Basal Ganglia

Definition and Terminology

The term basal ganglia originally referred to all masses of gray matter within the cerebrum, but now only includes subcortical nuclei that participate in control of movement with the cerebellum, corticospinal system, and brain stem motor nuclei.

Components: caudate, putamen, globus pallidus (GP), subthalamic nucleus, and substantia nigra

thalamus is not part of the basal ganglia, but many functions of the basal ganglia are mediated through the ventral anterior (VA) and ventral lateral (VL) nuclei of the thalamus
nuclei form part of the extrapyramidal motor system (not in pyramidal motor pathway) and indirectly control movement

Divisions of Basal Ganglia:

Lentincular Nucleus: putamen and globus pallidus (lens shaped)

Corpus Striatum: putamen, globus pallidus and caudate nucleus

Striatum: putamen and caudate nucleus

Topography

Lenticular Nucleus

together the putamen and globus pallidus form a wedge-shaped piece (putamen lateral, globus pallidus medial)

lateral medullary lamina – strip of myelinated fibers that separates the putamen from the globus pallidus

medial medullary lamina – strip of fibers that separates the internal (GPi) from external (GPe) globus pallidus
the globus pallidus is slightly darker than the putamen in myelin stained sections

Striatum

caudate and putamen originate embryologically from the same mass of cells; during development the caudate remains in the lateral wall of the lateral ventricle and develops into a C-shaped structure
in the adult, the caudate nucleus has three parts:

(1) an enlarged head that bulges into the anterior horn of the lateral ventricle
(2) a body that forms the lateral wall of the body of the ventricle
(3) a slender tail that borders the inferior horn of the ventricle

the caudate and putamen retain their embryological continuity just above the orbital surface of the frontal lobe

Subthalamic Nucleus and Substantia Nigra – both located in brainstem; substantia nigra is more caudal

Components of the Basal Ganglia

Main Neurotransmitters: Glutamate (Glu) Þ excitatory, GABA Þ inhibitory, Dopamine Þ inhibitory to the caudate and

putamen but excitatory to the substantia nigra

Component	Neurotrans	Afferent	Efferent
cortex	glutamate	-	caudate and putamen
striatum (caudate+putamen)	GABA, ACh, somatostatin	cortex	GPe, substantia nigra
ext. globus pallidus (GPe)	GABA	striatum	subthalamic nucleus via subthalamic fasciculus and GPi
int. globus pallidus (GPi)	GABA	GPe and subthalamic nucleus	thalamus
subthalamic nucleus	glutamate	GPe,motor and premotor cortices	GPi and GPe
substantia nigra – compact part (pars compacta, pigmented)	dopamine	-	lat. caudate nucleus and putamen; this dopamine modulates output of globus pallidus
substantia nigra – reticular part (pars reticulata,unpigmented)	GABA	striatum and subthalamic nuclei	medial caudate nucleus, putamen, VL/VA nucleus of thalamus
thalamus	glutamate	GPi and reticular part of subst.nigra	cortex

Connections of the Basal Ganglia – see figure below

(1) Primary Circuit: cortex Þ caudate and putamen Þ GP Þ thalamus (VA/VL) Þ cortex

primary input from the motor, sensory and association cortices projects to the caudate and putamen via glutamate

caudate and putamen transmit GABA to GPe and subsequently ß amount of GABA released from Gpe

less GABA is transmitted to GPi so GPi in turn transmits more GABA to thalamus and ß its release of glutamate

thalamus relays the information to the prefrontal and premotor cortices

(2) Substantia Nigra Circuit: striatum Þ substantia nigra Þ striatum

striatum projects to pars reticulata (of substantia nigra); pars compacta in turn projects back to the striatum
pars compacta axons release dopamine, which inhibits striatum
destruction of the nigrostriatal pathway is a major cause of Parkinson’s disease

(3) Globus pallidus – Subthalamic Nucleus Circuit: GPe Þ subthalamic nucleus Þ Gpi

GPe inhibits (GABA) the subthalamic nucleus via the subthalmic fasciculus

subthalamic nucleus in turn projects back to both segments of the GP
subthalmic nucleus also receives input from the motor and pre-motor cortices

Pathology of the Basal Ganglia – see figure below

definitions: dyskinesia Þ disorders of movement; dystonia Þ disorders of muscle tone

involuntary movements are often subdivided into tremors and the state of chorea, athetosi and ballismus

(1) Parkinson’s disease (PD) – most common disease of the basal ganglia

Pathology: loss of dopamine-containing cells of the substantia nigra and subsequent degeneration of dopamine projections to the striatum

Symptoms: rigidity, akinesia, tremor

Treatment: place lesion in GPi Þ ß inhibition to VA/VL so Ý output to cortex

amphetamines: Ý release of dopamine to caudate and putamen; cause hyperactivity, enhanced reactivity

(2) Huntington’s disease

Pathology: hereditary disorder involving widespread degeneration of cells of striatum and cerebral cortex

Symptoms: involuntary choreiform movements due to striatal degeneration; dementia due to cortical degeneration

(3) Hemiballismus

Pathology: contralateral subthalamic nucleus lesion

often in older people due to a stroke involving a small ganglionic branch of the posterior cerebral artery

Symptoms: wild flailing movements of one arm and leg

effects are contralateral to the lesion because the precortical projections (subthalamic nucleus Þ thalamus Þ cortex) are all ipsilateral; the cortex is concerned with motor control on the contralateral side of the body

Cerebellum Vs. Basal Ganglia

Basal Ganglia	Cerebellum
Receives input from all areas of cortex	Input primarily from sensory motor region
No sensory input	Receives sensory input
No projections to brainstem and vestibular nuclei	Projections to brainstem and vestibular nuclei
Initiation of movement	Modulation of movement
Lesion: tremor, rigidity, and chorea	Lesion: ataxia