Regulation of Posture and Movement

Introduction

Normal posture and movement depend on coordinated interactions between the spinal cord, brainstem, and higher motor centers. Descending control continuously modulates lower motor circuits, while disruption of this balance alters muscle tone, posture, reflex activity, and the execution of coordinated movements.

• Movement is produced by skeletal muscle contraction initiated through activation of spinal motor neurons.
• Spinal motor neurons receive continuous input from descending pathways originating in the cerebral cortex, brainstem, cerebellum, and basal ganglia.
• Voluntary movements are planned by the motor cortex, cerebellum, and basal ganglia before execution.
• Motor commands reach the spinal cord directly through the corticospinal tract and indirectly through brainstem descending pathways.
• The cerebellum and basal ganglia influence movement mainly by modifying descending motor signals rather than acting directly on spinal motor neurons.
• Upper motor neurons continuously adjust spinal motor neuron activity to meet changing functional demands.
• Supraspinal control serves three major functions:
  • Initiation and execution of voluntary movements.
  • Coordination and smooth execution of motor activity.
  • Maintenance of posture to provide a stable base for movement.

• Once movement begins, sensory receptors in muscles, tendons, joints, ligaments, and skin generate continuous feedback.
• Proprioceptive information reaches the cerebellum through the dorsal and ventral spinocerebellar tracts.
• The cerebellum compares intended movement with the actual performance and rapidly corrects motor errors.
• These corrective influences are transmitted mainly through brainstem descending pathways.
• Additional proprioceptive signals ascend through the dorsal column pathway to the sensory cortex.
• The sensory cortex communicates with the motor cortex, allowing ongoing modification of voluntary motor commands.
• Continuous sensory feedback improves movement accuracy, timing, and precision.
• Extrapyramidal pathways, particularly the vestibulospinal, reticulospinal, and tectospinal tracts, regulate posture, muscle tone, and automatic adjustments during movement.
• The cerebellum and basal ganglia strongly influence these pathways to ensure smooth, coordinated, and efficient motor performance.
• Integration of descending motor commands with continuous sensory feedback enables accurate movement while maintaining postural stability and balance throughout motor activity.

Levels of Integration

• Regulation of posture and movement is integrated at multiple levels of the central nervous system.
• The major levels include the spinal cord, medulla, midbrain, cerebral cortex, basal ganglia, and cerebellum.
• The spinal cord generates simple reflex responses through local neural circuits.
• Higher motor centers integrate sensory information to produce more complex and purposeful movements.
• Experimental interruption of the neuraxis has helped identify the functions of individual motor centers.
• When higher centers are disconnected, motor activity mediated by lower centers often becomes exaggerated.
• This phenomenon is known as the release phenomenon.
• Release phenomenon occurs because higher motor centers normally exert inhibitory control over lower motor circuits.
• Increased responsiveness of neurons below the lesion, known as denervation hypersensitivity, also contributes to enhanced motor activity.
• Together, these mechanisms increase reflex activity and alter muscle tone after damage to descending pathways.

Postural Reflexes

• Postural reflexes are automatic motor responses that maintain body alignment and stability.
• They provide a firm base for voluntary movements and continuously adjust posture during changes in body position.
• These reflexes are broadly classified into phasic and static postural reflexes.

Phasic or Dynamic Reflexes

• Phasic (dynamic) reflexes are brief responses that produce rapid postural corrections.
• They enable immediate adjustments to sudden changes in body position or external forces.
• Important examples include the phasic stretch reflex, righting reflexes, and vestibular placing reactions.
• These reflexes act together to maintain balance, preserve orientation, and support smooth execution of voluntary movement during everyday activities.

Tonic or Static Reflexes

• Tonic (static) reflexes produce sustained muscle contraction to maintain posture and body stability.
• They continuously adjust posture during movement.
• mportant examples include the tonic stretch reflex, tonic neck reflexes, and tonic labyrinthine reflexes.

