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SF2 - Test 3 > 3 - Extrapyramidal Systems > Flashcards

3 - Extrapyramidal Systems Flashcards

1
Q

Major contributors to the motor system:

Pyramidal Motor System (direct and indirect)

A

Planning and initiating voluntary motor movement and muscle tone

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2
Q

Major contributors to the motor system:

Cerebellum

A

Balance, equilibrium and real time motor adjustment

NO direct projection to the cortical spinal system

Clinical: Voluntary movement disorders (ipsilateral)

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3
Q

Major contributors to the motor system:

Extrapyramidal Motor System

A

Motor programming–plan, initiate, maintain

Habitual behaviors–procedural learning

NO direct projections to the cortical spinal system

Involuntary movement disorders (contralateral)

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4
Q

Where do Basal Ganglia and Cerebellum nuclei project?

A

To Thalamus

NOT direct to spinal cord

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5
Q

What connects basal ganglia to thalamus?

What type of signals does it send?

A

Globus Pallidus

Inhibitory ONLY; levels of this just change

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6
Q

What connects cerebellum to thalamus?

A

Deep cerebellar nuclei

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7
Q

Substantia Nigra:

Pars Compacta vs Pars Reticularis

A

Pars Compacta - neurons contain melanin

Parts Reticularis - neurons DONT contain melanin

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8
Q

Clinical:

Hypokinetic vs Hyperkinetic Disorders

A

Hypokinetic: Parkinson’s

Hyperkinetic: Huntingtons chorea, Ballismus dystonia

Movement disorder is always contralateral to the injury or lesion

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9
Q

Clinical: Parkinson’s Disease

Pathways?

A

Degeneration of the DA neurons in the SNc

Hypokinetic Disorder

Reduced excitation of the Direct (Go) excitatory pathway = hard to initiate movement

Reduced inhibitory drive of Indirect (No Go) inhibitory pathway = hard to release thalamus from inhibition to start movement

*Both pathways affected

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10
Q

Parkinson’s Disease

Motor Symptoms

A

Resting tremor

Cogwheel rigidity

Bradykinesia (slowness in movement)

- decreased size of handwriting, loss of voluntary movement

  • Unsteady gait, retropulsion
  • Speech and swalling disturbances
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11
Q

Parkinson’s Disease

Non-motor Symptoms

A

Sensory Abnormalities - Olfactory (often 1st), Parathesia (dermal sensation)

Autonomic Dysfunction

Depression/Anxiety/Sleep Disorders

Masked facies and ‘reptillian stare’

Dementia

Akathisia (restlessness)

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12
Q

Clinical: Tremor

General Definition and Differentiating Myoclonus?

A

Rhythmic or semi-rhythmic oscillating movements that can be fast or slow

  • -

Can differentiate from myoclonus in that tremor has both agonsit and antagonist muscles are activated; resulting in BIDIRECTIONAL movements

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13
Q

Clinical: Essential Tremor

A

Familial, benign, or senile tremor–most common

Effects upper extremities, head, tongue, lips, and vocal cords

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14
Q

Clinical: Resting Tremor

A

Occurs when limbs are relaxed and decrease in intensity or disappear when the limb is moved

Usually involves upper extremities, includes pill roll tremor

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15
Q

Clinical: Intention Tremor (Ataxic Tremor)

A

Produced with purposeful movement toward a target, such as lifting a finger to touch nose

Usually worsens as you get closer to target

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16
Q

Clinical: Postural Tremor

A

Occurs when the limbs are actively held in position against gravity and disappears at rest

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17
Q

UMN Lesion vs Basal Ganglio Lesion?

A

Rigity is key

UMN = clasp knife

Basal Ganglia = ratchet like interuptions; Cogwheel Rigidity

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18
Q

Clinical: Parkinson’s Pathology

Synucleinopathy?

Iron?

