DR HEMKIRAN SINGH
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BASAL NUCLEI
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Dr Hemkiran Singh
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DEFINITION: Large masses of grey matter situated in basal core
of white matter of each cerebral hemisphere
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• Collection of cell bodies of neurons within CNS = Nucleus
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• Collection of cell bodies of neurons within PNS = Ganglion
• Therefore Basal “Ganglia” is a misnomer, but it is still used
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• Correct term is Basal “Nuclei”
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Parts • Caudate nucleus +
Putamen =
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Caudate Nucleus SINGH Neostriatum (Striatum)
2. Putamen • Putamen + Globus
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3. Globus Pallidus
4. Substantia nigra (mid-brain) SINGH Pallidus =
Lentiform nucleus
5. Subthalamic nucleus (below
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thalamus)
* Claustrum & Amygdaloid nuclear complex
Caudate nucleus +
Lentiform nucleus =
Corpus striatum
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Amygdala + Claustrum =
Archistriatum
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Globus pallidus =
Paleostriatum
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Caudate nucleus +
Putamen = Neostriatum
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1. Caudate Nucleus
• C shaped
• Lies in concavity of Lateral ventricle
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• Wrapped around thalamus
• Has 3 parts
i. Head: in floor of anterior horn of
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Lateral ventricle
ii. Body: in floor of trunk of lateral
ventricle
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iii. Tail: in roof of inferior horn of
lateral ventricle
Tail ends anteriorly in Amygdaloid
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Nucleus
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Head of caudate nucleus
is visible in TS of brain
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It lies medial to anterior
limb of internal capsule,
in lateral wall/floor of
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anterior horn of lateral
ventricle
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2. Putamen &
3. Globus Pallidus
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Together form a biconvex lens like
structure = Lentiform nucleus
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Anterior limb of internal capsule
separates lentiform nucleus from
head of caudate nucleus
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Posterior limb of internal capsule
separates lentiform nucleus from
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Thalamus
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TS through brain at
level of Foramen of
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Monro, showing
internal capsule
and basal ganglia
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• Medial medullary lamina
separates medial part of
globus pallidus from its lateral
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part
• Lateral medullary lamina
separates lateral part of globus
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pallidus from putamen
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• Neo-Striatum (Caudate nucleus + Putamen) ,
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Subthalamic nucleus = AFFARENT PART of
Basal Nuclei
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Paleostriatum / Globus SINGH
Pallidus(internal/medial part) , Substantia
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nigra(reticular part) = EFFERENT PART of Basal
Nuclei
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Connections of Corpus striatum
1. AFFARENT: From cerebral cortex, thalamus, substantia nigra; end in
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caudate nucleus or putamen
i. Cortico-striate fibers: From ipsilateral cerebral cortex
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ii. Thalamo-striate fibers: medio-dorsal, intralaminar & midline
nuclei of Thalamus
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iii. Nigro-striate fibers: from substantia nigra (compact part/pars
compacta) of midbrain (they carry Dopamine synthesised in sub.
