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PSY3180 Neuropsychology > Lecture Week Four: Parkinson's Disease > Flashcards

Lecture Week Four: Parkinson's Disease Flashcards

1
Q

What is the Basal Ganglia, and where is it?

A

BG is a group of grey matter sub-cortical structures, adjacent to the thalamus.

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2
Q

What are the two subcortical motor systems that project to the cortex via the thalamus?

A
  • BGTC (basal ganglia thalamo-cortical) motor circuit

- The Cerebellar motor system

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3
Q

What are the three major components of the motor system in the brain?

A
  • Motor Cortex
  • Basal Ganglia
  • Cerebellum
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4
Q

Basal ganglia includes what structures? (5)

A
  • Caudate
  • Putamen
  • Globus pallidus
  • Subthalamic nucleus
  • Substantia nigra
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5
Q

All cerebellar output originates in the ____ ____ _____

A

All cerebellar output originates in the DEEP CEREBELLAR NUCLEI

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6
Q

The BGTC motor circuit is responsible for…

A

controlling the preparation and execution of motor plans/schemata

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7
Q

What is a motor program?

A

a set of motor commands needed to execute a simple motor act.

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8
Q

What BG circuit is involved in simultaneous movements, & execution of learned motor programs (e.g. walking)?

A

BGTC Motor Circuit

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9
Q

Without BG output, what is affected?

A

initiation, execution, & sequencing of automatic actions are affected.

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10
Q

How does the BG motor circuit work?

A

There are two pathways for the BG motor circuit:

  1. Direct: Premotor areas -> Putamen -> GPi/SNr -> Brainstem -> Spinal cord
  2. Indirect: Premotor areas -> Putamen -> GPe -> STN -> GPi/SNr -> Brianstem -> Spinal cord
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11
Q

In the BG motor circuit, what inhibits the thalamus?

A

the GPi and SNr

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12
Q

In terms of the BG motor circuit, (direct and indirect pathway), which pathway is mediated by D1-type dopamine receptors, and which is mediated by D2-type dopamine receptors?

A

Direct pathway = D1-type dopamine receptors

Indirect pathway = D2-type dopamine receptors

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13
Q

What are D1 and D2-type dopamine receptors responsible for?

A 
D1 = initiating behavioural responses
D2 = inhibiting behavioural responses
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14
Q

Is the Direct or Indirect BG pathway affected by early Parkinson’s Disease?

A

Direct pathway is affected

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15
Q

Is the Direct or Indirect BG pathway affected by early Huntington’s Disease?

A

Indirect pathway is affected

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16
Q

What does SNpc stand for?

A

The Substantia Nigra pars compacta (SNpc)

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17
Q

What is the SNpc?

A

A brain structure that is densely packed with large dopamine-containing
neurons.
• It receives GABAergic inhibitory input from the striatum.
• SNpc neurons project back to the caudate and putamen in a topographic manner.
• Action of the dopamine depends on the type of receptors -> dopamine then acts to modulate the excitatory corticostriatal input

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18
Q

The 5 parallel, segregated ‘basal ganglia thalamocortical (BGTC) circuits’ include:

A
  1. Skeletomotor circuit
  2. Oculomotor circuit
  3. DLPF circuit
  4. LOF circuit
  5. AC circuit
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19
Q

What kind of input occurs in the skeletomotor circuit?

A

premotor and somatosensory cortical input

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20
Q

What kind of input occurs in the oculomotor circuit?

A

Frontal eye field & cortical input

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21
Q

What kind of input occurs in the DLPF circuit?

A

input from the dorsolateral prefrontal cortex

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22
Q

What kind of input occurs in the LOF circuit?

A

input from the lateral orbitofrontal cortex

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23
Q

What kind of input occurs in the AC circuit?

A

input from the anterior cingulate and medial OFC

24
Q

What is the organisation/order of the skeletomotor circuit?

A

SMA + cortical inputs -> Putamen -> GPi/SNr -> Thalamus

25
Q

What is the organisation/order of the oculomotor circuit?

A

FEFs + cortical inputs -> Caudate -> GPi/SNr -> Thalamus

26
Q

What is the organisation/order of the Dorsolateral Prefrontal Cortical circuit?

A

DLPFC + cortical inputs -> Caudate -> GPi/SNr -> Thalamus

27
Q

What is the organisation/order of the Lateral Orbitofrontal Cortical circuit?

A

LOFC + cortical inputs -> Caudate -> GPi/SNr -> Thalamus

28
Q

What is the organisation/order of the Anterior Cingulate circuit?

A

AC + cortical inputs -> Ventral Striatum -> GPi/SNr -> Thalamus

29
Q

What are the main/only causes of BG dysfunction and/or damage?

A

Parkinson’s and Huntington’s Diseases

30
Q

Which disease is associated with damage to SNpc neurons?

A

Parkinson’s Disease, onset often occurs at age 65-70.

31
Q

In terms of Parkinson’s Disease-related degeneration of the SNpc, at what % of cell loss do symptoms normally appear?

A

Symptoms typically appear after around 70-80% of SNpc cell loss

32
Q

What is the main deficit or consequence that results due to PD?

A

The main deficit is dopaminergic cell loss in substantia nigra (which projects to the striatum), and the formation of Lewy bodies

33
Q

What neuroanatomical regions are affected by PD? (8)

A 
Putamen (part of the motor loop)
Medial olfactory area, 
Lateral hypothalamus,
Amygdala,  
Entorhinal, 
Cingulate, 
Hippocampal
Frontal cortices
34
Q

What is the most characteristic pathological marker of PD?

