BASAL GANGLIA
Basal Ganglia (Nuclei) Group of deep, interrelated subcortical N Accessory motor system  that  Functions usually  not  by itself but in close association with cerebral cortex & corticospinal motor control system  Most input signals from: cerebral cortex Most output signals back to: cerebral cortex
Anatomy Caudate Putamen Globus pallidus Substantia nigra Subthalamic nucleus
Anatomy Overview
Anatomy
The Putamen Circuit –  Executing  Patterns  of Motor Activity
The Putamen Circuit - Functions Putamen circuit + cerebral cortex Controls  complex patterns of motor activity Writing,  Cutting paper with scissors, Hammering nails  Shooting a basketball through a hoop, passing a football, Throwing a baseball  Most aspects of vocalization  Controlled movements of the eyes  And virtually any other skilled movements
The Putamen Circuit - Lesions Globus Pallidus:  Spontaneous, continuous  writhing movements  of a hand, an arm, the neck, or the face –  Athetosis Subthalamus:  Sudden  flailing movements  of an entire limb –  Hemiballismus Putamen:  Flicking movements  in hands, face, & other parts of body –  Chorea Substantia Nigra:  Common and extremely severe disease of  rigidity ,  akinesia , and  tremors  -  Parkinson ’ s disease
The Caudate Circuit –  Cognitive Control of Sequences of Motor Patterns Cognition  Most motor actions occur as a consequence of  cognition Caudate nucleus is pivotol
The Caudate Circuit Timing  and  Scaling  of movements
 
BG Circuit - Neurotransmitters
? What was common between  Yasir Arafat ,  Muhammad Ali  &  Adolph Hitler ?
Parkinson’s Disease Degenerative disorder of basal ganglia Dopamine depletion results from: Degeneration  dopamine nigrostriatal system Antipsychotic drugs that block dopamine receptors Toxic reaction to a chemical agent The Northern California drug dealer!* Severe carbon monoxide poisoning
Parkinson’s Disease – Clinical Tremor (involuntary tremor) Affects distal segments of limbs (hands and feet; head, neck, face, lips, tongue; or jaw) Characterized by rhythmic, alternating flexion & contraction movements (4-6 beats/minute) Disappears during voluntary movement Start unilateral- spread bilateral Rigidity  Resistance to movement of both flexors & extensors throughout the full range of motion Most evident during passive joint movement  involves jerky, cogwheel-type movements requiring considerable energy Start unilateral- spread bilateral
Parkinson’s Disease – Clinical Bradykinesia (slowness of movement) Movements: Are slow to initiate & perform Difficult to stop Are stiff & staccato in character instead of smooth While walking: Walking and turning  en bloc  is difficult Freezing spells take small, shuffling steps without swinging arms  Posture: Lean forward to maintain center of gravity Loss of postural reflexes – fall (often backward) Masked  face: Emotional & voluntary facial movements become limited Loss of blinking reflex  Failure to express emotion Throat: Tongue, palate, and throat muscles – rigid Drooling common Speech: slow and monotonous, without modulation and poorly articulated
Parkinson’s Disease – Clinical Advanced  Parkinsonian features: Dementia (similar to Alzheimer’s disease)  Falls  Fluctuations in motor function  Neuropsychiatric disorders Sleep disorders
 
 
Parkinson’s Disease – Treatment Nonpharmacologic Group support  Education Daily exercise, adequate nutrition  Botulism toxin injections Pharmacologic Antiparkinson drugs act by: Increasing functional ability of underactive dopaminergic system Increase dopamine levels (levodopa) Augment release of dopamine (amantadine) Function as dopamine agonists (bromocriptine) Inhibit metabolic breakdown of dopamine (selegiline) Reducing excessive influence of excitatory cholinergic neurons Anticholinergic drugs
Parkinson’s Disease – Treatment Surgical Thalamotomy or pallidectomy performed using stereotactic surgery
Overall Motor Control
 

