Parkinson's Disease Flashcards

1
Q

briefly describe the anatomy of the basal ganglia

A
  1. Striatum
    1. cuadate
    2. putamen
  2. Globus pallidus
    1. internus
    2. externus
  3. Substantia nigra
    1. compacta
    2. reticularis
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2
Q

what is the role of the basal ganglia?

A
  1. Motor control
    • initation and execution of movement
    • prevention of unwanted movements through inhibitory control
    • direct and indirect pathways that work together to help create desired movement
  2. Eye-movement loop
  3. Goal-directed behavior loop
  4. Social behavior loop
  5. Emotion loop
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3
Q

describe the direct pathway of basal ganlia control

A
  1. Thalamus, gone unchecked, sends constant excitatory signals to cortex to elicit movement
  2. GP, SN inhibit thalamus to prevent unwanted movement
  3. When movement is needed, cortex sends info to striatum, which in turn inhibits GP and SN
    • this opens gate for thalamus to resume excitatory projections to cortex to elicit movement
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4
Q

describe the indirect pathway of the basal ganglia

A
  1. When movement is NOT needed, cortex has striatum inhibit GPe, losing its usual ability to inhibit subthalamic nuclei
  2. Cortex then activates subthalamic nuclei, who’s job is to send excitatory signals to GPi and SN, which strengthens their inhibition of thalamus
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5
Q

describe regulation of the direct and indirect loops

A
  1. Substania Nigra pars compacta neurons have connections to the striatum
  2. those connections modulate activity of indirect pathway through dopamine release in striatum
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6
Q

List important BG neurotransmitter

A
  1. Dopamine
  2. Acetylcholine
  3. GABA
  4. Glutamate
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7
Q

where is dopamine made and what does it do?

A
  1. Made in substantia nigra pars compacta
  2. SNPC uses it to modulate striatum activity by releasing dopamine to impact both direct/indirect pathways
    • excitatory to striatum neurons in direct pathway
    • inhibitory to striatum in indirect pathway
    • dual effect = powerful decrease in suppression of thalamus BG → futher facilitation of movement
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8
Q

what is the role of ACh?

A
  1. inhibits dopamine when appropriate
  2. can quickly interrupt ongoing motor behavior in response to salient environment stimuli
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9
Q

what is the role of GABA and Glutamate?

A

both are primary NT in direct and indirect pathways

GABA → inhibitory

Glutamate → excitatory

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10
Q

List BG dysfunctions/disorders

A
  1. Parkinson’s Disease
    • Parkinsonisms
  2. Huntington’s Disease
  3. Tardive Dyskinesia
  4. Dystonia
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11
Q

List other causes of BG dysfunction

A
  1. CO poisoning
  2. Copper poisoning
  3. Drug OD
  4. Head injury
  5. Infection
  6. Liver disease
  7. Metabolic problems
  8. MS
  9. Side effects of certain meds
  10. Stroke
  11. Tumors
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12
Q

List the general S/S of BG dysfunctions

A
  1. Difficulty initiating, continuing or stopping movements
  2. Muscle tone abnormalities → rigidity
  3. Increased involuntary movements
    • Hemiballismus
    • Athetosis
    • Chorea
    • Tremor
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13
Q

define hemiballismus

A

rare hyperkinetic movement disoder (subtype of chorea)

characterized by violent involuntary limb movements, unilaterally

movements are wider and more intense than chorea

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14
Q

define athetosis

A

slow, involuntary, convoluted, writhing movements of the fingers, hands, toes, and feet and in some cases arms, legs, neck and tongue

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15
Q

define chorea

A

involuntary, irregular unpredictable muscle movements

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16
Q

What is Parkinson’s Disease?

A

idiopathic, slowly progressive degenerative disease with non-motor and motor symptoms

17
Q

List S/S of PD

A
  1. Parkinsonian gait
  2. Slowed movement
  3. Reduced arm swing
  4. Rigidity
  5. Freezing
  6. Shuffling steps
  7. Postural instability
  8. Asymmetric resting tremor
  9. Mask like face
18
Q

Describe incidence and prevalance of PD

A
  • 1-2% of persons > 60
    • incidience increases w/age
  • 1 million cases in US, 5-10 million world wide
  • Men > women (3:2)
  • Mean age of onset: early 60s
    • young onset (21-40) PD occurs in 5-10% of cases
  • decreased prevalence in black and Asian populations
19
Q

List and describe the 2 etiologic subgroups of PD

A
  1. Primary Parkinsonism (PD) → unknown etiology
    • hypothesis - complex interaction of factors
      • age, genetics, environment
  2. Secondary Parkinsonism
    • infectious/postcephalitic, atherosclerosis, toxic, drug-induced
20
Q

describe the pathophysiology of PD

A
  1. degeneration of dopaminergic neurons in BG
    • loss of DA stores in substania nigra
  2. As disease progresses, numerous other regions of brains involved as well as impaired modulation of other NTs
21
Q

How is PD clinically dx?

