ppt

1. NEUROANATOMY OF BASAL GANGLIA & ITS
RELEVANCE TO PSYCHIATRY
PRESENTER : Dr. ANUSUYA . M
CHAIR PERSON : Dr.SHANMUGAPRIYA.A.R

2. Basal Ganglia…
The term basal ganglia refers to a number of
subcortical nuclear masses embedded inside the
cerebral white matter in the inferior part of the
cerebral hemisphere,anterior & lateral to the
thalamus.

4. • Major structures:
• Caudate nucleus
• Putamen
• Globus pallidus(internal and external)
• Subthalamic nuclei
• Substantia nigra

5.  Amygdala is included within basal ganglia as it occupies
an important position and connection between the basal
ganglia and the limbic system
 Embryological evidence supports inclusion of the amygdala

6.  An additional term “ventral striatum” describes parts of
the
basal ganglia that are
1. Closest to limbic structures
2. Involved in cognitive and behavioural functions
 Nucleus accumbens ia major structure of ventral striatum
 It has a rich dopaminergic innervation arising from the
ventral
tegmental area and amygdala

9. • STRIATUM = Caudate nucleus +
Putamen.
• CORPUS STRIATUM =
Caudatenucleus+ Putamen+
Globus pallidus.
• LENTIFORM NUCLEUS = Putamen
+Globus pallidus

11. The nuclei of the basal
ganglia are shown from
the lateral perspective.
The caudate nucleus
includes the head, body
and tail. The lenticular
(lentiform) nucleus
consists of an apposition
of two nuclei – the
putamen laterally (seen
here) and the globus
pallidus medially (not
seen on this view).

12. • The basal ganglia of the
opposite side of the brain
are shown, so they are
being visualized from the
medial perspective. This
view therefore shows the
globus pallidus, which is
located medially, and its
two subdivisions (internal
and external segments).
• The putamen is located
more laterally. These
nuclei collectively form
the lentiform nucleus.

13. INPUTSTOTHE BASAL GANGLIA
STRIATUM ISTHE MAJOR RECIPIENTOF INPUTSTOTHE BASAL
GANGLIA.THREEMAJORAFFERENT PATHWAYSARE KNOWNTO
TERMINATE INTHESTRIATUM.
• CORTICOSTRIATAL
• NIGROSTRIATAL
• THALAMOSTRIATAL

14. TH -THALAMUS
PT – PUTAMEN
CD - CAUDATE NUCLEUS
CM –CENTRAL MEDIAN
NUCLEUS
SNC - SUBSTANCIA NIAGRA
PARSCOMPACTA
VS –VENTRALSTRIATUM
SNR – SUBSTANCIA NIAGRA
PARS RETICULATA
CORTICOSTRIATAL
PATHWAY
THALAMOSTRIATAL PATHWAY
NIGROSTRIATAL PATHWAY

15. CORTICOSTRIATAL PATHWAY

16. NIGROSTRIATAL PATHWAY:
THALAMOSTRIATAL PATHWAY:
Nigrostriatal
pathway
Thalamostriatal
pathway
Corticostriatal
pathway

17. Functions of BASAL GANGLIA
 Regulationof voluntary movement
 Learning of motorskills
 Execution of a particular movement
 Preparation of the body forthe movement

18.  Role in cognition, emotion, and oculomotorcontrol
 Behavior ,memory, attention, and reward processes
 Learning of associations between stimuli, actions and
rewards.
 Motivational modulation of motor behavior

19. Functional connections of basal ganglia
 In the motor loop cortical projections are to the putamen
 All other loops cortical projections are to thecaudate
 In cognitive loop
Frontal lobe
caudate
Globus
pallidus
Thalamus

20. be involved in the motor
expressionsof emotion
 The limbic loop
ORBITOFRONTAL
CORTEX
ANTERIOR CINGULATE
CORTEX
VENTRAL
STRIATUM
NUCLEUS
ACCUMBENS
VENTRAL
PALLIDUM
The limbic loop may
THALAMUS

21.  Theoculomotor loop
 The oculomotor connects cortical regions invoived in visual
attention and eye movement planning to caudate
FRONTAL EYE FIELD
POSTERIOR PARIETAL CORTEX
CAUDATE
SUBSTANTIA
NIGRA
THALAMUS

22. Three major pathways emerge from the basal
ganglia, which project onto various structures of
the brain, communicating with them.
1) Direct (excitatory)
2)Indirect (inhibitory)
3)Hyperdirect (inhibitory) pathways

23. •Cortex - Striatum (glu)
•Striatum - GPi/SNr (GABA
•GPi/SNr - Thalamus (GAB

24. Direct pathway
1) The direct pathway starts from the
cortex and projects to
the striatum (caudate nucleus and
putamen) with excitatory glutamatergic
(glu) neurons. The neurons from the
striatum, which are inhibitory GABAergic,
send their axons to the Gpi.

