Lecture on Basal Ganglia by Dr. Roomi

8/13/2019 Lecture on Basal Ganglia by Dr. Roomi

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PHYSIOLOGYOF

BASAL GANGLIA

By

Dr. Mudassar Ali Roomi (MBBS, M.Phil.)Assistant Professor Physiology


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BASAL GANGLIA

These are masses ofgrey matter present inthe white matter of

cerebral hemisphere. These include 5 nuclei:

1. Caudate nucleus

2. Putaman nucleus

3. Globus pallidus

4. Substantia nigra

5. Sub thalamic nucleus
http://www.google.com/url?sa=i&rct=j&q=basal%20ganglia&source=images&cd=&cad=rja&docid=GmwXQrOK4Hhf3M&tbnid=d8-JrmJvkUoMRM:&ved=0CAUQjRw&url=http://www.intechopen.com/books/basal-ganglia-an-integrative-view/clinical-motor-and-cognitive-neurobehavioral-relationships-in-the-basal-ganglia&ei=fNFSUeX7JsbYPe-6gLAP&bvm=bv.44342787,d.ZGU&psig=AFQjCNGjC0DpLkSEdIphhh37tw-D2tJc_Q&ust=1364468266865582


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BASAL GANGLIA

Caudate + putaman =corpus neostriatum.

Globus palidus makes

the paleostriatum.

Caudate is separatedfrom putaman byinternal capsule.

Putaman + globuspallidus = lentiform /lenticular nucleus.
http://www.google.com/url?sa=i&rct=j&q=basal%20ganglia&source=images&cd=&cad=rja&docid=GmwXQrOK4Hhf3M&tbnid=d8-JrmJvkUoMRM:&ved=0CAUQjRw&url=http://www.intechopen.com/books/basal-ganglia-an-integrative-view/clinical-motor-and-cognitive-neurobehavioral-relationships-in-the-basal-ganglia&ei=fNFSUeX7JsbYPe-6gLAP&bvm=bv.44342787,d.ZGU&psig=AFQjCNGjC0DpLkSEdIphhh37tw-D2tJc_Q&ust=1364468266865582


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CONNECTIONS OF BASAL GANGLIA:

(2 important circuits)

1. PUTAMAN CIRCUIT

2. CAUDATE CIRCUIT


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PUTAMAN CIRCUIT:

RECIEVES FIBERS FROM:

Pre motor area

Supplementary motor

area & Somatosensory areas

SENDS FIBERS TO:

Globus pallidus

V.A.T.N. & V.L.T.N.

Primary motor area,supplementary motorarea & pre motor areas.


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CAUDATE CIRCUIT

RECIEVES FIBERS FROM: Cerebral cortex (including:

pre motor &supplementary motorarea)

SENDS FIBERS TO: GLOBUS PALLIDUS

V.A.T.N. & V.L.T.N.premotor & supplementary

motor areas & to pre-frontal cortex.

Note: no fiber from thiscircuit go to primarymotor area.


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NEURO TRANSMITTERS IN BASAL GANGLIA

1) CORTICO-STRIATE FIBERSrelease ACETYLCHOLINEat their nerve endings

(cholinergic fibers).2) NIGRO-STRIATE FIBERS

(fibers which pass fromsubstantia nigra

caudate & putaman )secrete DOPAMINEattheir nerve endings(dopaminergic fibers).


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NEURO TRANSMITTERS IN BASAL GANGLIA:

3) fibers which pass fromcaudate & putamanglobus pallidus & substantianigra secrete GABA (GammaAmino Butyric Acid) at theirnerve endings.

4) fibers which pass from brainstembasal ganglia

secrete NOREPINEPHRINE,SEROTONIN & ENKEPHALINat their nerve endings.


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Here 3 neuro

transmitters are

important:

ACETYLCHOLINEexcitatory

DOPAMINE & GABA

inhibitory


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FUNCTIONS OF BASAL GANGLIA:

As ACCESSORY motor system.

Do not function independently but with

the help of CEREBRAL CORTEX &CORTICO-SPINAL SYSTEM.


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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 gangliadisturbed writing

appears that person is learning to write.


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2) COGNITIVE CONTROL OF MOTOR

ACTIVITY:

Basal ganglia + sensory input & information stored inthe brainCOGNITIVE CONTROL of motor activity.

Cognitive control = ?

It is pattern & sequence of eventsto achieve aspecific aim or goal, e.g.,

person walking on a roadsudden sight of a wildanimalsequence of movements to save life

(controlled by Basal ganglia).


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3) CONTROL OF EXTENT & TIMING OF

MOVEMENTS:

Basal ganglia helps to decide, that for HOWLONG the movements will occur & HOWRAPID 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.


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OTHER FUNCTIONS OF BASAL GANGLIA

Control of muscle tone

Control of automatic associated movements

e.g. movements of arms while running


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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.


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2) CHOREA:

Rapid dancing movement affecting hand,

arm or some other part of body.

Due to damage in CAUDATE & PUTAMAN.

2 types of Chorea:

1) HUNTINGTONS CHOREA

2) SYDENHAM / RHEUMATIC CHOREA

(complication of rheumatic fever).


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HUNTINGTONS CHOREA:

Hereditarydisorder.

Features manifest in 3rdor 4thdecade of life.

There is degeneration of GABA

secreting neurons in CAUDATE& PUTAMAN.

As GABA is inhibitory, due tolossoutburst of activity inGLOBUS PALLIDUS &SUBSTANTIA NIGRAdancingmovements.

Here (chorea + dementia): Notdue to loss of GABA but due todamage to cholinergic neuronsin cerebral cortex.


