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Cerebellum + basal ganglia are the two systems that modulate motor cortex demands for motor functions. These systems have no descending pathways, but they modulate movements. Hence disorders of these systems cause uncoordinated voluntary movements and presence of involuntary movements.

Basal ganglia

  • A group of nuclei for motor function
    • Defined as the corpus striatum (=caudate+lentiform), subthalamic nucleus (diencephalon) and substantia nigra (midbrain)
    • Modulate the motor areas of the cortex
      • Translate ideas into actual movement
      • Store data about the sequence of learned movements
    • Damage results in disorders of movement (too much or too little, eg. involuntary movement)
      • Ie: damage to extrapyramidal tracts causing disorders in fine tuning of movements
      • Vs. damage to pyramidal tracts resulting in paralysis
  • Notes:
    • The neostriatum is made up of the caudate nucleus and putamen – receives input from the cortex
      • caudate from association, putamen from motor
    • The pallidum is made up of the globus pallidus that is involved in output
    • The subthalamic nucleus and substantia nigra are regulatory


  • Composed of:
    • Medially – the caudate
      • Has a head, body and tail
      • Lines the walls of the anterior horn, body and inferior horn of the lateral ventricdle
    • Laterally– the putamen
      • Separated from globus pallidus by the lateral medullary lamina
      • Covered laterally by the external capsule
      • Note that the putamen starts a little bit before the GP (in sections), because it is bigger and doesn't sit in the bend of the internal capsule
    • In between – the internal capsule
      • Nucleus accumbens (ventral striatum) is the connection between the caudate and putamen (below the anterior limb of the internal capsule)
  • Inputs
    • Neocortex (sensorimotor to putamen, association to caudate)
      • Neurotransmitter is glutamate which has an excitatory effect
    • Substantia nigra pars compacta (the nigrostriate pathway)
      • Neurotransmitter is dopamine that excites D1 receptors and inhibits D2 receptors in putamen
  • Outputs
    • Globus pallidus (internal and external)
      • Neurotransmitter is GABA which has an inhibitory effect
    • Substantia nigra pars reticulata
      • Neurotransmitter is GABA which has an inhibitory effect
  • Note that (neo)striatum and corpus striatum are different things
  • Note that the internal capsule continues into the brainstem as the cerebral peduncle

Globus Pallidus

  • Two parts divided by medullary lamina
    • External(GPe)
      • Inputs from striatum (GABA, -ve)
      • Outputs to STN (GABA, -ve)
    • Internal(GPi)
      • Inputs from striatum (GABA, -ve), STN (Glut, +ve)
      • Outputs to VL (ventral lateral), CM (central medial) thalamus and brainstem reticular formation (GABA, -ve)

Subthalamic nucleus

  • Located between the thalamus and midbrain adjacent to the internal capsule
    • Inputs from GPe (GABA, -ve) o Outputs to GPi (Glut, +ve)

Substantia nigra

  • Located in the cerebral peduncle of the midbrain
    • 2 parts:
      • Ventrally/laterally: pars reticulata (SNr)
        • Midbrain continuation of the GPi with similar connections
      • Dorsally/medially: pars compacta (SNc)
        • Dopaminergic neurons projecting to striatum (+ve and –ve). Dopamine-producing cells are black, due to the byproduct of its synthesis which is neuromelanin.


  • There are two main feedback loops to the cerebral cortex that operate in parallel and have opposite effects
  • NOTE: at rest, GPi and GPe are active and exert inhibitory effects on the thalamus and STN so the motor cortex is quiet
  • Direct loop – excitatory to the cortex facilitating movement
    • Fibres from cortex excite the striatum (caudate/putamen/NAcc) which (via GABA) inhibits GPi
      • This causes disinhibition of GPi inhibition of the thalamus
      • Thus the thalamus excites the motor areas of cortex allowing action
  • Indirect loop – inhibitory to the cortex suppressing unnecessary movements
    • Fibres from the cortex excite the striatum which (via GABA) inhibits GPe
      • These project to the STN and thus this inhibition is disinhibited
  • This causes the STN to excite the GPi which causes further inhibition of the thalamus preventing unnecessary movement

User:Sameer Mahajan read above.

