The basal ganglia consist of several structures including the caudate nucleus, putamen, globus pallidus, substantia nigra, and subthalamic nucleus. They are located within the cerebral hemispheres and are involved in motor control and cognition. Two main circuits exist - the putamen circuit for executing movements and the caudate circuit for cognitive motor control. Diseases that impact the basal ganglia like Parkinson's and Huntington's result from dysfunction of neurotransmitter pathways and can cause both hyperkinetic and hypokinetic movement disorders. Common treatments involve replacing dopamine or modifying basal ganglia circuitry.

1. Basal ganglia

4. On each side of the brain, these ganglia
consist of the
• caudate nucleus,
• putamen,
• globus pallidus,
• substantia nigra, and
• subthalamic nucleus.
They are located mainly lateral to and
surrounding the thalamus, occupying a large
portion of the interior regions of both cerebral
hemispheres.

6. Two main circuits
• The Putamen Circuit
For executing learned patterns of movement.
• The Caudate Circuit
For Cognitive Control of Sequences of Motor
Patterns.

7. The term cognition means the thinking
processes of the brain, using both sensory input
to the brain plus information already stored in
memory.
Most of our motor actions occur as a
consequence of thoughts generated in the mind,
a process called cognitive control of motor
activity.
The caudate nucleus plays a major role in this
cognitive control of motor activity.

11. Functions of basal ganglia
• Function in association with the corticospinal system
to control complex patterns of motor
activity(cutting paper with scissors, hammering
nails, shooting a basketball through a hoop, passing
a football, throwing a baseball etc.
• Cognitive control of motor activity e.g. if a person
comes across a lion he will subconsciously plan 1)
turning away from the lion, (2) beginning to run, and
(3) even attempting to climb a tree
• To Change the Timing and to Scale the Intensity of
Movements

12. A lesions of the posterior parietal cortex
produce an inability to accurately perceive
objects through normally functioning
sensory mechanisms, a condition called
agnosia.

13. • In case of lesion in the right posterior parietal
cortex ,the patient's ability to copy the left side of
the drawings is severely impaired.
• Also, such a person will always try to avoid using
his or her left arm, left hand, or other portions of
his or her left body for the performance of tasks,
or even wash this side of the body (personal
neglect syndrome), almost not knowing that
these parts of his or her body exist.

14. Diseases of the Basal Ganglia in Humans
• Three distinct biochemical pathways in the basal
ganglia normally operate in a balanced fashion:
(1) the nigrostriatal dopaminergic system,
(2) the intrastriatal cholinergic system, and
(3) the GABAergic system, which projects from
the striatum to the globus pallidus and
substantia nigra.
• When one or more of these pathways become
dysfunctional, characteristic motor abnormalities
occur. Diseases of the basal ganglia lead to two
general types of disorders: hyperkinetic and
hypokinetic.

15. • Athetosis consists of slow, writhing movement
of the distal parts of the limbs.
• Chorea is characterized by rapid, flicking
movement of the extremities and facial
muscles.
• Ballism is associated with violent, flailing
movement of the limbs (ballistic movement).
• Akinesia is difficulty in initiating movement
and decreased spontaneous movement.
• Bradykinesia is slowness of movement.

16. Abnormal Function in the Putamen
Circuit: Athetosis, Hemiballismus, and
Chorea
• when a portion of the circuit is damaged or
blocked, certain patterns of movement become
severely abnormal.
• lesions in the globus pallidus frequently lead to
spontaneous and often continuous writhing
movements of a hand, an arm, the neck, or the
face-movements called athetosis.
• A lesion in the subthalamus often leads to
sudden flailing movements of an entire limb, a
condition called hemiballismus.

17. Huntington Disease
• An autosomal dominant inherited disease, with
the onset occurring most often in adult life(30-
40years).
• Death occurs 15 to 20 years after onset.
• The disease has been traced to a single gene
defect on chromosome 4. This gene encodes a
protein, huntingtin, the function of which is not
known. The codon (CAG) that encodes glutamine
is repeated many more times than normal.
• The disease affects men and women with equal
frequency.

18. Damage to GABnergic neurons of caudate
nucleus and putamen to the globus pallidus
external segment releases inhibition, permitting
the hyperkinetic features of the disease to
develop.
Signs and symptoms:
• Choreiform movements first appear as
involuntary movements of the extremities and
twitching of the face (facial grimacing). Later,
more muscle groups are involved. Speech
becomes slurred and then incomprehensible.
• Progressive dementia occurs with loss of
memory and intellectual capacity.

19. Parkinson Disease
• Has both hypokinetic and hyperkinetic features
• Is a progressive disease of unknown cause that
commences between the ages of 45 and 55
years.
• It is associated with neuronal degeneration in
the substantia nigra

20. • The dopamine secreted in the caudate nucleus
and putamen is an inhibitory transmitter;
• Destruction of the dopaminergic neurons in the
substantia nigra allow the caudate nucleus and
putamen to become overly active and possibly
cause continuous output of excitatory signals to
the corticospinal motor control system.
• These signals could overly excite many or all of
the muscles of the body, thus leading to rigidity.

21. Types of Parkinson disease
According to the cause
• Postencephalitic parkinsonism developed
following the viral encephalitis outbreak of 1916–17
in which damage occurred to the basal nuclei.
• Iatrogenic parkinsonism can be a side effect of
antipsychotic drugs (e.g., phenothiazines).
Meperidine analogues (used by drug addicts) and
poisoning from carbon monoxide and manganese
can also produce the symptoms of parkinsonism.
• Atherosclerotic parkinsonism can occur in elderly
hypertensive patients

22. • Tremor. This is the result of the alternating
contraction of agonists and antagonists. The
tremor is slow and occurs most obviously when
the limbs are at rest. It disappears during sleep.
• Rigidity. This differs from the rigidity caused by
lesions of the upper motor neurons in that it is
present to an equal extent in opposing muscle
groups.
• If the tremor is absent, the rigidity is felt as
resistance to passive movement and is
sometimes referred to as plastic rigidity (lead
pipe). If the tremor is present, the muscle
resistance is overcome as a series of jerks, called
cogwheel rigidity.

23. • Bradykinesia
• Akinesia
• Mask like face:The movements are slow, the
face is expressionless, and the voice is slurred
and unmodulated.
• Staccato and stiff movements. Swinging of
the arms in walking is lost.
• Postural disturbances. The patient stands with
a stoop, and his or her arms are flexed. The
patient walks by taking short steps and often is
unable to stop. In fact, he or she may break into
a shuffling run to maintain balance.

24. • There is no loss of muscle power and no loss of
sensibility. Since the corticospinal tracts are
normal, the superficial abdominal reflexes are
normal, and there is no Babinski response. The
deep tendon reflexes are normal.
• other motor symptoms including dysphagia
(impaired ability to swallow), speech disorders,
gait disturbances, and fatigue.

25. Treatment
• Treatment with L-Dopa
• Treatment with L-Deprenyl (inhibits monoamine
oxidase)
• Treatment with Transplanted Fetal Dopamine
Cells
• Treatment by Destroying Part of the Feedback
Circuitry in the Basal Ganglia