Cerebellum Flashcards
Describe the inputs to the cerebellum.
Afferent information:
vestibular
proprioceptive and skin receptor information
sensorimotor cortex (auditory system and visual system)
Describe in a broad sense the information processing of the cerebellar cortex and nuclei.
mossy and climbing fibers enter the cerebellar cortex …almost all info exits through Purkinje cells (which left alone have an inhibitory function) and they project to deep nuclei.
What is the overall role of the cerebellum.
coordination
correction of current movements to match those intended
Describe the outputs of the cerebellum.
Motor systems: vestibular nucleus thalamus red nucleus (reticular formation) NO DIRECT connection to the spinal cord
Describe the gross anatomy of the cerebellum.
Superior cerebellar peduncle (carrying info OUT)
Middle cerebellar peduncle (inferior and middle are carrying information mostly IN)
Inferior cerebellar peduncle
most of neurons in brain are in the cerebellum…TONS of processing taking place
sort of like a roof over the 4th ventricle
Vermis (anterior lobe)
Hemisphere (posterior lobe)
flocculus and nodulus …. damage to one section produces different clinical findings
Describe the afferents to the cerebellum. What are they called?
from cerebral cortex to pontine nuclei, pontocerebellar fibers will go through MCP and enter the cerebellar cortex (L cerebral cortex projects to right cerebellum)
afferent info coming from inferior olive, vestibular cochlear nuclei and DSCT and CCT to ICP and then cerebellar cortex
(all fibers coming in (afferent) are called “mossy” because of which neurons they will innervate in the cerebellum/where they end up except ONE - “climbing” fibers originates from inferior olive
Describe the somatotopic anatomy of the cerebellum.
midline (vermis) has to do with trunk movement (gait/balance) - projects to fastigal nucleus
hemispheres - have to do with activity of limbs (project to dentate nucleus)
flocconodular- vestibular eye movement
Where might there be a problem if someone has issues with their hand or leg on their right side of body?
Where might there be a problem if someone exhibits difficulty walking?
cerebellar function on RIGHT side of body
(SAME SIDE)
walking problem- cerebellar vermis
What do Perkinje cells do?
Info is mainly in hemispheres and Purkinje projects out to deep nuclei. Purkinje tend to inhibit these deep cerebellar nuclei
Describe the ICP afferents/efferents.
Afferents: inferior olivary nucleus (medulla), vestibular nuclei, spinal cord, trigeminal nucli, reticular formation
Cerebellar efferents:
vestibular nuclei
Decribe MCP afferents/efferents.
Afferents: cerebral cortex
No efferents
Cortex projects down to pontine nuclei which then cross over to cerebellum on the other side
Describe the main/notable afferents to the cerebellum. (Specific names)
Anterior spinocerebellar ascends in contralateral spinal cord (T12-L5) and terminates in vermis and intermediate zone - ipsilateral (SCP)
Pontocerebellar originates from pontine nuclei and terminates in anterior and posterior lobes - contralateral vermis - ipsilateral (ONLY ONE GOING THROUGH MCP)
-middle takes care of cortex
almost ALL come from the ICP
Describe the SCP afferents/efferents.
Afferents:
anterior spinocerebellar tract
Cerebellar efferents:
originate from deep cerebellar nuclei
-info with SCP crosses to the other side (cerebral cortex projects: L controls R side of body)
Describe what would happen with a lesion of R cerebellar or R cerebral cortex.
R cerebellar lesion - problem with R side of body
R cerebral lesion - problem w L side of body
Describe/diagram the flocculonodular lobe (input and output).
What are the clinical findings when it is damaged?
See diagram on slide 19.
(if problem there will be balance and coordination problems associated with the head - can affect eye movement, shaking eyes)
Describe/diagram the vermis (input and output).
What are the clinical findings when it is damaged?
See diagram on slide 20.
clinical findings: damage to vermis can result in walking with feet apart, can’t keep balance when sitting
Describe/diagram the cerebellar hemispheres (input and output).
See digram on slide 21.
lesion produce motor coordination problems with limbs (arm or leg may be uncoordinated)
Describe the layers of the cerebellum.
3 layers
molecular layer (outermost)
Purkinje cell layer (middle)
granular layer (inner layer)
Describe the molecular layer of the cerebellum.
mainly axons and dendrites (outermost layer)
Basket cells - axons synapse on the Purkinje cell body
Stellate cells - axons synapse on Purkinje cell dendrites
Describe the Purkinje cell layer.
middle layer
Purkinje cells- ONLY axons that leave the cerebellar cortex (major efferents!)
Describe the granular layer.
innermost layer before the white matter
Granular cells - send their axons into the molecular layer as parallel fibers (where all mossy fibers synapse)
Describe the functions and pathways of mossy fibers, climbing fibers, Purkinje cells.
mossy fibers synapse on granule cells and send long projections to granule layer, split into parallel fibers that go both ways and will interact with the dendrites of Purkinje cells. (if activate one parallel, minimal effect … can have thousands of parallel fibers per Purkinje)
-granule sends cell axon to molecular layer to divide up into a parallel fiber - it is excitatory exciting inhibition of Purkinje cell
Climbing fibers from contralateral inf. olivary nucleus will wrap around dendritic tree of Purkinje cells (have a 1:1 ratio with Purkinje cells… VERY specific, if activate one, SIGNIFICANT effect)
- climbing wraps around dendritic tree so when its turned on it REALLY turns on the inhibitory function of that one Purkinje cell.
satellite cells inhibit inhibition
Describe the dendritic tree.
You have a granule cell shooting up parallel fibers through rows of Purkinje cells lined up ( can have 1 axon with over 400 Purkinje cells lined up) … but have thousands of parallel fibers going through - so takes a bunch of granule cells to be activated to have an effect
Cerebellar diseases generally cause 3 principal deficits. Describe them.
- HYPOTONIA: diminished resistance to passive limb displacement, often called “lack of check”; results in overshooting and excessive rebound.
- ATAXIA: delay in the initiation of movement, errors in range and force of movements (dysmetria) and errors in the regularity and rate of repetitive movements (dysdiadochokinesia).
- INTENTION TREMOR: errors in position; most marked at the end of movements where the greatest precision is required.
