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NM II > Parkinson's Disease Pre Module and 101 > Flashcards

Parkinson's Disease Pre Module and 101 Flashcards

1
Q

The common age of dx:

A

60 years or older

4% of all with PD are under the age of 50

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2
Q

What 3 conditions fall under the description of “Parkinsonism”?

A

PD
Progressive Supranuclear Palsy
Multiple Systems Atrophy

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3
Q

What type of dementia can have parkinsonian features?

A

Lewy Body Dementia

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4
Q

Progressive Supranuclear Palsy signs and symptoms

A

-can’t look down due to impaired eye movements
-scared appearance
-severe postural extension
-falls in the first year- typically backward
-ONSET: over age 50

** WORSE PROGNOSIS THAN PD

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5
Q

Multiple Systems Atrophy signs and symptoms

A

-dysautonomia
-parkinsonian and/or
-cerebellar syndrome-ataxia, dysarthria -orthostatic hypotension: 30mm systolic or 15mm diastolic drop
-urinary system- urinary problems usually arise from degeneration in a part of the brainstem that controls urination. Symptoms such as incontinence, leakage, urinary frequency

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6
Q

Cardinal Signs of PD:

A

rigidity
bradykinesia
resting tremor
postural instability - usually occurs later in the disease process

SUPPORTIVE CRITERIA
-unilateral onset –> then BL
-progressive course
-persistent asymmetry affecting side of onset the most

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7
Q

Possible non-motor signs of Parksinson’s

A

-cognitive impairment - attention, dual task, dementia
-pain
-depression
-hallucinations
-olfactory loss
-dysautonomia
-sleep dysfunction
-fatigue

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8
Q

What is required for PD diagnosis?

A

-cardinal signs (bradykinesia plus one other)
-pos response to dop replacement (70-100% improvement)

-type using UPDRS:
–tremor dominant form
–postural instability and gait disorder form

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9
Q

What is the difference between the tremor-dominant form of PD and the postural instability and gait disorder form? (UPDRS)

A

the PIGD form -
-more problems with instability and gait dysfunction
-more likely to have cognitive deficits
-faster decline –> need medications earlier

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10
Q

What are 4 common medication types for individuals with PD?

A

DOPAMINE REPLACEMENT: precursor to DA, levodopa crosses the BBB and converts to dopamine; Carbidopa inhibits the breakdown of levodopa peripherally
ex: Sinemet-carbidopa/levodopa (helps prevent vomiting, GI side effects),
Rytary- extended-release carbidopa/levodopa

DOP. AGONIST increases the efficiency of dopamine already in the system —> may delay starting dopamine replacement
-Pramipexole
-Ropinirole
-Rotigotine patch
-Apomorphine (rescue)

DIFFERENT ADMINISTRATIONS POSSIBLE:
-enteral through jejunum tube (duopa)
-transdermal injection
-sublingual, inhaled and nasal spray preparations being studied

COMT INHIBITORS -slows down the breakdown of dopamine
-tolcapone
-entacapone
-opicapone

MAO-B INHIBITORS- slows the breakdown of dopamine –>
-may be used early in the disease
-may have a neuroprotective effect
-rasagiline
-selegiline

Anticholinergics - bind to and block ach receptors

Adenosine A2A Receptor Antagonist

Botulinum Toxin for dystonia

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11
Q

Deep brain stimulation for PD:

A

-for medication-resistant tremor

leads go under the skin and are implanted deep into the brain –> wires go through a burr hole in the skull

the pulse generator is under the clavicle at the anterior chest wall

has the potential to decrease the amount of meds needed

LEADS GO IN:
-globus pallidus
-subthalamic nucleus
-thalamus

SE
-cog impairment, worsened balance, dysarthria

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12
Q

GOLD STANDARD MEASURES USED TO DESCRIBE PD

A

UPDRS

Hoehn and yahr

(schwab and england - not listed as gold standard)

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13
Q

Performance measures for PD:

A

freezing of gait
PDQ-39
mobility and function

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14
Q

look to SG for Hoehn and Yahr Classifications

A

look there

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15
Q

UPDRS CATEGORIES AND TOTAL POINTS

A
  1. mentation, behavior, mood
  2. ADLs
  3. motor examination
  4. complications of meds

total score: 176 points
motor subscale: 108 points

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16
Q

PARKSINSON’S DIAGNOSIS

A

-a chronic, progressive, neurodegenerative condition that often presents later in life

MUST INCLUDE:

*UKPD Brain Bank Criteria
-bradykinesia must be present plus ONE: resting tremor, rigidity, postural instability(not caused by vision, vestibular, cerebellar dysfunction)
*UPDRS parts I-IV to assess progression, medication response
*Hoehn and Yahr Staging
*Time
*Carbidopa-Levodopa trial
*Imaging - MRI (rule out structural impairment), DAT scan
*autonomic test, smell test, skin biopsy (abnormal protein in ppl with PD)

SUPPORTIVE CRITERIA:
-unilateral onset, persistent asymmetry
-responsive to levodopa
progressive
-levodopa induced dyskinesia
-prodromal symptoms (RBD, loss of smell) –> before the major signs or symptoms start

EXCLUSION
-strokes/head injuries repeated
-anti-dopaminergic agent exposure
-encephalitis
-sustained remission
-poor response to L dopa
-other neurologic signs (cerebellar signs, early dementia, supranuclear palsy)

17
Q

epidemiology of PD

A

more in men 3:2

fastest growing neurodegenerative dod in terms of disability, prevalence, and death

RISK FACTORS
-age
-exposures- agent orange, pesticides
-reduced risk: cigarettes, caffeine