A

90% cases unknown origin

Degeneration of DA neurons in the SNc indicated by loss of melanin-containing neurons

Type of proteinopathy caused by protein misfolding and involves presence of Lewy Bodies that positively stain for alpha-synuclein

- - -

Abnormal accumulation of iron in the melanin-containing degenerating neurons

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19
Q

Clinical: Parkinson’s Treatment Strategies

Drugs / Side Effects

A

Drugs:

Levodopa + carbidopa

MAO inhibitors (slow breakdown of DA)

COMT inhibitors (slow breakdown of L-dopa)

Side Effects:

  1. Dyskinesia/hypokinesia: on-off phenomena due to high dose followed by decreeasing drug levels
  2. L-dopa induced dyskinesia after long-term use of L-Dopa
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20
Q

Clinical: Parkinson’s Disease Treatment Strategies

Surgery

A

Thalamotomy - radiofrequency ablation

Deep Brain Stimulation (DBS) - electrodes implated contralateral; pulse generator provides high-frequency electrical stimulation

Symptoms: Dysarthria and balance

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21
Q

Clinical: Wilson’s Disease

A

Copper metabolism disease that causes progressive degeneration of the LIVER and BASAL GANGLIA

Present earlier in life (20s)

Symptoms:

Rings in cornea

Wing beating tremor

rigidity, bradykinesia, impaired speech, psychiatric symptoms, abnormal liver panel

22
Q

Clinical: Huntington’s Disease

A

Autosomal dominant linked to expansion of CAG triplet repeat sequency

Progressive Striatal Neurodegenerative Disease

Targets: Striatum (caudate/putamen), particularly enkephalin-containing neurons in indirect pathways

***Net effect is INCREASED thalamic EXCITATION due to REDUCED INHIBITION through the Indirect pathway***

LOSS OF CONTROL OF INDIRECT PATHWAY

23
Q

Clinical: Huntington’s Disease Symptoms

A

Hyperkinetic Disorder that includes all 4 basal ganglia functions (movement, eye control, emotion, cognition)

Symptoms show 30-40

Symptoms:

Choreiform Movement

Athetosis

Psychiatric disturbances (depression, anciety, OCD, manic-like behavior)

Dystonic posturing

Tics

Dementia

24
Q

Clinical: Chorea Movements

A

Fluid or jerky involuntary movements of varying qyality

Can be mistaken for fidgeting

Severe: Frantic, constantly occurring movements that interrupt voluntary movements

Hemi-chorea is observed with contralateral infarct, hemorrghage, tumor, abscess, or focal lesion

25
Q

Clinical: Athetosis

A

Slower form of chorea, characterized by continuous, involuntary writing movements that prevent maintains of stable posture

26
Q

Clinical: Dystonia

A

Abnormal or distorted posturing of the limbs, trunk, or face due to sustained contraction of muscles (Charlie Horse)

Painful; can result in hypertophy

Can be generalized (whole body), unilateral, or focused

27
Q

Clinical: Tics

Example?

A

Urge to perform a sudden brief action

Motor tics: face, neck, eye blinks, and less often in extremities

Vocal tics: brief grunts, coughing barking

Example: Tourette’s Syndrom

28
Q

Clinical: Ballismus

A

Wild flinging movement of the extremities

Subthalamic Nucleus Lesion, results in net INCREASE in thalamic EXCITATION due to REDUCED INHIBITION via the INDIRECT PATHWAYS = HYPERKINETIC effect

29
Q

Clinical: Hemiballismus

A

Unilateral (contralateral to lesion) flinging movements to to unilateral lesion to one subthalamic nucleus

Usually Stoke, hemorrhage, tumor, infection, or inflammation

30
Q

Clinical: Causes of Disease of Direct/In Direct Pathway

Stroke/Infarct

A

Anterior and Middle Cerebral Arteries supply Striatum

Anterior Choroidal Arteries supple the striatum

Posterior Cerebral Artery supplies the SN

31
Q

Clinical: Causes of Disease of Direct/In Direct Pathway

Medication

A

D2 Antagonists (no-go, inhibitory) such as anti-psychotics can result in irrecversible development of tardive dyskinesia

(involuntary movement of the tongue lips, face, trunk, and extremities)

32
Q

Clinical: Causes of Disease of Direct/In Direct Pathway

Other Causes

A

Tumor

Carbon Monoxide Poisoning

Pesticides

33
Q

What is the rough transmission of neural signals through the body movement loop?

