxing Injury

A

punched from in front

First hit FRONTAL LOBE then hit OCCIPITAL LOBE

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6
Q

Contusion

A

**can result in hemorrhage : need to do imaging if there is a bleed can go into a coma from the pressure of blood in brain, need to be observed closely

anatomical structural injury
can be associated with coup and contracoup mechanism of injury

can be severe and extensive
can be mild with just edema and resolve 2-4 days

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7
Q

Sequela to TBI

A

problems can vary in severity

  • anterograde amnesia: amnesia prior to incident will be more common
  • retrograde amnesia is more severe: not learning new information
  • loss of mental flexibility -more rigid in thinking
  • attention and concentration deficits : short attention, impair learning
  • rate of new learning impaired
  • HIGHER LEVEL THINKING IMPAIRED: problem solving impaired
  • Can return to work and social interaction impaired in 50% of severe TBI patients–higher level tasks are difficult
  • -FRONTAL LOBE DEFICITS: behavioral issues
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8
Q

Meningitis

signs and sx

A

CNS infection

caused by bacterial or viral infection of pia and arachnoid
–better to have bacterial for treatment
MEDICAL EMERGENCY: can die

  • signs and sx*
    1. headache
    2. fever
    3. confusion
    4. stiff neck
    5. sensory changes
    6. red spotting on skin, especially extremities (6-12 hours)
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9
Q

Acute Meningitis

A

if acute: THIS IS AN EMERGENCY: all structures bathed by CSF is exposed to infection –> GO TO THE EMERGENCY ROOM

-college setting common (often give vaccine)

there are flu symptoms, red spots on skin, especially extremities
antibodies build up and lead to severe vascular changes in extremities: ie gangrene

bacterial: take antibiotics (within 6-12 hours)
viral: some medications

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10
Q

Flu symptoms with red spots on skin

A

GO TO THE EMERGENCY ROOM

SEVERE MENINGITIS

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11
Q

Chronic Meningitis

A

less severe than acute, pick up what it is: if bacterial use antibiotic, if viral treat the symptoms

slow progression of sx–blood born bacteria

dx: lumbar puncture and CSF analysis and blood cultures

Bacterial causes:

1) CNS trauma or surgery (especially if skull fracture)
2) ear infection
3) Lyme disease
4) HIV

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12
Q

Regional Meninitis

A

if someone gets flu sx ask if traveled recently

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13
Q

Etiology of sx in Meningitis

A

response to infection is increase CSF production with obstruction of BF

Results in cerebral edema, inflammation of blood vessels

Can cause hydrocephalus (increased fluid)
MR
CNS involvement
motor deficits and seizures

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14
Q

Encephalitis

A

brain inflamed–> they need to see the doctor

Can be bacterial or viral, meninges are affected

Sx

1) impaired consciousness, confusion
2) Fever, headache, seizures, weakness
3) Any CNS signs +/or CNS involvement

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15
Q

What causes encephalitits?

A
  1. Mumps
  2. Regional Virus
  3. Bacteria

Can get proressive neuroloical decline after

  1. Herpes Simplex Encephalitis: (herpes simplex virus gets into the CNS) headache, personality changes seizures
  2. St. Louis Encephelitis
  3. West Nile encephalitis
  4. Post Infectious Encephalitis: ie had chicken pox/ measles / mumps / german measles / flu
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16
Q

Lyme Disease

cause

Initial Signs (3)
Secondary Signs
Third-Neurological Symptoms (3)

A

caused by tick bites from mice, deer ticks
**CAN GET PNS AND CNS INVOLVEMENT FROM IT

Initial signs:

1) large circular lesion
2) red rash
3) flu like symptoms

Secondary Signs

1) Arthritis in 2/3 of untreated patients
* *need to be treated to not get this**

Third: Neuro Sx

1) Plexitis (plexopathy, can happen to both plexus)
2) Bell’s Palsy
3) Cardiac Arrhythmia’s

Dx: bloodwork
Tx: Antibiotics early

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17
Q

HIV/AIDS

what it does

sx (6)

sx if untreated

A

Destroys myelin in CNS (can also have PNS involvement)

-early sx like MS: weakness, sensory disturbances, demyelinating neuropathies, 
like Meningitis (not AIDS, but a variety of opportunist organisms) 

If untreated late onset of symptoms:

  • AIDS dementia
  • PERIPHERAL neuropathy
  • Myopathies
  • Cerebrovascular complications
  • Seizures
  • Encephalopathies (diffuse brain disease)
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18
Q

Toxic and Metabolic

alcohol

A

Alcohol: CNS depressor: chronic use can cause CNS and PNS involvement
–overdose can cause tremor, respiratory failure, coma, hallucination, ataxia

Etiology:

  • Vitamin B (thiamine) needed to synthesize high levels of alcohol
  • Causes deficiency: in thiamine and other B vitamins needed for nerve function
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19
Q

Wernicke Korsakof Syndrome

A

BC deficient in vitamin B

1) eye movement disorders, nystamus
2) ataxic gait
3) mental status changes: quiet confusion, perceptual disorders, selective memory loss
4) inability to learn new information. Short term memory very impaired. Lon term memory is better.

