CNS Unit 11 Cerebellum and Basal Ganglia Flashcards

1
Q

Where does the Cerebellum receive sensory Information from?
Where does it send information back to?

A

From the brain and spinal cord about body position and movement (Rate, Timing and Force)

  • Exerts it influence by sending information back to motor systems of the cortex and brainstem to correct the movement
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2
Q

What is the Main Role of the Cerebellum?

A

To detect any movement that deviates from the intended cortical commands

“Error detector-movement corrector”

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3
Q

What are the 3 Major Functions of the Cerebellum?

A

Synergy of Movement
- Properly grouping movements for the performance of selective response and also has a role in motor learning

Maintenance of Upright Posture
- With respects to one’s position in space

Maintenance of Tone
- Maintaining tension/firmness (ie tone) during a muscle contraction

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4
Q

What are the Functional Regions of the Cerebellum, what are their functions and what motor pathway influences them?

A
  • Lateral Hemisphere
    -Function: Motor Planning for extremities
    -Motor Pathways influenced: Lateral corticospinal tract
  • Intermediate Hemisphere:
    -Function: Distal Limb Coordination
    -Motor Pathway Influenced: Lateral corticospinal tract
  • Vermis and Flocculondular Lobe:
    -Function: Proximal limb and Truck Coordination ; Balance and Vestibulo-ocular reflexes
    -Motor Pathway Influenced: Anterior Corticospoinal tract, reticulospinal tract, vestibulospinal tract and tectospinal tract
    (This is for prox. limb and trunk coordination)
    Medial Longitudinal Fasciculus
    (This is for balance and vestibulo-ocular reflexes)
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5
Q

What are the Deep Cerebellar Nuclei, and what is their function?

A

“Dont Eat Greasy Food”
- Dentate: Input from lateral regions. (This is the largest, its active just before voluntary movements, and works on our extremities)
- Emboliform: Input from intermediate regions
- Globase: Input from intermediate regions
- Fastigial: Input from medial regions (Often works together with the Vestibular Neclei, they tend to influence the vermis and flocculonodular lobes, they exert influence over the trunk)

  • Vestibular Nuclei (Brainstem): Function in some ways like deep cerebellar nuclei, input from inferior vermis and flocculi

The Emboliform and Globase together make the Interposed Nuclei (These movements are active during and in relation to the movement, they work mainly on our limbs)

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6
Q

In the Cerebellum, what are two kinds of Synaptic Inputs?

A
  • Mossy Fibers, these climb up and as they enter the molecular layer they bifurcate and turn into parallel fibers, become inverwoven with in Purkinje cells and thats how they synapse, these Purkinje cells send information down and out to our Deep Cerebellar Nuclei and Vestibular Nuclei
  • Climbing Fibers, similar to mossy fibers

  • Mossy Fibers receives input from Pontine nuclei and other sources
  • Climing Fibers receives input from inferior olivary nucleus
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7
Q

What are the Principles of Cerebellar lesions?

A
  • Ataxia is Ipsilateral to the side of the lesion
  • Midline lesions cause unsteady gait (Truncal Ataxia) and eye movement abnormailites
  • Lesions to lateral vermis cause limb ataxia (Appendicular Ataxia)
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8
Q

What are the Cerebellar Output Pathways?

A

Pathways from the cerebellum to the lateral motor systems and periphery are double crossed. (This is why deficits and coordination occur ipsilateral to the lesion)

  • Lesions of the vermis dont cause unilateral deficits because medial motor systems influence the proximal trunk musculature bilaterally
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9
Q

What are the Cerebellar Input Pathways?

A

2 Major Input Pathways

  • Pontocerebellar Fibers: Mostly from primary sensory and motor cortex and part of visual cortex (via corticopontine fibers). {Senses relayed from the pons to the cerebellum}
  • Spinocerebellar Pathways (This has 4 tracts)
    -Dorsal Spinocerebellar Tract (LE) and Cuneocerebellar Tract (UE): Unconscious proprioception of limb movements
    -Ventral Spinocerebellar Tract (LE) and Rostral Spinocerebellar Tract (UE): Reflect the amount of activity of the inter-neurons in descending pathways
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10
Q

What are the 3 branches of Arteries that supply the Cerebellum?

A
  • SCA
  • AICA
  • PICA
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11
Q

What are the S/S of a Cerebellar Artery Infarct?

A
  • Vertigo
  • Nausea and Vomiting
  • Horizontal Nystagmus
  • Limb Ataxia
  • Unsteady Gait
  • Headache
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12
Q

What would happen if there was an AICA infarct?

A

There would be unilateral hearing loss

AICA supplies internal auditory artery

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13
Q

SCA infarcts mostly involve what? What would this cause?

A
  • Involves mostly the cerebellum and spare the lateral brainstem
  • Ipsilateral ataxia with little/no brainstem signs
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14
Q

What would happen if the Cerebellum Swells?