25. 2) The neurons of Gpi are inhibited that
is they seceret less GABA. The
inhibition on thalamus from Gpi
becomes less.
The fibers that travel from the GPi to the
thalamus, form two white matter
fascicles called ansa lenticularis and
lenticular fasciculus, that fuse into one
pathway called thalamic fasciculus just

26. 3) From the thalamus, excitatory
pathways go to the cortex (prefrontal,
premotor and supplementary cortex)
where they affect the planning of the
movement by synapsing with the neurons
of the corticospinal and corticobulbar
tracts in the brainstem and spinal cord.

27. This entire system functions on the principle of positive
feedback. Since the two of the inhibitory synapses are serially
connected, that means that the first inhibitory neuron
(striatum) suppresses the activity of the second inhibitory
neuron (Gpi).
As a result there is reduction of the inhibitory influence that
the Gpi has over the thalamus, so-called disinhibition of the
thalamus.
So the final function of the direct pathway of the basal ganglia
is to excite the motor cortex or to increase the motor activity.

30. Indirect pathway
This pathway begins (like the direct pathway) from the cortex, projecting to
the striatum. Instead of sending axons directly to the GPi and SNr, they
project to the external globus pallidus.
The neurons from the GPe send inhibitory fibers to the subthalamic
nucleus instead of sending directly to the thalamus (hence its name
“indirect”).
From the subthalamic nucleus, neurons send their axons to the GPi/SNr and
then continue as the direct pathway with GABAergic inhibitory neurons to
the thalamus and glutamate excitatory efferents to the cortex.

31. So, functionally, the striatum inhibits the external
globus pallidus, and that causes disinhibition of the
subthalamic nucleus.
The neurons of the subthalamus become more active,
and they excite the internal segment of the globus
pallidus which in the end, inhibits the thalamic nuclei.
The final result of this pathway is a decreased activity of
the cortical motor neurons and suppression of the
extemporaneous( PERFORMED) movement

33. Hyperdirect pathway:
Neurons from the cortex directly project to the SN,
conveying strong excitatory signals to the GPi with
shorter conduction time than the direct and indirect
pathway, bypassing the striatum which then excites the
Gpi thus suppressing thalamic activity on the cerebral
cortex and increasing inhibitory influences on the upper
motor neurons.
As a result, together with the indirect pathway, only
the selected motor program is executed and other
competing motor programs are canceled.

35. In summary, when a given motor pattern is
computed by the cortex, it is first conveyed to
the basal ganglia via glutamatergic projections
to the striatum, with the purpose of releasing
the intended movement and suppressing the
unintended ones.
The direct pathway funnels the information
from the striatum to Gpi via GABAergic
inhibitory projections thus selectively reducing
its activity and firing from the thalamocortical
neurons to initiate the movement

36. Along with the initial signal to the striatum, the cerebral
cortex suppresses competing motor programs by
the indirect and hyperdirect pathways.
When excited by the glutamatergic inputs of the cerebral
cortex, striatum sends inhibitory signals to the GPe which
normally exerts GABAergic inhibition on the STN.
Therefore, the glutamatergic excitatory neurons of the
STN can then excite the Gpi thus suppressing thalamic
activity on the cerebral cortex and increasing inhibitory
influences on the upper motor neurons.

37. The activity of the direct and indirect pathways
are modulated by D1 and D2 dopamine
receptors contained in the substantia nigra,
pars compacta.
The hyperdirect pathway bypasses the striatum
and therefore the substantia nigra does not
play any role in its regulation.

