Cerebellum Flashcards

You may prefer our related Brainscape-certified flashcards:
1
Q

What is the general function of the cerebellum? What do lesions result in?

A

Evaluate disparities between intention and action and generate correction signals to the cortex and brainstem.

Lesions results in loss of spatial accuracy and temporal coordination of movement as well as impairment of balance and loss of muscle tone. Sensation and strength of muscle contraction are not impacted.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Describe the general anatomy of the cerebellum.

A
  • Grey matter on the outside, white matter on the inside
  • Invaginations are called folia
  • Two transverse fissures: primary fissure divides anterior and posterior lobes, posterolateral fissure divides posterior lobe from flocculonodular lobe
  • Deep cerebellar nuclei receive input from cerebellar cortex
  • Three peduncles containing incoming and outgoing information
  • Three mediolateral regions: vermis and two hemispheres
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How is the cerebellum divided functionally?

A

Central vermis and the lateral and intermediate zones in each hemisphere

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How is the cerebellum divided anatomically?

A

Primary fissure divides the anterior and posterior lobes and the posterolateral fissure separates the foculonodular lobe.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Describe the input system from the inferior olive.

A

The inferior olive projects climbing fibers into the cerebellar cortex via the inferior cerebellar peduncle which wrap around the dendrites of the Purinje cell, making hundreds of synapses. If it fires an action potential, it is guaranteed to stimulate the Purkinje cell. There is little divergence in this pathway.

The inferior olive received inputs from the spino-olivary pathway (travels with spinothalamic) as well as from the cortex. It is responsible for comparing the actual movement with the intended movement.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Describe the how the cerebellum receives the rest of it’s input (non-olivary)

A

Mossy fibers make up the rest of the input to the cerebellum and consist of axons from the spinocerebellar tracts, pontine nuclei, vestibular nuclei, cortex, etc. This is a largely divergent system in which each mossy fiber terminates on granule cells which send their axons into the Purkinje layer (parallel fibers) to synapse on hundreds of Purkinje cells, however, they only synapse on a single Purkinje cell once or twice (i.e. activation is not guaranteed).

Input from the spinal cord enters through the inferior cerebellar peduncle while input from the cortex enters in the middle cerebellar peduncle.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the only output of the cerebellar cortex? Where do these nuclei project?

A

The cerebellar cortex projects only to deep cerebellar nuclei (except for the vestibulocerebellum)

  • Cerebrocerebellum projects to dentate nucleus which projects to the motor and premotor cortices (motor planning)
  • The paravermis projects to the interposed nuclei which project to the lateral decending systems for motor execution
  • The vermis projects to the fastigial nuclei which project to medial descending systems for motor execution as well
  • The vestibulocerebellum (floculonodular lobe) projects to vestibular nuclei which regulate balance and eye movement
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Describe the somatosensory map of the spinocerebellum.

A

The limbs are represented in the intermediate portions of the hemispheres while the axial muscles and the head are represented in the vermis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the functions of the spinocerebellum and cerebrocerebellum? How do they project?

A

The spinocerebellum compares motor commands with motor execution and corrects them during movement:

  • Limbs: interposed nuclei –> VL –> M1 (contralateral projection via SCP)
  • Axial: fastigial nuclei –> red nucleus –> rubrospinal/corticospinal tract

The cerebrocerebellum is active during planning prior to movement:

  • Dentate –> VL –> association, premotor, M1 (contralateral projeciton via SCP)

The vestibulocerebellum projects to the vestibular nuclei via the ICP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What cerebrocognitive funtions does the cerebellum have?

A

The dentate nucleus becomes more active when an individual is asked to do sensory discrimination. It is also important in adapting the motor system to a task that requires adaptation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the three types of cerebellar symptoms after a lesion?

A
  • Hypotonia: lack of resistance to passive displacement of limbs
  • Ataxia: lack of coordation with resprect to eye movements, walking, initiating movements, dysdiadochokinesia, dysmetria, decomposition of movement
  • Intentional tremor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the basal ganglia and what do they do?

A

The basal ganglia are a cluster of neuronal cell bodies at the base of the brain in the CNS which modulate movement, cognition, and behavior.

  • Striatum: caudate and putamen
  • Pallidum: globus pallidus interna and externa
  • Substantia nigra: pars compacta and pars reticularis
  • Subthalamic nuclei
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How are the basal ganglia connected to the rest of the brain?

A

Cortex signals to the caudate/putament which projects to the substantia nigra and the globus pallidus. The signal is then sent to the thalamus and back to the cortex.

Nuclei within the basal ganglia modulate the signal and send it back to the cortex via the thalamus.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Describe the direct and indirect circuitry in the basal ganglia.

A

In the direct pathway, the cortex signals the the striatum which activates the GPi or SNr (normally inhibits VA/VL of the thalamus). The thalamus projects back to the cerebral cortex.

In the indirect pathway, the cortex excites the striatum which inhibits the globus pallidus externa which is normally inhibiting in subthalamic nucleus. STN can now excite the GPi/SNr which inhibits signlaing to the thalamus and subsequent cortical activation.

The substantia nigra pars compacta excites the direct pathway and inhibits the indirect pathway which facilitates movement.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Which neurotransmitters are released by each component of the basal ganglia?

A

The striatum receives stimuli from the cortex and inhibits the GPi/SNr via GABA in the direct pathway as well as GPe via GABA in the indirect pathway. GPe releases GABA onto the subthalamic nucleus which activates the GPi/SNr using glutamate. The GPi/SNr inhibits VA/VL of the thalamus with GABA. The thalamus projects excitatory inputs back to the cortex. The SNc activates the direct pathway of the striatum (D1 receptor) and inactivates the indirect pathway of the striatum (D2 receptor) using dopamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How does cholinergic transmission impact the activity of the thalamic neurons? Dopaminergic?