Spinal Integration

• The spinal cord is a major center for integrating motor activity, posture, and reflex responses.
• It performs several essential functions required for normal movement.
• Spinal neural circuits generate spinal reflexes, which produce rapid and automatic responses to sensory stimuli.
• A typical example is the withdrawal reflex, which protects the body from harmful stimuli.
• The spinal cord also regulates muscle tone through local neural circuits.
• Activity of gamma motor neurons alters muscle spindle sensitivity, thereby adjusting muscle tone.
• Gamma motor neuron activity is strongly influenced by descending pathways from higher motor centers.
• The spinal cord contains central pattern generators, which are neural networks capable of producing rhythmic movements such as walking.
• These networks generate basic locomotor patterns even without continuous sensory input, although normal locomotion requires supraspinal modulation.
• The tonic stretch reflex integrated within the spinal cord provides sustained muscle contraction for maintaining posture and balance.

Spinal Preparation

• The contribution of the spinal cord to motor control has been studied using the spinal preparation model in experimental animals.
• In this preparation, the spinal cord is transected below the brainstem to eliminate descending influences while preserving spinal circuitry.
• Transection below the cervical region preserves diaphragmatic function, whereas lower thoracic transection better maintains cardiovascular stability.
• Three characteristic stages follow spinal cord transection.
• The initial stage of spinal shock is marked by flaccidity and loss of reflex activity below the lesion.
• This is followed by the stage of recovery, during which spinal reflexes gradually return and become increasingly active.
• The final stage of failure is characterized by progressive deterioration of spinal function.
• These observations demonstrate the essential role of descending pathways in regulating spinal motor activity, muscle tone, posture, and coordinated movement.

Stage of Shock

• Spinal shock begins immediately after complete transection of the spinal cord.
• It is characterized by a temporary loss of spinal reflex activity below the level of the lesion.
• During this phase, voluntary movement and all sensory functions below the injury are absent.
• The initial stage is also called the stage of flaccidity because muscles lose their normal tone.
• The duration of spinal shock varies among species and is related to the degree of dependence on supraspinal control.
• In humans, spinal shock generally lasts 1–4 weeks, although the duration varies with the severity and level of injury.

Mechanism of Shock

• The exact mechanism is not completely understood.
• The most widely accepted explanation is the sudden loss of descending facilitatory influences from higher motor centers.
• This interruption markedly reduces the excitability of spinal motor neurons and interneurons.
• Species with greater supraspinal control exhibit more prolonged spinal shock.
• Experimental studies show that a second spinal transection below the original lesion does not reproduce spinal shock, supporting the role of loss of descending input.
• Electrophysiological studies demonstrate a marked reduction in motor neuron excitability during the acute stage.

Features of Shock

• Muscles become flaccid because spinal motor neurons temporarily lose excitatory input.
• Deep tendon and superficial reflexes are absent (areflexia).
• Complete loss of sensation (anesthesia) occurs below the lesion.
• Voluntary motor function is completely abolished.

Features at the Level of the Lesion

• Patients may experience localized pain due to injury of spinal tissues and nerve roots.

Other Features

• The urinary bladder and rectum become atonic, causing urinary retention and bowel dysfunction.
• Bladder sphincter function may recover earlier than detrusor muscle activity.
• Penile erection is usually absent during the acute phase because spinal autonomic reflexes are suppressed.
• Lesions above the thoracolumbar sympathetic outflow may produce marked hypotension due to loss of sympathetic vasoconstrictor activity.
• Injuries below the lower thoracic region have a smaller effect on systemic blood pressure because most sympathetic outflow remains intact.
• Paralysis of limb muscles abolishes the muscle pump, reducing venous return and cardiac output.
• Consequently, the lower limbs may become cold, cyanotic, and edematous because of impaired circulation.
• High thoracic lesions may interrupt visceral sensory pathways, reducing awareness of abdominal distension or discomfort.
• Recovery from spinal shock is indicated by the gradual reappearance of spinal reflexes, reflecting restoration of intrinsic spinal neuronal activity despite persistent interruption of descending pathways.

Stage of Recovery

Smooth Muscle Function

• The stage of recovery begins after spinal shock as spinal reflexes gradually return below the level of the lesion.
• Recovery occurs progressively over days to weeks and reflects restoration of intrinsic spinal cord activity.
• Smooth muscle function returns before skeletal muscle function.
• The urinary sphincter regains activity earlier than the detrusor muscle, although bladder emptying remains impaired initially.
• Blood vessels gradually recover vascular tone, leading to progressive normalization of blood pressure.

