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Transcript
Neuroscience 7c - Basal Ganglia and Cerebellum
Anil Chopra
1. Draw a diagram of the component structures of the basal ganglia and indicate how
they interact.
2. Know the clinical signs of Parkinson’s disease and Huntington’s disease.
3. Explain which structures degenerate in Parkinson’s disease (PD) and Huntington’s
disease (HD) and differentiate between the clinical signs of HD and PD.
4. Explain the “Alexander and Crutcher’s hypothesis” to describe the function of
basal ganglia and how this can help to explain the symptoms seen in HD and PD.
5. Explain how the cerebellum contributes to the co-ordination of movement
6. Know the relevance of the pathways into and out of the cerebellum
7. Understand how the cellular organisation of the cerebellum relates to its
functioning.
8. Define ataxia and explain how lesions in specific areas of the cerebellum relate to
effects in the specific parts of the body.
Both the basal ganglia and the thalamus act on
the motor cortex to allow for smooth coordinated movement. Lesions in these areas
result in movement disorders.
Motor cortex
via
thalamus
via
thalamus
basal ganglia
cerebellum
motor neurons & interneurons
spinal cord
Basal Ganglia
caudate
nucleus
putamen
globus pallidus
GPe
GPi
subthalamic
nucleus (STN)
forebrain
coronal view
substantia
nigra
midbrain
Parts of the Basal Ganglia
The basal ganglia lies in the deep white matter of the cerebral cortex and consists of:
 Caudate
 Putamen (together with caudeate nucleus mane striatum).
 Internal and external segments of the globus pallidus (GPi and GPe)
 Pars reticulata and pars compacta of the substantia nigra (SNr and SNc)
 Subthalamic nucleus (STN)
The nuclei modify movements on a minute to minute basis. They communicate with
the motor cortex and the thalamus. The basal ganglia is normally inhibitory, as
opposed to the cerebellum which is excitatory. The balance between the basal ganglia
and cerebellum leads to smooth co-ordinated movements.
Circuit of Basal Ganglia
Diagram shows:
Gutamatergic pathways as red (stimulatory)
Dopaminergic pathways as magenta (stimulatory)
GABA pathways as blue (inhibitory)
 Cerebral cortex stimulates striatum
 Pars compacta of substantia nigra stimulates striatum
 Striatum inhibit external globus pallidus, internal
globus pallidus and pars reticular of the substantia
nigra DIRECTLY.
 Striatum also inhibit internal globus pallidus
INDIRECTLY via the external globus pallidus 
subthalamic nucleus  internal globus pallidus.
 Internal globus pallidus and pars reticulum of the
substantia nigra project to  thalamus. They are the
only outputs to the system.
 The thalamus projects to the cerebral cortex.
(Specifically the premotor area and the supplementary
motor area – the two regions involved in planning
movement).
The thalamus is inhibited normally, however, when the cerebral cortex wants to
initiate a movement, it sets off a chain reaction which results in the inhibition of the
nuclei that are inhibiting the thalamus. The thalamus therefore becomes stimulated
and stimulates the parts of the cortex involved with the planning of a movement.
Parkinson’s Disease
In Parkinson’s
disease, the pars compacta
of the subsatntia nigra does
not stimulate the striatum as
much (due to problem with
SNc or dopamine receptors on
the striatum) and the thalamus
is inhibited resulting in its
inability to stimulate the
pemotor/supplementary motor
areas (PMA/SMA) of the cortex.
Symptoms of Parkinson’s Disease
 Bradykinesia-sloweness of movements.
o Difficulty in small movements: doing up buttons, handling a knife
o Face hypomimic (expressionless, mask-like)
o Akinesia- difficulty in the initiation of movements. Needs external sensory
triggers to initiate movement: e.g. a visual trigger because cannot initiate
movements internally.
 Tremor at rest - usually starts in one hand (asymmetry) “pill rolling” tremor,
tends to spread with time to other parts of the body.
 Rigidity - (no to be confused with spasticity) a type of resistance to passive
movements. To the physician passively moving the patient’s limb feels like
bending a lead pipe- lead pipe rigidity
 Gait slow, small steps, reduced arm swing.
Huntington’s Disease
Huntington’s disease is caused by a defective “Huntington Gene” on chromosome 4.
This results in the degradation of the spiny GABAergic neurons in the striatum. It is
an autosomal dominant disease.
Symptoms of Huntington’s Disease
 Choreic movements (Chorea): Rapid jerky involuntary movements of the body.
o These normally affect the hands and face at first.
o They can be masked into
socially acceptable
movements at first but they
gradually increase over time
and cause great distress to
patients.