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20
Q

Toxic Metabolic disorders

A

Alcohol is CNS depressant and chronic use cause CNS/PNS involve

Wernicke Korsakoff Syndrome–deficient in vitamin B
Polyneuropathy–sensory and motor demyelination and or degeneration
Optic Neuropathy
Cerebellar Ataxias

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21
Q

Concussion –when go back to activity

A

make sure no residual sins before go back to activity

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22
Q

Hepatic encephalopathy

A

lead to acute hepatic coma
acute hepatic failure–failure to detoxify metabolites, which have strong effect on many cerebral metabolic processes
–PNS and CNS (bc not able to break down the toxins)

-usually due to dialysis

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23
Q

Heavy Metals

A
  • lead, mercury, arsenic
  • all areas of CNS can be affected (where heavy metals collect)
  • can result in optic atrophy, mental retardation, learning disabilities
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24
Q

Depression vs Dementia vs Delirium

A

Depression: mood disorder–depressed mood and low E

Dementia: global decline intellectual function that cant tx with a medication

Delirium: REVERSIBLE, disturbance of consciousness and cognition due to metabolic, infectious, or toxic factors (including medication)

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25
Q

Depression

A

at least 2 week period of depressed mood or loss of interest in normal activities

+ 4 other related sx

1) change appetite +/or sleep, fatigue
2) psychomotor agitation or retardation
3) worthless of guilt feelings
4) suicide thouhts
5) cognitive disturbances –difficult to concentrate and/or impaired memory , may seem confused

subacute or gradual onset (depend on cause)

Improve in cognitive sx with tx*

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26
Q

How does Dementia present clinically

A

Dementia clinically presents as a progressive decline in intellectual and cognitive function

—Occurs in 5-10% of people above 65 years

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27
Q

What is the most common form of Dementia

A

AD is the most common cause of dementia among people 65 and older

Estimates indicate 4.5 million people have AD and rates increase with increasing age

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28
Q

Does dementia have to progress to AD?

A

Dementia, a loss of intellectual capacity and memory can be nonprogressive and without progressing to AD

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29
Q

5 Signs of Dementia

A

1) Getting lost when walking
2) Cant fill out checks or balance check books
3) Forget common names, things to do
4) Cannot find bathroom-“incontinent”—deemed incontinent because they couldn’t remember where the bathroom is and had an accident
5) Blank stare –truly blank secondary to loss of associated areas: they are not visually processing with the higher cortical function association area (first memory in temporal lobe but then other areas are affected too)

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30
Q

Presentation and Progression of Dementia

A

1) Memory loss/difficulty with complicated intellectual function.
* Especially short term memory loss (temporal lobe is the area first involved)
2) Later presents with increased general confusion and speech deficits. Progress to severe difficulty in reading, writing, following directions and engaging in simple conversations.
3) Motor function decline is usually at the end stage of Alzheimers disease. Motor function decline does NOT occur with dementia. (motor units the last involved, closely monitor AD patient because they may wander and don’t remember who they are and how to get back)

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31
Q

Does motor function decline with dementia?

A

NO

Motor function decline is usually at the end stage of Alzheimers disease. Motor function decline does NOT occur with dementia. (motor units the last involved, closely monitor AD patient because they may wander and don’t remember who they are and how to get back)

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32
Q

Assessment of Dementia: Mini Mental State Exam

A

–Is patient A&O x 3? (person, place and time)

–Can patient count by 3, 7’s backwards?

–Can patient follow 2 step commands?

–Can patient remember 4 objects?
First tell them that you will have them remember it so they notice it first

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33
Q

Functional Assessment Staging Tool: FAST

A

Stage 1: no functional loss

Stage 2: subjective loss ie world difficulties only

Stage 3: impairment in demanding situations ie employment

Stage 4: mild AD: ie difficulty with everyday tasks

Stage 5: moderate AD: requires prompting/assistance with ADL

Stage 6: moderate AD: requires prompting/assistance with ADL

Stage 7: ie incontinence, difficulty walking, unable to speak, smile, and swallow

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34
Q

Why do you need to do a CAT scan on a patient with dementia?

A

to rule out a TREATABLE cause of the cognitive or intellectual decline

—Stroke, tumor, something pathological that is treatable

—Cerebral atrophy also occurs in healthy elderly

—Help to rule out tumor, CVA

—Enlarged cortical sulci

—Enlarged ventricles (ie CSF, atrophy, it is abnormal can be different causes)

—Neuronal loss in association areas (cell loss indicates pathalogy)

—Better to do a clinical assessment for diagnosis, CAT scan is used for ruling out

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35
Q

When a patient has dementia, what do we need to assess for?

A

1) Stroke, tumor, something pathological that is treatable
2) Cerebral atrophy occurs in healthy elderly
3) Tumor, CVA etiologies
4) Enlarged cortical sulci

5) Enlarged ventricles
(ie CSF, atrophy, it is abnormal can be different causes)

6) Neuronal loss in association areas
(cell loss indicates pathalogy)

7) Better to do a clinical assessment for diagnosis, CAT scan is used for ruling out

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36
Q

What are causes of Dementia (5)

A

1) AD accounts for 65% of dementia.

2) Dementia is related to TBI
BUT: AD is not related to TBI

3) Dementia is not part of normal aging being accelerated, incidence
- -INCREASE between 65-80
- -DECREASE in ppl over 90

4) Incidence: FEMALES more than males
5) LOW EDUCATION reveals higher incidence compared to someone with a college education

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37
Q

Is AD related to TBI?

A

Dementia is related to TBI

BUT AD is not related to TBI

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38
Q

What pathologies can cause Dementia?

A

1) MULTI-INFARCT dementia:
presents with a segmental decline in intellectual ability with each new lesion: lacunar strokes –do a CT scan

2) Chronic infectious processes:
hypoglycemia, AIDs

3) can develop in later stages of PD

4) dementia with LEWY BODIES:
PD like presentation with early onset of dementia

5) NEUROTOXIC AGENTS:
heavy metals, aluminum, drugs

6) ACUTE ONSET:
reversible (cardiac arrhythmia, post anesthesia-temporary, depression-can present
like dementia)

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39
Q

Can acute onset dementia

be reversed?

A

YES

cardiac arrhythmia

post anesthesia-temporary,

depression-can present
like dementia

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40
Q

Normal pressure hydrocephalus

  1. mechanism
  2. cause
A

1) due to blockage of CSF flow, ventricles enlarge and produce CNS decline.
2) Due to TBI, meningitis, hemorrhage.

–>restriction in flow of CSF and uptake of CSF, if in a kid, skull enlarges and not increase pressure. If fused skull the ventricles enlarge more and more. Spinal tap and measure pressure considered normal, they are increasing ventricle size, brain is declining in size.

