The basal ganglia are subcortical brain structures involved in motor control and include the corpus striatum, amygdaloid body, and claustrum. The corpus striatum contains the caudate nucleus and lentiform nucleus, which regulate muscle tone and movement. Damage to the basal ganglia can cause movement disorders like Parkinson's disease due to reduced dopamine in the corpus striatum.

1. BASAL GANGLIA ANATOMY DR.SHAZIA ZAHRA.S

2. BASAL GANGLIA
The basal ganglia or basal nuclei are subcortical, intracerebral masses of grey
matter forming important parts of the extra-pyramidal system.
Principally involved in the control of posture and movements (primarily by inhibiting
motor functions)
They include the following:
1. CORPUS STRIATUM (which is partially divided by the internal capsule into two
nuclei:
-The Caudate Nucleus
-The Lentiform Nucleus (Anatomically the putamen and globus pallidus are
together called lentiform nucleus)
2. AMYGDALOID BODY
3. CLAUSTRUM
The four nuclei (caudate, lentiform, amygdaloid and claustrum are joined to the
cortex at the anterior perforated substance.

3. CORPUS STRIATUM
• It lies lateral to thalamus
• It is divided completely by internal capsule into caudate
and lentiform nucleus.
• Bands of grey matter pass from lentiform nucleus across
the internal capsule to the caudate nucleus, giving the
striated appearance hence,the name corpus striatum.
• It comprises the caudate and lentiform nucleus

4. CAUDATE NUCLEUS
-It is a large C-shaped or comma shaped grey
mass
-It has a head, body and tail.
HEAD: (anterior) large, & rounded and forms the
lateral wall of anterior horn of lateral ventricle.
-Completely separated from the putamen by the
internal capsule except rostrally where it is
continuous with the putamen through and
beneath the anterior limb of internal capsule.
-The most ventral part of the corpus striatum is
called the nucleus accumbens, which has
connections with the limbic system

5. BODY: Long and narrow continuous
with head,lies in the floor of lateral
ventricle.
TAIL : Long, narrow and
tapering,descends posteriorly into the
temporal lobe and lies in the roof of
inferior horn of lateral ventricle

6. LENTIFORM NUCLEUS
 it is a three sided wedge shaped
mass of grey matter, with a convex
outer surface and an apex which lies
against the genu of the internal
capsule
 It is divided into a:
-Larger darker lateral portion called
Putamen contains small cells and
-smaller,lighter portion called
globus pallidus
made up of large (motor cells)

7. MORPHOLOGICAL DIVISION OF
CORPUS STRIATUM
o The paleostriatum is the older and
primitive part. It is represented by the
globus pallidus (pallidium)
o the Neostriatum is more recent in
development. It is represented by the
caudate nucleus and the putamen of
the lentiform nucleus. The neostriatum
is often called the striatum

8. CONNECTIONS OF CORPUS
STRIATUM

9. FUNCTIONS OF CORPUS STRIATUM
 The corpus striatum regulates muscle tone and thus helps in
smoothening voluntary movements.
 It controls automatic associated movements, like the swinging of
arms during walking. Similarly it controls the coordinated movements
of different parts of the body for emotional expression
 It influences the precentral motor cortex which is supposed to
control the extra pyramidal activities of the body.
 These do not receive any sensory input from spinal cord unlike the
cerebellum. Basal ganglia contributive to the cognitive function of the
brain
 These helps cortex in execution of learned patterns of movements
subconsciously

10. CONT..
 Corpus striatum,cerebellum and motor areas of cerebrum jointly are
responsible for planning, execution and control of movements,
 Corpus striatum and cerebellum without sending fibres to spinal
cord modify the effect on spinal cord through projections to motor
cortex and extra pyramidal fibres.
 Basal ganglia and cerebellum do not initiate movements but are able
to adjust motor commands.

11. AMYGDALOD BODY
This is a nuclear mass in the temporal lobe, lying anterio superior to
the inferior horn of the lateral ventricle.
Topographically it is continuous with the tail of the caudate nucleus,
but functionally it is related to the stria terminalis. It is a part of
limbic system
It is continuous with the cortex of the uncus,the limen insulae and the
anterior perforated substance.
AFFERENTS: From the Olfactory tract
Efferents: Gives rise to stria terminalis which ends in the anterior
commissure, the anterior perforated substance & in hypothalamic
nuclei

12. CLAUSTRUM
It is saucer shaped nucleus situated between the
putamen and the insula, with which it is coextensive.
Inferiorly, it is thickest and continuous with the
anterior perforated substance.

13. DYSFUNCTION OF BASAL GANGLIA
o Lesions of basal ganglia and cerebellum do
not cause paralysis. These produce abnormal
movements or posture or changes in tone.
o PARKINSON: Lesion of corpus Striatum
o CHOREA: Occurs due to disease of caudate
nucleus
o ATHETOSIS: Occurs due to lesion in
putamen: Is aform of movement disorder
which is slow repetative writhing in nature
o BALLISMUS: Due to disease of subthalamic
nucleus: Characterised by irregular
movements of trunk, girdles & both the
limbs

14. CAUSES
Condition that cause injury to the
brain can damage the basal
ganglia include:
• Carbon monoxide poisoning
• Drug overuse
• Head injury
• Liver disease
• Infection
• Metabolic problem
•Multiple sclerosis
• Poisoning with cu/
manganese/other heavy metals
• Drug side effects
• Tumours

