Basal ganglia

5. Basal Ganglia
Dr. Sai Sailesh Kumar G
Associate Professor
Department of Physiology
R.D. Gardi Medical College, Ujjain, Madhya Pradesh.
Email: dr.goothy@gmail.com

6. Functional anatomy
 Basal ganglia consists of
1. Corpus striatum
2.Claustrum
3. Amygdaloid body

7. Functional anatomy
 Corpus striatum is further divided into
Caudate nucleus
Lentiform nucleus
Lentiform nucleus is further divided into outer part-putamen and
inner part-globus pallidus
Globus pallidus is further divided into inner and outer segments

10. Functional anatomy
 The structure, functions and connections of putamen and
caudate nucleus is same so they both collectively called as
striatum or neo striatum
Striatum = Caudate nucleus + Putamen
Globus pallidus send major efferents of basal ganglia so it is
called as pallidum or paleo striatum

11. Functional anatomy
 Claustrum is present between putamen and insular cortex
Its functions are not properly known
Amygdaloid body is connected with limbic system and discussed
along with limbic system
Subthalamic nucleus is present lateral to hypothalamus
Substansia nigra consists of pars reticularis and pars compacta

15. Functional anatomy
 Basal ganglia consists of
Caudate nucleus
Lentiform nucleus ( GP and Putamen)
Subthalamic nucleus
Sunstantia Nigra ( Pars compacta and pars reticularis)

16. Afferent connections
 Cortico-striate fibers
All parts of cerebral cortex send axons to the caudate nucleus
and putamen
The largest input is from the sensory-motor cortex
Glutamate is the neurotransmitter

17. Afferent connections
 Thalamostriate fibers
The intralaminar nucleus of thalamus send large number of
axons to caudate nucleus and putamen

18. Afferent connections
 Nigrostriate fibers
Neurons in the substantia nigra send axons to the caudate
nucleus and putamen
Dopamine is neuro transmitter
These fibers are inhibitory in function

19. Afferent connections
 Brainstem striatal fibers
Ascending fibers from brain stem end in the caudate nucleus and
putamen
Serotonin is neurotransmitter
These fibers are inhibitory

20. Afferent connections

21. Efferent connections
 Striatopallidal fibers
Pass from caudate nucleus and putamen to globus pallidus
Gamma aminobutyric acid (GABA) as neuro transmitter

22. Efferent connections
 Striato nigral fibers
Pass from caudate nucleus and putamen to substantia nigra
GABA or Ach or substance P as neurotransmitter

23. Efferent connections

24. Striatum- Substantia nigra connections
 Nigrostriate fibers - Dopamine
Striatonigral fibers - GABA

25. Striatum- Substantia nigra connections

26. Striatonigral and nigrostriate pathways
 Striatonigral pathway – Neuro transmitter is GABA- inhibitory
Neurotransmitter
Nigro striate pathway neurotransmitter is dopamine which is an
inhibitory neurotransmitter to the striatum.
Striato nigral pathway indirectly stimulates the striatum by
inhibiting dopamine release

27. Striatonigral and nigrostriate pathways
 Cortico striate pathway- glutamate is N.T ( stimulatory)
Thalamo striate pathway – glutamate is N.T ( stimulatory)
Nigro striate pathway- dopamine is N.T ( inhibitory)
The interplay between these N.T helps to regulate the muscle
tone and also block involuntary movements during the execution
of a particular act.

28. Functions
 The precise functions of basal ganglia is not properly known.
Basal ganglia is an accessory motor system that functions in
close association with cerebral cortex and cortico spinal motor
control systems
Helps to plan and control complex patterns of muscle
movements
Example writing alphabets

29. Functions
Example writing alphabets
When basal ganglia damaged, ones writing becomes crude as if
one were learning how to write for the first time
Other patterns that need basal ganglia are cutting paper with
scissors, hammering nails, shooting a basketball, passing a
football, throwing a baseball, vocalization, controlled movements
of eyes any other skilled movements.