***SURGICAL PLACEMENT OF SHUNT

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41
Q

Normal pressure hydrocephalus

presentation

diff dx

A

PRESENTATION
1) Gait apraxia as 1st sign, initiation severely affected

2) Dementia
3) Incontinance
4) Possible LE spasticity (wont see this in PD)

DIFFERENTIAL DIAGNOSIS

  1. fast onset
  2. no tremor
  3. no rigidity
  4. Lumbar puncture→normal CSF pressure!!

***SURGICAL PLACEMENT OF SHUNT
–>restriction flow/uptake CSF,
if kid, skull enlarges not increase pressure.
If fused skull ventricles enlarge more and more.
Spinal tap and measure pressure considered normal, they are increasing ventricle size
BRAIN IS DECLINING IN SIZE

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42
Q

Which is most to least common form of Dementia

AD, Mixed vascular AD, vascular ADm others

A

AD–> Mixed vascular AD –> Vascular Dementia –> other types

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43
Q

Gait apraxia is the first sign of what condition?

A

Normal pressure hydrocephalus

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44
Q

How is Normal pressure hydrocephalus treated?

A

Surgical placement of shunt

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45
Q

5 frequent sx when patient dx with AD?

A

1) Apathetic Syndrome:
s unique syndrome
Was the most frequent

2) Affective Syndrome: there will be anxiety and depression—will see one, will see the other: very agitated vs quiet and withdrawn
3) Psychomotor: agitation, irritability and aberrant motor behavior: they need good structure and consistency because they cannot deal with the change of anything being different, there is consistent staffing, consistent schedule,
4) Psychotic: delusions and hallucinations
5) Manic: dis-inhibition and euphoria

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46
Q

Preclinical AD:

Where first signs of AD are noticed

A

Signs of AD are first noticed in the

1) ENTORHINAL CORTEX, –> then proceed to the
2) HIPPOCAMPUS –>Hippocampus and then
3) TEMPORAL LOBE

These changes before see symptoms

Affected regions begin to shrink as nerve cells die

Changes can begin 10-20 years before symptoms appear

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47
Q

How long does it take after brain changes for sx to appear?

A

Changes can begin 10-20 years before symptoms appear

brain changes before see symptoms

Affected regions begin to shrink as nerve cells die

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48
Q

Mild to moderate AD:

A

AD spreads through the brain. The CEREBRAL CORTEX begins to shrink as more and more neurons stop working and die

1) Mild AD signs: can include memory loss, confusion, trouble handling money, poor judgment, mood changes and increased anxiety
2) Moderate AD signs: can include increased memory loss and confusion, problems recognizing people, difficulty with language and thoughts, restlessness, agitation, wandering, and repetitive statements
3) In severe AD, extreme shrinkage occurs in the brain. Patients are completely dependent on others for care
4) If bed-bound they are susceptible to skin breakdown, contractures, often go into fetal position

–Symptoms can include weight loss, seizures, skin infections, groaning, moaning, grunting, increased sleeping, loss of bladder and bowel control

5) Death usually occurs from aspiration pneumonia or other infections
- –Caregivers can turn to a hospice for help and palliative care

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49
Q

What causes:

AD spreads through the brain. The CEREBRAL CORTEX begins to shrink as more and more neurons stop working and die

A

higher cortical function involvement, decline in function, some degree of cell death leads to this: difficulty in understanding and in memory. Some frontal lobe: restlessness, how they interact with people

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50
Q

Mild AD signs

A

Mild AD signs: can include

memory loss

confusion

trouble handling money

poor judgment

mood changes

increased anxiety

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51
Q

Moderate AD signs

A

Moderate AD signs: can include

increased memory loss and confusion

problems recognizing people,

difficulty with language and thoughts,

restlessness,

agitation,

wandering,

repetitive statements

52
Q

Severe AD

A

extreme shrinkage occurs in the brain. Patients are completely dependent on others for care

—If bed-bound they are susceptible to skin breakdown, contractures, often go into fetal position

–Symptoms can include weight loss, seizures, skin infections, groaning, moaning, grunting, increased sleeping, loss of bladder and bowel control

53
Q

3 Stages of AD

A

1) Mild AD signs: can include memory loss, confusion, trouble handling money, poor judgment, mood changes and increased anxiety
2) Moderate AD signs: can include increased memory loss and confusion, problems recognizing people, difficulty with language and thoughts, restlessness, agitation, wandering, and repetitive statements
3) In severe AD, extreme shrinkage occurs in the brain. Patients are completely dependent on others for care

—If bed-bound they are susceptible to skin breakdown, contractures, often go into fetal position

–Symptoms can include weight loss, seizures, skin infections, groaning, moaning, grunting, increased sleeping, loss of bladder and bowel control

5) Death usually occurs from aspiration pneumonia or other infections
- –Caregivers can turn to a hospice for help and palliative care

54
Q

Two abnormal brain structures associated with AD

A

1) Neurofibillary tangles: breakdown in structural architecture of neuron axons
2) Beta-amyloid plaques: extracellular “scar tissue” that results from neuron cell death (drug trials on anti-amyloid plaque therapy)

  • –Nerves cannot fire, conduct,
  • –Breaking down of neurons, scar tissue that forms around neurons
  • –The whole nerve structure is starting to breakdown
  • –Plaques and tangles block nerve conduction
55
Q

Cause of neurofibillary tangles in AD

A

Neurons have an internal support structure partly made up of microtubules. A protein called tau helps stabilize microtubules. In AD, tau changes causing microtubules to collapse and tau proteins clump together to form neurofibillary tangles.

56
Q

Beta amyloid plaques

A

1) Amyloid precursor protein (APP)is the precursor to amyloid plaque.
2) APP sticks through the neuron membrane
3) Enzymes cut the APP into fragments of protein, including beta amyloid
4) Beta amyloid fragments come together in clumps to form plaques
5) In AD many of these clumps form disrupting the function of neurons. Thus affects the hippocampus and other areas of the cerebral cortex.

