Motor Areas Pyramidal System

Figure 13.11

organization of motor subsystems

Introduction Basal ganglia motor related signals to the motor cortex are inhibitory Cerebellar motor related signals to the motor cortex are excitatory Balance of these systems allows for smooth, coordinated movement

Motor system includes Tracts eg. Corticospinal (pyramidal) (Skillful voluntary movement) Corticobulbar and Bulbospinal (Extrapyramidal) Basal Ganglia (regulator) Cerebellum (regulator)

Cerebral Cortex CEREBRAL CORTEX BASAL GANGLIA Corticospinal tracts THALAMIUS Corticobulbar tracts BRAIN STEM CEREBELLUM Bulbospinal tracts SENSORY INPUT SPINAL CORD FINAL COMMON PATH

Major Motor Pathways 1. Corticospinal (cortex to spinal cord) a) Lateral – distal limb muscles (fine manipulations). b) Ventral – trunk and upper leg muscles (posture / locomotion). 2. Corticobulbar (cortex to pons, 5th, 7th, 10th and 12th cranial nerves) – control of face and tongue muscles; upper face both contralateral, lower face contralateral 3. Ventromedial (brain stem to spinal cord) – trunk and proximal limb muscles (posture, sneezing, breathing, muscle tone) 4. Rubrospinal (red nucleus to spinal cord) – modulation of motor movement (limb movement independent of trunk movement)

Components of motor neurons Upper motor neuron (corticospinal & corticobulbar). Starts from motor cortex and ends in Cranial nerve nucleus (corticobulbar). Anterior horn of spinal cord in opposite side(corticospinal tracts). Lower Motor Neuron Starts from anterior horn of spinal cord and ends in appropriate muscle of the same side. eg. All peripheral motor nerves.

MOTOR TRACTS & LOWER MOTOR NEURON MOTOR CORTEX MIDBRAIN & RED NUCLEUS (Rubrospinal Tract) UPPER MOTOR NEURON (Corticospinal Tracts) VESTIBULAR NUCLEI (Vestibulospinal Tract) PONS & MEDULLA RETICULAR FORMATION (Reticulospinal Tracts) LOWER (ALPHA) MOTOR NEURON THE FINAL COMMON PATHWAY SKELETAL MUSCLE

Somatic Motor System Interactions of the sensory and motor systems enable voluntary movement.

Steps in Motor Action

Levels of motor control Cerebral cortex Brain stem Spinal cord and cranial motor nuclei

Includes Cortical Motor Areas Primary Motor Cortex (M-I) Supplementary Motor Area (M-II) Premotor Cortex (PMC) Frontal Eye Field Area Broca’s Area for speech

Motor cortex Primary motor cortex ( M1) Premotor area (PMA) Supplementary motor area (SMA) Note: All the three projects directly to the spinal cord via corticospinal tract. Premotor and supplementary motor cortex also project to primary motor cortex and is involved in coordinating & planning complex sequences of movement (motor learning).

Primary Motor Cortex (M-I) Location :- Immediately anterior to the central sulcus and extends to the medial surface of hemisphere also known as Broadmann’s area 4. Description: Body is represented as up side down and stretched on the medial surface where pelvic and leg muscles are represented. Hand and mouth has a greater area of representation and is large because of frequently used (skill).

Body map: human body spatially represented Where on cortex; upside down

Primary Motor Cortex (M-I) controls the musculature of the opposite side of the body. Face area is bilaterally represented. Functions:- Is used in execution of skilled movements and the direction, force and velocity of movements. Lesions:- Ability to control fine movements is lost. Ablation of M-I alone cause hypotonia not spasticity.

Supplementary Motor Area (M-II) Location: Found in lateral and medial aspect of the Frontal lobe. Function: It works together with premotor cortex. Involved in programming of motor sequences. Lesions: Reduces ability in performing complex activity.