38. NIGROSTRIATAL PATHWAY: (Modulation)
In direct pathway the neurons from SNpc ascend up to
the striatum & release dopamine that acts on the D1
receptors that are excitatory.
As a result with excitatory glutamatergic neurons
there is an extra inhibition on Gpi (less GABA)
leading to less Inhibition of thalamus
The final result is increase in the motor activity.

39. In indirect pathway the neurons from SNpc ascend up
to the striatum & release dopamine that acts on the D2
receptors that are inhibitory.
As a result Gpe is inhibited producing less GABA causing
more Inhibition over subthalamic nucleus and Gpi.
The final result is disinhibition of thalamus leading to
increase in the unwanted motor activity.

40. Disorders of the basal ganglia
Hypertonic-Hypokinetic :
Disorders caused by disturbance of the
indirect loop that causes a loss of the
inhibition of the thalamic neurons resulting
in excess cortical activity and movement.
1) Tremor
2) Chorea
3) Hemiballismus
4) Ballismus
5) Huntington’s disease
6) Tics and Dystonia

41. 2) Hypotonic-Hyperkinetic.
Disorders resulting from the degeneration
of the neurons that form the direct pathway.
Since this is the pathway that serves for the
planning of the movement, the problems
that patients will have been presented in two
forms - Bradykinesia (slow movement) or
Akinesia ( inability to move at all )
1) Parkinson’s disease
2) Essential tremor (ET)

42. PARKINSON’S DISEASE

43. CHARACTERISTICTRIAD :-
RESTING TREMOR, RIGIDITY,BRADYKINESIA.
ALSO ASSOCIATED WITH GAIT & POSTURAL
DISTURBANCES

44. THANK YOU

45. Psychiatric manifestations in PD
• 70% of patients with PD exhibit
psychatric symptoms
• Depression is the most frequently found in up
to 50% cases
• Anxiety disorders are found in upto 40%
of patients with PD
• Apathy it is related to dysfunction of
forebrain dopaminergic system
• Psychotic symptoms occur in up to 40% of
patients with PD mainly related to
treatment with dopaminergic and
anticholinergic medications

46. WILSON’S DISEASE
NEUROLOGICAL FINDINGS
• TREMOR
• DYSTONIA
• RIGIDITY
• CHOREOATHETOSIS
• BRADYKINESIA
• MASKED FACIES
• MICROGRAPHIA
PSYCHIATRIC MANIFESTATIONS
• PERSONALITY CHANGES
• DEPRESSION
• SUICIDALITY
• ANXIETY DISORDERS
• PSYCHOTIC DISORDERS

47. HUNTINGTON’S DISEASE

48. • In huntingtons disease there is loss of
ENKergic neurons in the striatum
which project primarily to Gpe
• Loss of these neurons leads to inhibition
of STN
• Excitation of thalamus leading to
increased thalamocortical activity and
hyperkinesis ( chorea)

49. • TREMORS
TYPESOFTREMORS
• RESTTREMOR
• POSTURALTREMOR
• INTENTIONTREMOR

50. • CHOREA:

51. • DYSTONIA:

52. • HEMIBALISMUS:

53. • ATHETOSIS:

54. DOPAMINE – ACETYLCHOLINE HYPOTHESIS
• There is always a reciprocal balance b/w dopamine
and acetylcholine in striatum.
• Dopamine neurons make postsynaptic connections
on cholinergic interneurons in nigrostriatal pathway.
• Dopamine acting at D2 receptors normally inhibits
acetylcholine release from post synaptic nigrostriatal
cholinergic neurons.
• When D2 blockers are given, dopamine no longer
suppreses the release of Ach ,thus disinhibiting Ach
release from cholinergic neurons.

55. Cont…
• In turn leading to more excitation of post synaptic
muscuranic cholinergic receptors on GABAnergic
neurons leading in inhibition of movements & to
symptoms of Drug induced movement disorders.
• The normal balance b/w Dopamine and acetylcholine
in striatum can be restored with anticholinergics that
blocks the release of acetylcholine at muscuranic
cholinergic receptors.

