faculty of medicine dr zaïd mansour brain control of movement
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Faculty of Medicine Dr Zaïd Mansour Brain control of movement. Motor control hierarchy. Strategy , sensory information generates a mental image of the body and its relationship to the environment. - PowerPoint PPT PresentationTRANSCRIPT
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Faculty of MedicineDr Zaïd Mansour
Brain control of movement
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1. Strategy, sensory information generates a mental image of the body and its relationship to the environment.
2. Tactics, tactical decisions are based on the memory of sensory information from past movements.
3. Execution, sensory feedback is used to maintain posture, muscle length, and tension before and after each voluntary movement.
Motor control hierarchy
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How does the brain communicate with the SC:-Lateral pathways-Ventromedial pathways
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The lateral pathways-Corticospinal tract-Rubrospinal tract
The rubrospinal tract facilitatesmotor neurons in the cervical spinal cordsupplying the flexor muscles
of the upper extremities.
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The ventromedial pathways:-Vestibular tracts-Tectospinal tract-Reticulospinal tracts
Vestibulospinal tarcts:-Medial VST: bilateral connection to neck muscles (stability of the head)-Lateral VST: ipsilateral connection as far down as the lumbar region
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The tectospinal tract
The superior colliculus receives inputs fromthe retina, visual cortex, somatosensory and auditory information
It constructs a map of the world around us for directing the head and eye movements towards the appropriate target
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The reticulospinal tacts
-The pontine (medial) RS tract:Enhances the antigravity muscles
-The medullary (lateral) RS tract:Liberates the antigravity muscles
Both tracts are controlled by descending tracts from the cerebral cortex
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Motor cortex
-Area 4 (primary motor cortex, M1)-Area 6Premotor area (PMA)Supplementary motor area (SMA)
Area 6 ------ Area 4What actions are desired ---- how the actions will be carried out
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Somatotopic map of the human motor cortex
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Strategy- Motor area 6- Posterior parietal cortex- Prefrontal cortex
The posterior parietal cortex receivesinputs from:-The primary somatosensory cortical areas-Visual cortexPer Roland:when the subjects were asked only to mentally rehearse the movement without actually moving
the finger, area 6 remained active, but area 4 did not.
Edward EvartsCells in the SMA typically increase their discharge rates about a second before the execution of a movement in either hand.
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The prefrotal cortex:-Abstract thinking-Decision making-Anticipation
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Decorticate posture (decorticate rigidity, flexor posturing, mummy baby)Patients with decorticate posturing present with the arms flexed, or bent inward on the chest, the hands are clenched into fists, and the legs extended and feet turned inward. - Flexion in the UL: disinhibition of the red nucleus, the rubrospinal tract and medullary reticulospinal tract biased flexion outweighs the medial and lateral vestibulospinal and pontine reticulospinal tract biased extension in the upper extremities.- Extension in the LL: the pontine reticulospinal and the medial and lateral vestibulospinal biased extension tracts greatly overwhelm the medullary reticulospinal biased flexion tract.
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Decerebrate posturing (decerebrate rigidity, or extensor posturing)It describes the involuntary extension of the upper extremities in response to external stimuli. In decerebrate posturing, the head is arched back, the arms are extended by the sides, and the legs are extended. A hallmark of decerebrate posturing is extended elbows. The arms and legs are extended and rotated internally. The patient is rigid, with the teeth clenched.Damage below the level of the red nucleus
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The Basal Ganglia
Loop: cortex BG thalamus cortex
Function: selection and initiation of willed movements
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Basal Ganglia
Cortex ------Striatum ------Globus pallidus -------VLo -------Cortex (SMA)
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Basal Ganglia Motor Loop:Putamen ---- (inhib) GP ---- (inhib) VLo ---- (excit) SMAConsequence: cortical activation of the putamen leads to excitation of the SMA
How?At rest, neurons in the GP are spontaneously active and thus inhibit VLoCortical activation (l) excites putamen neurons, which (2) inhibit globus pallidus neurons, which (3) release the cells in VLo from inhibition, allowing them to become active. (4) The activity in VLn boosts the activity of the SMA.
