Movement & Brain Mechanisms

हालचाल आणि में द ू यंत्रणा

1. Why Is Movement Complex? (हालचाल जटिल का आहे ?)

Movement involves immense neural computation. The brain processes current sensory input and
stored memories to generate commands, ultimately carried out at the neuromuscular junction (NMJ)
where motor neurons cause muscle contraction.

The motor systems serve multiple roles:

•​ Moving through and manipulating the world
•​ Verbal and non-verbal (gesture) communication
•​ Maintaining posture and balance
•​ Controlling smooth muscles for autonomic functions (breathing, gut movement)
•​ Controlling saccadic eye movements for visual tracking

A useful example: picking up a raspberry. This deceptively simple action requires:

•​ Visual cortex: locates the fruit
•​ Frontal motor regions: plan the movement
•​ Spinal cord + motor neurons: generate arm/hand contraction
•​ Sensory receptors (fingers): relay tactile and proprioceptive feedback
•​ Basal ganglia: judge grasp force
•​ Cerebellum: regulate timing and accuracy
Two key control strategies:
•​ Feedback control — ongoing movement monitored by sensory systems (proprioception, touch,
vision) and adjusted in real time. Limited to slow movements (sensory loop takes 150–200 ms).
•​ Feedforward control — movement predicted from past experience BEFORE it occurs. Uses stored
motor programmes. Improves with practice. The cerebellum is key here.

2. Complete Movement Pathway (संपर्ण

ू हालचाल मार्ग)
From intention to muscle contraction — step by step:
Step Structure Role
1. Intention Prefrontal Cortex Decides to act; sets goal

2. Planning SMA / Premotor Cortex Sequences & prepares motor programme

3. Gating Basal Ganglia → Thalamus Selects desired movement; suppresses others

4. Cerebellum → Thalamus Predicts & corrects errors; feedforward control

Timing/Correc
tion

5. Motor Primary Motor Cortex (M1) Upper motor neurons fire; enters corticospinal tract
Command

6. Brainstem Reticulospinal / Adjusts posture & proximal muscle tone

Vestibulospinal
 7. Spinal Cord Anterior Horn (α-MN) Final common pathway; CPG modulates rhythm

8. NMJ Acetylcholine → nAChR ACh released; end-plate potential triggers contraction

9. Contraction Muscle (extrafusal fibres) Sliding filament → muscle shortens → movement

10. Feedback Proprioceptors → Sensory data corrects ongoing & future commands
Cerebellum

3. Key Brain Areas & Structures (मख्

ु य में द ू क्षेत्रे आणि रचना)

Structure Role Injury Effect

Prefrontal Cortex Decision to act; goal-setting Cannot initiate purposeful
action

SMA Self-initiated sequential planning Difficulty with internally

generated sequences

Premotor Cortex Externally-cued movement prep Difficulty with cue-triggered

(PMC) movements

Primary Motor Cortex Executes commands via CST; somatotopic Contralateral weakness /
(M1) map (homunculus) paralysis

Corticospinal Tract Main voluntary pathway UMN→LMN; Spasticity, hyperreflexia,

(CST) decussates at medullary pyramids Babinski sign

Basal Ganglia Action selection via direct (GO) / indirect Parkinson's (hypo) or
(STOP) pathways; dopamine-modulated Huntington's (hyper)
 Substantia Nigra (SNc) Produces dopamine → modulates basal Parkinson's disease
ganglia

Cerebellum Coordination, timing, error correction via Ataxia, dysmetria, intention

internal models; compares efference copy to tremor
actual movement

Thalamus (VLo/VLc) Motor relay: BG & cerebellum → cortex Disrupted motor

timing/selection

Spinal Cord (α-MN) Final common pathway (LMN); motor units; Flaccid paralysis, atrophy,
CPGs for rhythmic movement areflexia

Neuromuscular ACh → nAChR → end-plate potential → Myasthenia gravis, botulism

Junction contraction

1.​ The Primary Motor Cortex (M1)

The primary motor cortex occupies the precentral gyrus of the frontal lobe. Pioneering work by Wilder
Penfield, who electrically stimulated the motor cortex in awake epilepsy surgery patients, revealed its
somatotopic organisation.

The Motor Homunculus:

Different parts of M1 control different muscle groups, forming a topographical 'map' of the body called
the motor homunculus. Crucially, body parts are NOT equally represented — cortical space is
proportional to the precision of control needed, not body size.
•​ Hands, fingertips, lips and tongue → disproportionately large cortical areas (fine motor control)
•​ Trunk and proximal limbs → smaller areas (gross motor)
•​ Legs and feet → represented medially (on the top/inner surface of the hemisphere)
•​ Face → represented laterally (on the outer surface, most inferior part of the strip)

Important nuances from Sussex text:

•​ The homunculus is a simplification — Penfield himself noted overlap between facial, arm/trunk,
and leg regions
•​ Modern analyses show a fractured somatotopic organisation with neurons controlling different
body parts intermingled
•​ This leads to the question: does M1 control individual muscles, or movements?
 2.​ Basal Ganglia — GO / STOP Pathways (बेसल गँग्लिया — GO / STOP मार्ग)
The basal ganglia are five interconnected nuclei located within the forebrain, below the cerebral cortex.
They modulate motor function at the highest level, acting as a gating system that selects desired
movements and suppresses competing or unwanted ones.
Beyond motor control, they are involved in: action selection, associative learning, habit formation,
motivation, emotions, and reinforcement learning. The basal ganglia gate movement via two opposing
pathways modulated by dopamine from the substantia nigra:

Direct Pathway (GO):

Cortex → Striatum → GPi/SNr → Thalamus disinhibited → Motor cortex excited → Movement
facilitated
•​ Dopamine on D1 receptors ENHANCES this pathway

Indirect Pathway (STOP):

Cortex → Striatum → GPe → STN → GPi → Thalamus inhibited → Motor cortex suppressed →
Movement blocked
•​ Dopamine on D2 receptors SUPPRESSES this pathway
•​ Loss of dopamine (Parkinson's) = indirect dominates = too little movement
•​ Loss of indirect pathway neurons (Huntington's) = insufficient STOP = too much movement

Dopamine is the key modulator:

●​ Dopamine on D1 receptors → activates direct pathway → GO signal

●​ Dopamine on D2 receptors → suppresses indirect pathway → removes STOP signal
●​ In Parkinson's disease, dopamine neurons in the substantia nigra die → indirect pathway
dominates → excessive movement suppression → tremor, rigidity, bradykinesia

3.​ Cerebellum — Error Correction (सेरेबेलम — त्रट

ु ी दरु
ु स्ती)
It is located at the back of the brain, just above the brainstem. Despite its size and neuronal richness,
the cerebellum is not necessary for the direct execution of movement — rather, it is essential for the
coordination, timing, scaling, and precision of movement.
The cerebellum enables predictive (feedforward) motor control through internal models. Over
repeated practice of a movement:
•​ An internal model (motor programme) of the movement is learned
•​ The next time that movement is needed, the cerebellar model generates the appropriate
commands predictively
•​ This is why movements become more accurate and 'automated' with practice — hitting a tennis
ball, typing, playing piano

The cerebellum works by comparing intended movement with actual movement:

•​ Receives efference copy (corollary discharge) — a copy of the motor command
•​ Receives sensory feedback from proprioceptors about actual movement
•​ Computes motor error = difference between predicted and actual outcome
•​ Sends corrective signals back to motor cortex via thalamus (VLc)
•​ Builds internal models over practice → movements become automatic and precise

4.​ Spinal Cord Essentials (पाठीचा कणा — मख्

ु य मद्
ु दे )
The spinal cord is far more than a passive relay cable from brain to muscles. It is an active executive
organ that contains the motor neurons, processes sensory feedback, generates reflex responses, and
produces rhythmic movement patterns independently.
A cross-section reveals two distinct zones:
•​ White matter (outer): contains ascending and descending axon tracts — both sensory and motor
•​ Grey matter (inner, butterfly-shaped): contains neuronal cell bodies
The spinal cord is divided into four regions:
•​ Cervical (C1–C8): neck, arms, hands — damage here causes quadriplegia
•​ Thoracic (T1–T12): trunk, chest wall, upper abdomen
•​ Lumbar (L1–L5): legs — damage here causes paraplegia
•​ Sacral (S1–S5): bladder, bowel, lower legs, sexual function

•​ Motor unit = 1 alpha motor neuron + all muscle fibres it innervates (smallest unit of motor output)
•​ Size principle: slow (fatigue-resistant) → fast fatigue-resistant → fast fatigable — recruited in order
•​ Central Pattern Generators (CPGs): spinal interneuron circuits that generate rhythmic movements
(walking, running) WITHOUT brain input. Basis for step training in spinal cord injury.

Central Pattern Generators (CPGs)

More than 100 years ago, Sherrington (1910) and Brown (1911) demonstrated that the spinal cord,
completely disconnected from the brain, could produce rhythmic stepping movements in cats. This
established the concept of central pattern generators.

CPGs are circuits of interneurons in the spinal cord that can generate coordinated, rhythmic
movements (walking, running, chewing, swimming) without requiring continuous input from the brain.
•​ CPGs ensure that extensor and flexor muscles work in concert for fluid, reciprocal movement
•​ They can select between gaits — walking and running require different muscle timing, stance
duration, and joint angles
•​ Descending inputs from higher centres (primarily M1) signal the CPG to select between gaits
•​ Sensory feedback from muscles (proprioception) and the environment shapes CPG activity in real
time

4. Movement Disorders — Quick Reference (हालचाल विकार — संक्षिप्त संदर्भ)

Disorder (विकार) Structure Affected Mechanism Key Signs

Stroke (पक्षाघात) M1 / Internal CST interrupted Spastic hemiplegia, Babinski
Capsule (UMN) contralaterally sign, hyperreflexia
Parkinson's Substantia Nigra Indirect pathway dominant Bradykinesia, resting tremor
Disease (dopamine loss) → GPi over-inhibits thalamus (3–5 Hz), rigidity
(पार्कि न्सन्स रोग)

Huntington's Striatum (indirect STN under-activated → Chorea, cognitive &

Disease pathway) excessive cortex output psychiatric decline
(हं टिग्ं टन्स रोग)

Cerebellar Ataxia Cerebellum Loss of error correction & Dysmetria, intention tremor,
(सेरेबेलर timing ataxic gait
अटॅ क्सिया)

ALS / MND (मोटर Both UMN & LMN Progressive degeneration of Spasticity + atrophy +
न्यरू ॉन रोग) both motor neuron types fasciculations

Myasthenia NMJ (nAChR Reduced receptors → weak Fatigable weakness, ptosis,

Gravis antibodies) end-plate potential diplopia
(मायस्थेनिया
ग्रेव्हिस)

Spinal Cord Injury Spinal cord below Severed descending + Paralysis, sensory loss,
(मेरूरज्जू दख
ु ापत) lesion ascending tracts autonomic dysfunction