57
Q

Prognosis with AD

  • lifespan
  • is progression related to age of initial diagnosis?
A

—An average of 8 years life span following diagnosis

—After age 80, 15% of the population has mild dementia but not necessarily AD

—Progression not related to age of initial diagnosis (not increase with age?)

58
Q

Medical Treatment Options for Patients with AD and Dementia (5)

A

1) Medications for mild to moderate AD: slow the progression for a period of time

Aricept: acytelcholine-esterase inhibitor (boosts Ach)

Exelon

Reminyl

2) Clinical Trials for a Vaccine
3) Anti-oxidants (vitamins) and folic acid-but not more is better, don’t want too high toxic dosages
4) Medications that prevent formation of beta amyloid plaque
5) Homocysteine: an amino acid has been implicated in AD and heart disease: some people believe it plays a role in AD

59
Q

Treatment of Patients with AD and Dementia: guide to PT

A

1) Based upon symptoms. If true agitation use medications, if depressed treat depression.
2) If nervous energy channel the energy—get them doing stuff, ambulate, to release the agitation
3) Patients with dementia are very concrete “jump in the car”—instruct family members on being clear in their communication
4) Don’t confront them on errors, they will forget anyway. Constant corrections just belittle the patient, move on
5) Break a task into small steps: if they are not thrilled about doing something, first walk into bathroom, then lets brush teeth, then lets go into the tub: because they don’t want to take the bath, do a progression of activities to reach the end goal works much smoother in nice easy simple steps that they can handle

Use nonverbal communication –easier to interpret than verbal cuing

60
Q

AD Prevention

A

1) Physical exercise decreased incidence
2) Mental exercise, mental stimulation decrease incidence
3) Humor

4) Reduction of risk factors:
i. HTN
ii. Smoking
iii. cardiovascular disease

61
Q

PT Intervention AD and Dementia

A

1) Early in the progression –manage the symptoms as discussed earlier
- –Remind them of what they forgot, help orient them
- –If they say their family hasn’t come and they were there that morning, remind them that they were there but recognize that they do not remember

2) As dementia worsens, safety evaluation and closer supervision of the patient
- -They may need supervision: get distracted, forget where they are
- –They may not be safe to live at home alone
- –Go to put something on the stove and forget it was there, or turn on bath and forget

  • **Maintain functional independence as long as possible
  • Even if they need supervision
  • This is a key factor
  • As long as you can keep someone ambulatory the secondary issues of becoming WC or bedbound can be prevented: contractures, skin breakdown, respiratory issues.

Work with the patient and put the walker in front of them and hope they go into automatic pilot to walk because verbal cues will be hard, use more nonverbal cues, help them maneuver the walker, VC is harder for them to process

***When mobility ceases, prevent skin breakdown, prevent contracture development, ensure proper nutrition and hygiene

62
Q

Tips

PT Intervention AD and Dementia

A

a. Know your patient, you can only notice changes in thought and behavior if you know how the patient usually behaves
b. Most confused elderly: patients feel frightened and helpless, they often try to defend themselves by becoming combative, do not take it personally if patient is verbally or physically abusive to you
c. Speak to the patient in low tones, soothing voices are easier for the hearing impaired
d. Try to maintain consistent staffing through primary care—consistency
e. Orient patient every morning, tell them the date, month, year, and season, remind them where they are and why—help them be grounded
f. Check on confused patients frequently. This reassures them and provides opportunity to orient them
g. Ask the family to bring familiar belongings, pictures, clothing, and personal property decrease patient fear—ie a special chair
h. Protect patient from harmful substances and falls
i. Do not startle patient or approach without warning or approach from behind if patient is known to strike out
j. Personal supervision
k. Know what medications the patient is taking, even a small dose change or new drug introduction may cause confusion

***Restraints are a last resort (even a seatbelt patient cannot get open, bedrails), never use as punish

63
Q

Should restraints be used to punish a patient with AD?

A

NEVER

64
Q

Nun studies on AD

A
  • Autopsies of elderly nuns revealed many had no clinical signs of dementia, but had many microscopic markers associated with AD (lacunar strokes, associated with early AD)
  • Brain’s of nuns with one or two pin sized strokes and markers associated with AD, had a 93% chance of signs of dementia prior to death
65
Q

How bad are cognitive changes with aging?

A

Not as bad as we are led to believe, many abilities well preserved

Common problems: memory—most common complaint of older adults

Word finding: processing speed, executive functions, planning, organizing problem solving, etc.

66
Q

Depression vs Dementia vs Delirium in the elderly

A

Depression: mood disorder with pathologically depressed mood and low energy

Dementia: progressive cognitive impairment that results in impaired ADL

Delirium: REVERSIBLE disturbance of consciousness and cognition due to metabolic, infectious, or toxic factors (including medications)

67
Q

Depression

what are the criteria

A

***Note that there is improvement in cognitive sx with tx

1) At least 2 WEEK period of depressed mood or loss of interest in normal activities

plus:
1) change in appetite/sleep, fatigue

2) psychomotor agitation or retardation
3) worthless or guilt feeling
4) suicide thoughts
5) cognitive disturbance –difficulty concentration +/or impaired memory. May appear confused.
* can be subacute or gradual onset depending on cause

68
Q

Cause of depression

A

25% of inpatients

  • painful conditions
  • lower income, socially isolated individuals, loss of loved ones
  • memory loss may be selective with short term memory loss
  • poor attention, lack of motivation, drive

IT IS TREATABLE BUT MUST BE RECOGNIZED

69
Q

Delirium

A

RAPID ONSET: hours/2-3 days

REVERSIBLE and FLUCTUATES

Acute impairment of cognitive function and consciousness

-caused by intrinsic loss of homeostasis
May be due to medications, fever, ETOH, acute medical condition

-not due to pre-existing conditions

70
Q

Types of Delirium

3

A

1) Hyperactive:
patient is very alert, increased psychomotor activity. AGITATED. Too Alert