A

“The Cerebellum would push laterally and down”

  • This would compress the 4th Ventricle, which can lead to hydrocephalus and increased intracrainal pressure
  • The brainstem can potentially herniate through the foramen magnum
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15
Q

What would be the S/S of Cerebellar Hemorrhage?

A
  • Headache
  • Nausea/ Vomiting
  • Ataxia
  • Nystagus

Sometimes initially presents only with GI symptoms of n/v (fatal gastroenteritis)

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16
Q

What would happen if there was a Large Cerebellar Hemorrhage?

A
  • The 4th ventricle can become involved and can cause hydrocephalus, it can cause CN 7 palsy and impaired consciousness
  • This may eventually cause brainstem compression and death
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17
Q

What are the Clinical Findings and Localization of Cerebellar Lesions?

A
  • Ataxia (lack of order)
  • Dysrhythmia (abnormal timing)
  • Dysdiadochokinesia (abnormal rapid alternating movement, RAM)
  • Dysmetria (abnormal trajectories)
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18
Q

What is the difference between Truncal Ataxia and Appendicular Ataxia?

A
  • Truncal Ataxia: this is the result from lesions of vermis or the most medial part of the cerebellum, medial motor systems get affected which control our trunk in an upright position, particularlly while walking. These patients have a wide based unsteady gait
  • Appendicular Ataxia: this is the result from lesions of the intermediate and the lateral cerebellum. This affects the lateral motor systems (Lateral corticospinal tract and rubrospinal tract), these deal with our extremities. These patient sometimes have an intention tremor

Lesions often involve both vermis and hemispheres, so truncal and appendicular ataxia can coexist in the same patient

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19
Q

What do lesions of the Cerebellar Hemisphere or Cerebellar Peduncles cause?

A

Ipsilateral Ataxia of the extremities

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20
Q

What can False Localization of Ataxia be caused by?

A

Lesions outside of the cerebellum that involve cerebellum input or output pathways

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21
Q

What are S/S of Cerebellar Disorders?

A
  • Nausea/Vomiting
  • Vertigo
  • Slurred speech
  • unsteadiness
  • uncoordinated limb movement
  • headaches on side of lesion
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22
Q

With Cerebellar Disorders, what can an UMN and LMN lesion cause?

A
  • UMN lesion can cause slow, clumsy movements of extremities
  • LMN lesions can cause weakness
23
Q

With Cerebellar Disorders, severe loss of position sense (DCML) can cause?

A

Ataxia

24
Q

With Cerebellar Disorders, Basal Ganglia dysfunctions can cause?

A

Slow, clumsy movements or gait unsteadiness

25
Q

How do you test for Appendicular Ataxia?

A

Watch for Dysmetria and Dysrhythmia

  • Finger to nose
  • Heel-shin test
  • Rapid foot tapping
  • Rapid hand movements
  • Percision finger tap
  • Overshoot test

Finger to Nose and Heel-Shin are the best known test

26
Q

How do you test for Truncal Ataxia?

A

Pts will have a wide-base, and unsteady gait

  • Tandem Gait (Heel to Toe gait), Patients tend to falll or deviate towards the side of the lesion
  • Romberg Test
27
Q

For adults, what are the most common causes of Acute Ataxia?

A

Toxins or Stroke

28
Q

For Adults, what are common causes of Chronic Ataxia?

A
  • Cerebrovascular Disease
  • Brain METs
  • Muliple Sclerosis
  • Chronic Toxic Exposure
29
Q

For Children, what are common causes of Acute Ataxia?

A
  • Accidental drug ingestion
  • Cerebrolitis
  • Migrain Headaches
30
Q

What is Spinocelleballar Ataxia?

A

This is a hereditary ataxia that can occur in both children and adults

31
Q

With the Basal Ganglia, what structures make up the Striatum?

A

Caudate and Pudamen

32
Q

With the Basal Ganglia, what structures make up the Lenticular Nucleus?

A

Putament and Globus Pallidus

33
Q

Use the Image

Going from lateral to medial, what are the structures of the Basal Ganglia? What are some non-BG structures that we may also see?

A

Non-BG structures:
- Insular Cortex: Most lateral structure
- Extreme Capsule
- Claustrum
- External Capsule

BG structures:
- Putamen (most lateral of BG)
- Globus Pallidus
- Internal Capsule
- Caudate Nucleus
- Thalamus

34
Q

The Basal Ganglia receives input from what?

A

Input from Cortex, via the Striatum

remember the striatum is made of the putamen and caudate nucleus

35
Q

The Basal Ganglia’s sends Output where?

A

Output to Thalamus, via the Globus Pallidus internal segment (GBi) and Substantia Nigra (Pars reticula) (SNr)

The SNr is gonna send outputs to our head and our neck

35
Q

What are the 2 pathways that exist from input to output BG nuclei?

A

Direct and Indirect Pathways

36
Q

What is the role of the Thalamus?

A

The Thalamus tells the body to Move It and Go

How much we move and go depends on how much the Basal Ganglia inhibits the thalamus

37
Q

Does the Basal Ganglia Inhibit or excit the Thalamus?

