Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
54 Cards in this Set
- Front
- Back
What does the cerebellum do?
|
Motor Control: synergy of muscle action, muscle tone, equilibrium
|
|
From where does the cerebellum receive sensory input?
|
From muscles and joints (proprioception); from vestibular apparatus (makes adjustments).
|
|
What are the 4 pair of deep cerebellar nuclei?
|
Dentate - emboliform - globose - fastigial
(located in cerebellar medullary center) (E&G = interposed nucleus) |
|
What types of cells are in the molecular layer in the cerebellum?
|
Stellate and basket cells
|
|
What types of cells are in the granule layer in the cerebellum?
|
Granule and Golgi cells
|
|
What are the 3 layers of the cerebellar cortex?
|
1. Molecular
2. Purkinje 3. Granular |
|
From which fibers do granule cells receive input?
|
Mossy fibers
|
|
What is the NT of granule cells?
|
Glutamate (excitatory)
|
|
From which fibers do Purkinje cells receive input?
|
Parallel and climbing fibers
|
|
Where do the myelinated axons of Purkinje cells terminate?
|
In the deep nuclei (almost exclusively)
REMEMBER: Purkinje cell axons carry the sole output of cerebellar cortex. |
|
What is the NT associated with Purkinje cells?
|
GABA (often with peptide co-transmitter)
|
|
What are basket/Golgi/stellate cells?
What is the NT involved? |
Inhibitory interneurons
GABA |
|
What is the NT of mossy fibers?
|
ACh (excitatory to both Purk cells and deep nuclei)
|
|
Where do climbing fibers exclusively originate?
|
contralateral inferior olivary complex
(= olivocerebellar fibers) |
|
What is the NT of climbing fibers?
|
Aspartate (excitatory)
|
|
What is the bottom line of cerebellar circuitry? (see slide 8)
|
Excitatory afferents drive both cerebellar cortex and the deep nuclei. The complex circuitry in cortex refines or modulates the excitatory output of the deep nuclei, which then indirectly influences LMNs via the motor thalamus (VL), motor cerebral cortex, reticular formation, vestibular nuclei and red nucleus.
|
|
What are the only excitatory neurons in the cerebellar cortex?
|
Granule cells
|
|
Where are afferents to the deep nuclei from?
|
1. Extra-cerebellar source: Collateral branches of mossy and climbing fibers (excitatory)
2. Purkinje cells: "neurons in specific cerebellar areas project to specific deep nuclei" (inhibitory) |
|
Where do the vermal areas and flocculus project?
|
Fatigial nucleus
|
|
Where do paravermal areas (intermediate zone) project?
|
Globose and Emboliform nuclei
|
|
Where do lateral hemispheres project?
|
To dentate nucleus
|
|
Where is the most cerebellar output form?
What is the exception? |
Deep cerebellar nuclei
Flocculonodular lobe + cortex of uvula |
|
Describe the MCP:
|
Entirely afferent
Only pontocerebellar |
|
Describe the ICP:
|
Primarily afferent
|
|
What are the afferents in the ICP?
|
Dorsal spinocerebellar
Cuneocerebellar Olivocerebellar Vestibulocerebellar Trigeminocerebellar Reticulocerebellar |
|
What are the efferents in the ICP?
Where do they go? |
Fastigial nuclei
Flocculonodular Lobe Vermal areas of cortex * Go to vestibular nuclei and reticular formation |
|
Describe the SCP:
|
Primarily efferent.