A

Lewy Bodies; which are abnormal aggregations of protein that develop inside nerve cells. They have a spherical structure, and contain filaments and degenerating organelles.

35
Q

How does the brain try and compensate for the substantial Nigrostriatal Degeneration (70-80%) due to PD?

A

Remaining survivor neurons produce an increased dopamine output

36
Q

What ways does PD affect the BG motor circuits? (3)

And, what is the overall net result?

A

• In PD there is an underactive motor circuit (not as excitable as it should be)
• Loss of dopamine from the SNpc leads to over inhibition of the GPe in the indirect pathway (so that output nuclei are over activated)
• Reduced dopamine also leads to reduced activity along the direct inhibitory projection from the putamen to GPi/SNR (causes akinesia and rigidity)
• Net result - decreased thalamic output –
hypokinesia or decreased motor activity

37
Q

What are the suspected causes of PD?

A

Genetic predisposition (5-10% of cases are familial), and Genetic Mutation that forms the following abnormal proteins; parkin, ubiquitin, and a-synuclein.

38
Q

What mutated protein is a major component of PD Lewy Bodies?

A

a-synuclein

39
Q

What external factors can cause mutations in the a-synuclein gene?

A

toxins like industrial chemicals, carbon monoxide, herbicides, and pesticides

40
Q

What is levodopa?

A

Also known as L-dopa, it is a precursor for dopamine. It crosses the blood brain barrier and directly metabolizes into dopamine and helps stimulate the release of dopamine. It alleviates tremors, bradykinesia, and rigidity.

41
Q

When does L-dopa dose need to be increased?

A

More L-dopa is needed when more neurons die due to PD. More side-effects also occur.

42
Q

What is Pallidotomy?

A

A surgical procedure that creates a lesion in the ventral or internal portion of the globus pallidus. PD-related dopamine decreases cause the pallidum to become overactive, lessioning the GP structure arrests this accessive activity.

43
Q

who might have a Pallidotomy?

A

patients who are experiencing difficulty with the PD drugs

44
Q

Patients receiving deep brain stimulation to the globus pallidus and subthalamic nucleus show…

A
  • Improved motor functioning,
  • Increased metabolism in the
    premotor cortex and cerebellum.
  • Alleviates PD symptoms without negative effects.
45
Q

What are stem cells?

A

A renewable source of tissue that can be coaxed to become different cell types of the body

46
Q

What are the best-known stem cells?

A 
Embryonic stem (ES) cells. found
within an early-stage embryo. These cells can generate all the major cell types of the body (they are “pluripotent”).
47
Q

What do adult stem cells do?

A

adult stem cells help with maintenance and repair by becoming specialized cells types of the tissue or organ where they originate

48
Q

What has been the level of response (%) in PD patients who received Stem Cell Therapy?

A

After 3 years of stem cell therapy, recipients under 60 yrs had improved 30% and older patients by 14%

49
Q

What is one major hurdle to stem cell therapy for Parkinson’s Disease?

A

Work is still needed to generate robust cells, in both quality and quantity, that can also survive and function appropriately in a host brain

50
Q

How are cues used in rehabilitation therapies for PD?

A

Internal cueing mechanisms (via globus pallidus) are damaged and patients rely on cues to direct movements. Two major external cues are used in clinics:

  • Tape cues on a walkway allow patients to increase their stride length
  • Metronomes act as cues to initiate movements and also act as rhythmical music therapy for PD patient’s homes.
51
Q

Finish these facts about PD:
– A form of _________ ___________ dementia
– Attacks the _____ ______ (mainly the _______ ______) and the _________ system
– Slowed _____ ______ and ______ function
– Is not common under ___ years
– Average age at onset is ___ years
– PD is a ______ disorder; there are a range of clinical features

A

FACTS:
– A form of sub-cortical neurodegenerative dementia
– Attacks the basal ganglia (mainly the substantia nigra) and the dopaminergic system
– Slowed general motor and cognitive function
– Is not common under 40 years
– Average age at onset is 65 years
– PD is a heterogeneous disorder; there are a range of clinical features

52
Q

What are the 7 motor symptoms of PD?

A

– Resting tremor
– Bradykinesia (difficulty executing movements)
– Akinesia (difficulty initiating movements)
– Muscular rigidity & impaired balance
– Stooped posture, small, shuffling steps, poor arm swing
– Micrographia (progressive shrinking of writing)
– “Masked face” (expressionless face)

53
Q

What are the 5 Executive Functioning difficulties in PD?

A 
– changing mental set
– maintaining mental set
– set-shifting
– verbal fluency
– planning and organizing
54
Q

What happens to language and speech in PD patients?

A 
General language processing and sentence structure is intact (no aphasia or linguistic impairment).
Some problems with:
- Understanding grammatical complexity
- Articulation
- Bursts of speech
- Compulsive word repetition
55
Q

What happens to memory in PD patients?

A

Memory function is relatively spared in PD. May show recall deficits on:

  • paired associative learning,
  • visual reproduction of geometrical designs
    (note: PD patients still show encoding and registration of this material, just impaired recall)
56
Q

Do people with Parkinson’s Disease often have good insight on their problem?

A

Yes!

57
Q

What happens to Visual-Spatial skills in PD patients? (4)

A

Evident impairment.

  • Poor visual spatial activity on motor and non-motor tasks
  • Impaired ability to do matching, drawing of lines, and following targets on a screen
  • Slowed eye initiation and execution
  • Overshoot targets and have hypo reflexivity

PSY3180 Neuropsychology (11 decks)

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