Cns basal ganglia

  • 1.
  • 2.
    Basal Ganglia (Nuclei)Group of deep, interrelated subcortical N Accessory motor system that Functions usually not by itself but in close association with cerebral cortex & corticospinal motor control system Most input signals from: cerebral cortex Most output signals back to: cerebral cortex
  • 3.
    Anatomy Caudate PutamenGlobus pallidus Substantia nigra Subthalamic nucleus
  • 4.
  • 5.
  • 6.
    The Putamen Circuit– Executing Patterns of Motor Activity
  • 7.
    The Putamen Circuit- Functions Putamen circuit + cerebral cortex Controls complex patterns of motor activity Writing, Cutting paper with scissors, Hammering nails Shooting a basketball through a hoop, passing a football, Throwing a baseball Most aspects of vocalization Controlled movements of the eyes And virtually any other skilled movements
  • 8.
    The Putamen Circuit- Lesions Globus Pallidus: Spontaneous, continuous writhing movements of a hand, an arm, the neck, or the face – Athetosis Subthalamus: Sudden flailing movements of an entire limb – Hemiballismus Putamen: Flicking movements in hands, face, & other parts of body – Chorea Substantia Nigra: Common and extremely severe disease of rigidity , akinesia , and tremors - Parkinson ’ s disease
  • 9.
    The Caudate Circuit– Cognitive Control of Sequences of Motor Patterns Cognition Most motor actions occur as a consequence of cognition Caudate nucleus is pivotol
  • 10.
    The Caudate CircuitTiming and Scaling of movements
  • 11.
  • 12.
    BG Circuit -Neurotransmitters
  • 13.
    ? What wascommon between Yasir Arafat , Muhammad Ali & Adolph Hitler ?
  • 14.
    Parkinson’s Disease Degenerativedisorder of basal ganglia Dopamine depletion results from: Degeneration dopamine nigrostriatal system Antipsychotic drugs that block dopamine receptors Toxic reaction to a chemical agent The Northern California drug dealer!* Severe carbon monoxide poisoning
  • 15.
    Parkinson’s Disease –Clinical Tremor (involuntary tremor) Affects distal segments of limbs (hands and feet; head, neck, face, lips, tongue; or jaw) Characterized by rhythmic, alternating flexion & contraction movements (4-6 beats/minute) Disappears during voluntary movement Start unilateral- spread bilateral Rigidity Resistance to movement of both flexors & extensors throughout the full range of motion Most evident during passive joint movement involves jerky, cogwheel-type movements requiring considerable energy Start unilateral- spread bilateral
  • 16.
    Parkinson’s Disease –Clinical Bradykinesia (slowness of movement) Movements: Are slow to initiate & perform Difficult to stop Are stiff & staccato in character instead of smooth While walking: Walking and turning en bloc is difficult Freezing spells take small, shuffling steps without swinging arms Posture: Lean forward to maintain center of gravity Loss of postural reflexes – fall (often backward) Masked face: Emotional & voluntary facial movements become limited Loss of blinking reflex Failure to express emotion Throat: Tongue, palate, and throat muscles – rigid Drooling common Speech: slow and monotonous, without modulation and poorly articulated
  • 17.
    Parkinson’s Disease –Clinical Advanced Parkinsonian features: Dementia (similar to Alzheimer’s disease) Falls Fluctuations in motor function Neuropsychiatric disorders Sleep disorders
  • 18.
  • 19.
  • 20.
    Parkinson’s Disease –Treatment Nonpharmacologic Group support Education Daily exercise, adequate nutrition Botulism toxin injections Pharmacologic Antiparkinson drugs act by: Increasing functional ability of underactive dopaminergic system Increase dopamine levels (levodopa) Augment release of dopamine (amantadine) Function as dopamine agonists (bromocriptine) Inhibit metabolic breakdown of dopamine (selegiline) Reducing excessive influence of excitatory cholinergic neurons Anticholinergic drugs
  • 21.
    Parkinson’s Disease –Treatment Surgical Thalamotomy or pallidectomy performed using stereotactic surgery
  • 22.
  • 23.

Editor's Notes

  • #4 2 main jobs: 1) helping motor cortex execute PATTERNS of complex movements 2) Helping cortex plan (‘think’) complex motor movements
  • #5 Note the internal capsule tucked in between basal ganglia, cortex and thalamus
  • #7 the putamen circuit has its inputs mainly from those parts of the brain adjacent to the primary motor cortex but not much from the primary motor cortex itself. Then its outputs do go mainly back to the primary motor cortex or closely associated premotor and supplementary cortex. Functioning in close association with this primary putamen circuit are ancillary circuits that pass from the putamen through the external globus pallidus, the subthalamus, and the substantia nigra—finally returning to the motor cortex by way of the thalamus.
  • #10 concerned with putting together sequential patterns of movement lasting 5 or more seconds instead of exciting individual muscle movements.
  • #12 Ref: berne p190-191…xcellent circuit diagrams of basal ganglia in parkinson and huntington’s
  • #15 *Parkinsonism is also seen as a complication of treatment with the phenothiazine group of tranquilizer drugs and other drugs that block D2 receptors. It can be produced in rapid and dramatic form by injection of 1-methyl-4-phenyl-1,2,5,6-tetrahydropyridine (MPTP). This effect was discovered by chance when a drug dealer in northern California supplied some of his clients with a homemade preparation of synthetic heroin that contained MPTP. MPTP is a prodrug that is metabolized in astrocytes by the enzyme MOA-B to produce a potent oxidant, 1-methyl-4-phenylpyridinium (MPP+). In rodents, MPP+ is rapidly removed from the brain, but in primates it is removed more slowly and is taken up by the dopamine transporter into dopaminergic neurons in the substantia nigra, which it destroys without affecting other dopaminergic neurons to any appreciable degree. Consequently, MPTP can be used to produce parkinsonism in monkeys, and its availability has accelerated research on the function of the basal ganglia.