Cortical Input ->

Striatum ->

Pallidum ->

Thalamus ->

A

Cortical Input: Motor, Premotor, Somatosensory

Striatum: Putamen

Pallidum: Lateral Globus Pallidus, Internal Segment

Thalamus: Ventral Lateral, and Ventral Anterior Nuclei

Cycles back to cortical targets

34
Q
A
35
Q

What separates the Striatum/Neostriatum?

What compromises the Neostriatum?

A

Separated by the internal capsule

Neostriatum = Caudate + Putamen

36
Q

What comprises Lentiform Nucleus?

A

Lentiform Nucleus = Putamen+Globus Pallidus

37
Q

What comprises the Corpus Striatum?

A

Corpus Striatum =

Caudate+Putamen+Globus Pallidus

*Principle component of the extrapyramidal system*

38
Q

What are GPe and GPi?

A

Globus Pallidus External, Globus Pallidus Internal

Globus Pallidus allows Basal Ganglia to send inhibitory signals to the Thalamus

39
Q

Neurotransmitters:

Major Input + Type?

Major Output + Type?

A

Input:

Glutamate (excitatory)

Dopamine (modulatory)

Output:

GABA (inhibitory)

40
Q

What is the main neurotransmitter of the following:

Cortico-Striatal Pathway

Nigro-Striatal Pathway

Thalamo-Striatal Pathway

A

Cortico-Striatal = Glutamate (excitatory)

Nigro-Striatal = Dopamine (modulatory)

Thalamo-Striatal = Glutamate (excitatory)

41
Q

What can be said for the activity of GPi (Globus Pallidus Internal) neurons?

A

They are inhibitory and tonically active (No-Go Indirect path)

42
Q

Direct Pathway - GO

Travel Path?

Net Effect?

Neurotransmitter + Receptor

End Result

A

Travel: Striatum direct to Globus Pallidus Int. (GPi) or Pars Reticularis (SNr)

Net: Facilitates Movement; excitations through thalamic connections to motor/pre-motor cortex

NT / RX: Dopamine + D1-receptors (excitatory)

**DECREASE Direct = Decrease GO = INCREASE Inhibition (Thalamus) = LESS movement**

43
Q

Indirect Pathway - NO GO

Travel Path?

Net Effect?

Neurotransmitter + Receptor

End Result

A

Travel: Striatum direct to Globus Pallidus Ext. (GPe) and Subthalamic nucleus to Globus Pallidus Int. (GPi) or Pars Compacta (SNc)

Net: Inhibits movement through thalamic connections to motor/pre-motor cortex

NT / RX: Dopamine + D2-receptors (inhibitory)

**DECREASE Indirect = Decrease NO-GO = DECREASE Inhibition (Thalamus) = MORE movement**

44
Q

What three nuclei make up the corpus striatum?

A

Caudate

Putamen

Glubus Pallidus

45
Q

What are 3 incoming projections to the neostriatum and what neurotransmitter do they use?

A
  1. Cortico-Striatal: Glutamate (+)
  2. Nigro-Striatal: Dopamine
  3. Thalamo-Striatal: Glutamate (+)
46
Q

What are two major outputs from the neostriatum and what neurotransmitters do they use?

A
  1. Glubus Pallidus - Thalamus
  2. Neostriatum - SNr

Both NT’s are GABAergic Inhibitory

47
Q

Are D1 or D2 receptors excitatory and what is this kind of neuron?

A

D1 = Excitatory

Neurotransmitter = Dopamine

D2 = Inhibitory

Neurotransmitter = Dopamine

Medium Spiny Neurons

48
Q

What is the Parkinson’s Triad of Symptom, and what nuclei are affected?

A
  1. Resting tremor
  2. Cogwheel Rigidity
  3. Bradykinesia (slowness in movement)
    - - -

Dopaminergic Neurons from SNc

49
Q

What symptoms differentiate PD, Wilson’s and Huntington’s

A

Parkinson’s: Olfactory dysfunction, Reptillian stare, speech/swalling

Wilsons: Wing Beating, Corneal Rings

Huntington: Choreiform movement, Tics

50
Q
A

SF2 - Test 3 (25 decks)

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