Reflex Responses

• Reflex activity reappears in a predictable sequence.
• The earliest response is usually a slight flexor withdrawal reflex following a painful stimulus.
• Adductor muscle reflexes may also reappear during the early recovery phase.
• In some patients, the knee jerk is among the first deep tendon reflexes to return.

Mechanism of Recovery

• The precise mechanism is not completely understood.
• Recovery is believed to result from increased effectiveness of local spinal circuits.
• Axonal sprouting from sensory afferents and spinal interneurons creates new synaptic connections.
• These newly formed connections occupy synaptic sites that were previously supplied by interrupted descending fibers.
• Enhanced spinal excitability gradually restores reflex function despite persistent loss of supraspinal input.

Muscle Tone and Size

• Skeletal muscle tone gradually returns, usually within 2–3 weeks in humans.
• Tone commonly reappears first in the lower limb flexor muscles, followed by the upper limbs and trunk.
• Extensor muscles recover more slowly, producing a characteristic flexed posture of the lower limbs.
• This posture is often described as paraplegia in flexion.
• Continuous reflex activity helps preserve muscle bulk, reducing severe muscle wasting despite paralysis.

Reflex Movements

• Involuntary flexor spasms develop as spinal reflexes recover.
• Flexor muscle contraction occurs with simultaneous reciprocal inhibition of extensor muscles.
• Painful stimulation of the foot elicits a strong withdrawal response with flexion of the hip and knee.
• An extensor plantar response (Babinski sign) is commonly present because of loss of corticospinal control.

Flexor Reflex

• The flexor withdrawal reflex is usually the first spinal reflex to recover after spinal shock.
• A painful stimulus to the lateral sole produces a Babinski response, flexion of the hip and knee, and thigh abduction.
• Simultaneous reciprocal inhibition relaxes antagonist muscles.
• This protective reflex rapidly withdraws the limb from a potentially harmful stimulus.

H6: Mass Reflex

• In advanced recovery, strong cutaneous stimulation may trigger a mass reflex.
• This widespread response includes bilateral flexor spasms and contraction of the abdominal muscles.
• Reflex emptying of the urinary bladder and bowel may occur due to activation of spinal autonomic pathways.
• Profuse sweating below the level of the lesion may accompany the response.
• The mass reflex usually appears several months after spinal cord injury, indicating marked enhancement of spinal reflex activity.

Coitus Reflex

• The coital reflex is a spinal reflex triggered by stimulation of the glans penis or surrounding genital skin.
• The response includes penile erection, contraction of the cremaster muscle causing testicular elevation, and contraction of the dartos muscle, producing wrinkling of the scrotal skin.
• Hip flexor and thigh abductor muscles may also contract during the reflex.
• Reflex seminal emission may occur, but complete sexual intercourse usually remains impaired because voluntary motor control is absent.

Deep Reflexes

• Deep tendon reflexes gradually return after recovery of the flexor withdrawal reflex.
• The knee jerk usually reappears within 1–5 weeks.
• Early quadriceps contraction is brief, causing the limb to relax rapidly after the reflex response.
• The ankle jerk returns later and may be accompanied by mild ankle clonus.

Extensor Responses

• Extensor muscle tone increases gradually over several months.
• Progressive extensor spasticity causes the lower limbs to assume an extended posture, known as paraplegia in extension.
• Knee and ankle tendon reflexes become markedly exaggerated.
• Passive stretching of the limbs may trigger powerful reflex extension involving both lower limbs.
• Simultaneous contraction of flexor and extensor muscles increases limb rigidity.
• The previously observed mass reflex often becomes less prominent during this stage.
• Genital stimulation continues to evoke spinal genital reflexes, although seminal emission may be absent.