A

The BG inhibits the thalamus
- Input to thalamus is inhibitory via GPi and SNr

The brain contributes to how much BG inhibits thalamus via the direct and indirect pathways

38
Q

With the Basal Ganglia, describe the Direct Pathway.

A
  • The cortex releases Glutamate, this is going to be very excitatory. (The striatum is going to be excited)
  • Because the striatum is excited, its going to release GABA (which is inhibited)
  • When GABA is inhibited, the GPi and SNr are inhibited. This will then not release anymore GABA to the Thalamus.
  • This means that the Thalamus is not going to be inhibited
  • Thalamus not inhibited (Disinhibited) = Movement

In other words, The Direct Pathway results in Movement

39
Q

With the Basal Ganglia, describe the Indirect Pathway.

A
  • The Cortex is going to release Glutamate, however the substantia nigra par compacta releases dopamine which is inhibitory
  • Because of the the Striatum sends out an inhibitory GABA to the Globus Pallidus Externus segment, this then does not inhibit the Subthalamic nucleus
  • This then causes the Subthalamic Nucleus to release Glutamate, which is going to excite the Globus Pallidus internal segment and Substantia nigra par reticularis
  • GPi and SNr then release GABA which is inhibitory to the Thalamus
  • When the Thalamus is inhibited, we dont move

In other word the Indirect pathway results in No or reduction movement

40
Q

What are the Four Parallel Channels of the Basal Ganglia?
What are the structures associated and what do they do?

A

In the Dorsal Striatum
- Motor Channel
-Regulation of movement
-Somatosensory cortex; Primary motor cortex; Premotor cortex
- Oculomotor Channel
-Regulation of eye movements
-Posterior parietal cortex; prefrontal cortex
- Prefrontal Channel
-Cognitive Processes
-Posterior parietal cortex; premotor cortex

In the Ventral Striatum
- Limbic Channel
-Regulation of emotions and motivational drives (thought to play a key role in neurobehavioral and psychiatic disorders)
-

41
Q

Patients with Basal Ganglia lesion can have either Hypokinetic Movement or Hyperkinetic Movement. What is the difference between them?

A

Hyperkinetic Movement disorders are typified by Huntington’s Disease, in which uncontrolled involuntary movement produce a random pattern of jerks and twist

Hypokinetic Movement disorders are typified by Parkinsons Disease, which is characterized by rigidity, slowness and marked difficulty initiating movement

42
Q

What is the cause of Huntington Pathology?

A
  • When the inhibitory effect of Striatum and Globus Pallidus Externus (GPe) decreases (inhibition on GPe is removed) and therefore, GPe further inhibits the Subthalamic nucleus (STN)
  • STN cannot activate the GBi/SNr and therefore they do not inhibit the thalamus as much
  • Hyperkinetic Movement
43
Q

What are the Clinical Presentations of Parkinson’s Disease?

A
  • Bradykinesia/Hypokinesia
  • 4-Hz resting tremor
  • Postureal Instability
  • Rigidity

Asymmetrical presentation at onset

44
Q

What are Secondary Presentations for Parkinson’s Disease?

A
  • Infrequent blinking
  • Reduced arm swing
  • Expressionless face (“masking”)
  • Soft, monotonous voice
  • Impairment of alternating movement
45
Q

With PD, what is Froment’s Maneuver?

A

When voluntary activity and resistance against gravity increases the rigidity

46
Q

With PD, what is Truncal Hypertonus (Flexed Posture)?

A

The patient has increased tone in their trunk

47
Q

What are features that we would NOT see with PD?

A
  • Significant weakness
  • Spasticity
  • Hyper- or hyporeflexia
  • Babinski sign
  • Sensory loss
48
Q

How is a person diagnosed with PD?

A
  • Classical Triad: Tremor, Rigidity, alkinesia
  • Asymmetry of signs
  • Resting tremor
  • Good response to Levodopa
49
Q

What are the Signs for Parkinsonism?

A
  • No resting tremor
  • Symmetrical from onset
  • No or minimal response to levodopa
  • Early dementia
  • Marked autonomic signs
  • Ataxia
  • Corticospinal signs
50
Q

Which Pathway of the Basal Ganglia takes over?

A

The indirect pathway

51
Q

What is Huntington’s Disease?

A
  • An autosomal dominant neurogenerative condition
  • Affects all 4 channels of the Basal Ganglia
  • Causes progressive atrophy of striatu -> Caudate Nucleus
52
Q

What are the Characteristics of Huntington’s Disease?

A
  • Abnormalities of body movements (Chorea, eye movements), emotions and cognition
  • Onset of 30-50 year old (can pass to children), initial symptoms include subtle chorea and behavioral disturbances
  • Other signs: Tics, athetosis, and dystonic posturing
53
Q

What are Gross Pathological Changes with Huntington’s Disease?

A
  • On the right the Caudate Nucleus has degenerated to much, which leads to enlarged lateral ventricals
  • The Sulci are also much deeper on the right, due to degeneration of the gray matter
Normal is to the Left