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nigra to caudate nucleus & Putamen; they have inhibitory effect
on basal nuclei)
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2. EFFERENT: Most efferents arise from Globus pallidus, but
some from substantia nigra too
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i. To Thalamus: ventral anterior & ventral-lateral nuclei
(which project to motor & premotor areas)
a) Ansa lenticularis: loops around posterior limb of internal
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capsule
b) Fasciculus lenticularis: passes thorugh internal capsule
c) a and b unite to form Thalamic fasciculus
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ii. To subthalamus: reciprocal connections with it via
subthalamic fasciculus
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AFFARENT
1. Corticostriate
2. Thalamostriate
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3. Nigrostriate
EFFERNT
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1. Pallido-thalamic (ansa
lenticularis, fasciculus lenticularis,
thalamic fasciculus)
2. Pallido-subthalamic: subthalamic
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fasciculus
3. To red nucleus, reticular
formation, substantia nigra
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HEMKIRAN SINGH
SINGH
FUNCTIONS OF BASAL NUCLEI
1. Planning and programming of voluntary movements
2. Determine how rapidly a movement is to be performed and how large the
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movement must be
3. Decrease muscle tone and inhibit unwanted muscular activity
4. Regulate the muscle tone and thus helps in smoothening the voluntary motor
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activities of the body
5. Control automatic associated movements, like swinging of arms during
walking
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6. Control reflex muscular activity
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7. Control group of movements for emotional expression
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Disorders of basal ganglia
• Lead to:
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1. Difficulty in starting voluntary movements (bradykinesia)
2. Slowness of wanted movements (hypokinesia)
3. Occurrence of unwanted involuntary movements (hyperkinesia)
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4. Increase in muscle tone (rigidity)
Examples:
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1. Parkinsonism
2. Chorea
3. Athitosis
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4. Hemiballismus
5. Wilson’s disease (hepatolenticular degneration)
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Parkinsonism
• Neurodegenerative disorder, after 50 years of age
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• deficiency of the neurotransmitter dopamine in the corpus
striatum following a lesion in substantia nigra and/or its
projections (nigrostriate fibres)
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• Dopamine causes Inhibition of cells within the corpus striatum
• Parkisonism is a “Release phenomenon” due to lack of
inhibitory influences following dopamine deficiency
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• Triad of symptoms
1. Akinesia/bradykinesia
2. Tremors (resting)
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3. Rigidity (increased tone)
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Difference beween substantia nigra in a normal person (left) v/s a
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person with Parkinson’s disease (PD) (right) – reduction in pigment in
substantia nigra compacta in PD
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Chracteristic features of
Parkinsonism:
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TRIAD of Bradykinesia,
Tremors and rigidity
1. Resting tremors (eg:
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pill rolling movements);
diminish on doing any
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voluntary movements,
exaggerated by
emotional excitation
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2. Lead pipe rigidity/ Cog wheel
rigidity: due to increased tone of
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muscles; physician feels
resistance to passive movement
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of a joint throughout the motion Lead pipe rigidity
* (different from clasp knife
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rigidity of Upper Motor Neuron
palsy in which there is initial
resistance, followed by sudden
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decrease in resistance) Clasp knife rigidity
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3. Stooped-posture: Caused by rigidity;
back Is flexed, arms adducted and flexed,
and knees bent
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4. Bradykinesia: slowing-down of
movements and absence of associated
movements, such as arm-swinging. During
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walking, difficulty in getting up from chair;
difficulty in initiating movements
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Treatment:
Medical – L-dopa (precursor of Dopamine)
Surgical – Placing small lesions (stereo-tactic surgery) in globus pallidus &
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thalamus); striatal implants of Dopamine containing neurons of fetal origin
Latest: Electrodes in globus pallidus/thalamus – Deep brain stimulation
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5. Shuffling gait
(stiff, short steps, SINGH
because of
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increased rigidity SINGH
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6. Mask like face
(hypomimia): loss of
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facial expression, due
to lack of control of
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muscles for emotional
expression.
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7. Other motor features: reduced eye blinking, drooling,
hypophonia (soft voice), dysphagia, freezing of gait,
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micrographia (abnormally small, cramped handwriting)
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CHOREA
• Quick(jerky) , irregular, involuntary, purposeless
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movements
• Involve tongue, face, limbs
• Eg: swift grimaces, sudden movements of head or
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limbs
• 2 types: Sydenham’s chorea, Huntington’s chorea
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ATHETOSIS
• Slow, sinuous writhing movements
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• Distal segments of limbs (fingers, toes)
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BALLISMUS
• Violent blast of irregular movements
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• Involve proximal muscles of limbs , trunk, girdles
• Eg: limb suddenly flies out in all directions out of
control
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• Maybe one limb is involved (monoballismus), or both
limbs of one side (hemiballismus)
• Caused by vascular lesion of subthalamic nucleus
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WILSON’S DISEASE/ HEPATOLENTICULAR DEGENERATION
• Deposition of copper in liver & brain (esp basal nuclei)
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• Kayser Fleischer rings(by copper deposition) in cornea
• Clinical picture might closely ersemble parkinsonism
• Dystonia, tremors, incoordination
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