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CEREBELLUM Largest part of hind
brain.
LOCATION:
Posterior cranial
fossa behind pons &
medulla.
ANATOMY: Covered
above by meninges(Tentorium
Cerebelli).
Has 2 hemispheres
joined by Vermis.
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LOBES: 3
1) anterior lobe
2) posterior / middlelobe
3) flocculo nodular lobe
FISSURES: 2
1) Primary fissure (vshaped). Part ofcerebellum above thisfissure is anterior lobe.
2) Uvulo-nodular fissure(separates posteriorlobe from flocculonodular lobe)
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Topographical representation: Vermis &
Intermediate zone of cerebellar
hemisphere.
Each cerebellar hemisphere has 2 zones,
intermediate zone & lateral zone.
Axial parts of body represented in
Vermis.
Limbs & facial region Intermediate
zone.
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AFFERENTS TO TOPOGRAPHICALREPRESENTATION:
Corresponding areas of motor cortex.
Corresponding parts of the body &
Brain stem
EFFERENTS:
Cerebral cortex Red nucleus
Reticular formation
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VERMIS: 10 Primary lobules.
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I LINGULA
II CENTRAL LOBULE
III CENTRAL LOBULE
IV CULMEN
V DECLIVE
VI SIMPLE LOBULE
VII FOLIUM TUBER.
VIII PYRAMID
IX UVULA
X NODULE
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Cerebellum has:
1) cortex cerebellar (grey matter on periphery)
2) white matter core (having deep cerebellarnuclei, 4 on each side, from lateral to medialside:
DENTATE, EMBOLIFORM, GLOBASE &FESTIGEAL. (Lateral medial) BUT DEGF! (dont eat greasy food)
EMBOLIFORM + GLOBASE = NUCLEUS
INTERPOSITUS.
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MOTOR OUTPUT FROMCEREBELLUM: Axons of neurons in deep cerebellar
nuclei motor output.
From dentate + interpositus leave via
SUPERIOR CEREBELLAR PEDUNCLE.
From fastigial nucleus leave via
INFERIOR CEREBELLAR PEDUNCLE.
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F G E D
( N.I)
SUPERIOR
CEREBELLAR PEDUNCLE
INFERIOR
CEREBELLAR PEDUNCLE
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CEREBELLAR CORTEX: 3 LAYERS:
Outermost molecular layer
2nd layer purkinje cells layer
3rd later granular layer
PURKINJE
CELL
AXONS
DENDRITES
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MOLECULAR LAYER: STELLATE CELLS
BASKET CELLS
Large no. ofdendrites & nerve
fibers from deeper
layers.
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PURKINJE CELL LAYER: Single layer. Flask shaped cells.
From top of cells arise dendrites 1, 2 (withoutdendritic spines, i.e., smooth)
& 3 branches (with dendrite spines).
From base of cells axons white matter acquiresmyelin sheath.
Most nerve fibers from purkinje cells
synapse onto
deep nuclear cells.
Only few fibers bypass deep nuclear cells go tovestibular nuclei.
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GRANULAR LAYER: Granule cells having Multiple dendrites
synapse with incoming
Mossy fibers.
Their axons pass into
molecular layer
end into a T termination.
These fibers alsosynapse with golgi cells,
basket cells & stallate
cells.
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WHITE MATTER OFCEREBELLUM: 3 TYPES OF FIBERS:
INTRINSIC FIBERS
AFFERENT FIBERS
EFFERENT FIBERS
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INTRINSIC FIBERS: Pass between cerebellar cortex & vermis.
Also pass from 1 cerebellar hemisphere
to other. They remain in the cerebellum.
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AFFERENT FIBERS: 2 TYPES:
CLIMBING FIBERS (come from inferior
olivary nucleus) MOSSY FIBERS (all the other afferent
fibers except the climbing are called
Mossy fibers).
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EFFERENT FIBERS: Start as axons of purkinje cells.
Most of these axons synapse onto deep
nuclear cells.
From deep nuclear cells, efferent fibers arise
go to different parts of CNS .
Only few purkinje fibers bypass deep nuclear
cells go to vestibular nuclei (these are from
vermis & flocculo-nodular lobe).
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There is a neuronal circuit in cerebellum.
Millions of functional units.
Each functional unit consist of a purkinje cell &a deep nuclear cell.
Climbing fibers give collaterals, which synapsewith deep nuclear cells.
collaterals from climbing fibers excite deepnuclear cells.
Climbing fibers pass to molecular layersynapse with dendrites ofpurkinje cells.
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Mossy fibers collaterals synapsewith deep nuclear cells.
Mossy fibers granular layersynapse with dendrites of granule cell.
1 climbing fibercan synapse with about 10 purkinje cells.
1 mossy fibercan synapse with 100s ofgranule cells.
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Excitatory:
deep nuclear cells Granule cells
Inhibitory:
Purkinje cells
Basket cells
Golgi cells
Stellate cells
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When deep nuclear cells are to be excited, itsthrough COLLATERALS from climbing &mossy fibers.
When inhibited, its through purkinje cells.
Purkinje cells & deep nuclear cells discharge
continuously (50-100 impulses/sec).
This is the neuronal circuit in the cerebellum.
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BASIC FUNCTION OF CEREBELLUM: To control timing of turn-on signals to agonists
& turn-off signals to antagonists at the onset ofa movement & then
To control timing of turn-off signal to agonists &turn-on signals to antagonists at the end of a
movement.
Basic disturbance in cerebellar disease
ATAXIA / INCOORDINATION OF
MOVEMENT.
