Basal Ganglia 2011

8/6/2019 Basal Ganglia 2011

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BASAL GANGLIADr. TDS


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The pleasant aroma of freshly brewed coffeeand baked cinnamon rolls are enough tomotivate anyone of us to walk toward the

coffee and cinnamon rolls and taste them bylifting the coffee cup and roll to take a sip anda few bites

Tasting the cinnamon roll may elicit certainfacial expressions that may indicate to thoselooking at us that we are enjoying the delicious

tasting cinnamon roll.


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Furthermore, the warm cinnamon aroma may

evoke fond memories of the first time we

tasted a cinnamon roll

In this example, the olfactory system

(mediating the sense of smell), the limbic

system (processing emotions and memory),

and the basal ganglia involved in movement

are all interconnected


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Basal ganglia are involved in the planning and

programming of movement or, more broadly,

in the processes by which an abstract thought

is converted into voluntary action (initiates)


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Much of the output of the basal ganglia, which

is mediated through the thalamus, is to reduceor dampen the excitatory input to the cerebral

cortex


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. When there is a disruption of this mechanism,

disturbances in motor function ensue

Discharge patterns of the basal ganglia become

excessive, abnormal slowing of movements

Lesions of the basal ganglia produce a reduced

output, presence of abnormal, involuntarymovements that occur during periods of rest


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BASAL GANGLIA STRIATUM

(NEOSTRIATUM)

VENTRAL

STRIATUM

LENTICULAR

NUCLEUS

CORPUS

STRIATUM

Caudate nucleus

Putamen

Globus pallidus

Subthalamicnucleus (of

ventral

thalamus)

Substantia nigra

(ofthemesencephalon

Caudate nucleus

Putamen

Ventralportion

ofcaudate

Nucleus

Putamen

Anteriorperforated

substance

Nucleus

accumbens

Putamen

Globus pallidus

Caudate

nucleus

Putamen

Globus pallidus


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Componentsofthe Basal Ganglia

Input Nuclei Corpus Striatum

Caudate

Putamen

Output Nuclei GlobusPallidus Interna

SubstantiaNigraPars Reticulata*

Intermediate Nuclei GlobusPallidus Externa SubthalamicNucleus*

SubstantiaNigraParsCompacta*


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Afferentsto Striatum

Sensory cortex

Motor cortex

Substantia nigra Intralaminar nucleiofThalamus


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The putamen appears to be concerned

primarily with motor functions

The caudate nucleus, is involved with

cognitive aspects of movement, eye

movements, and emotional correlates of

movement


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Efferentsfrom Striatum

Globuspallidus

Substantia nigra


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Afferentsto Globuspallidus

Caudate nucleus

Putamen

Subthalamic nucleus


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EFFERENTS FROM GLOBUS

PALLIDU

S SUBTHALAMICNUCLEUS

SUBSTANTIA NIGRA

THALAMUS (VA and VL)


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Functions

1. Planning and programming of movements

that is conversion of idea into action

2. Provides postural background for anymovement

3. Regulation of muscle tone

4. Helps to bring about subconsciousmovements like facial expressions


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PathwaysofMotor Loop

DirectPathway

Overall Excitatory

IndirectPathway Overall Inhibitory


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DirectPathway

CORTEX

PUTAMEN

(GPe)

(STN)

GP interna

VA/VL THALAMUS

Glutamate (+)

Glutamate (+)GABA (-)

GABA (-)


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IndirectPathway

CORTEX

PUTAMEN

GP externa

STN

GP interna

VA/VL THALAMUS

Glutamate (+)

GABA (-)

Glutamate (+) GABA (-)

GABA (-)

Glutamate (+)


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Modulatory RoleofDopamine

Activation of the dopaminergic pathway

excites the direct pathway but inhibits the

indirect pathway

Excites the facilitatory (direct) pathway via its

excitatory effects on dopamine D1

receptors in

regions of the neostriatum that project to the

medial pallidal segment


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Inhibiting the inhibitory (indirect) pathway

that projects initially to the lateral pallidalsegment because of the inhibitory effects on

dopamine D2 receptors in the neostriatum


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Movement Disorders

Hyperkinetic

Hemiballismus

Huntingtons DiseaseChorea

Hypokinetic

Parkinsons Disease

Drug Induced (Neuroleptics, MPTP)


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Parkinson's Disease


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Parkinson Disease

Neurological disease affecting over four millionpatients worldwide, over1.5 million people inthe U.S..