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3) HEMIBALISMUS:

involuntary, violent

movement affecting 1

side of body / 1 limb.

Here is damage toSUBTHALAMIC

NUCLEUS. ***
http://www.google.com/url?sa=i&rct=j&q=hemiballismus&source=images&cd=&cad=rja&docid=Zf7-LcbUUHsMfM&tbnid=Z863B6Xal-Lj8M:&ved=0CAUQjRw&url=http://www.terapisehat.com/2010/08/chorea-athetosis-dan-hemiballismus.html&ei=mNxSUeLtDsrUPOz8gaAI&bvm=bv.44342787,d.ZGU&psig=AFQjCNFPOknCd8ykxtS9T5BDHT_Ap8PKQQ&ust=1364471307835305


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4) PARKINSONS DISEASE (PARALYSIS AGITANS)

1STdiscovered by JAMESPARKINSON.

CAUSE: degeneration ofDOPAMINE secreting

neurons in SUBSTANTIANIGRA

DOPAMINE deficiency inCAUDATE & PUTAMAN (

by 50% or even less)

No release of

DOPAMINE from NIGROSTRIATE fibers.


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NORMALLY:

ACETYLCHOLINE =DOPAMINE or

EXCITATORY INFLUENCE =

INHIBITORY INFLUENCE(on caudate & putaman).

In this disease, due todopamine deficiencythis balance is disturbed

excitation of caudate &putamanfeatures ofParkinsonism.
http://www.google.com/url?sa=i&rct=j&q=parkinson+disease+symptoms&source=images&cd=&cad=rja&docid=_Zr8PaLX3Hd-BM&tbnid=b_wa2pZIamGIDM:&ved=0CAUQjRw&url=http://www.anti-agingfirewalls.com/2012/06/30/a-stem-cell-cure-for-parkinsons-disease-so-close-and-yet-so-far-away/&ei=Q9tSUabsLsXaOdaMgGA&bvm=bv.44342787,d.ZGU&psig=AFQjCNFO1L3BSeLVIeABHNgyh5e-n3YQ0Q&ust=1364470941260175


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CAUSES OF PARKINSONISM:

1) IDIOPATHIC: (Cause ?)

In old age dopamine secretion & dopamine

receptorsdecrease.

2) TRAUMA: TO BASAL GANGLIA:

Mohammad Ali (boxer)


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3) COMPLICATION OF TREATMENT WITH

PHENOTHIAZINE DERIVATIVES:

Increased dose over long duration.

4) COMPLICATION OF INFLUENZA:

During 1stworld war, epidemic of influenza

complicationParkinsonism (in many complicatedcases).


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FEATURES OF PARKINSONISM:

*IMBALANCE BETWEEN

EXCITATORY &

INHIBITORYINFLUENCE

OF ACETYLCHOLINE &DOPAMINE

(respectively) DUE TO

LOSS OF DOPAMINE.
http://www.google.com/url?sa=i&rct=j&q=parkinson+disease&source=images&cd=&cad=rja&docid=S2ZHkBU7bRZ12M&tbnid=WJghj_HnLWqkmM:&ved=0CAUQjRw&url=http://commons.wikimedia.org/wiki/File:Sir_William_Richard_Gowers_Parkinson_Disease_sketch_1886.jpg&ei=jNpSUYqXFoTbPauEgLgO&bvm=bv.44342787,d.ZGU&psig=AFQjCNEcfXFZXJqWfDBxQP6NA8-goZBRZQ&ust=1364470755311822


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1) AKINESIA OR BRADYKINESIA:

Inability to initiate movement.

or patient is very slow to initiate movement.


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2) RIGIDITY:

LEAD PIPE RIGIDITY:

When a limb is passively flexedfeeling of

bending of a lead pipecontinuous

resistance.

Rigidity due toincreased motor neuron

discharge to both AGONISTS & ANTAGONISTS

(Tug of war between them).

LEAD PIPE


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3) TREMORS:

(PILL ROLLING TREMORS)

REGULAR, RHYTHMIC, ALTERNATE CONTRACTION ofAGONISTS & ANTAGONISTS.

Tremors involve: fingers & hand & may involvetongue & lips.

STATIC TREMORS (at rest)

Absent in sleep.

Worst in emotional state & when patient is conscious

that someone is watching him.


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Due to rigidityback is flexed, arms are

flexed & adducted & knees are bent.

In severe casesmarked rigiditypatient

can be moved like a statue !


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4) GAIT:

Short steps.

Unable to stop the movement.

Person chases his own shadow.

5) FACIAL EXPRESSION:

MASK LIKE FACE.

Loss of facial expression.

6) DECREASED ASSOCIATIVE MOVEMENTS:

DECREASED 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).


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BASIC PRINCIPLES OF TREATMENT:

There is dopamine deficiency, so we give

LEVO-DOPA(it can cross blood brain barrier &

in brain: levo-dopadopamine

Anti cholinergic drugsinhibit over activity

of Acetylcholine.

Sometimes drugs fail. Treatment is then

electro-coagulation of thalamic nuclei (VLTN &

VATN are important).


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WILSONS DISEASE OR HEPATO-LENTICULAR

DEGENERATION: (another lesion of basal ganglia)

Due to HEREDITORY AUTOSOMAL RECESSIVEDISORDER of COPPER METABOLISM.

In these patients, plasma Ceruloplasmin level

is lowcopper deposition in body tissues:(liver & lentiform nucleus)hepatic cirrnosis& effects due to damage to lentiform nucleus(PUTAMAN + GLOBUS PALLIDUS).


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Lecture on Basal Ganglia by Dr. Roomi

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Lecture on Basal Ganglia by Dr. Roomi