This presentation is intended to address the basic anatomy of basal ganglia, the
arrangements and functioning of various circuits concerned with basal ganglia and
certain applied aspects related to movement disorders explained by basal ganglia
It was as early as 1664 when two first clear identification of distinct subcortical
structures was published by English anatomist, Thomas Willis. At the beginning of
20th century there were serious attempts to provide detailed comparative descriptions
of Corpus Striatum (Wilson, 1914 and Cajal 1911). The corpus striatum then came
to be recognized as a major component of extra pyramidal system. It was recognized
that lesions of these would result in disorders of motor function in Humans (Wilson
1914, Vogt 1911).
Anatomy of basal ganglia
Basal ganglia include subcortical structures of grey mater which are situated in
core of each hemisphere. It includes corpus striatum, sub thalamic nucleus, substantia
nigra and pedenculopontine nucleus.
- 1. Corpus striatum
It consists of caudate nucleus and lentiform nucleus. The lentiform nucleus is further
divided into putamen and globus pallidus. The caudate nucleus and putamen are functionally
related and forms the striatum. The globus pallidus forms the pallidum. The striatum
is further divided into dorsal striatum ( Cuadate nucleus and putamen) and ventral
striatum ( nucleus accumbens).
The pallidum is divided into dorsal pallidum and ventral pallidum which includes
anterior perforated substance. The globus pallidus is further divided into globus
pallidus externa (GPe) and globus pallidus interna (GPi). Most of the cells of striatum
are medium spiny nerves (MSN) and contain GABA, substance-P and encephalin. The
encephalinergic neurons possess D2 receptors and substance –P neuron have D1 dopamine
receptors over them. These neuron are chief source of striatal efferents to pallidum.
The aspiny neurons contain acetyl choline and are mostly interneurons. The globus
pallidus contain large multipolar neurons. GABA is the neurotransmitter in both
internal and external GP.
- 2. Subthalamic nucleus (STN)
It is a biconvex mass of grey mater, which lies below hypothalamus. It is involved
in indirect circuit of basal ganglia
- 3.Substantia Nigra
It is a pigmented sheet of nerve cells which extends along entire length of midbrain.
It consist of 2 parts: pars reticulata (SNr) and pars compacta (SNc). The SNr is
one of the chief output nucleus of basal ganglia. The projection fibers from SNr
to thalamus appears to be GABA ergic. The SNc has dopaminergic neurons which sent
afferent to dorsal striatum, via mesolimbic dopaminergic system to ventral striatum,
prefrontal cortex and anterior cingulated gyrus.
- 4.Pedunculopontine nucleu (PPN)
They lie in midbrain and are influenced by both direct and indirect pathways converging
on GP1 and SNr. It influences the skeletomotor systems by activating the reticulospinal
Functionally the striatum can be considered to be afferent input to basal ganglia.
The Gpi and SNr are chief output nuclei of the basal ganglia. Striatum receives
input from most of the neocortex. The corticostriatal fibres are glutaminergic and
excitatory. The striatum also receives dopaminergic fibres from SNc. Most of the
efferent fibre from dorsal striatum pass to dorsal pallidum as striato-pallidal
The output fibres from pallidum are arranged in 2 discrete bandles:
The fibres from thalamic nuclei, which are glutaminergic project to pre-motor and
supplimentery motor areas of cerebral cortex.
- 1.Fascicular lenticularis: Fibres from Gpi occupies forel
- 2.Ansa Lenticularis: Arise from Gpi and Gpe and joint
together in prerubral field to form the thalamic fasiculus and occupies the forel
field H-1. It terminates in ventral anterior (VA) and Ventral lateral(VL) nuclei
of thalamus. The striato pallidal and pallidothalamic fibers are GABA ergic.
The direct connection between putamen and Gpi and SNr is called direct pathway.
There is also and indirect pathway where putamen is connected to Gpi and SNr through
STN. Here fibres from putamen go to GPr an then to STN and to SNr and Gpi. The connections
between STN to Gpi and SNr are excitatory and glutaminergic. A remarkable consequence
of activation of MSN is that basal ganglia output is decreased when direct pathway
is stimulated resulting in disinhibition of thalamus and cortical excitation. The
basal ganglia output is increased when the indirect pathway is stimulated thereby
inhibiting the thalamus and leading to cortical inhibition.
Role of Dopamine in basal ganglia
Dopaminergic projection to striatum facilitates transmission over direct pathway
via activation of D1 receptor and inhibits transmission over indirect pathway via
the D2 receptors. This enables dopamine released in striatum to modulated costico-striatal
The overall effect of dopamine released in striatum appears to be a reduction in
basal ganglia output leading by disinhibition to increased activity of thalmo-cortical
fibres. This facilitates movements.
Dopamine also has a role in synaptic plasticity within the striatum being implicated
in both long term potentiation (LTP) and long term depression (LTD) Dopaminergic
neurons may play an important in determining which striatal synapses should be strengthened
or weakened. This is critical in autonomous learning (implicit memory).
Unlike all other basal ganglia circuits dopaminergic neurons do not show activity
changes in relation to movements but they discharge in relation to probability and
imminence of behavioral reinforcement.
of basal ganglia:
There is parallel organization of basal ganglia circuits. There is paucity of inter
neurons or axon collaterals in basal ganglia nuclei. Hence the flux of information
in different circuits remain seggregated.