Autonomic Reflexes

• The micturition reflex becomes hyperactive, producing reflex bladder emptying.
• Because bladder contraction is incomplete, residual urine remains after voiding.
• Persistent bladder overactivity may lead to spastic neurogenic bladder, characterized by reduced bladder capacity, wall hypertrophy, and fibrosis.
• The defecation reflex also returns, but bowel evacuation is often incomplete.
• Resting blood pressure usually returns to normal, although impaired autonomic regulation may cause exaggerated fluctuations during physiological stress.
• Sweating below the level of the lesion gradually returns, improving skin temperature regulation and overall skin health.

Supporting Reactions

• Supporting reactions are automatic spinal responses that help maintain body support after reflex activity has recovered.
• Two types are recognized: positive supporting reaction and negative supporting reaction.

Positive Supporting Reaction

• The positive supporting reaction is initiated by tactile stimulation of the sole of the foot.
• The stimulated limb extends and becomes rigid, allowing it to support body weight.
• Both cutaneous and proprioceptive afferents contribute to this response.
• Activation of extensor muscles converts the limb into a stable weight-bearing structure.
• Other limbs also become rigid, improving overall postural stability.
• This reaction demonstrates the ability of spinal circuits to generate coordinated postural responses independently of the brain.

Negative Supporting Reaction

• The negative supporting reaction is the active disappearance of the positive supporting reaction.
• Stretch of extensor muscles contributes to termination of the supporting response.
• This mechanism allows transition from a rigid supporting posture to the next phase of movement.

Locomotion Generator

• The ability of spinal animals to stand and perform stepping movements indicates the presence of intrinsic spinal locomotor circuits.
• These circuits are known as central pattern generators.
• Central pattern generators are networks of spinal interneurons that generate rhythmic motor activity without continuous sensory input.
• Separate locomotor generators are present in the cervical and lumbar enlargements for coordinated upper and lower limb movements.
• They produce alternating activation of flexor and extensor muscles, creating the rhythmic pattern required for walking.
• Experimental stimulation with excitatory neurotransmitters can activate these spinal networks and produce stepping movements.
• Under normal conditions, central pattern generators receive activating signals from the mesencephalic locomotor region in the midbrain.
• After spinal cord transection, loss of descending input prevents spontaneous activation, so external sensory or experimental stimulation is required to initiate locomotor activity.

Stage of Failure

• The stage of failure may develop in chronic spinal cord injury because of prolonged immobilization, poor nutrition, recurrent infections, and inadequate nursing care.
• Reflex activity gradually declines as the threshold for spinal reflexes increases.
• The mass reflex disappears, and reflexes become difficult to elicit.
• Progressive muscle wasting and flaccidity develop because of prolonged inactivity.
• Persistent pressure over bony prominences causes pressure ulcers, which heal poorly and increase the risk of systemic infection.
• Prolonged immobilization promotes bone loss, leading to hypercalciuria and urinary tract stone formation.
• Recurrent urinary infections, sepsis, and renal complications are major causes of morbidity and mortality.
• Early rehabilitation, optimal nutrition, infection control, pressure-relieving measures, and appropriate medical care improve long-term survival and lity of life.

Medullary Integration

• The medulla is an important center for integrating tonic postural reflexes and maintaining muscle tone.
• Its role has been investigated experimentally using the decerebrate preparation, produced by transection between the superior and inferior colliculi.
• This procedure removes higher motor influences while preserving many brainstem motor pathways.

Features of Decerebrate Preparation

• Unlike spinal cord transection, spinal shock does not occur after decerebration.
• Marked extensor rigidity develops immediately after the lesion.
• The limbs become fully extended, and the trunk and neck are hyperextended because of excessive extensor muscle activity.
• Righting reflexes are absent, preventing the animal from restoring its normal posture.
• Tonic postural reflexes remain intact and are often exaggerated.

Mechanism of Decerebrate Rigidity

• Decerebrate rigidity results from excessive activation of spinal motor circuits controlling extensor muscles.
• Two major mechanisms contribute to this increased muscle tone:
  • Increased excitability of motor neuron pools.
  • Increased discharge of gamma motor neurons, which enhances muscle spindle sensitivity.

• Enhanced spindle sensitivity strengthens the stretch reflex, producing sustained extensor muscle contraction.