 Dementia develops later.
 Death usually after 10-15
years.
Cerebellum
It is divided horizontally into 3 lobes:
- Anterior lobe
- Posterior lobe
- Flocculonodular lobe
It is also vertically into 3 regions:
- vermis
- intermediate cerebellum
-
Deep cerebellum nuclei
Superior
cerebellar
peduncle
pon
s
Middle
cerebellar
peduncle
Dentate
nucleus
interpose
fastigi
d
al
Inferior
cerebellar
peduncle
l
ateral cerebellum
Purkinje
cells
Granule
cell
layer
Parallel
fibers
magnified
granule
Mossy
fibers
Climbing
fibers
Purkinje cell
To deep
axons
nuclei
Layers of the Cerebellum:
 Molecular layer - Cell free – contains only axons and dendrites.
 Purkinje cell layer - Its axons are the only output of the cerebellum to the deep nuclei.
 Granule cell layer - Granule cells send the axons up to the molecular layer where they end
in a T and run parallel to the surface- parallel fibers- and synapse with Purkinje cells.
 Mossy fibers : these are the inputs to the cerebellum:
- 1. spinal cord
- 2. vestibular nuclei
- 3. brainstem reticular formation
- 4. deep pontine nuclei.
 Climbing fibers - second source of input- from inferior olivary nuclei.
Pathways Into and out of the Cerebellum
There are 3 highways into and out of the cerebellum - the inferior, middle and
superior cerebellar peduncles. There are 3 deep nuclei: Fastigal nucleus (involved in balance; has connections with vestibular and reticular nuclei)
 Interposed involved in voluntary movements with projections to the thalamus & red nucleus
 Dentate also involved in voluntary movements with projections to the thalamus &
red nucleus
There are 3 sources of input: Mossy fibres from the spinocerebellar pathways
 Climbing fibres from the inferior olive
 Mossy fibres from the pons bring information from the cerebral cortex and are
known as corticopontine connections and cross over after synapsing at the pons
Functions of the Cerbellar Divisions
The cerebellum is involved in the co-ordination of movement. It compares what you
thought you were going to do (according to the motor cortex) with what you are
actually about to do (according to proprioceptive feedback). The Basic Circuit is the
same in all parts of the cerebellum and has 3 parts to it:
» Direct path – input projects directly to motor systems via deep cerebellar nuclei
» Indirect side loop – mossy fibres input to granular cells through parallel fibres, to
Purkinje cells and back to the cerebellar nuclei. This circuit is used
to correct reflex responses
Climbing fibres input – to Purkinje cells. This is the error detection
input. This circuit is used for learning movements
Vestibulo-cerebellum:
- flocculonodular lobe
Input: vestibular nuclei and vestibular nerve
Output: Purkinje cell axons  to legs, trunk, and eye muscles
Function: It regulates gait and posture. It also coordinates head movements with eye movements.
Disorders:
a) ataxic gait:- wide based stance (looks drunk)
b) imbalance when eyes closed (Romberg sign)
c) nystagmus
Spinocerebellum
- vermis projects to fastigial nucleus
- intermediate projects to interposed nucleus
Input: spinal cord (somatosensory & muscle afferents) via dorsal and ventral spino-cerebellar tracts
Output: Purkinje cells axons to fastigial and interposed nuclei and (via red nucleus,
vestibular nuclei and reticular nuclei) to spinal cord.
Function: tunes motor execution by adjusting muscle tone.
Disorder: hypotonia
Cerebrocerebellum
- lateral cerebellum projects to dentate nuclei
Input: from cerebral cortex via pontine nuclei (mossy fibers) and inferior olive (climbing fibers).
Output: Purkinje cells axons to dentate nuclei and via thalamus to motor & premotor
cerebral cortex.
Function: tactics and coordination of skilled movements.
Disorders:
a) Inability to perform complex movements involving several muscle groups (dysmetria)
b) Inability to coordinate rapid alternating movements (dysdiadochokinesia)
c) Deficits are ipsilateral
Ataxia
The cerebellum is involved in co-ordinating movements and damage results in incurordination or ataxia. Lesions affect the same side of the body as the damage in the
cerebellum and are related to functional areas.
 Flocculonodular lobe lesion results in impaired balance, but co-ordination is ok
 Vermus/intermediate area lesions such as from alcoholic cerebellar degeneration
result in ataxia or proximal muscles and disorders of gait
 Lesions of the cerebellar hemispheres result in hypotonia and intention tremor,
especially in distal muscles