-peak: 85-89 years old

18
Q

pathophysiology of PD

A

MACRO
-small changes macroscopically

loss of neurons in substantia nigra pars compacta (brainstem) and locus coeruleus

-the death of DA neurons in substantia nigra (basal ganglia)
-30% loss–> motor symptoms onset
-dopamine throughout the striatum is lost (basal ganglia)

MICROSCOPICALLY
alpha-synuclein protein –> aggregates into lewy bodies with mutation

19
Q

Substantia nigra and connection with caudate and putamen of basal ganglia

A

the DA neurons of the substantia nigra project to the caudate and putamen of the striatum (BG) –> this pathway makes up the nigrostriatal pathway

20
Q

Genetics of PD

A

the complex interaction between genetics and enviro

~15% genetic

LRRK2, GBA, PARK2, PINK1 gene

-may help to determine if someone is a candidate for DBS

21
Q

COMMON MOTOR SYMPTOMS

A

resting tremor –> less likely essential tremor

bradykinesia –> slower, smaller movements
–decrement of movement
–interruptions/hesitations

rigidity

postural instability

decreased stride

festination- tiny steps

-FOG

-stooped posture–> camptocormia (abnormal trunk flexion), pisa syndrome (lateral flexion, stooping)

-dystonia–> toe curling, muscle cramps, big toe extension with other phalanx flexion (striatal toe)

22
Q

non-motor symptoms

A

psychiatric–> anxiety, dep, apathy

cog impairment (at 20 years of dod –> 80% have dementia)
–PD-MCI, PD-dementia

-dysautonomia
–constipation
–urinary incontinence
–orthostatic hypotension

-dec sense of smell–> hyposmia/anosmia

-fatigue

-sialorrhea (decreased swallowing reflex –> drooling

-hypophonia, dysarthria –> quiet speech, dec muscle strength of muscles needed for speech

-pain

-sleep: insomnia, Rem sleep behavior disorder (RBD), RLS/PLMS (restless leg/periodic limb movements of sleep

ophthalmology
-convergence insufficiency
-saccadic intrusions
-eyelid opening apraxia

autonomic
-neurogenic orthostatic hypotension
- hyperhidrosis

23
Q

RBD characteristics

A

act out dreams

can happen 10-20 years before diagnosis of the condition

24
Q

Symptoms of pre-motor/prodromal period

A

constipation

RBD

EDS- excessive daytime

sleepiness

hyposmia

depression

25
Q

What is is a symptom of PD that usually only happens in the mid-advanced stages of PD?

A

psychosis

26
Q

Describe the typical progression and clinical course from preclinical phase onward:

A

preclinical phase -2 - (-6 )years

the onset of levodopa therapy/diagnosis–> honeymoon period - 0-3 years

motor complication period- 3-8 years

resistant symptoms - 8-15 years

cognitive decline ~15-20 years

27
Q

What is a DAT scan?

A

dopamine transporter scan

SPECT scan

Ioflupane I 123 injection

tags DA transporters in striatum–> demonstrates integrity of nigrostriatal nerve terminals

-loss of neurons, loss of signal

-cannot distinguish between other forms of PD

28
Q

Differential diagnosis for PD

A

TAUOPATHIES
-progressive supranuclear palsy (early falls, wheelchair sign, can’t look down)
-cortical basal syndrome/degeneration

SYNUCLEINOPATHIES
-multisystem atrophy (dysautonomia, possible cerebellar signs)
-dementia with LB (early dementia, cognitive fluctuation)

TOXINS
-pesticides
-MPTP (contaminated synthetic heroine)
-agent orange
-manganese, lead
-alcohol withdrawal

DRUG-INDUCED
-dopamine antagonist anti-psychotics
-VMAT2 inhibitors
-lithium
-valproic acdid

29
Q

types of tremors not related to PD

A

essential tremor
dystonic tremor
holmes/rubral/midbrain/cerebellar outflow tremor

30
Q

What other disorders did we learn about that can parkinsonian like symptoms?

A

AD

HD

Spinocerebellar ataxia

31
Q

What is the only disease modifying therapy for parkinson’s

A

exercise

(diet and sleep are two other lifestyle modifications)

32
Q

SEs dopaminergic therapy

A

 GI distress (nausea, vomiting)
 Dyskinesias - involuntary, erratic, writhing movements of the face, arms, legs
or trunk. Choreiform
 Orthostatic hypotension
 Decreased B12/folate absorption
 Impulse control disorders (more so with the dopamine agonists)
 Hallucinations
 Dopamine dysregulation syndrome (DDS) (can become addicted)
 Parkinsonism-Hyperpyrexia Syndrome (acute withdrawal, neuroleptic-like
malignant syndrome)

33
Q

non-motor treatment

A

 Anti-depressants/anxiolytics
 Bowel regimen
 Anticholinesterase Inhibitors (donepezil, rivastigmine) –> MAY HELP Freezing of Gait
 Sleep
 RLS/PLMS (ropinrole,
gabapentin, etc)
 RBD (melatonin, clonazepam)  Sialorrhea
 Botulinum toxin injections,
atropine drops

34
Q

Focused ultrasound - advanced therapy

A

With focused ultrasound (FUS), doctors use ultrasound beams to destroy brain cells that cause movement problems. (It’s a bit like using a magnifying glass to focus sunlight rays on a leaf to make a tiny hole.)

permanent lesion via sonification

working towards bilateral treatment

less cog impairment possible

35
Q

Duopa

A

A Carbidopa Levodopa Gel that
is continuously delivered by a
pump through a J tube to the
small intestine

more regulated and on time

bypasses the stomach

enteral admin

NM II (13 decks)

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