2) Hypoactive: reduced alertness and activity. Lethargic
3) Mixed: fluctuate btwn hyperactive and hypoactive

52% of pts with delirium are mixed

71
Q

Triggers for delirium

A
  1. Drugs, Sedatives, narcotics, drug withdrawel
  2. CNS neurological conditions
  3. Stress, sleep deprivation, physical restraints
  4. hypoxia, anemia
  5. any loss of internal homeostasis
72
Q

PT interventions for patients with depression

A
  1. staff aware and agree on the status
  2. see patients LATER IN THE DAY (morning usually worse)
  3. acknowledge patient’s feelings and PRAISE accomplishments (ADL, therapy)
  4. EXERCISE seems to help

**focus on what they can do

73
Q

PT interventions for patients with delirium

A
  1. ADL & activities meaningful/helpful to the patient
  2. work with nursing on time for PT
  3. limit the ENVIRONMENT and create a STABLE, FAMILIAR ENVIRONMENT
  4. EYE CONTACT,
    be CALM and RESPECTFUL
74
Q

Parkinson’s Disease

where in brain

etiology

progression

age of onset

A

BASAL GANGLIA: planning and initiation of movement, muscle tone (rigidity), posture, movement, and walking
—–Basal ganglia (part of the extra-pyramidal system) interacts with the pyramidal system and cerebellum to control movement.

Etiology PD: probably genetic + environmental

Progression is variable: 10-15 yrs (dx –> death)

1% of population over age 50yrs, onset in 50s
5-25/100,000

75
Q

NEUROLOGICAL PRESENTATION IN PD

A

1) Bradykinesia: (negative sign) slowness / poverty of movement
2) Rigidity: (positive sign) Cogwheel rigidity (rachet-like), like a second hand on a watch

3) Resting Tremor: (positive sign)
5-7 hz: usually distally-in hands.
Pill rolling of thumb and fingers

4) Deficits of normal postural and equilibrium reactions: fall without protective reaction or blinking

5) Deficits in initiation of movement (negative sign)
- -Akinesia: mask face
- -WS deficit
- -self initiated activities all reduced (motor, speech)

6) Festinating Gait: (positive sign) Increased speed of gait with difficulty stopping “chasing COG” (small slow steps)
7) Freezing: (Negative sign) Motor Blocks (block to maintain motor pattern)

76
Q

PD:

Bradykinesia:

is it a +/- sign

what is it

A

(negative sign)

slowness / poverty of movement

slowness of movement, less fluid movement, progress to lack of movement and cannot initiate movement

77
Q

PD:

Rigidity:

is it a +/- sign

what is it

A

(positive sign)

Cogwheel rigidity (rachet-like), like a second hand on a watch

does NOT melt away as go through the range

(not spasticity)

78
Q

PD:

Resting Tremor:

is it a +/- sign

what is it

A

(positive sign)

5-7 hz: usually distally-in hands.
Pill rolling of thumb and fingers

TREMOR STOPS WHEN START TO MOVE: SEE IT WHEN NOT MOVING THE LIMB

(this is different from cerebellum intentional tremor)

79
Q

PD

Posture/Eqb rxns

A

Deficits of normal postural and equilibrium reactions: fall without protective reaction or blinking

80
Q

PD:

Initiation of movement

is it a +/- sign

what is it

A

(negative sign)

  • -Akinesia: mask face
  • -WS deficit
  • -self initiated activities all reduced (motor, speech)
81
Q

PD:

Festinating Gait

is it a +/- sign

what is it

A

(positive sign)

Increased speed of gait with difficulty stopping “chasing COG” (small slow steps)

82
Q

PD:

Freezing:

is it a +/- sign

what is it

A

(Negative sign)

Motor Blocks (block to maintain motor pattern)

83
Q

PD• bradykinesia

A

o slow movement
o poverty of movement
o negative sign
o slow movement progressing to lack of movement and unable to initiate movement

84
Q

PD• rigidity

A
o	not spasticity 
o	cogwheel rigidity
o	alpha motor neuron output
•	move a limb 
•	rachet like
•	feel through the full ROM doesn’t melt away 
o	positive sign
85
Q

PD• resting tremor

A

o positive sign
o not intentional like in cerebellar involvement
o usually distally in the hand
• pill rolling of thumb and fingers
o when they are resting
• ask them to reach forward and it stops
o tremor is one of the early findings

86
Q

Neuro Presentations

A

deficits of normal postural and equilibrium reactions
o head down without moving
o cannot initiate a correction
• they are aware of it

lack of equilibrium and posture reactions
o they will fall like when you cut down a tree
o no protective reactions
o don’t even see them blink
o loss of the equilibrium reactions
lack protective extension

Deficits in initiation of movement
o negative sign
o akinesia, masked face

no internal drive to change facial expression
o cannot initiate movement without some kind of cueing
o weight shifting deficit
o self-initiated activities all reduced: motor and speech

festinating gait 
o	positive sign 
o	small steps increased speed of gait with difficulty stopping 
o	chasing COG 
o	small steps like chasing COG 
o	accelerate and cannot stop 

freezing
o negative sign
o MOTOR BLOCKS
o Walking slower and smaller steps and when need to turn or change the pattern of walking or walking straight
—-They step on like glue and they get stuck to the floor and cant get moving
o Block to maintaining the motor pattern

87
Q

Unified Parkinson’s Disease Rating Scale

what does it do?

What test coralates with it?

what three sections?