Direct and indirect loops


  • At rest, GP cells are active and releasing inhibitory GABA to the thalamus (to reduce its excitement of the motor cortex)
  • When you want to move, you send an excitatory command from the cortex to the putamen. The putamen projects inhibitory GABA neurons to the GPi. This is the direct loop. Net effect is to excite cells in the motor cortex (facilitating/enhancing movement)


  • Overall, net effect is to suppress a particular movement (read above)
  • Note that putaminal cells with D1 receptors stimulate the direct pathway. Putaminal cells with D2 receptors inhibit the indirect pathway.



For more information read this.


  • Hyperkinetic disorders - too much thalamic activity caused by poor basal ganglia modulation
    • Excessive involuntary movements resulting from decreased activity (damage) of STN, which interrupts the indirect pathway
      • This causes a lack of inhibition on the thalamus by GPi
      • May result from a lesion of STN or the striatum
    • EG: Hemiballismus – sudden flailing movements of contralateral limbs – STN lesion (e.g. secondary to PCA occlusion)
    • EG: Chorea – dance-like, jerky, purposeless movements of limbs, face, tongue
      • Results from degeneration of D2 GABA cells in the striatum (particularly the putamen)
      • Can be caused by Huntington’s chorea (genetic autosomal dominant) - do genetic testing, also affects frontal lob
    • Athetosis – slow writhing movements of trunk and proximal limbs with varying spasticity. Striatal damage.
      • Eg: cerebral palsy
      • Often combined with chorea – choreoathetosis
  • Hypokinetic disorders
    • Characterised by a slowness of movement
    • EG: Parkinson’s disease; due to decreased activity in the direct pathway and an increased activity in the indirect pathway (due to dopamine withdrawal)
      • Results from degeneration of dopaminergic nigrostriate neurons
        • These excite the direct path or inhibit the indirect path
        • Thus, degeneration results in reduced cortical motor activity and less movement
      • Characteristics:
        • Bradykinesia (hypokinesia) – difficulty starting, carrying out and stopping movements; although people notice tremors in PD, the main pathology is lack of movement. (Note they can show that the basal ganglia are active just before movement).
          • Expressionless (mask) face, reduced arm movements while walking
        • Rigidity – flexors and extensors affected, cogwheel
        • Resting tremor – rhythmic nodding and hand movements (pill-rolling), diminish during voluntary movements
          • Interneurons lose regulation
        • Abnormal posture – postural reflex are impaired, stooped, poor balance
        • Click here to see Parkinsonian Gait
          • When you first ask them to move, it takes a while for them to start. Once they've started moving, it takes them a moment to stop in response to what you ask.
      • Treatment
        • L-Dopa, if lesions removal – eg. pallidotomy, deep brain stimulation (DBS)
          • L-Dopa is given instead of dopamine, which can't cross the BBB
          • Over time it becomes less an less effective, because there is a disease process killing off STN neurons, so there are less and less that can be activated by L-Dopa. Eventually, the increase in dose causes involuntary movements: take drug --> involuntary movements --> window of normality --> freeze up. Over time, window of normality decreases
          • Best way to fix intractable PD, is to put electrode in STN and use a frequency that blocks the inhibitory effect of the STN, to cut the indirect pathway and free up the pathway for movement


Other circuits

  • There are other feedback loops through the basal ganglia concerned with cognition and mood
    • Mood (limbic) circuit: begin sand ends in the anterior part of the cingulate gyrus and involves nucleus accumbens
    • Cognitive loop begins and ends in the prefrontal cortex
    • These other feedback loops can explain why cognitive and behavioural changes often appear in late stage bg disease (PD and Huntington’s chorea)
  • Caudate nucleus has a big head because it receives a lot of input from the prefrontal cortex, to which it also projects (feedback loop to the prefrontal cortex). Therefore as chorea and PD progress, you get cognitive impairment.

To study the loop, start off with GPi and GPe active, and then add in the other neurons to see the effects of the two pathways.

Note also that the cerebellum acts on the cortex re: movement. See next week