15. PARKINSON DISEASE
Chronic and progressive movement disorder,
Primarily affects the neurons of basal ganglia
Syndrome that consists of slowing down in the intiation & execution of
movement(bradykinesia) increased muscle tone(rigidity),tremor and
impaired postural reflexes
Drug induced-long term use of phenothiazines
Neuro toxins(cyanide,CO)
Arterioscleriosis

16. ETIOLOGY

17. PD
Destruction of dopamine producing
neurons within basal ganglia
Reduces the amount of available
striatal dopamine(inhibitory effects)
Increase in acetylcholine(excitatory)
Inadequately balanced Ach excitatory
activity
Difficulty in controlling movements

18. CLASSIFICATION & SYMPTOMS

19. SYMP
THREE CARDINAL SYMPTOMS
1. Resting tremors: Mc first
symptom,most evident one
hand with arm rest- usually
unilateral becomes bilateral
worsens with stress
2. Bradykinesia (generalized
slowness of movement)
3. Muscle rigidity
Symptoms worsens as disease
progresses
Patient also suffer from non-
motor symptoms such as:
1. Cognitive impairment
2. Olfactory impairment
3. dysphagia
4. GI dysfunction
5. Sleep disturbances
6. Depression

20. SECONDARY PARKINSONISM
Associated with drugs,
stroke, tumour, infection
or exposure to toxins
such as carbon monoxide
or maganese

21. DRUG INDUCED PARKINSONISM
S/E of some drugs, esp those
affects the dopamine levels in
the brain, can actually cause
symptoms of parkinsonism
Although tremor and postural
instability may be less severe.this
condition may be difficult to
distinguish from the Parkinson’s
disease.
Medications that can cause are:
o Anti-psycotics
o Metaclopromide
o Reserpine
o Tetrabenazine
o Some ca channel blockers
o Stimulants such as
amphetamines and cocaine
oUsually after stopping those
medications parkinsonism
gradually disappears

22. VASCULAR PARKINSONISM
• Multiple small stroke can cause
parkinsonism
• Pt with this disorder are more likely to
present with gait difficulty than tumour, & are
more likely to have symptoms that are worse
in the lower part of the body.
• Some will also report the abrupt onset of
symp or give a H/O step wise deterioration
• Dopamine is tried to improve patient
mobility although the results are often not as
successful.
• VP is static or very slowly progressive when

23. PARKINSONISM PLUS SYNDROMES

24. DIAGNOSIS AND TREATMENT
1. Neurological examination
2. Brain scans and other labs are also
sometimes carried out to detect other
disease resembling PD
3. Neuro protective Therapy
4. Symptomatic :Levodopa, anti
cholinergics (benztropine)
5. Antiglutametergics
6. Monoamine oxidase inhibitor,
Dopamine agonist, Adenosine A2
receptor antagonist
7. Levodopa resistant symp: Botulinim
toxin injection
Surgical treatment (Deep brain
stimulation)
Cell replacement therapies.

25. CONT..

26. HUNTINGTON’S DISEASE
Is a neurodegenerative disorder that causes the progressive breakdown of
nerve cells in the brain especially damage in Basal ganglia
Autosomal-dominant disorder and is an inherited progressive
neurodegenerative disorder characterized by choreiform movements,
psychiatric problems, and dementia. It is caused by a cytosine-adenine-
guanine (CAG) trinucleotide repeat expansion in the huntingtin (HTT) gene
on chromosome 4p and inherited in an autosomal-dominant pattern. The
pathophysiology of HD is not fully understood, although it is thought to be
related to toxicity of the mutant huntingtin protein. As there is no known
cure, treatment is symptomatic and remains supportive.
Age at presentation: 30’s -40 years or later
When disease onset begins at 20 know as JEVENILE HD

27. ETIO-PATHOGENESIS

28. SYMPTOMS
ADULT ONSET: most common
forms and severe forms
CHILDHOOD ONSET: occurs at
young age
Symptoms of Parkinsonism

29. DIAGNOSIS
CT BRAIN
MRI BRAIN
PET(isotope)scan of brain
DNA testing for chromosome 4 defect
Tetrabenazine-to treat chorea
Haloperidol-Anti psychotics
Clonazepam-To alleviate choreic
movements & control hallucinations &
delusion
Tranquilizers, Lithium- for severe
mood swings

30. TREATMENT

31. QUESTIONS
A 64-year-old man with a history of Parkinson's disease is reviewed
in clinic and a decision has been made to start him on cabergoline.
Which one of the following adverse effects is most strongly
associated with this drug?
1.optic neuritis
2. transient rise in liver function test
3. Pulmonary fibrosis
4. Renal failure
5.Thrombocytopenia

32. PULMONARY FIBROSIS
Dopamine receptor agonists
e.g. bromocriptine, ropinirole, cabergoline, apomorphine
ergot-derived dopamine receptor agonists (bromocriptine,
cabergoline) have been associated with pulmonary, retroperitoneal
and cardiac fibrosis. The Committee on Safety of Medicines advice
that an echocardiogram, ESR, creatinine and chest x-ray should be
obtained prior to treatment and patients should be closely monitored
patients should be warned about the potential for dopamine receptor
agonists to cause impulse control disorders and excessive daytime
somnolence
more likely than levodopa to cause hallucinations in older patients.
Nasal congestion and postural hypotension are also seen in some
patients

33. Q2

34. ANS

35. Q3

36. ANS