A

tool used to monitor status +/or progression of the disease

  • STATUS and PROGRESSION of PD
  • BERG is the only test that correlates with this scale*
  1. Mentation, behavior and Mood
    (intellectual impair, thought disorder, depression, motivation/initiative)
  2. ADL
    (speech, salivation, swallowing, handwriting, cutting food and handling utensils, dressing, hygiene, bed mobility, falling, freezing, walking, tremor, sensory complaints)
  3. Motor
    (speech, facial expression, tremor at rest, action /postural of hands , rigidity, finger taps, hand movements, rapid alternate movements of hands, leg agility, arising from chair, posture, gait, postural stability, bradykinesia and hypokinesia)

Dyskeniesias–% of day, disabling, painful, early morning dystonia

Clinical Fluctuations: on off periods
Other complications : anorexia, nausea, vomitting, sleep disturbances, systomatic orthosasis)

88
Q

What is the Hoehn and Yahr Scale:

A

system for describing how the symptoms of Parkinson’s disease progress.

STAGE 1: Mild Unilateral Disease:

1) impaired Diadochokinesis (rapid alternating: they have slow movements)
2) decreased FASCIAL EXPRESSION, INITIATION of movements, speech VOLUME, some equilibrium REACTIONS
3) Slight rigidity

STAGE 2: bilateral involvement

1) independent ADL
2) impaired posture, postural changes,
3) Tremor
4) Bradykinesia, decreased spontaneous movements
5) No facial expressions
6) shuffling gait, difficulty turning
7) Depression

Stage 3: bilateral involvement, moderate difficulty in ADL

1) BALANCE IMPAIRED
2) loss of equilibrium reactions
3) Bradykinesia, akinesia
4) retropulsion: forward chasing of COG: smaller more rapid steps with trunk flexed forward
5) FREEZING during gait
6) horrendous turning during gait
7) difficulty with dressing (initiation-not apraxia), ADL difficult

Stage 4:
Stage 5:

89
Q

Hoehn and Yahr Scale:

Stage 1:

A

Mild UNILATERAL Disease:

1) impaired Diadochokinesis (rapid alternating: they have slow movements)
2) decreased FASCIAL EXPRESSION
3) decreased INITIATION of movements,
4) decreased speech VOLUME
5) loss of some EQUILIBRIUM REACTIONS
6) Slight RIGIDITY

90
Q

Hoehn and Yahr Scale:

Stage 1:

How is their Balance, Gait, ADL?

A

Balance ok

Gait Ok

ADL ok

91
Q

Hoehn and Yahr Scale:

Stage 2:

A

STAGE 2: bilateral involvement

1) independent ADL
2) IMPAIRED POSTURE, postural changes,
3) BILATERAL RESTING TREMOR
4) BRADYKINESIA, DECREASED SPONTANEOUS movements
5) NO FACIALl expressions
6) SHUFFLING gait, difficulty TURNING
7) DEPRESSION

92
Q

Hoehn and Yahr Scale:

Stage 2:

How is their Balance, Gait, ADL?

A

BILATERAL INVOLVEMENT

Postural changes (more flexed)

Gait Changes (shuffling gait, difficulty turning, less armswing, less trunk rotation)

FUNCTIONAL FOR ADL

93
Q

Hoehn and Yahr Scale:

Stage 3

A

BILATERAL INVOLVEMENT; MODERATE DIFFICULTY IN ADL

1) BALANCE IMPAIRED
2) loss of equilibrium reactions (no protective reactions)
3) Bradykinesia, akinesia

4) retropulsion: forward chasing of COG:
smaller more rapid steps with trunk flexed forward

5) FREEZING during gait (they know what they want to do but cant do it)
6) horrendous turning during gait
7) difficulty with dressing (initiation-not apraxia), ADL DIFFICULT

94
Q

Hoehn and Yahr Scale:

STAGE 3

How is their Balance, Gait, ADL?

A

BILATERAL INVOLVEMENT; MODERATE DIFFICULTY IN ADL

Impaired Balance

Impaired gait: retropulsion, freezing, bad turning

ADL: difficult

95
Q

Hoehn and Yahr Scale:

Stage 4:

A

SEVERE DISABILITY, MARKED GAIT DISTURBANCE

1) RIGIDITY increased
2) worse bradykinesia–>AKINESIA
3) bed mobility difficult (not weakness, a motor control issue)
4) “poor” balance
5) decreased dexterity
* ALL ADL DECREASED*

96
Q

Hoehn and Yahr Scale:

Stage 5:

A

CONFINED TO WC OR BED

1) non-ambulatory
2) severe rigidity
3) bradykinesia, akinetic: very few voluntary movements
4) Flexion posture
5) Drooling, dysphagia (eating difficult)
6) Decubeti (bed position, contractures and skin breakdown)
7) respiratory function decreased due to akinesia

AKINESIA: few voluntary movements

97
Q

Complications and Side Effects of PD

  1. Dyskinesia
  2. Psychiatric
  3. Sleep disturbances
  4. Weaning off effect between doses
  5. on/off phenomenon
A
  1. Dyskinesia: choreaform movements, due to dopamine overuse
  2. Psychiatric: drug levels nightmare, hallucination (auditory, visual)
  3. Sleep disturbances: secondary to medications (because of hallucinations, nightmares…)
  4. Weaning off effect between doses: important to postpone initiation of drug therapy
  5. On/Off Phenomenon: severe fluctuation of movement ability NOT related to dosage
98
Q

Which of these complications and side effects of PD are NOT related to dosage?

  1. Dyskinesia
  2. Psychiatric
  3. Sleep disturbances
  4. Weaning off effect between doses
  5. on/off phenomenon
A

on/off phenomenon

When someone is having an off period, this can be related to diet and protein intake, it is important to spread out protein intake in the day when on the medication

99
Q

Complications of PD

  1. Dementia
  2. Micrographia
  3. ANS dysfunction
  4. Orthostatic Hyotenstion
  5. Bowel and blader dysfunction
A

Dementia: in 25% of PD pts

Micrographia: very small writing: look at the old things they wrote to track the effect on this motor task

ANS Dysfunction:

  • sweating
  • constipation (mobility disorder in GI too)
  • excessive salvation
  • ->drooling: Self initiation of swallowing reflex is impaired causing drooling

Orthostatic hypotension

  • *Monitor this in activities, make family aware
  • *Get them up slowly: long sit, dangling edge of bed, stand up slowly,
  • *Compression stockings
  • *Ankle pumps
  • *Night light

Bowel and blader dysfunction
decreased GI motility: decreased peristalsis in GI

100
Q

Orthostatic Hypotension in Parkinsons

How much reduced BP?

