Physiology chapters
Basal ganglia
What the basal ganglia do, how their direct and indirect circuits and neurotransmitters work, and why their failure causes Parkinson's disease, Huntington's disease, chorea, athetosis and hemiballismus.
- The basal ganglia select wanted movements and suppress unwanted ones, working in loops with the cortex and thalamus.
- The direct pathway increases movement; the indirect pathway decreases it; dopamine from the substantia nigra boosts the first and damps the second.
- Too little movement: Parkinson's (dopamine loss). Too much: chorea (Huntington's), athetosis, hemiballismus (subthalamic nucleus).
On this page
Overview
The basal ganglia are a group of deep nuclei that work with the motor cortex. They do not send fibres to the spinal cord. Instead, they act through loops with the cortex and thalamus.
Their job is to help start wanted movements, suppress unwanted ones, and control the force and timing of movement. They are also involved in learning motor habits.
For the structures themselves, see the anatomy page on the basal ganglia.
Components
- Striatum: caudate nucleus and putamen. The main input station.
- Globus pallidus: external (GPe) and internal (GPi) segments.
- Subthalamic nucleus.
- Substantia nigra: pars compacta (makes dopamine) and pars reticulata.
The main output comes from the GPi and substantia nigra pars reticulata. It is inhibitory (GABA) and goes to the thalamus.
Two main circuits
- Putamen circuit: controls learned patterns of movement (writing, cutting with scissors). Input from motor and sensory cortex.
- Caudate circuit: cognitive control of movement: planning what to do and in what order, based on memory and thought. Input from association cortex.
Direct and indirect pathways
The GPi constantly inhibits the thalamus. The thalamus excites the motor cortex. So the GPi acts like a brake on movement.
Direct pathway: releases the brake
Cortex → excites striatum → striatum inhibits GPi → GPi inhibits the thalamus less → thalamus excites the cortex → more movement.
Indirect pathway: presses the brake
Cortex → excites striatum → striatum inhibits GPe → GPe inhibits the subthalamic nucleus less → subthalamic nucleus excites GPi → GPi inhibits the thalamus more → less movement.
Direct pathway increases movement. Indirect pathway decreases movement. The subthalamic nucleus belongs to the indirect pathway.
Role of dopamine
Dopamine from the substantia nigra pars compacta travels to the striatum in the nigrostriatal pathway.
- It excites the direct pathway (D1 receptors).
- It inhibits the indirect pathway (D2 receptors).
Both effects increase movement.
Neurotransmitters
| Transmitter | Where |
|---|---|
| Dopamine | Substantia nigra → striatum |
| GABA | Striatum → globus pallidus and substantia nigra; GPi → thalamus (inhibitory) |
| Acetylcholine | Interneurons within the striatum |
| Glutamate | Cortex → striatum; subthalamic nucleus → GPi (excitatory) |
Dopamine and acetylcholine have opposite effects in the striatum and are normally in balance.
Disorders of the basal ganglia
Parkinson's disease
How it happens: degeneration of dopamine neurons in the substantia nigra pars compacta. The direct pathway weakens and the indirect pathway becomes overactive, so the thalamus is over-inhibited.
What you see:
- Bradykinesia: slowness and difficulty starting movement.
- Rigidity: "lead-pipe", or "cogwheel" when tremor is added.
- Resting tremor: about 3–6 per second, "pill-rolling", which lessens with movement.
- Stooped posture, shuffling gait, expressionless face, small handwriting.
Treatment: levodopa (crosses the blood-brain barrier and is turned into dopamine), dopamine agonists, MAO-B inhibitors, and anticholinergic drugs to restore the dopamine-acetylcholine balance.
Dopamine itself does not cross the blood-brain barrier, so levodopa is given instead. Anticholinergics help because loss of dopamine leaves striatal acetylcholine relatively overactive.
Huntington's disease
How it happens: an autosomal dominant CAG repeat expansion causes loss of GABA-producing neurons in the caudate and putamen (especially those of the indirect pathway), and of acetylcholine neurons. With the brake weakened, the thalamus is over-active.
What you see: chorea (quick, jerky, dance-like movements), then dementia and personality change, usually starting in mid-life.
Chorea
Quick, irregular, jerky movements that flit from one part to another. Seen in Huntington's disease and in Sydenham's chorea after rheumatic fever.
Athetosis
Slow, writhing, twisting movements, mainly of the hands and fingers. Linked with damage to the globus pallidus and putamen, for example after brain injury around birth.
Hemiballismus
How it happens: a small stroke in the subthalamic nucleus.
What you see: sudden, violent, flinging movements of the arm and leg on the opposite side.
Lesion of the subthalamic nucleus → contralateral hemiballismus.
Tremor of the basal ganglia (Parkinson's) is present at rest; tremor of the cerebellum is an intention tremor, worse on movement.
Expect: the components, the direct and indirect pathways and their effect on movement, the action of dopamine on D1 and D2 receptors, transmitter changes in Parkinson's and Huntington's disease, why anticholinergics and levodopa work, and the lesion site in hemiballismus.
Quick revision
- Main loop: cortex → striatum → GPi → thalamus → cortex.
- GPi output is inhibitory (GABA) to the thalamus.
- Direct pathway increases movement; indirect pathway decreases it.
- Dopamine: D1 excites direct, D2 inhibits indirect; net effect, more movement.
- Parkinson's: nigrostriatal dopamine loss; bradykinesia, rigidity, resting tremor.
- Huntington's: loss of striatal GABA neurons; chorea.
- Hemiballismus: contralateral subthalamic nucleus.
Written by The House Job from standard physiology references (Guyton and Hall Textbook of Medical Physiology; BRS Physiology).
FAQ
What is the function of the basal ganglia?
They help start wanted movements, suppress unwanted ones, and control the force and sequence of movements.
What is the defect in Parkinson's disease?
Loss of dopamine-producing neurons in the substantia nigra pars compacta.
Why is levodopa given instead of dopamine?
Dopamine does not cross the blood-brain barrier, but levodopa does and is converted to dopamine in the brain.
What causes hemiballismus?
A lesion of the subthalamic nucleus on the opposite side.