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Basal Ganglia:Function: facilitation of the initiation of willed movementsHypokinesia: increased inhibition of the thalamus by the BGHyperkinesia: decreased inhibition of the thalamus by the BG
Substantia nigra is divided into SNr (reticulata) and SNc (compacta)
Direct pathway:Cortex (stimulates) → Striatum (inhibits) → "SNr-GPi" complex (less inhibition of thalamus) → Thalamus (stimulates) → Cortex (stimulates) → Muscles → (hyperkinetic state)
Indirect pathway:Cortex (stimulates) → Striatum (inhibits) → GPe (less inhibition of STN) → STN (stimulates) → "SNr-GPi" complex (inhibits) → Thalamus (is stimulating less) → Cortex (is stimulating less) → Muscles, etc. → (hypokinetic state)
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Connectivity diagram showing excitatory glutamatergic pathways as red, inhibitory GABAergic pathways as blue, and modulatory dopaminergic as magenta
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Parkinson’s disease:
affects about 1 % of all people over age 50
Triad of : resting tremor, bradykinesia and rigidity
Cause: degeneration of the substantia nigra
The pathological hallmark of PD is a loss of the pigmented, dopaminergic neurons of the substantia nigra pars compacta, with the appearance of intracellular inclusions known as Lewy bodies
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Parkinson’s disease:
shuffling gait:short, uncertain steps,with minimal flexionand toes dragging
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Normal situation:
Substantia nigra (dopamine)----(excit) putamen----(inhib) GP----(inhib) VLo----(excit) SMA
PD: bradykinesia
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Treatment of PD:-L Dopa ( (L-dihydroxyphenylalanine)+ carbidopa or benserazide
-Dopamine-Receptor Agonistsbromocriptine (PARLODEL) and pergolide(PERMAX); and two newer, more selective compounds, ropinirole (REQUIP) and pramipexole (MIRPEX).
-Catechol-O-Methyltransferase (COMT) Inhibitors: tolcapone (TASMAR) and entacapone (COMTAN).
-Selective MAO-B Inhibitors: selegiline (ELDEPRYL), & rasagiline (Azilect)
Apomorphine (APOKYN) is a dopaminergic agonist that can be administered by subcutaneous injection
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Huntington’s disease:-Is a fatal autosomal dominant disorder-Prevalence: 10 case per 100, 000-Mutation in the Huntington’s gene on the short arm of chromosome 4(repeat codon CAG, CAG sequence encoding glutamine, exceeds a threshold value, 35)-Dyskinesia, dementia, mood & personality disorders-Degeneration in the BG (caudate, putamen, GP) and cortex-BG degeneration leads to chorea (spontaneous, uncontrollable and purposeless movements of various parts of the body) as a result of loss of the inhibitory output to the thalamus
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HDAtrophy of BG & cortex
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Hemiballismus:
- violent, flinging movements of the extremities- it is caused by damage to the subthalamic nucleus- loss of excitatory drive to the globus pallidus facilitates VLn
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Cerebellum10% of the total volume of the brain50% of the total number of neurons in the CNSCoordination of movement Vermis -------------- ventromedial descending pathwaysCerebellar hemispheres --------- lateral pathways
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The motor loop through the lateral cerebellum
Cortex----Pons----Cerebellum----VLc----Motor Cortex
The cortico-ponto-cerebellar projection contains about 20 million axons; that is 20 times more than in the pyramidal tract
Execution of planned, voluntary, multijoint movements
Practice makes perfect !The cerebellum acts as the brain inside for skilled movements.
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The motor loop through the lateral cerebellum
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Tremor:
-Physiological tremor-Resting tremor-Intention tremor
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Resting tremor postural tremor intention tremor
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TicsTics are brief, repetitive, stereotyped, coordinated movements occurring at irregular intervals. Examples include repetitive winking, grimacing, and shoulder shrugging. Causes: drugs such as phenothiazines and amphetamines.
ChoreaChoreiform movements are brief, rapid, jerky, irregular, and unpredictable. They occur at rest or interrupt normal coordinated movements. Unlike tics, they seldom repeat themselves. The face, head, lower arms, and hands are often involved. Causes include Sydenham’s chorea (with rheumatic fever) and Huntington’s disease.
AthetosisAthetoid movements are slower and more twisting and writhing than choreiform movements, and have a larger amplitude. They most commonly involve the face and the distal extremities. Athetosis is often associated with spasticity. Causes include cerebral palsy.
DystoniaDystonic movements are somewhat similar to athetoid movements, but often involve larger portions of the body, including the trunk. Twisted postures may result. Causes include drugs such as phenothiazines, spasmodic torticollis.