30. Putamen circuit
1. From premotor and supplementary motor areas of motor cortex and
somatosensory areas of sensory cortex to putamen
2. From putamen to the internal portion of GP
3. From GP to venteroanterior and venterolateral nucleus of thalamus
4. From thalamus to primary motor cortex and premotor and
supplementary motor areas of cortex

32. Putamen circuit
Helps to execute learned pattens of movements
How?
Little is known about this function
Damage of circuit, certain patterns of movements becomes abnormal
Lesion of GP, leads to spontaneous and continuous writing
movements of hand, arm, neck and face.
These movements are called athetosis

34. Putamen circuit
Lesion to subthalamic nucleus, sudden flailing movements of
entire limb, called as hemiballismus
Multiple small lesions in putamen leads to flickering movements
in hands, face and other parts of body, called as chorea.
Lesion to substantia nigra leads to common and extremely
severe disease called Parkinson’s disease.

36. Caudate circuit
Signals pass from cerebral cortex to caudate nucleus
Next transmitted to the internal globus pallidus
Then to relay nucleus of venteroanterior and ventero lateral nucleus of
thalamus
Finally back to the prefrontal, premotor and supplementary motor
areas of cerebral cortex.
Almost none returning to primary motor cortex.

38. Caudate circuit
Important for cognitive functions
Thinking process of brain
Thoughts generated in brain
Motor action occurs
When we saw a lion if basal ganglia is intact, immediately we will turn away
from lion, run and even climb a tree
If basal ganglia are damaged the individual will takes longer and longer time
to think what to do………Lion will do by that time

39. Timing and scale the intensity of movements
To control movements two important capabilities of brain are
1. Determine how rapidly the movement is performed
2. Control how large the movement will be
We can write letter “a” slowly and rapidly
We can also write small a on paper and large A on the blackboard
The proportional characteristics of the letter remains same

40. Timing and scale the intensity of movements
In patients with basal ganglia lesion, these timing and scaling of
movements is almost absent
Basal ganglia functions in close association with cerebral cortex.
One important area is posterior parietal cortex
Lesion of posterior parietal cortex causes agnosia (inability to
recognize the objects or persons)

41. Timing and scale the intensity of movements
Patient with right parietal cortex lesion try to copy drawings
Ability to copy left side of drawing is severely impaired
Such a person also avoid using his left side arm, hand or other
portions of his left side body for performance of task or washing
this side of the body ( personal neglect syndrome)
He lost sense that side body exists

43. Functions of specific neurotransmitters
Dopamine pathway from substantia nigra to striatum
GABA pathway from striatum to substantia nigra
Ach pathway from cortex to striatum
Multiple general pathways from brian stem secrete norepinephrine,
serotonin, enkephalins and other N.T
Multiple glutamate pathways that provides most of excitatory signals
balances inhibitory signals by dopamine, GABA, serotonin pathways

44. Parkinson’s disease
Paralysis agitans
Hypokinetic and hyperkinetic features
Described by James Parkinson
Destruction of substantia nigra portion (pars compacta)
This portion sends dopaminergic neurons to the striatum
Damage of nigrostriatal pathway

45. Parkinson’s disease
First disease identified as being due to a deficiency in a specific
neurotransmitter
Estimated to occur in 1-2% of individuals over the age of 65
Hypokinetic – Akinesia, bradykinesia
Hyperkinetic- resting tremor, cogwheel rigidity
There is a decrease in normal, unconscious movements such as
swinging arms during walking

46. Parkinson’s disease
Tremor is present at rest
Disappear with activity

47. Parkinson’s disease
 Rigidity of much of the musculature of the body
 Mask-like face – No facial expressions
 Involuntary tremors of involved areas even when the person is resting ( resting tremors)
 Akinesia – serious difficulty in initiating a movement
 Bradykinesia- slowness of movements
 Postural instability caused by impaired postural reflexes leading to poor balance and falls
 Dysphagia – difficulty in swallowing
 Speech disorders
 Gait disturbances
 Fatigue

49. Parkinson’s disease
The cause of these abnormal motor effects is unknown
Dopamine is an inhibitory N.T
Damage to the nigrostriatal pathway causes the striatum to be overly
active
Continuous output of excitatory signals to the corticospinal motor
system
Overly excite many muscles - rigidity

50. Parkinson’s disease
The cause of these abnormal motor effects is unknown
Dopamine is an inhibitory N.T
Damage to the nigrostriatal pathway causes the striatum to be overly
active
Continuous output of excitatory signals to the corticospinal motor
system
Overly excite many muscles - rigidity

51. Parkinson’s disease – non motor symptoms
Most notably depression
hyposmia or rapid eye movement sleep behavior disorder (RBD)
Constipation
Autonomic disorders
Cognitive dysfunction
 Screening these early non-motor features might be one approach
towards early 'preclinical' diagnosis of PD.