Basal ganglia can be considered as a family of re-entrant loops that are organized
in parallel, each taking origin from specific region of cerebral cortex then this
input going to specific areas of basal ganglia which are returned back to same cortical
fields via the thalamus. There are 4 functional circuits.
- 1.Skeletomotor circuits
- 2.Oculomotor circuits.
- 3.prefrontal (cognitive) circuit
- 4.Limbic circuit
- Skeletomotor circuit
It begins in motor and pre- motor areas of frontal lobe and somatosensory field
of parietal lobe. The striatal position of circuit lies mainly in putamen. Costicostriatal
projection are glutaminergic and excitatory. The MSN of striatum are GABA ergic
in nature and inhibitory. It projects to Gpi and SNr via the direct pathway and
to Gpe via indirect pathway. The MSN discharge in relation to planning or execution
of movements. The aspiny interneurons discharge spontaneously.
The information from striatum may be channeled through direct and indirect pathways.
Cortically initiated activation of direct pathway result in positive feed back at
cortical level and activation of indirect pathway to negative feed back.
- Oculomotor loop
Orginates from frontal eye field and supplementary eye fields. The impulses then
go to body of caudate nucleus. The striatum sends inhibitory control over substantia
nigra which further inhibits superior colliculis.
- Prefrontal circuit (cognitive loop)
Originates from pre- frontal cortex and goes to head of caudate nucleus and then
finally back to pre- frontal cortex.
- Limbic circuit
Arises from anterior cingulated gyrus with basal ganglia components lying in ventral
striatum and ventral palladium.
The number of striatal neurons receiving cortical afferent is much smaller than
the number of cortical afferents sending these projection. Also the number of output
neurons in striatum is larger than the number of target neurons of Gpi and SNr.
This funneling of information may permit recombination of cortical input. This serves
to modulate cortical activity.
Normally a tonic high frequency inhibiting output of basal ganglia suppress the
thalamo-cortical neurons thereby restraining any movements. A movement is facilitated
when there is a phasic activation of direct pathway thereby activating thalamo-cortical
neuron. There is a temporal interplay between activity of direct and indirect output
which helps to scale certain movement parameters such as amplitude or velocity during
a movement. This is called scaling hypothesis. The motor circuit may also act to
compare the intended movement from cerebral cortex with proprioceptive feed back.
A signal from the comparator would be then projected back to pre-central motor area
Basal ganglia output may act to focus the cortical selection of movements. This
fecilitates wanted movements and inhibit unwanted movements. By amplifying phasic
activity both direct and indirect pathways. The basal ganglia helps to sharpen the
contrast in activity in areas of cortex governing wanted and unwanted movements.
Basal ganglia and movement
There are 2 types of movement disorders:
- A)Hypokinetic (Parkinsonism)
- B)Hyperkinetic ( chorea, dystonia, Tic etc..)
In general hypokinetic movement disorder is characterized by increased indirect
pathway activity and hyperkinetic movement disorder by increased direct pathway
The above can be explained by parkinsonism and chorea as clinical paradigms.
It is a prototype of hypokinetic movement disorder characterized by bradykinesia,
rigidity and tremors. Loss of dopaminergic neuronal input from SNc to striatum leads
to overall increase in indirect pathway activity and decreased activity in direct
pathway. This enhances inhibitory influence over the thalamus which inhibits the
thalamocortical projection akinesia is due to increased inhibition of supplementary
motor area. Early position of Berietschaft potential is small in patients with parkinsonism.
Abnormalities in neuronal activity in basal ganglia eventually leads to abnormalities
in spinal cord via the PPN and reticulospinal tract. There is inhibition of Ib interneurons
through the reticulospinal tract. This leads to disinhibition of motor neurons
and rigidity. Tremors of parkinson’s disease is supposed to be due to oscillatory
discharge in thalamic nuclei. Recently it has been postulated to be due to unmasking
of pacemaker like activity of basal ganglia due to loss of dopaminergic neurons.
This is a typical hyperkinetic disorder where there are non-sterotyped jerky quasipurposive
involuntary movements affecting the limbs or trunk. Caudate nucleus is affected.
Pathologically striatal neurons projecting to Gpe are specifically involved. This
leads to reduced inhibition of neuron of Gpe. This further leads to increased inhibition
of STN and Gpi/SNr through indirect pathway. This leads to reduced output to thalamus
and increased activity of thalamocortical neurons and excessive movements.
Therapeutic implication- Deep Brain stimulation(DBS)
DBS is high frequency stimulation of certain nuclei like STN and Gpi used in treatment
of PD. In parkinsonian state studies have showed that dopamine depleation in striatum
results in hyperactivity of STN and in turn increased activity of Gpi and SNr. The
over activity in these two structures induces a tonic inhibitory influence on motor
thalamic nuclei which results in hypoactivity of cortical neurons. High frequency
stimulation of STN and Gpi induces a deactivation of basal ganglia output structures
that liberates motor thalamic nuclei from tonic GABA ergic influence. The direct
effect of DBS is supposed to inhibit the structure stimulated by 2 mechanisms :
depolarization block and neuronal jamming. Direct action by release of neurotransmitter
release has also been postulated.
Basal ganglia are a group of subcortical and brain stem nuclei, which are involved
in programming, planning, initiation and smooth execution of movements. There are
direct and indirect pathways within the basal ganglia, which may be selectively
involved leading to hypo or hyperkinetic movement disorders. Targeting certain specific
nuclei like STN and Gpi by DBS is of therapeutic benefit in advanced Parkinson’s