Cause?

A

Reduced systolic BP at least 20mmHg or diastolic BP of at least 10mmHg within 3 minutes of standing

1) Many drugs aggravate OH.
Antiparkinsonian drugs, diuretics, antihypertensive and antidepressants

2) Patients want to control incontinence and drink less: cause decreased blood volume and other problems

PT: compression stockings, progressive upright activities, appropriate fluid intake

  • *Monitor in activities, make family aware
  • *Get them up slowly: long sit, dangling edge of bed, stand up slowly,
  • *Compression stockings
  • *Ankle pumps
  • *Night light
101
Q

What is the pathology of Parkinsons?

A

Degeneration of neurons in substantia nigra and deficit of dopaminergic influences to the corpus striatum
(caudate nucleus, globus pallidus and putamen)

For symptoms to be present 80% of these substantia nigra cells have died

[Imbalance of dopaminergic and cholinergic systems when lose dopamine producing neurons

When develop PD and lose dopamine producing neurons have an imbalance in dopaminergic and cholanirgic systems]

102
Q

Medications used in PD

A

classifications of Medications used—
try to improve uptake and availability of dopamine produced and keep it viable or active, make receptor sites more sensitive to dopamine, improve the balance. Use these medications as long as possible

1) Levodopa Replacement: Sinemet
become dopamine in the brain, has a peripheral inhibitor to help prevent it from being broken down and converted before it crosses the BBB

2) Dopamine agonists: stimulate dopamine receptor sites
Ie bromocriptine (parlodel)

3) Anticholinergics: restore balance between Ach and Dopamine
i. Benzotropine (Cogentin) or Artane

d. MAO-B Inhibitors: block the brain enzyme that breaks down levodopa
i. Selegiline or Deprenyl

103
Q

Sinemet

A

for parkinsons

LEVADOPA REPLACEMENT: Sinemet

10: 100 =
10 peripheral inhibitor: 100 levodopa that is then converted to dopamine
—-Carbidopa (inhibitor) : levadopa

High concentrations in the periphery–> side effects nausea and vomiting

—-Dopamine agonists. They activate dopamine receptors directly. Used in early stage of intervention and later stage when higher levels of Levadopa are problematic

Some patient go right to this but that is not ideal, if replace right away and not working they increase the dose of the dopamine replacement more and more and after a while this produces more side effects. The longer you can produce balance by what is present or decreasing the imbalance by stopping cholinergic then don’t need to start immediately with the replacement therapy

It needs to become dopamine in the brain so it has a peripheral inhibitor to help prevent it from being broken down and converted before it crosses the BBB

104
Q

parlodel

A

Parkinsons:

Dopamine agonists: stimulate dopamine receptor sites

Ie bromocriptine

105
Q

Cogentin/Artane

A

Parkinsons

Anticholinergics: restore balance between Ach and Dopamine

106
Q

Selegiline / Deprenyl

A

MAO-B Inhibitors: block the brain enzyme that breaks down levodopa

107
Q

Parkinsons Pharmacology: which is used when

A

1) ANTICHOLINERGICS:
Ach to dominate when low dopamine: early on ANTICHOLINERGICS to balance dopamine and Ach

2) REPLACEMENT THERAPY:
Later dopamine too low: REPLACEMENT THERAPY needed
Levodopa + peripheral inhibitors until BBB, then convert to dopamine

108
Q

What is the on/off phenomenon in Parkinsons?

A

on - off phenomenon
- decreased GI motility or levadopa compete with large AA for transport across the intestinal wall

Off periods –> prevent by taking levadopa with less food / LOW PROTEIN (AA prevent levadopa absorption)

Also help to use controlled release formulation (Sinemet CR)

109
Q

Surgical Management of PD

A
  1. PREVIOUS SURGICAL STRATEGIES:
    - —Adrenal gland implant into caudate nucleus, to produce dopamine
    - –Fetal tissue grafts also shown to “take” with resultant decreases in medication requirements and decreased symptoms
  2. PALLIDOTOMY: started first
    - –Produce small lesion in globus pallidus part of cholenrgic system
    - –Lesions that disrupt the primary pathways that are cholinergic mediated in the basal ganglia and therefore help to restore balance between the two systems
  3. DEEP BRAIN STIMULATION: more done
    - –Electrical inhibition of Ach pathways between globus pallidus, thalamus, and or subthalmic nuclei that are overactive due to loss of dopaminergic control
    - –Uses a small stimulator to inhibit to create a balance
110
Q

What are the PT interventions for parkinsons?

6

A

1) Evidence based effectiveness of STRENGTHEN, FLEXIBILITY, BALANCE training
2) Greatest 6 month carryover when coupled with CUEING patients

3) Strength training : due to decreased MU recruitment
- –Even though presented as strong, had decreased motor unit recruitment and synchronization of firing the motor units

4) Flexibility: general conditioning exercise, PNF
- –Trunk movement, gives rotation

5) AAROM, trunk rotation, stationary bike, treadmill, prolonged walks
- –Stationary bike: fluidity of movement
- –Any kind of aerobic conditioning is important

6) Home assessment and ADL
- –What barriers they have

111
Q

Summarize how to manage Parkinson’s

A

Tx:
inpatient, community based, outpatient, homecare, individualized exercise

1) At diagnosis they should prevent inactivity, prevent fear of move or fall, maintain physical capacity and improve physical capacity
- can be in any setting
- consider starting drug therapy — better to wait

3) Most ppl start meds if tremors is a big problem because PT cannot help that

**Stage 2: bilateral involve but not loss of balance yet: prevent falls, reduce chorea limitations, transfers, posture (not the flexed posture): do extension Mckenzie exercise, work on balance and dynamic and stepping in diagonals and protective reactions

**Later on work to maintain and to prevent contractures and deformities when wc and bed bound

112
Q

How to assess a patient with Parkinsons

Which of these are sensitive indicators?