Role of Reticulospinal Pathways

• The brainstem reticular formation contains both facilitatory and inhibitory motor regions.
• The pontine reticulospinal tract provides a continuous facilitatory influence on spinal motor neurons, especially extensor muscles.
• The medullary reticulospinal tract exerts an inhibitory influence on spinal motor activity.
• Normal posture depends on a balance between these opposing descending pathways.

Influence of Higher Motor Centers

• The cerebral cortex, basal ganglia, and cerebellum enhance the activity of inhibitory neurons in the medullary reticular formation.
• Although the basal ganglia act indirectly through cortical and brainstem connections, they contribute to suppression of excessive muscle tone.
• The cerebellum also supports inhibitory control by influencing brainstem motor centers.

Effect of Midcollicular Transection

• A midcollicular lesion interrupts descending input from the cerebral cortex and basal ganglia to the medullary reticular formation.
• Consequently, inhibitory output from the medullary reticulospinal tract is markedly reduced.
• In contrast, the pontine reticulospinal tract continues to discharge spontaneously.
• The resulting imbalance favors excessive facilitatory influence on spinal motor neurons.
• Increased gamma motor neuron activity enhances stretch reflexes and extensor muscle tone.
• The combined increase in motor neuron excitability and spindle sensitivity produces the characteristic decerebrate rigidity seen after midbrain transection.

Importance of Decerebrate Rigidity

• Decerebrate rigidity predominantly affects extensor muscles, producing marked increase in muscle tone.
• Antigravity muscles, mainly the lower limb extensors in humans, are essential for maintaining upright posture against gravity.
• Sustained extensor tone is a normal component of static postural reflexes.
• Excessive extensor rigidity after decerebration demonstrates the important role of medullary motor centers in regulating antigravity muscle tone and maintaining postural stability through descending brainstem pathways.

Medullary Reflexes

• The medulla integrates several static postural reflexes that are essential for maintaining posture and muscle tone.
• These reflexes become more prominent after a midcollicular lesion because inhibitory influences from higher centers are lost.
• Major medullary postural reflexes include extensor rigidity, tonic labyrinthine reflexes, and tonic neck reflexes.

Extensor Rigidity

• Extensor muscle tone is a key postural mechanism that enables the body to resist gravity and maintain an upright position.
• This tone is generated mainly through the combined actions of the reticulospinal and vestibulospinal tracts.
• The reticulospinal tract regulates muscle tone primarily by altering gamma motor neuron activity and muscle spindle sensitivity.
• The vestibulospinal tract acts mainly by facilitating alpha motor neurons supplying extensor muscles.
• Together, these descending pathways ensure appropriate antigravity muscle activity and stable postural control.

Tonic Labyrinthine Reflexes

• Tonic labyrinthine reflexes are static postural reflexes that adjust muscle tone according to body position relative to gravity.
• These reflexes are best demonstrated in decerebrate preparations, where the animal cannot restore its normal posture.

Receptors

The otolith organs of the vestibular apparatus serve as the sensory receptors.

Stimulus

The primary stimulus is the effect of gravity on the otolith organs during changes in body position.

Reflex Pathway

Reflex responses are transmitted mainly through the vestibulospinal tracts.

Response

• Extensor muscle rigidity is greatest when the animal is in the supine position.
• Extensor tone progressively decreases when the body is turned sideways.
• Rigidity is least in the prone position.
• These reflexes continuously adjust muscle tone in response to head and body orientation.

Importance

They are essential for maintaining posture, balance, and stable body alignment against gravity.

Table 130.1: Righting reflexes (RR).

Righting Reflex	Primary Stimulus	Main Receptor	Principal Integration Center	Functional Response
Labyrinthine	Head tilt due to gravity	Otolith organs (vestibular apparatus)	Midbrain	Maintains the head in an upright position.
Neck	Stretch of neck muscles	Muscle spindles	Midbrain	Sequentially aligns the shoulders, thorax, and pelvis with the head.
Body-on-Head	Pressure on one side of the body	Cutaneous exteroceptors	Midbrain	Restores normal head position.
Body-on-Body	Lateral body pressure	Cutaneous exteroceptors	Midbrain	Corrects body posture even when the head remains tilted.
Limb	Stretch of limb muscles	Muscle spindles	Midbrain (red nucleus)	Assists restoration of normal body posture.
Optical	Visual orientation cues	Retinal photoreceptors	Visual cortex	Uses visual input to maintain normal head position.