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CONNECTIONS OF CEREBELLUMTHROUGH 3 PEDUNCLES: AFFERENT
EFFERENT
Superior peduncle
midbrainMiddle peduncle
pons
Inferior peduncle
medulla
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INFERIOR CEREBELLAR PEDUNCLECONNECTIONS: AFFERENTS:
Posterior spino-cerebellar tract.
Cuneo-cerebellar tract (from cuneate nucleus).
Vestibulo-cerebellar fibers (from vestibular
nuclei).
Reticulo cerebellar (from reticular formation).
Olivo-cerebellar (from inferior olivary nucleus).
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EFFERENTS:
Cerebello-vestibular
Cerebello-reticular
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MIDDLE PEDUNCLE:Mainly AFFERENTS (Ponto-cerebellar
fibers).
These fibers arise from pontine nuclei &
cross over to opposite side middlecerebellar peduncle.
These fibers are part of cortico-ponto-cerebellar pathway.
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SUPERIOR PEDUNCLE: AFFERENTS:
Anterior spino-
cerebellar tract.
Rubro-cerebellartract (from red
nucleus).
Tecto-cerebellar
(from tectum of
midbrain).
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EFFERENTS:
To Red nucleus, then to thalamic nucleithen to Cerebral cortex.
Other fibers go directly ventro-lateral & ventro anterior thalamic nuclei cerebral cortex
.
Some basal ganglia.
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CEREBELLUM HASRECIPROCAL CONNECTIONS 1) CEREBRAL CORTEX
2) RETICULAR FORMATION
3) VESTIBULAR NUCLEI
4) RED NUCLEUS
AFFERENTS EFFERENTS
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FUNCTIONS OFCEREBELLUM: Functionally divided into 3 parts:
1) lateral zone
2) intermediate zone
3) flocculo-nodular lobe & vermis.
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LATERAL ZONE:FUNCTION No body representation.
Also called cerebro-cerebellum (extensive
connections with cerebral cortex).
Program & plan movement. Plans sequence & timing of each component of
movement.
Smooth progress of movement, e-g, eating thecurry & bread (bread curry mouth).
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*cerebellum does not INITIATE
movement BUT COORDINATES it.
In cerebellar disease loss of smooth
progression of movements.
Extra motor predictive function.
Helps to access timing of movement.
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INTERMEDIATE ZONE: FUNCTION Also called spino-cerebellum, due toconnection with spinal cord.
Face & limbs are represented.
Coordination of movements (distal part oflimbs).
Acts as a comparator.
Compares intended plan of movement withactually performed movement.
In case of discrepancy, corrective signals aresent.
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Cerebellum gets intended plan ofmovement from motor cortex & also from
red nucleus.
Fig shows cerebral & cerebellar control of
voluntary movements involving especially
intermediate zone & its associated
nucleus interpositus.
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It recieves information actually performed
movements from PROPRIOCEPTORSthrough spino-cerebellar tracts.
Compared & corrected via signalsthrough red nucleus & thalamic nuclei to
motor cortex.
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Also controls: rate, range & direction of
movement.
Damping function.
Prevents pendular movements & tremors
(pendular knee jerk in case of disease)
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Also controls very rapid movements like
typing (ballistic movements).
Also controls very rapid eye movement
(reading & when a person in a moving
vehicle, fixate the outside scene).
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FUNCTION OF FLOCCOLONODULARLOBE & VERMIS: Controls posture & equilibrium.
Also concerned with motion sickness.
Controls stretch reflex & muscle tone.
Normal influence is facilitatory on stretch reflex& muscle tone.
From here purkinje nerve fibers vest nuclei(bypass deep nuclear cells)
Also called vestibulo-cerebellum due toconnection with vestibular nuclei.
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CEREBELLAR DISEASE: Involvement of cerebellar cortex & 1 or
more of deep cerebellar nuclei.
*No muscle paralysis & no sensory lossoccurs. (MCQ)
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FEATURES:1) ATAXIA: Incoordinate movements due to defect in
control of RANGE, DIRECTION, RATE &
TIMING of movement. Asynergia (no synergism between
agonists & antagonists; normal
synergism = when agonists contract,antagonists relax).
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2) DYSMETRIA & PASTPOINTING: Inability to control range or extent of
movement.
Dysmetria also manifest as pastpointing.
When patient tries to touch an object
hand overshoots (past pointing).
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3) ADIADOCOKINESIA /DYSDIADOCOKINESIA: Inability to perform RAPID, ALTERNATE,
OPPOSITE movement (rapid supination
& pronation of arm).
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4) DRUNKEN GATE /STAGGERING GATE: Patient walks on a broad base.
SPECIFIC POSTURE: Head is rotated &
flexed towards the side of lesion.
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5) SLURRED SPEECH: Due to dysarthria ( disordered
articulation).
Incoordination of muscles of articulation. Some words or syllables are spoken loud
& others are spoken in weak tone.
Some are held for long period & someare spoken short.
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6) INTENTION TREMORS /ACTION TREMORS: Absent at rest.
Appear when patient performs some
voluntary action. Example of drinking water from a cup.
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7) REBOUNDPHENOMENON: Patient cannot stop a movement
abruptly.
Example of flexion of elbow may hithis face.
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8) DECOMPOSITION OFMOVEMENTS: Patient is not able to perform actions
involving simultaneous movement at
more than 1 joint. Movements are broken into components.
Loss of smooth progression of 1
movement to other.
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9) NYSTAGMUS: Rhythmic rapid movement of eyeballs
when eyes are focused on 1 side.
Cerebellum has a damping function,which is disturbed.
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10) PENDULAR KNEEJERK: Due to loss of damping function of
intermediate zone of cerebellum.
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11) HYPOTONIA: Due to loss of excitatory action of
cerebellum on stretch reflex & muscle
tone.