52. Parkinson’s disease - Treatment
Administration of L-Dopa ameliorates many symptoms
Especially rigidity and akinesia
L-Dopa is converted to dopamine in brain and restore normal
balance between the N.T
Administration of dopamine has not produce similar effect
because dopamine can not cross BBB

53. Parkinson’s disease - Treatment
Administration of L-deprenyl
Inhibits monoamino oxidase
Responsible for destruction of dopamine secreted
So dopamine remains longer time in basal ganglia
A combination of L-dopa and L-deprenyl is more helpful
treatment

54. Parkinson’s disease - Treatment
Surgical treatment by making lesions in globus pallidus
(pallidotomy) or in subthalamic nucleus helps to restore the
output balance towards normal
Implant dopamine-secreting tissues in or near basal ganglia

56. HOME ABOUT • ISSUES • JOURNAL POLICIES • USERFUL INFO • CONTACT US
HOME ARCHIVES VOL 10 NO 3 (2019 ):VOLUME 10 ISSUE 3 Original Articles
Effect of caloric vestibular stimulation in a paraquat-induced
parkinsonian mouse model
Sai Sailesh Kumar Coothy
Assistant Professor & HOD, Department of Physiology, Vishnu Dental
College, Bhimavaram, West Godavari District-AndhraPradesh, India
Srilatha Coothy
Assistant Professor, Department of Biochemistry, Vishnu Dental College,
Bhimavaram, West Godavari District-AndhraPradesh.India
DOI:h tt p s://d oi.org/10.26452/ijrp s.vl0 i3.1
430
it!PDF
@ LATEX

57. HOME ABOUT • ISSUES • JOURNAL POLICIES • USERFUL INFO • CONTACT US
HOME ARCHIVES VOL10 NO 1 (2019}:VOLUME 10 ISSUE1 Original Articles
Effect of caloric vestibular stimulation on brain
neurotransmitters in an MPTP-induced mouse model of
Parkinson's disease
Kumar Sai Sailesh
Department of Physiology, Vishnu Dental College, Bhimavaram, West
Godavari District, Andhra Pradesh, India
Archana R
Department of Physiology, Saveetha Medical College, Saveetha Institute of
Medical and Technical Sciences, Thandalam , Chennai, Tamil Nadu, India
PDF

69. Huntington’s disease (Huntington’s chorea)
Autosomal dominant hereditary disorder
Symptoms start at 30- 40 years
Starts with flicking movements in individual muscles
Then progressive severe distortional movements in entire body
Severe dementia develops along with motor dysfunctions

70. Huntington’s disease (Huntington’s chorea)
Damage of strionigral pathway
Loss of cell bodies of GABA secreting neurons
GABA pathway inhibits substantia nigra and GP
Loss of inhibition leads to outburst of signals from SN and GP
Cause distortional movements

71. Huntington’s disease (Huntington’s chorea)
Dementia may not be due to loss of GABAergic neurons
It may be due to loss of Ach secreting neurons especially in the
thinking areas of cortex
The abnormal gene that cause disease has been found
The abnormal protein cause the disease is Huntington
How this protein cause disease is not known

72. A 69-year-old man went to consult his physician. He had tremors in his
hands and fingers. His face was inexpressive. When he was invited to
enter the physician’s office, he had difficulty standing up. He walked
slowly into the office. There was no sensory loss. The stretch reflex was
normal. Muscles exhibited rigidity.

73. 1. Identify this condition
2. Discuss the physiological basis of this condition
3. Describe the connections of basal ganglia
4. Discuss the functions of basal ganglia