Basal Ganglia

BASAL GANGLIA:
Masses of grey matter present in white matter of cerebral hemisphere. Includes 5 nuclei: CAUDATE PUTAMAN GLOBUS PALLIDUS SUBSTANTIA NIGRA & SUB THALAMIC NUCLEUS
CAUDATE + PUTAMAN = CORPUS STRIATUM. CAUDATE internal capsule PUTAMAN. PUTAMAN + GLOBUS PALLIDUS = LENTIFORM / LENTICULAR NUCLEUS.
CONNECTIONS OF BASAL GANGLIA: (2 important circuits)

1) PUTAMAN CIRCUIT 2) CAUDATE CIRCUIT
PUTAMAN CIRCUIT:
RECIEVES FIBERS FROM: Pre motor area Supplementary motor area & Somatic sensory areas
SENDS FIBERS TO: Globus pallidus V.A.T.N. & V.L.T.N. Primary motor area, supplementary motor area & pre motor areas.
Additional connections of putaman circuit:

Fibers from putaman Globus pallidus SUBSTANTIA NIGRA THALAMIC NUCLEI CEREBRAL CORTEX. Some fibers from putaman GLOBUS PALLIDUS SUBTHALAMIC NUCLEUS THALAMIC NUCLEI CEREBRAL CORTEX. Some fibers from putaman GLOBUS PALLIDUS SUBTHALAMIC NUCLEUS BACK TO PUTAMAN. (lot k budhu ghar ko aay)
CAUDATE CIRCUIT:
RECIEVES FIBERS FROM: Cerebral cortex (including: pre motor & supplementary motor area)
SENDS FIBERS TO: GLOBUS PALLIDUS V.A.T.N. & V.L.T.N. pre motor & supplementary motor areas & to pre-frontal cortex. * NO FIBER FROM THIS CIRCUIT PRIMARY MOTOR AREA.
NEURO TRANSMITTERS IN BASAL GANGLIA:

1) CORTICO-STRIATE FIBERS ACETYLCHOLINE at nerve endings (cholinergic fibers). 2) NIGRO-STRIATE FIBERS (fibers which pass from substantia nigra caudate & putaman ) DOPAMINE at nerve endings (dopaminergic fibers).
3) fibers which pass from CAUDATE & PUTAMAN GLOBUS PALLIDUS & SUBSTANTIA NIGRA GABA (Gamma Amino Butyric Acid) at nerve endings. 4) fibers which pass from BRAIN STEM BASAL GANGLIA NOREPINEPHRINE, SEROTONIN & ENCHAFFARINES at nerve endings.
Here 3 neuro transmitters are important: ACETYLCHOLINE excitatory DOPAMINE & GABA inhibitory
FUNCTIONS OF BASAL GANGLIA:

As ACCESSORY motor system. Do not function independently but with the help of CEREBRAL CORTEX & CORTICO-SPINAL SYSTEM.
1) CONTROL OF COMPLEX & SKILLED MOVEMENTS:

BASAL GANGLIA with the help of CEREBRAL CORTEX & CORTICO-SPINAL SYSTEM control complex & skilled movements: WRITING, STITCHING, PLAYING BASKET BALL, HAMMERING THE NAIL & CUTTING DESIGN WITH SCISSORS. In damage to basal ganglia disturbed writing appears that person is learning to write.
2) COGNITIVE CONTROL OF MOTOR ACTIVITY:

Basal ganglia + sensory input & information stored in the brain COGNITIVE CONTROL of motor activity. Cognitive control = ? It is pattern & sequence of events to achieve a specific aim or goal, e.g., person walking on a road sudden sight of a wild animal sequence of movements to save life (controlled by Basal ganglia).
3) CONTROL OF EXTENT & TIMING OF MOVEMENTS:

Basal ganglia helps to decide, that for HOW LONG the movements will occur & HOW RAPID the movement will be (EXTENT OF MOVEMENT). e.g. while writing: RANGE: x OR X SPEED: rapid: or slow:
Basal ganglia function in close cooperation with posterior parietal cortex.
LESIONS OF BASAL GANGLIA: 1) ATHETOSIS:

Continuous, slow writhing movements affecting hand, arm, face or may be neck. It is due to damage to GLOBUS PALLIDUS.
2) CHOREA:
Rapid dancing movement affecting hand, arm or some other part of body. Damage is in CAUDATE & PUTAMAN. 2 types of Chorea: 1) HUNTINGTONS CHOREA 2) SYDENHAM / RHEUMATIC CHOREA (complication of rheumatic fever).
HUNTINGTONS CHOREA: Hereditary disorder. Features manifest in 3rd or 4th decade of life. There is degeneration of GABA secreting neurons in CAUDATE & PUTAMAN. As GABA is inhibitory, due to loss outburst of activity in GLOBUS PALLIDUS & SUBSTANTIA NIGRA dancing movements. Here (chorea + dementia): Not due to loss of GABA but due to damage to cholinergic neurons in cerebral cortex.
3) HEMIBALISMUS:
Continuous, violent movement affecting 1 side of body / 1 limb. Here is damage to SUBTHALAMIC NUCLEUS.
4) PARKINSONS DISEASE OR PARALYSIS AGITANS:

1ST discovered by JAMES PARKINSON. CAUSE: degeneration of DOPAMINE secreting neurons in PARS COMPACTA of SUBSTANTIA NIGRA DOPAMINE deficiency in CAUDATE & PUTAMAN ( by 50% or even less) No release of DOPAMINE from NIGRO STRIATE fibers.
NORMALLY: ACETYLCHOLINE = DOPAMINE or EXCITATORY INFLUENCE = INHIBITORY INFLUENCE (on caudate & putaman). In this disease, due to dopamine deficiency this balance is disturbed excitation of caudate & putaman features of Parkinsonism.
CAUSES OF PARKINSONISM:
1) IDIOPATHIC: (Cause ?) In old age dopamine secretion & dopamine receptors decrease. 2) TRAUMA: TO BASAL GANGLIA: Mohammad Ali (boxer) He looks like a butterfly & fights like a bee---- Mohammad---Mohammad Ali !
3) COMPLICATION OF TREATMENT WITH PHENOTHIAZINE DERIVATIVES: Increased dose over long duration.
4) COMPLICATION OF INFLUENZA: During 1st world war, epidemic of influenza complication Parkinsonism (in many complicated cases).
FEATURES OF PARKINSONISM:
*IMBALANCE BETWEEN EXCITATORY & INHIBITORY INFLUENCE OF ACETYLCHOLINE & DOPAMINE (respectively) DUE TO LOSS OF DOPAMINE.
1) AKINESIA:
Inability to initiate movement. or patient is very slow to initiate movement. DHAKKA START !
2) RIGIDITY: COG WHEEL RIGIDITY:

When 1 limb is passively flexed intermittent resistance to flexion (small wheel moves the larger wheel intermittently).
1 2 (RA-HUT) or COG WHEEL
2) RIGIDITY: LEAD PIPE RIGIDITY:

When a limb is passively flexed feeling of bending of a lead pipe continuous resistance. Rigidity due to increased motor neuron discharge to both AGONISTS & ANTAGONISTS (Tug of war between them).
LEAD PIPE
3) TREMORS: (PILL ROLLING TREMORS)

REGULAR, RHYTHMIC, ALTERNATE CONTRACTION of AGONISTS & ANTAGONISTS. Tremors involve: fingers & hand & may involve tongue & lips. STATIC TREMORS (at rest) Absent in sleep. Worst in emotional state & when patient is conscious that someone is watching him.
Due to rigidity back is flexed, arms are flexed & adducted & knees are bent. In severe cases marked rigidity patient can be moved like a statue !
4) GAIT:
Short steps. Unable to stop the movement (DHAKKA STOP). Person chases his own shadow.
5) FACIAL EXPRESSION:
MASK LIKE FACE. Loss of facial expression.
6) DECREASED ASSOCIATIVE MOVEMENTS:

Like swinging of arms while walking.
7) SUPERFICIAL ABDOMINAL REFLEX:

Present.
8) TENDON JERKS:
Difficult to be elicited due to rigidity.
9) BABINSKI SIGN:
Not present.
10) *MUSCLE PARALYSIS & *SENSORY LOSS:

ABSENT (like in cerebellar disease, but present in Brown Sequard syndrome).
BASIC PRINCIPLES OF TREATMENT:

There is dopamine deficiency, so we give LEVO-DOPA (it can cross blood brain barrier & in brain: levo-dopa dopamine Anti cholinergic drugs inhibit over activity of Acetylcholine. Sometimes drugs fail. Treatment is then electro-coagulation of thalamic nuclei (VLTN & VATN are important).
WILSONS DISEASE OR HEPATOLENTICULAR DEGENERATION: (another lesion of basal ganglia)

Due to HEREDITORY AUTOSOMAL RECESSIVE DISORDER of COPPER METABOLISM. In these patients, plasma seroplasmin level is low copper deposition in body tissues: (liver & lentiform nucleus) hepatic cirrnosis & effects due to damage to lentiform nucleus (PUTAMAN + GLOBUS PALLIDUS).

Basal Ganglia

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BASAL GANGLIA:

CONNECTIONS OF BASAL GANGLIA: (2 important circuits)

Additional connections of putaman circuit:

NEURO TRANSMITTERS IN BASAL GANGLIA:

FUNCTIONS OF BASAL GANGLIA:

1) CONTROL OF COMPLEX & SKILLED MOVEMENTS:

2) COGNITIVE CONTROL OF MOTOR ACTIVITY:

3) CONTROL OF EXTENT & TIMING OF MOVEMENTS:

LESIONS OF BASAL GANGLIA: 1) ATHETOSIS:

4) PARKINSONS DISEASE OR PARALYSIS AGITANS:

2) RIGIDITY: COG WHEEL RIGIDITY:

2) RIGIDITY: LEAD PIPE RIGIDITY:

3) TREMORS: (PILL ROLLING TREMORS)

6) DECREASED ASSOCIATIVE MOVEMENTS:

7) SUPERFICIAL ABDOMINAL REFLEX:

10) MUSCLE PARALYSIS & SENSORY LOSS:

BASIC PRINCIPLES OF TREATMENT:

WILSONS DISEASE OR HEPATOLENTICULAR DEGENERATION: (another lesion of basal ganglia)

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