Workshop: Movement

Voluntary movement involves the higher centres of the cerebral cortex, cerebellum and basal ganglia.

idea → program → execution → feedback → idea/program/execution (cycle)

Idea of voluntary movement = supplementary motor area, association areas and limbic system

Program for voluntary movement = primary motor cortex, premotor area, supplementary motor area

Execution of voluntary movement = pyramidal tract, extrapyrimidal tract and motor neurons → movement of skeletal muscle

feedback for voluntary movement = sensory systems, cerebellum, thalamus, basal nuclei and brainstem

Voluntary motor impulses arise in the motor area of the cerebral cortex and synapse with motor neurons in the spinal cord. The axons form pyramidal tracts which cross over in the medulla oblongata.

Density of muscle innervation is proportional to the complexity of movement.

The cerebellum is involved in coordination of movement as well as control of posture. Cerebellum dysfunction can result in ataxia or an intention tremor. Ataxia presents as poor balance, unsteady walking and a tendency to fall over. Intention tremor is due to poor adjustment of motor signal resulting in oscillating movements.

The basal ganglia consists of the striatum, globus pallidus and substantia nigra. It’s responsible for initiation of movement, fine movement and coordinated movement.

Substantia nigra projects inhibitory dopaminergic neurons to the striatum and receives inhibitory GABAergic neurons from the striatum.

The corpus striatum projects inhibitory GABAergic neurons to the substantia nigra and globus pallidus and receives inhibitory dopaminergic neurons from the substantia nigra, Inhibitory cholinergic interneurons are found within the corpus striatum.

The globus pallidus receives inhibitory GABAergic neurons from the striatum and projects inhibitory GABAergic neurons to the thalamus.

The thalamus receives inhibitory GABAergic neurons from the globus pallidus and projects excitatory glutamatergic neurons to the cortex.

The cortex receives excitatory glutamatergic neurons from the thalamus and projects excitatory glutamatergic neurons to the striatum and spinal cord.

Diseases of the basal ganglia may be hyperkinetic, dyskinetic or hypokinetic. Examples include Parkinson’s and Huntington’s.

Characteristics of Parkinson’s disease include tremor, slow movements and stiff/inflexible muscles. It’s caused by Lewy bodies and loss of neurons in the substantia nigra leading to dopamine reduction. Both genetic and environmental factors contribute to disease development.

Parkinson’s can be treated with physiotherapy, medication (dopamine agonist/MAO-B inhibitor), or in some cases surgeries including deep brain stimulation, thalamotomy or pallidotomy are used.

Huntington’s is a primarily genetic disorder which affects 1 in 20,000 people. It arises due to degeneration of cholinergic neurons in the striatum and cerebral cortex, and GABAergic neurons in stiatopallidal and striatonigral pathways. This results in chorea, dementia and eventually death. Typically to initiate movement the cortex sends a signal to the basal ganglia to release inhibition. In Huntingtons this initiation or reinstatement of inhibition can be erratic and uncontrolled.

Chorea is a type of dyskinesia characterized by rapid, jerky involuntary body movements.

Huntingtons can be treated with tetrabenazine and/or antipsychotics and benzodiazepines, as well as with physical therapies and different modifications.

Tetrabenazine may work by depleting monoamines and inhibiting VMAT2.

Antipsychotics/benzodiazepines are positive allosteric modulators of some GABA receptors.