Premotor Cortex (PMC) Location: Functions: Broadmann’s area 6. It lies immediately anterior to primary motor cortex. It is more extensive than primary motor cortex (about 6 times) Functions: It works with the help of basal ganglia, thalamus, primary motor cortex, posterior parietal cortex. It plays role in planning and anticipation of a specific motor act.

Lesion: Its lesion do not cause paralysis but only Slowing of the complex limb movement. Lesion may result in loss of short-term or Working memory.

White matter of the spinal cord Ascending pathways: Sensory information by multi-neuron chains from body up to more rostral regions of CNS Dorsal column Spinothalamic tracts Spinocerebellar tracts Descending pathways: Motor instructions from brain to more caudal regions of the CNS. Pyramidal (corticospinal) most important to know. All others (“extrapyramidal”).

Functions of pyramidal tract Controls primarily distal muscles which are finely controlling the skilled movements of thumb & fingers on the opposite side. eg. Painting, writing, picking up of a small object etc. Effect of lesion: loss of distal motor function in opposite side. Pure corticospinal tract lesion cause hypotonia instead of spasticity. The reason is that pure pyramidal tract lesion is very rare, and spasticity is due to loss of inhibitory control of extrapyramidal tract.

Some Descending Pathways Synapse with ventral (anterior) horn interneurons Pyramidal tracts: Lateral corticospinal – cross in pyramids of medulla; voluntary motor to limb muscles Ventral (anterior) corticospinal – cross at spinal cord; voluntary to axial muscles (Trunk and upper leg muscles). “Extrapyramidal” tracts: one example

Somatic Motor Clinical signs Position sense test Clonus Babinski sign Enhanced deep tendon responses Spasticity Clasp knife response

Position sense With the client’s eyes closed, the clinician manipulates the client’s right thumb. He is asked to point his left thumb in the same direction as his right thumb. The clinician switches sides and he is no longer able to perform the task.

Clonus A series of fast, involuntary contractions symptomatic of damage to upper motor neurons.

Babinski reflex An extension of the great toe, sometimes with fanning of the other toes, in response to stroking of the sole of the foot. It is a normal reflex in infants, but it is usually associated with a disturbance of the pyramidal tract in children and adults.

Enhanced Deep Tendon Reflexes An unusually vigorous patellar tendon reflex may be observed following upper motor neuron damage, often in conjunction with heightened muscle tone (spasticity) and clonus.

-Spasticity (hypertonia) is a feature of altered muscle performance,occurring in disorders of the central nervous system which give rise to the Upper Motor Neuron Syndrome (UMNS ). - It can be defined as increased resistance to passive stretch. -Patients complain of stiffness & inability to relax -Muscles become permanently "tight" or spastic. When there is a loss of descending inhibition from the brain to BRAIN STEM EXCITATORY CENTERS,vestibulospinal &reticulospinal EXCITATORY signals cause muscles to become overactive, & spastic . - The condition can interfere with walking, movement, or speech.

Spasticity The man exhibits spasticity of the right side, while the woman exhibits spasticity of the left side.

Clasp knife response Initially there is great resistance to extension of the joint, followed by a gradual “melting” of the resistance as continued, steady pressure is applied.

Features of upper motor neurone disease 1) Paralysis affect movement rather than muscles. 2) No remarkable muscle wasting, but disuse atrophy 3) Spasticity ( hypertonia ) , frequently called “ clasp-knife spasticity ” 4) Clonus Repetitive jerky motions (clonus), especially when limb moved & stretched suddenly 5) exaggerated tendon jerks 6) Extensor plantar reflex = Babinski sign ( dorsiflexion of the big toe and fanning out of the other toes ) 7) Absent abdominal reflexes

Features of lower motor neurone disease 1) Weakness and decreased muscle tone (Flaccid paralysis) 2) Remarkable muscle wasting. 3) Absent tendon jerks. 4) Negative extensor plantar reflex (Babinski sign). 5) Present abdominal reflexes.