While it can affect individuals at any age, it ismost common in the elderly.

The average age of onset is 55 years, althoughapproximately 10 percent of cases affect thoseunder age 40.


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Appears Later in Life

Continuous Progressive Neurological

Disease, thereby causing increasing disability

of movement no cure


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Etiology

Cerebral atherosclerosis

Viral encephalitis Side effects of several antipsychotic drugs

(i.e., phenothiazides, butyrophenones,

reserpine)


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Environmentalfactorsand neurotoxins

Pesticides, herbicides, industrial chemicals -

contain substances that inhibit complex I in the

mitochondria


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UsuallyOther Accompanied Autonomic Deficits Seen

Later in Disease Process:

Orthostatic Hypotension

Dementia

Dystonia

Ophthalmoplegia

Affective Disorders


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Parkinson Disease Neurochemistry

Loss of Dopaminergic (DA) Cells Located in

Basal Ganglia; most symptoms do not appear

until striata DA levels decline by at least 70-

80%.


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CORTEX

PUTAMEN

(GPe)

(STN)

GP interna

VA/VL THALAMUS

Glutamate (+)

Glu(+)GABA (-)

GABA (-)

Parkinsons Disease

(--)

CORTEX

PUTAMEN

GP externa

STN

GP interna

VA/VL THALAMUS

Glutamate (+)

GABA (-)

GABA (-)

GABA (-)

Glutamate (+)

DA(+)

Glu(+)


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Imbalance primarily between the excitatory

neurotransmitter Acetylcholine and inhibitory

neurotransmitter Dopamine in the Basal

Ganglia

ACh

DA


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Drug Therapy

Drug Therapy Against Parkinson

Disease Is Aimed at Bringing the

Basal Ganglia Back to Balance

DecreaseCholinergic Activity Within BasalGangliaandthisCan Be Done Two Ways:

Activating Dopamine receptorsin SubstantiaNigrafeedingback toCholinergicCellsin the

striatum Turn offtheCholinergicCells, Then Things Are

Brought Back to Balance

Antagonize Acetylcholine receptors


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Agentsthat Increase Dopaminefunctions

Increasing the synthesis of dopamine - l-Dopa

Inhibiting the catabolism of dopamine selegiline

Stimulating the release of dopamine amphetamine

Stimulating the dopamine receptor sites directly -bromocriptine&pramipexole

Blocking the uptake and enhancing the release of dopamine -amantadine


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Chorea

Chorea ischaracterizedby rapid,involuntary

"dancing" movements


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Huntingtons Disease

Autosomal dominant Loss of cholinergic and GABAergic neurons in

the striatum

Trinucleotide repeat defect on chromosome 4 Characterized by multiple quick, random

movements most prominent in the

appendicular muscles.

Athetosis (slow, wormlike, involuntary

writhing movements) most noticeable in the

fingers and hands.


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Huntingtons Disease

CORTEX

PUTAMEN

GP externa

STN

GP interna

VA/VL THALAMUS

Glutamate (+)

GABA (-)

Glutamate (+) GABA (-)

GABA (-)

Glutamate (+)

+


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Hemiballismus

Wild flinging movements of half of the body

Injury usually to STN


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CORTEX

PUTAMEN

GP externa

STN

GP interna

VA/VL THALAMUS

Glutamate (+)

GABA (-)

GABA (-)

GABA (-)

Glutamate (+)

Glutamate (+)

Hemiballismus

+


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THANKYOU

Basal Ganglia 2011

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