Tonic Neck Reflexes

• Tonic neck reflexes are postural reflexes that alter muscle tone when the position of the head changes relative to the trunk.
• These reflexes help maintain postural stability by coordinating the activity of the neck, trunk, and limb muscles.

Receptors

The primary receptors are muscle spindles located in the upper cervical muscles, which detect changes in neck muscle length.

Stimulus

The stimulus is a change in the position of the head relative to the body, causing stretch of cervical proprioceptors.

Reflex Pathway

Sensory signals are transmitted to the brainstem, where they are integrated mainly through the reticulospinal and tectospinal pathways.

Response

• Flexion of the head produces flexion of the upper limbs and extension of the lower limbs.
• Extension of the head causes extension of the upper limbs and flexion of the lower limbs.
• Rotation of the head to one side extends the limbs on the same side and flexes the limbs on the opposite side.
• These coordinated responses redistribute muscle tone to support balance during changes in head orientation.

Importance

• Tonic neck reflexes are especially important in quadrupedal animals because they assist in maintaining a stable posture during movement and while changing the direction of gaze.
• For example, looking upward increases extensor tone in the upper limbs, whereas looking downward increases extensor tone in the lower limbs, helping the body remain balanced.
• In healthy adult humans, these reflexes are largely suppressed by higher brain centers but may reappear in certain neurological disorders involving loss of cortical inhibition.

Midbrain Integration

Midbrain mainly integrates the phasic postural reflexes. These are righting reflexes, vestibular placing reflex and grasp reflex. Central pattern generator for locomotion (CPG) is situated in midbrain (mesencepahlic generator for locomotion) that drives the spinal CPG.

Midbrain Preparation

The midbrain is an important center for integrating phasic postural reflexes, which help maintain body orientation during movement.

Features of Midbrain Animal

• These reflexes produce rapid, coordinated adjustments that restore normal posture after changes in body position.
• The midbrain integrates righting reflexes, the vestibular placing reflex, and the grasp reflex.
• It also contains the mesencephalic locomotor region, which activates spinal central pattern generators responsible for rhythmic locomotor movements.
• Central pattern generators within the spinal cord generate alternating patterns of flexor and extensor muscle activity required for walking.
• Signals from the midbrain initiate and regulate these spinal circuits to produce coordinated locomotion.
• Experimental studies of midbrain function are performed by creating a section at the upper border of the midbrain, producing a preparation known as a midbrain animal.
• Unlike decerebrate preparations, this preparation does not exhibit spinal shock because the spinal cord remains functionally active.
• Extensor muscle rigidity is present when the animal is at rest.
• This rigidity decreases or disappears during voluntary locomotor activity because phasic postural reflexes become active.
• The animal retains the ability to restore normal body orientation after displacement.
• The grasp reflex and vestibular placing reflex also remain functional, demonstrating preservation of important postural mechanisms.

Midbrain Reflexes

Righting Reflexes

• Righting reflexes are a group of coordinated reflexes that restore the normal position of the head and body after displacement.
• Their primary function is to maintain the head upright, stabilize posture, and keep the visual axis aligned with the surroundings.
• These reflexes depend on information from the vestibular apparatus, proprioceptors, cutaneous receptors, and visual receptors.
• They are activated by head tilt, neck muscle stretch, pressure on the body or limbs, and visual orientation cues.
• Most righting reflexes are integrated within the midbrain, whereas optical righting depends on intact cerebral cortical function.

Labyrinthine Righting Reflex

• The labyrinthine righting reflex is initiated when head tilt stimulates the otolith organs of the vestibular apparatus.
• Reflex activation contracts neck muscles to restore the head to a horizontal position despite body tilt.

Body on Head Righting Reflex

• The body-on-head righting reflex is triggered by pressure on one side of the body.
• Cutaneous receptors initiate head correction even when vestibular input is absent.