A

Cholinergic transmission activates the indirect pathway which results in inhibition of the thalalmic neurons. Dopaminergic transmission activates the direct pathway which causes excitation of thalamic neurons.

17
Q

What is dopamine involved in in the brain? Accordingly, what side effects can dopaminergic drugs have? What is the rate limiting step in its synthesis?

A
  • Mesocortical: schizophrenia
  • Mesolimbic: reward
  • Nigrostriatal: PD
  • Tuberoinfundibular: prolactin

Dopaminergic drugs can cause psychosis, impulsivity, addiction, etc. The rate limiting step in the synthesis of dopamine is the conversion of L-tyrosine to L-Dopa via tyrosine hydroxylase.

18
Q

What is causes Parkinson’s disease? What are they symptoms and why do these present?

A

PD is due to a slow progressive brain degeneration related to the accumulation of the protein alpha-synuclein in cytoplasmic aggregates called Lewy bodies. Lewy body formation spreads progressively through the brain starting in the brainstem–by the time motor symptoms appear, about 80% of neurons in the substantia nigra pars compacta are gone.

Symptoms include bradykinesia, rigidity, resting tremor, stooped/unstable posture, shuffling gait, cogwheel rigidity, masked face, depression, constipation, urinary symptoms, sleep disorders, hyposmia

Slowed motor activity occurs due to decreased inhibitory signal from the SNc resulting in excess activation of the GPi/SNr leading to excess inhibition of the thalamus.

19
Q

What is the main therapy for Parkinson’s disease?

A

Dopamine replacement with levodopa alleviates some of the symptoms. Dopamine is not used directly because it causes severe systemic side effects and does not cross the blood brain barrier. It’s precursor, L-dopa, does. L-dopa is given with carbidopa to inhibit its conversion to dopamine in the periphery.

Other therapies include dopamine receptor agonists, blocking dopamine metabolism, muscarinic cholinergic antagonists (activate indirect pathway)

20
Q

What is the main problem in Huntington’s disease? How is it treated?

A

HD involves the selective loss of medium spiny GABAergic neurons of the striatum whose output is through the indirect pathway. This leads to increased inhibition of the GPi/SNr by the direct pathway beause the STN is suppressed (by GPe) and cannot activate SPi/SNr. Decreased thalamic suppression results in chorea, athetosis, mental decline, and personality changes.

Nothing is available to stop the progression of HD. Blocking dopamine can provide symptomatic treatment and decrease choreiform movements. Antidepressants are available for personality changes.

21
Q

Which structures may be involved in conditions characterized by abnormal voluntary movements or by presence of excessive involuntary movements?

A

Dysfunction among basal ganglia, cerebellum, and other CNS areas. Movement can by either hypo or hyperkinetic.

22
Q

What is chorea?

A

Irregular, rapid, random movements that flow from one body part to another. Chorea that is low amplitude and affects distal muscles is called athetosis while chorea that is proximal and high amplitude is called ballismus (hemiballismus is due to lesions of subthalamic nuceli)

23
Q

What are tremors? What kinds of tremors exist?

A

Tremors are rhythmical and sinusoidal movements. Rest tremors are seen in PD, postural tremors are seen with ET and PD, kinetic tremors are seen with ET and cerebellar problems.

24
Q

What are the distinguishing features of PD and ET?

A

Parkinson’s Disease

  • Asymmetrical, rest tremor predominates over postural/action tremor, bradykinesia, cogwheel rigidity, micrographia, shuffling gait, family history may or may not be present

Essential tremor

  • Symmetrical, postural/action tremor more so than rest tremor, no bradykinesia, no rigidity, shaky-graphia, normal gait, likely family history
25
Q

What is myoclonus? How is it different from tremor?

A

Myoclonus is like a tremor but is irregular and has a fast and slow phase. Can be:

  • Physiologic: hypnic jerks
  • Hereditary: essential, epileptic, degenerative
  • Secondary: metabolic, drugs, lesion, degenerative
26
Q

What is a tic? What is unique about it?

A

A tic is an abrupt, brief, stereotyped, forewarned movement that is suppressible. Can be motor or vocal.

27
Q

What is dystonia?

A

Sustained muscle contractions with twisting postures or abnormal postures that are patterned and usually directional

28
Q

What is Parkinsonism?

A

A group of clinically related disorders involving rigidity, akinesia/bradykinesia, and basal ganglia pathology

Examples include PD, multiple systems atrophy, progressive supranuclear palsy, and secondary parkinsonism.

29
Q

Describe the pathology of PD.

A

In Parkinson’s disease the substantia nigra shows a loss of pigment, glial proliferation, microglial inflammation, and Lewy bodies with alpha-synuclein in neurons (round eosinophilc cytoplasmic inclusions).

30
Q

What are the atypical parkinsonian syndromes?

A
  • Multiple systems atrophy: autonomic failure
  • Progressive supranuclear palsy: ophthalmoparesis (“surprised face”)
  • Corticobasal degeneration: apraxia, dystonia
  • Wilson’s disease: young onset dystonia
31
Q

What is the major complication of Levodopa therapy?

A
  • Motor fluctuations: short halflife, end of dose wearing off, sudden on-off
  • Dyskinesias: peak dose corea and end of dose dystonia
  • Visual hallucinations
32
Q

What is a different treatment for Parkinsonism?

A

Deep brain stimulation which works by interrupting the inhibitory output coming from the GPi and SNr which releases the thalamus and allows more rapid movement and less muscle rigidity.

33
Q

What types of eye movements are there?

A

Voluntary:

  • Conjugate eye movements: smooth pursuit, optokinetic, vestibular, saccades
  • Disjunctive: vergence

Involuntary

  • Fixation movements