56. DRUG-INDUCED MOVEMENT DISORDERS

57. NEUROLEPTIC INDUCED PARKINSONISM
CLASSICTRIAD

58. NEUROLEPTIC INDUCED ACUTE DYSTONIA
OCCURS IN UPTO 10% PATIENTSMORE COMMON INYOUNG MEN

59. NEUROLEPTIC-INDUCED ACUTE AKATHISIA

60. NEUROLEPTIC-INDUCEDTARDIVE DYSKINESIA

61. THE ROLE OF THE BASAL GANGLIA IN
PSYCHIATRIC DISORDER
1. OCD
2. ADHD
3. Schizophreia
4. Depression
5. Addiction

62. Obsessive-compulsive disorder [OCD]
• There is evidence of basal ganglia dysfunction
from imaging studies of OCD
• Both reduced and increased volumes of
caudate nuclei are reported
• Increased caudate metabolism has been
found to reduce after effective treatment
of OCD

63. • OCD symptoms are mediated by hyperactivity in
orbitofrontal-subcortical circuits due to an imbalance
of tone between direct and indirect striatopallidal
pathways. Imaging studies point to the importance of
limbic-orbitofrontal-basal ganglia- thalamocortical
circuits in the pathogenesis
of OCD

64. • The basal ganglia serves as
• motor pattern generators in brainstem
• cognitive pattern generators in the cerebral cortex
• The loop neocortex-basal ganglia-thalamus- neocortex
plays a role in establishing
• cognitive habits
• motor habits
• Thus cortical basal ganglia loop dysfunction in OCD
reflects
• repetitive actions(compulsion)
• repetitive thoughts(obsessions)

65. Tourette syndrome
 It is often associated with OCD
 There is decrease in globus pallidus
volume.
 There was abnormal basal ganglia
assymetry found in boys with TS.
 Disturbed caudate function causes
abnormal activation of frontal lobe and
thalamus.(OCD,ADHD,TS)

66. ADHD
• This condition linked clinically and genetically to GTS and
OCD
• There is evidence from neuroimaging studies of striatal
dysfunction in patients with ADHD
• Defecits in response inhibition &attention in ADHD has
been associated with smaller volumes and lower activation
of B/L caudate.

67. OCD,GTS,ADHD
• Disturbed caudate function in these disorders result in
abnormal activation of the frontal lobes and thalamus via
dorsal lateral prefrontal and orbitofrontal circuits
• This results in overlapping clinical features of these
disorders

68. Schizophrenia
• In striatum anomalies of dopamine synthesis,storage and release
have been reported.
• There is elevation in striatal D2 receptors
• Increased D2 receptors activity and synthesis is also seen in 1st
degree relatives of schizophrenia.
• It is correlated with the prodromal symptoms in schizophrenia,as a
predictor of psychotic episode and risk factor for the disease.
• There is volumetric increase of caudate putamen complex in
schizophrenia patients.

69. Depression
 Limbic circuit and prefrontal circuits have been implicated to
have a role in pathophysiology of depression.
 Dopamine system is said to have a role in depression as
there is psychomotor retardation in depression which
mimics bradykinesia in parkinson’s disease.
 MRI studies have reported increased incidence of caudate
hyperintensity in elderly depressed patients.
 Cerebrovascular insufficiency in subcortical and basal
ganglia structures may precipitate some cases of late onset
affective disturbances.

70. LATE ONSET DEPRESSION:
• MRI studies have reported increased
incidence of caudate hyperintensities
in elderly depressed patients
• The presence of subcortical
hyperintensities may be associated with
poor prognosis
• Cerebrovascular insufficiency in subcortical
and basal ganglia structures may precipitate
some cases of late onset affective
disturbance

71. Addiction
• Connections of the orbitofrontal cortex-
ventral tegmental area- nucleus
accumbens- thalamus are important for
drug reinforcement and addiction
• This circuit is important in the
compulsive aspect of drug taking
behaviour

72. Early cocaine withdrawal
• Cocaine misusers after abstinence
showed significantly lower dopamine
D2receptor activities in the striatum
• Reduction in dopamine transmission is
associated with the anhedonia of acute drug
withdrawal &relapse to drug is to avoid the
anhedonic (hypodopaminergic) state
associated with withdrawal.

73. REFERENCES
 Comprehensive textbook of psychiatry 10th edition
 Inderbir singh’s textbook of human neuroanatomy
 Stahl’s Essential Psychopathology
 Lishman’s organic psychiatry
 Ganong’s review of medical physiology.
 Gray's Anatomy (41tst ed.). Edinburgh: Elsevier
Churchill Livingston.
 Internet Refernces