Carries output of dentate/globose/emboliform nuclei to red nucleus and thalamus. Afferent component: VSCT |
|
Which structures make up the vestibulocerebellum?
|
Flocculonodular lobe and uvula
|
|
What is the input and output to the vestibulocerebellum?
|
In: from vest nerve/nuclei
Out: vestibulocerebellar cortex influences LMNs indirectly (via RF, vest nuc, fastigial nuclei) |
|
What is the function of the vestibulocerebellum?
|
Maintains balance/equil (by adjusting muscle tone in axial and neck muscles & controlling eye mov't) in response to vestibular stimulation.
|
|
What makes up the spinocerebellum?
|
Medial cerebellum
Most of vermis + paravermal (medial hemisphere zone) |
|
What is the input / output to spinocerebellum?
|
In: from SC tracts (DSCT, VSCT, CCT)
Out: from spinocerebellar cortex --> fastigial nuclei (from vermal areas) OR globose and emboliform nuclei (from paravermal areas) |
|
How does the spinocerebellum indirectly influence LMNs?
|
(see page 6)
|
|
What is the function of the spinocerebellum?
|
Influences muscle tone and synergy of movements (especially of limbs) during stereotyped activities such as walking and during changes in posture. Impact primarily on axial and proximal limb muscles.
|
|
What makes up the neocerebellum?
|
Lateral portions of hemispheres
|
|
Describe input/output of neocerebellum:
|
In: indirectly from cerebral cortex via pontocerebellar or olivocrebellar tracts.
Out: to dentate nuclei, influences LMNs indirectly via thalamus --> motor cortex (via CST and CBT) OR Red nuclei (via RST) |
|
What is the function of the neocerebellum?
|
Planning/programming of complex movements and adjustments in muscle tone (required for non-stereotyped/learned/skilled mov't). Impact = on limb muscles (especially distally)
|
|
What's the bottom line of how cerebellum works with other CNS structures to achieve motor control?
|
Cerebellum acts as a comparator: It compares what the motor cortex is telling the muscles to do with what they are actually doing. In response, the cerebellum makes the appropriate adjustments via its connections with motor cortex (via thalamus) and with brain stem nuclei (vestibular and reticular formation) which give rise to tracts that will influence lower motor neurons.
|
|
What do cerebellar lesions produce?
|
Motor disturbances w/o voluntary paralysis.
|
|
How does midline cerebellar damage occur?
|
From damage to vermis, sometimes extending into spinocerebellum or flocculonodular lobe (vest.C)
Ex. Medulloblastoma, chronic alcoholism |
|
What are S/S of midline damage?
|
Bilateral!
Dysequilbrium, ataxic (wide) gait, swaying side-side, positional nystagmus, obstructed CSF flow |
|
How does neocerebellar syndrome occur?
|
Damage to cerebellar hemispheres or its connections (cerebellar cortex, deep nuclei, med center, peduncles).
|
|
When is neocerebellar syndrome most severe?
|
When deep nuclei or SCP are involved.
(If spared, most deficits are compensated for w/time by intact regions) |
|
What are the S/S of neocerebellar syndrome?
|
Deficits superimposed on basically intact volitional mov't - usually involving fine control (ex. force, range, rate, direction of mov't)
* Abn mov't greatest when muscles are being used (ex. intention tremor) * Unilateral lesion? Deficits ipsilateral. |
|
Ataxia
|
Intermittent or jerky movements due to errors in rate, force and direction; often used in reference to gait. Look for associated signs to differentiate from ataxia due to lesions elsewhere.
|
|
Nystagmus
|
Ataxia of ocular muscles
|
|
Hypotonia/Hyporeflexia
|
Pendular knee jerks: damping of the reflex is slowed, so there is more than the usual number of swings.
|
|
Asthenia
|
Weakness; tire easily d/t hypotonia
|
|
Asynergy/dyssynergy
|
Decomposition of movement; complex movements are broken down into their basic components. Lack of cooperation between closely related muscle groups; heel-to-shin test.
|
|
Dysarthria/scanning speech
|
Asynergy in muscles used for speech; thick and monotonous; irregular volume and rhythm.
|
|
Dysmetria
|
Past-pointing; abnormal range of movement; finger-to-nose test.
|
|
Dysdiadochokinesia or adiadochokinesia
|
Abnormality in rapidly alternating movements; combination of asthenia, dysergia and dysmetria.
|
|
Intention tremor
|
Occurs during mov't
|
|
Rebound
|
Delay in stopping the mov't
|