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Applied Pathophysiology > Parkinson's Disease > Flashcards

Parkinson's Disease Flashcards

1
Q

What is Parkinson’s Disease?

A

is the 2 most common neurodegenerative disease (after Alzheimer’s disease). Parkinson’s disease is IDIOPATHIC, usually occurs late in life, and is characterized by a variable combo of:
- resting tremor
- rigidity
- slow movements (& difficulty initiating movements)
- shuffling, slow gait
- masked facial expressions

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2
Q

Parkinson’s disease is…

A

CHRONIC & PROGRESSIVE disorder produced by loss of dopaminergic neurons within the basal ganglia (in partic. the substantia nigra!)

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3
Q

What is Parkinsonism?

A

a syndrome of symptoms comparable to Parkinson’s disease (variable
the basal ganglia.
combination of: tremor, rigidity, bradykinesia, gait disturbances) that are caused by loss of dopaminergic neurons due to toxins, vascular damage or inflammatory changes. May occur earlier in life.

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4
Q

What are PD’s symptoms?

A
  • RESTING tremor
  • rigidity (‘cogwheel rigidity’)
  • slow movements & difficulty initiating movements (“bradykinesia”)
  • shuffling, slow gait, stooped unsteady posture
  • masked facial expressions

also often:
- depressed mood
- cognitive impairment

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5
Q

Symptoms may have…

A

have “ON” and “OFF” periods where a patient fluctuates
* cognitive impairment
Also often:
between relatively symptom free (= on) vs. incapacitated (=off).

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6
Q

What is the prevalence & impact of PD?

A
  • majority are >65
  • & in long-term care
  • symptoms at younger age –> increased delay for diagnosis
  • MALES are more likely
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7
Q

Parkinson’s disease is:

A

a CHRONIC and PROGRESSIVE produced by loss of:
DOPAMINERGIC NEURONS within the basal ganglia.

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8
Q

What are apart of the Basal Ganglia?

A
  • Caudate Nucleus
  • Putamen
    Globus pallidus:
  • External segment
  • Internal segment

Subthalamic nucleus

Substantia nigra

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9
Q

What is the loop?

A

Cortex –> Basal Ganglia –> Thalamus –> Cortex

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10
Q

What is Voluntary Movements?

A

are produced by the corticospinal tract (=corticobulbospinal tract)

Frontal cortex areas important in motor planning project to and activate the “primary motor cortex” which elicits movement on the CONTRAlateral side of the body

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11
Q

Where does the Basal Ganglia receive input from?

A

the motor cortex, and project (via the thalamus) back to influence and alter activity in areas of motor plan, and initiating the cortex producing the
the movement.

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12
Q

What are Basal Ganglia imp. for?

A

for the PLANNING, INITIATION, & SMOOTH EXECUTION of movements accomplished by the cortiospinal tract

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13
Q

What are Basal Ganglia?

A

several interconnected nuclei located at the “base” of the cerebral cortices.

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14
Q

What is Basal Ganglia comprised of?

A

Caudate nucleus
Putamen
Globus Pallidus
Subthalamic nucleus
*Substantia Nigra (imp. for PD)

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15
Q

Where does the Basal Ganglia receive input from?

A

areas of motor cortex

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16
Q

Where does the Basal Ganglia project back to?

A

motor cortex via the thalamus

17
Q

What is Basal Ganglia imp. for?

A

smooth initiation & execution of motor programs

18
Q

What are 3 Basal Ganglia dyfunctions?

A
  1. HYPOkinetic movement disorders (ex: PD)
  2. HYPERkinetic movement disorders (ex: Huntington’s disease, maybe Tourette’s)
  3. Dystonia (like a hyperkinetic, but is muscle contraction that may produce an altered posture, or altered head or limb position)
19
Q

What is PD treated with?

A

drugs aimed at increasing dopaminergic activity
- sometimes effectiveness decreases over time b/c of postsynaptic changes (ex: receptor desensitization/internalization)

20
Q

What connects the substantia nigra dopaminergic neurons to other basal ganglia nuclei?

A

nigrostriatal tract

21
Q

There are many ______ interconnections?

A

basal ganglia

22
Q

What is the “direct pathway”?

A

removes inhibition from the thalamus –> ENHANCED activity in the motor cortices

23
Q

What is the “indirect pathway?”