6MWT, 2MWT, TUG, FRT,

A

1) 6MWT is more sensitive indicator of changes compared to the 2MWT
2) Time Up and Go is not sensitive
3) Functional Reach is proportional to Hoehn and Yard scale

113
Q

Can parkinson pt benefit from rehab?

A

Patients with moderate to severe PD can make clinically relevant improvements in function with a 3 WEEK length of stay in an inpatient rehab hospital with a interdisciplinary movement disorder program

For short periods of time at different times, have them continue on their own

114
Q

What is the basis for using external cues in patients with Parkinsons?

ie sensory cues—visual, auditory, tactile

A

1) Patients with PD have a deficit with internal cue production
- -Issue of self cue to do the movement
- -No internal generator saying it is time to get up and walk now
- -Low carryover, need it continuously, need to have family member educated to cue also

2) They rely on external cues to enhance motor performance
3) Most individuals use visual information when trying to improve motor performance

***These are sensory cues which are utilized by the patient to cue the motor system: they replace internal cues. In order to better function we use external cues to replace the lack of internal cues. They help the patients and therapists to overcome the movement deficits which limit function

115
Q

Why do parkinsons patients need cueing?

A

Normal Function of the Basal Ganglia

1) Helps to generate internal cues
:Need a WS to take a first step, they cannot preset this motor system

2) Involved in the periphery stages of movement
3) Presetting the motor system
4) Planning the movement

defect in
Dysfunction: inability to generate these internal cues

Disruption in the ability to perform sequential movements

116
Q

Why do external cues help patients with parkinsons?

A

Tap into the motor system bypassing basal ganglia
—->they use other systems in movement ie the cerebellum, so the visual cues etc are used to just bypass the basal ganglia need to use it

External cues:

  1. Replace the deficit of internally generated motor patterns:
    - —–they lose the motor pattern and they stop, have them focus and concentrate
  2. Provides external ‘pace’ to maintain movement
  3. Improves concentration on single component of movement pattern
117
Q

Examples of External Cues used for parkinsons

A

Auditory Cues: rhythm/metronome set pace, FIRE

Visual Cues: stripe helps (horizontal and evenly spaced), paper balls, able to catch a ball bc external cue but not throw it,

raised curb/obstacle can freeze

*example of tactile cue on hips to WS when tell them to take a step, holding a box to carry it somewhere can be a cue, ball on walker to kick if they freeze,

118
Q

Tx techniques in Parkinsons

1) Relaxation techniques
2) Rhythm and auditory cues facilitate movement
3) Marching + verbal cues
4) Clapping, movement, metronome
5) Mental rehearsal before the movement

A

1) Relaxation techniques
–Because they have high tone, rigidity
Do this before working on movement and flexibility

2) Rhythm and auditory cues facilitate movement

3) Marching with verbal cues
- -(military commands): step step step step (in beat and not loud enough, don’t be too gentle and polite if you want this effect it is loud)

4) Clapping, movement, metronome

5) Mental rehearsal before the movement
- –Fires the AHC and betz cells in motor cortex even though there is no movement, helps to wire the system to function better

119
Q

Role of Exercise in Parkinsons

A

1) Review of strengthening, aerobic exercise, flexibility and general mobility, task specific exercises for patients with PD
2) Prevent deconditioning prevalent in patients with chronic progressive neurological diseases!
3) Apply general principles of specificity of training combined with neuroplasty

4) Role of exercise:
Complexity/challenging
—>Progressive hierarchies: real world task specific practice
—>Promote continuous use (success) in everyday activities
Feedback/motivation: empower/reinforce

120
Q

LSVT

purpose

A

lee silverman voice therapy/training: start this big excursion movements from stage one to prevent the less and less ranges and smaller movements and low vital capacity and soft speech etc

1) Forced “normal” USE: bigger/faster whole body movements
- –Single Focus on attention to BIG EFFORT to fight bradykinesia
- –Think BIG for ALL tasks, disciplines, environments
- –Exaggerated exercise, exaggerated performance of ADL

2) Intensive Practice
- –Total time of practice: 16 of 1 hour individual sessions: 4x per week
- –Increased energy expenditure
- –High effort for larger movements
- –Repetitious daily exercises

121
Q

What is LSVT BIG

A

Developed from the lee silverman voice treatment approach of loud, overly expressive speech therapy for improving vocalization

LSVT Big: focuses on intensive exercising of high amplitude movements of increasing complexity for this same population

Goal is to improve movement perception and recalibrate disturbed sealing of moving amplitudes

Program is 4x per week for 4 weeks, each session is one hour in duration

122
Q

Why we use Forced Use-Intense Exercise for parkinsons?

A

1) Increased release of dopamine
2) Increased dopamine receptor uptake
3) Increased neurotrophic factors that are neuroprotective
3) Must be continued for long term efffects (just like meds must be maintained)

Ie tandom cycling – constant pedaling at high 80+ RPMs. Aerobic (65-80% target HR): active with assistive (pt 25%: therapist 75%): get to high rate of cycling with aerobic stress on pt to improve their functional status

123
Q

Parkinsons

Evidence re: PT/Rehab—carryover for function

A

1) Cuing strategies to improve gait
2) Cognitive strategies to improve transfers
3) Exercises to improve balance
4) Training of joint mobility and muscle power
5) Treadmill training
6) Specificity of training

124
Q

Motor Blocks and External Cues

in parkinsons

top 6

A
Start hesitation 86%**
On turning 45%
At doorway  25%
On open runway: 23%
At destination 18%
Other non gait 11%
125
Q

Parkinsons:

triggers of motor block

A

1) Inability to tap into motor program: help them initiate it
2) Inability to change motor program: what cues will help them, cue them, turn to the left,
3) Loss of internal pace mechanism