A
  1. Clinical exam → dx of exclusion
  2. may do a levodopa/carbidopa trial
    • most recent guidelines are shifting away from this
  3. Some pts will undergo SPECT scan
    • dopamine transporter scan (DaTscan)
  4. Only definitive way to dx PD is post-mortem exam of the brain
22
Q

List the 4 cardinal PD motor symptoms

A
  1. Bradykinesia, Akinesia, Hypokinesia
  2. Rigidity
  3. Tremor
  4. Postural Instability
23
Q

T/F: motor symptoms appear early on in the disease progression

A

FALSE

motor symptoms do not appear until - 60% neurodegeneration has already occured in BG

24
Q

describe the motor symptoms of bradykinesia, akinesia, hypokinesia

A
  1. Spontaneous and purposeful movements affected
  2. initiation, alteration in direction, stoppage all affected
  3. Complex tasks > simple commands
25
Q

what is the difference between bradykinesia, akinesia, hypokinesia?

A
  1. Bradykinesia → slowing/reducing of movement
    • cardinal feature of all parkinsosim disorders
    • multifactorial
    • result of insufficient recruitment of muscle force during movement
    • BG’s perception of how much force it wants to generate decreases
  2. Akinesia → complete loss of movement
    • will see in face
    • loss of arm swing in gait
  3. Hypokinesia → reduced movements
    • thought to be an issue w/force production
    • noticeable during writing tasks → letters look small and barely legible
    • minimal trunk movement during gait
26
Q

T/F: bradykinesia, akinesia, and hypokinesia are often the most disabiling symptom of PD?

A

TRUE

27
Q

describe the PD motor impairment → rigidity

A
  1. felt uniformly in all directions
    • asymmetrical early on in disease → eventual whole-body involvement (including trunk)
  2. usually seen proximally first
  3. leads to increased cognitive load, emotional stress energy expenditure of movements
    • long-term effects = decreased ROM, contractures, postural deformities
  4. Types:
    • lead pipe → sustained resistance
    • cogwheel → jerky, ratchet-like (lead pipe + tremor)
28
Q

describe the motor impairment → tremor

A
  1. resting tremor early on (can see kinetic as disease progresses)
  2. hands and foot most common, can see in head, neck, jaw or tongue
  3. tends to be mild, low frequency
  4. 70% of PD pts will experience a tremor at some point in the disease progression
  5. progression in 2 ways:
    • resting to moving tremor
    • travel to bilateral involvement
29
Q

describe the motor impairment → postural instability

A
  1. abnormal and inflexible postural responses
  2. smaller functional LOS
  3. difficulties w/self-initiated movements
  4. reduced anticipatory postural adjustments and control
  5. abnormal patterns of coactivation
  6. midline disorientation
  7. additional contributing factors:
    • rigidity
    • weakness
    • loss of ROM
    • freezing
    • meds AE
30
Q

What are the implications of PD Postural Instability?

A
  1. Pts with PD are 9x more likely to fall
  2. Falls become increasingly prevalent as disease progresses to the middle stages
    • disappear in late stages as pts become immobile
31
Q

what are the biggest overall risk factors for falls in PD pts?

A
  1. postural instability
  2. disease severity
  3. gait impairments (most notably Freezing of gait)

Other:

dementia, depression, postural hypotension, involuntary movements from long-term med use

32
Q

List additional motor symptoms of PD (outside of the 4 cardinal symptoms)

A
  1. Weakness
    • many potential causes:
      • decrease in torque production at all speeds
      • dopamine related?
      • EMG: delayed MU recruitment, asynchronization
      • disuse weakness common
      • Fatigue
  2. Breakdown of complex motor planning
    • sequential movements
    • transitioning between movements