Neck Righting Reflex

• The neck righting reflex is activated after the head has returned to the normal position while the trunk remains rotated.
• Stretch of cervical muscles produces sequential rotation of the thorax, abdomen, and pelvis until the body is aligned with the head.

Body on Body Righting Reflex

The body-on-body righting reflex corrects body position through pressure receptors in the skin, even if head movement is prevented.

Limb Righting Reflex

The limb righting reflex is initiated by proprioceptive input from the limbs and contributes to restoration of normal body posture.

Optical Righting Reflex

• The optical righting reflex uses visual information to orient the head correctly in space.
• This visual reflex requires an intact visual cortex and complements vestibular and proprioceptive mechanisms.
• Together, these reflexes maintain balance, stabilize gaze, improve locomotor efficiency, and protect the body from loss of equilibrium during changes in position.
• The grasp reflex is a primitive postural reflex triggered when an object touches or approaches the limbs.
• The limbs automatically grasp the object and extend to improve body support and stability.
• This reflex helps animals maintain posture and facilitates standing.
• In humans, the grasp reflex is normally present during infancy and is suppressed as the nervous system matures.

Vestibular Placing Reaction

• The vestibular placing reaction prepares the body for safe landing during rapid downward movement.
• Vestibular receptors detect linear acceleration of the body.
• Reflex impulses travel mainly through the vestibulospinal tract.
• The response includes extension of the upper limbs and spreading of the toes, improving balance and stability during landing.

Mesencephalic Locomotion Generator

• The mesencephalic locomotor region is a midbrain center that initiates and regulates locomotion.
• It activates spinal central pattern generators, which produce rhythmic muscle activity required for walking.
• Motor commands from the cerebral cortex reach this region through corticobulbar pathways.
• Descending signals are transmitted mainly through the reticulospinal tract to influence spinal motor neurons.
• This system initiates locomotion and rapidly modifies movement during activities such as running and swimming.
• The midbrain also coordinates phasic postural reflexes to maintain balance during movement.

Cortical Integration

• The cerebral cortex is the highest center for planning, initiating, and regulating voluntary movement.
• Before movement begins, the motor cortex develops an initial motor plan.
• This plan is refined through continuous interaction with the basal ganglia and cerebellum, which optimize the sequence, timing, force, and accuracy of movement.
• The motor cortex also communicates with the sensory and association cortices to incorporate sensory feedback and environmental information.
• The premotor cortex and supplementary motor area participate in preparing and organizing appropriate motor patterns.
• After processing is complete, motor commands descend to spinal motor neurons through descending motor pathways to produce coordinated muscle activity.

Decortication

• Experimental removal of the cerebral cortex is known as decortication, and the resulting preparation is called a decorticate animal.
• Decortication is used to study the specific contribution of the cerebral cortex to posture, movement, and motor learning.

Features of Decorticate Animal

• Decorticate animals do not exhibit spinal shock because the spinal cord and brainstem remain functionally connected.
• Brainstem-mediated postural reflexes, including righting reflexes and other midbrain reflexes, remain intact.

Decorticate Rigidity

• Decorticate rigidity is mild and is usually present only when the animal is at rest.
• This rigidity decreases or disappears during active movement because phasic postural reflexes become functional.
• Loss of cortical inhibition increases activity in descending pathways that influence gamma motor neurons, producing increased muscle tone.
• Voluntary movements that require planning, precision, and adaptation are markedly impaired.

Hopping and Placing Reactions

• Hopping reactions are severely affected after decortication.
• Normally, when the body is displaced sideways, rapid corrective steps are taken to restore balance.
• This automatic stepping response is greatly reduced without cortical control.
• Placing reactions are also impaired.
• Under normal conditions, the limbs are accurately positioned on a supporting surface after corrective stepping.
• Loss of cortical integration reduces the accuracy and effectiveness of these adjustments.
• These findings indicate that the cerebral cortex plays an essential role in integrating hopping and placing reactions.
• Learned motor responses and conditioned reflexes disappear after decortication because cortical circuits required for motor learning are absent.
• However, some conditioned responses can gradually be re-established through repeated training.
• The animal cannot effectively modify behavior based on previous experience.
• Basic homeostatic functions remain intact because the hypothalamus and brainstem are preserved.
• Regulation of body temperature, cardiovascular function, respiration, and other autonomic activities continues normally.
• Functional organization of postural control follows a hierarchical pattern.
• The spinal cord integrates simple spinal and supporting reflexes.
• The medulla coordinates static antigravity postural reflexes.
• The midbrain integrates righting reflexes that restore body orientation.
• The cerebral cortex integrates complex postural adjustments, voluntary movements, hopping reactions, placing reactions, and motor learning.