A

ends up inhibiting the thalamus –> DECREASED activity in the motor cortices

24
Q

What pathway is PD?

A

reduced activity in the direct pathway, and
increased activity in the indirect pathway
(–> slow movements = “bradykinesia”)

INDIRECT

25
Q

What pathway is Huntington’s disease?

A

reduced activity in the indirect pathway, and
increased activity in the direct pathway
(–>excessive movements = “hyperkinesia”)

26
Q

What causes the loss of dopaminergic neurons?

A

Parkinson’s disease is most often IDIOPATHIC (=cause unknown).
-denoted idiopathic Parkinson’s disease (IPD)

27
Q

There are known causes of Parkinsonism, such as:

A
  1. Drugs (partic. antipsychotics)
    - largely dopamine antagonists (that –> Parkinsonism)
    - usually resolves after drug use stopped
  2. Toxins (ex: MPTP, & pesticide “rotenone”)
    - impurity in synthetic opioid production –> caused Parkinsonism in drug users
    - has been used as a tool for research
    - IRREVERSIBLE damage to dopaminergic neurons
    - one mech is known to be due to –> mitochondrial dysfunction & free radical production
  3. Infections
    - post-encephalic syndrom
    - viral illness that causes degeneration of substantial nigria neurons
  4. Injury/trauma
    - substantia nigra neurons may be particularly susceptible to trauma
    - boxers are ~4x more likely to develop Parkinsonism!
28
Q

Loss of dopaminergic neurons is…

A

PROGRESSIVE & largely SUB-CLINICAL (meaning we’re not gonna know)

*Symptoms don’t show up until SN cells are ~80% gone! (only 20% present)

29
Q

What is the treatment of PD?

A
  • There is NO CURE for Parkinson’s disease.
  • Treatment goal is to MINIMIZE the symptoms (i.e. facilitate function).
  1. Pharmacological
  2. Deep Brain Stimulation
  3. Therapy
30
Q

What is the Pharmacological Treatment Strategies for PD?

A
  • Increase dopamine:
    ‐ L‐DOPA (levodopa)
    ‐crosses the blood brain barrier (dopamine does not) ‐increases dopamine release at remaining synapses
    ‐given in conjunction with DOPA Decarboxylase Inhibitor (ex: Carbidopa)
  • Decrease dopamine breakdown:
  • monoamine oxidase inhibitors
  • Dopamine agonists (more SE’S)
  • do not rely on release from dopaminergic neurons (activate postsynaptic receptors directly)
  • can –> more prolonged stimulation of dopaminergic receptors
  • Anticholinergics
  • may be beneficial (alter balance of activity in basal ganglia, & also in cortex)
  • may not be tolerated well in the elderly (various side effects, & exacerbates memory loss & confusion that might already be present - like Dementia)
31
Q

Why would you want to increase dopamine by L-DOPA?

A

‐because DOPA Decarboxylase is also in the peripheral nervous
system (and levodopa would get converted to dopamine there)
–> side effects!
‐CARBIDOPA doesn’t cross BBB, so reduces conversion in the PNS
‐COMT INHIBITORS (catechol‐O‐methyl transferase) also decrease levodopa breakdown in the periphery

‐ L‐DOPA (levodopa) (cont’d)
‐ usually provides a FEW YEARS of therapeutic efficacy.

32
Q

Why isn’t L-DOPA a cure?

A
  • relies on DOPAMINERGIC neurons (that continue to degenerate)
  • high dopamine release from the synapses that are left may stimulate mech’s to turn down those synapses (ex: receptor internalization, desensitization etc.)

ALSO, L-DOPA treatment can –> DYSKINESIA
(unwanted dysfunctional movements: tic’s, chorea, etc.)

33
Q

What is the Deep Brain Stimulation for PD?

A
  • Implanted electrodes in thalamus or basal ganglia
  • Electrical stimulation using an implanted stimulator can be very effective for relieving some symptoms
  • May require bilateral electrodes & stimulation (uni or bilateral)
34
Q

What is the Therapy for PD?

A
  • Physical therapy, Occupational therapy
  • Musical gait therapy
  • auditory rhythm may help activate the basal ganglia rhythmically

Applied Pathophysiology (34 decks)

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