Final Flashcards

Question

Depression

Answer 1

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*

Answer 2

Dementia clinically presents as a progressive decline in intellectual and cognitive function ---Occurs in 5-10% of people above 65 years

Answer 3

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

Answer 4

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

Answer 5

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)

Answer 6

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)

Answer 7

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)

Answer 8

--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

Answer 9

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

Answer 10

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

Answer 11

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

Answer 12

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

Answer 13

Dementia is related to TBI | BUT AD is not related to TBI

Answer 14

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)

Answer 15

YES cardiac arrhythmia post anesthesia-temporary, depression-can present like dementia

Answer 16

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

Answer 17

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

Answer 18

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

Answer 19

Normal pressure hydrocephalus

Answer 20

Surgical placement of shunt

Answer 21

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

Answer 22

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

Answer 23

Changes can begin 10-20 years before symptoms appear brain changes before see symptoms Affected regions begin to shrink as nerve cells die

Answer 24

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

Answer 25

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

Answer 26

Mild AD signs: can include memory loss confusion trouble handling money poor judgment mood changes increased anxiety

Answer 27

Moderate AD signs: can include increased memory loss and confusion problems recognizing people, difficulty with language and thoughts, restlessness, agitation, wandering, repetitive statements

Answer 28

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

Answer 29

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

Answer 30

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

Answer 31

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.

Answer 32

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.

Answer 33

---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?)

Answer 34

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

Answer 35

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

Answer 36

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

Answer 37

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

Answer 38

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

Answer 39

- 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

Answer 40

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.

Answer 41

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)

Answer 42

***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

Answer 43

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

Answer 44

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

Answer 45

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

Answer 46

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

Answer 47

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

Answer 48

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

Answer 49

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

Answer 50

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)

Answer 51

(negative sign) slowness / poverty of movement slowness of movement, less fluid movement, progress to lack of movement and cannot initiate movement

Answer 52

(positive sign) Cogwheel rigidity (rachet-like), like a second hand on a watch does NOT melt away as go through the range (not spasticity)

Answer 53

(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)

Answer 54

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

Answer 55

(negative sign) - -Akinesia: mask face - -WS deficit - -self initiated activities all reduced (motor, speech)

Answer 56

(positive sign) Increased speed of gait with difficulty stopping "chasing COG" (small slow steps)

Answer 57

(Negative sign) Motor Blocks (block to maintain motor pattern)

Answer 58

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

Answer 59

``` 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 ```

Answer 60

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

Answer 61

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

Answer 62

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)

Answer 63

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:

Answer 64

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

Answer 65

Balance ok Gait Ok ADL ok

Answer 66

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

Answer 67

BILATERAL INVOLVEMENT Postural changes (more flexed) Gait Changes (shuffling gait, difficulty turning, less armswing, less trunk rotation) FUNCTIONAL FOR ADL

Answer 68

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

Answer 69

BILATERAL INVOLVEMENT; MODERATE DIFFICULTY IN ADL Impaired Balance Impaired gait: retropulsion, freezing, bad turning ADL: difficult

Answer 70

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*

Answer 71

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

Answer 72

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

Answer 73

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

Answer 74

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

Answer 75

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

Answer 76

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]

Answer 77

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

Answer 78

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

Answer 79

Parkinsons: Dopamine agonists: stimulate dopamine receptor sites Ie bromocriptine

Answer 80

Parkinsons Anticholinergics: restore balance between Ach and Dopamine

Answer 81

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

Answer 82

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

Answer 83

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)

Answer 84

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 2. 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

Answer 85

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

Answer 86

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

Answer 87

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

Answer 88

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

Answer 89

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

Answer 90

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

Answer 91

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

Answer 92

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,

Answer 93

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

Answer 94

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

Answer 95

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

Answer 96

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

Answer 97

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

Answer 98

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

Answer 99

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

Answer 100

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