Table 130.2: Integration of motor functions at various levels of CNS as studied in different preparations.

Central Nervous System Level	Major Integrated Motor Functions
Spinal cord	Spinal reflexes are preserved.
Medulla	Integrates antigravity reflexes for postural support.
Midbrain	Integrates righting reflexes and maintains postural orientation.
Cerebral cortex	Supports conditioned reflexes, hopping, placing reactions, and complex voluntary motor control.

Cortical Motor Areas

• Cortical motor areas are specialized regions of the cerebral cortex responsible for planning, initiating, and coordinating voluntary movements.
• These areas include the primary motor cortex, premotor cortex, supplementary motor area, somatosensory cortex, and frontal eye field.

Primary Motor Cortex

• The primary motor cortex is located in the precentral gyrus and corresponds to Brodmann area 4.
• It is the principal origin of the corticospinal and corticobulbar tracts, which control voluntary skeletal muscle activity.

Connections

• The primary motor cortex generates motor commands required for precise, purposeful movements.
• It communicates extensively with the premotor cortex, supplementary motor area, thalamus, somatosensory cortex, brainstem, and spinal cord.
• Continuous sensory feedback allows ongoing modification and refinement of motor output.
• Motor pathways arising from the cerebral cortex primarily control muscles on the opposite side of the body because most fibers cross in the lower brainstem.

Motor Homunculus

• The body is represented in an orderly pattern within the primary motor cortex, forming the motor homunculus.
• The lower limb is represented near the medial surface, whereas the face is represented in the lateral part of the precentral gyrus.
• Most body regions have predominantly contralateral cortical representation, while muscles of the face receive varying degrees of bilateral cortical input.
• The size of each cortical representation reflects the precision and complexity of voluntary movement rather than the physical size of the body part.
• The hands and fingers occupy a disproportionately large cortical area because they perform highly skilled movements.
• The lips, tongue, and jaw also have extensive cortical representation to support precise movements required for speech and feeding.
• This organized cortical arrangement enables accurate control of fine motor activities and coordinated voluntary movement.

Premotor Cortex

• The premotor cortex corresponds mainly to the lateral part of Brodmann area 6.
• It receives input from the supplementary motor area and primary motor cortex.
• It projects to brainstem centers involved in postural control.
• It establishes appropriate posture before voluntary movement, facilitating efficient and coordinated motor execution.

Supplementary Motor Area

• The supplementary motor area occupies the medial part of Brodmann area 6.
• It receives sensory information from the primary somatosensory cortex.
• This region plans and organizes complex sequences of voluntary movements before their execution.
• It is particularly important for coordinated movements involving both hands.
• Damage to this area impairs performance of complex and bimanual motor tasks.

Primary Somatosensory Cortex

• The primary somatosensory cortex provides continuous sensory feedback to motor regions during movement.
• It contributes to accurate execution of learned motor skills and coordinated movement sequences.
• Corticospinal fibers arising from this cortex mainly terminate in the dorsal horn of the spinal cord, where they modulate incoming sensory signals.
• Injury to the somatosensory cortex disrupts skilled activities that depend on learned movement patterns.

Posterior Parietal Cortex

• The posterior parietal cortex integrates visual, proprioceptive, and tactile information to guide purposeful movements.
• It communicates extensively with the motor cortex and also contributes fibers to the corticospinal tract.

Frontal Eye Field

• The frontal eye field corresponds to Brodmann area 8.
• It coordinates voluntary eye movements by influencing the pontine gaze centers and the superior colliculus, which helps generate accurate saccadic eye movements.