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Subcortical structures: the cerebellum, basal ganglia, and thalamus 

Subcortical structures: the cerebellum, basal ganglia, and thalamus

Subcortical structures: the cerebellum, basal ganglia, and thalamus

Mark J. Edwards

and Penelope Talelli


Update: A link to video material relating to movement disorders has been added to this chapter.

Updated on 24 Sep 2015. The previous version of this content can be found here.
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date: 28 April 2017

Less is known of the function of the cerebellum, thalamus and basal ganglia than of other structures in the brain, but there is an increasing appreciation of their complex role in motor and nonmotor functions of the entire nervous system. These structures exercise functions that far exceed their previously assumed supporting parts as simple ‘relay stations’ between cortex and spinal cord.

The subcortical structures receive massive different inputs from the cerebral cortex and peripheral sense organs and stretch receptors. Through recurrent feedback loops this information is integrated and shaped to provide output which contributes to scaling, sequencing and timing of movement, as well as learning and automatization of motor and nonmotor behaviours.


Functional neuroanatomy—the cerebellum can roughly be divided into (1) vestibulocerebellum—integration of vestibular information, (2) spinocerebellum—integration of sensory information from the body, (3) pontocerebellum—integration of information from the cortex regarding planned or on-going movement.

Function—these are proposed to be as follows: (1) a timing device for movement, (2) facilitation of motor learning, and (3) facilitation and correct scaling and harmonization of muscle activity.

Clinical features of cerebellar lesions—these include impairment of movement with dysmetria (‘past-pointing’), dysdiadochokinesia, truncal and gait ataxia (in midline vermal lesions), dysarthria, and abnormal eye movements (commonly nystagmus).

Basal ganglia

Functional neuroanatomy—the basal ganglia participate in multiple parallel loops which take information from different (mainly cortical) areas and then feedback (mainly) to those same areas. Input is mainly from the striatum; output comes almost exclusively from either the globus pallidus interna or the substantia nigra pars reticulate, which send inhibitory projections to the thalamus; dopamine is the main neurotransmitter that regulates activity.

Function—four main roles are hypothesized: (1) release of desired movement from inhibitory control, (2) inhibition of undesired movement, (3) facilitation of sequential automatic movements, (4) integration of attentional, reward and emotional information into movement and learning.

Clinical features of basal ganglia lesions—these include rigidity, akinesia, and dystonia.


Functional neuroanatomy—the thalamus receives afferent input from the special senses, basal ganglia, cerebellum, cortex and brainstem reticular formation; efferent output is mainly directed to cortical areas and striatum.

Function—the main thalamic functions are thought to include (1) modulation of sensory information by integration of brainstem (in particular reticular activating complex) and relevant cortical information; and (2) modulation of cortical activity via cortico-thalamocortical loops.

Clinical features of thalamic lesions—these include (1) sensory abnormalities—ranging from loss to deep-seated, severe pain; (2) motor disorders—e.g. hemiplegia; and (3) movement abnormalities—e.g. myoclonus, dystonia—usually in the context of lesions also involving the basal ganglia.

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