lecture on basal ganglia by dr. roomi
TRANSCRIPT
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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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http://www.google.com/url?sa=i&rct=j&q=boxer+muhammad+ali&source=images&cd=&cad=rja&docid=o1rGTTapIEdy-M&tbnid=hYjUZOCP80NDIM:&ved=0CAUQjRw&url=http://www.cnn.com/2009/SPORT/09/03/muhammad.ali.ennis.ireland/&ei=GdxSUYuJGsWUO5eugPAG&bvm=bv.44342787,d.ZGU&psig=AFQjCNHlU6vEEDCVOYxRSBleziemGl8QfQ&ust=1364471136294279http://www.google.com/url?sa=i&rct=j&q=chaudary+shujat+hussain&source=images&cd=&cad=rja&docid=h68Atwc4Gvab1M&tbnid=wXAW-PDx5vfAjM:&ved=0CAUQjRw&url=http://electionsmeter.com/polls/chaudhry-shujaat-hussain&ei=rNtSUd_DKcjaOe31gZAO&bvm=bv.44342787,d.ZGU&psig=AFQjCNHrUtPgOtnkg0jBLG1Y7cu76uMneg&ust=1364471064643555http://www.google.com/url?sa=i&rct=j&q=parkinson+disease&source=images&cd=&cad=rja&docid=NwbE1nUHrWkqvM&tbnid=5gSk7eD50RZyBM:&ved=0CAUQjRw&url=http://bio349.biota.utoronto.ca/20089/20089bio349graham/parkinsons/&ei=_NpSUZ3hKYnAO4zvgNAO&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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