5IntroductionBasal ganglia motor related signals to the motor cortex are inhibitoryCerebellar motor related signals to the motor cortex are excitatoryBalance of these systems allows for smooth, coordinated movement
6Motor system includes Tracts eg. Corticospinal (pyramidal) (Skillful voluntary movement)Corticobulbar and Bulbospinal (Extrapyramidal)Basal Ganglia (regulator)Cerebellum (regulator)
8Major 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 contralateral3. Ventromedial (brain stem to spinal cord) – trunk and proximallimb muscles (posture, sneezing, breathing, muscle tone)4. Rubrospinal (red nucleus to spinal cord) – modulation of motor movement (limb movement independent of trunk movement)
10Components of motor neurons Upper motor neuron (corticospinal & corticobulbar).Starts from motor cortex and ends inCranial nerve nucleus (corticobulbar).Anterior horn of spinal cord in opposite side(corticospinal tracts).Lower Motor NeuronStarts from anterior horn of spinal cord and ends inappropriate muscle of the same side.eg. All peripheral motor nerves.
11MOTOR TRACTS & LOWER MOTOR NEURON MOTOR CORTEXMIDBRAIN &RED NUCLEUS(Rubrospinal Tract)UPPER MOTOR NEURON(Corticospinal Tracts)VESTIBULAR NUCLEI(Vestibulospinal Tract)PONS & MEDULLARETICULAR FORMATION(Reticulospinal Tracts)LOWER (ALPHA) MOTOR NEURONTHE FINAL COMMON PATHWAYSKELETALMUSCLE
12Somatic Motor SystemInteractions of the sensory and motor systems enable voluntary movement.
18Motor 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).
19Primary Motor Cortex (M-I) Location :-Immediately anterior to the central sulcus and extendsto the medial surface of hemisphere also known asBroadmann’s area 4.Description:Body is represented as up side down and stretched onthe medial surface where pelvic and leg muscles arerepresented. Hand and mouth has a greater area ofrepresentation and is large because of frequently used(skill).
20Body map: human body spatially represented Where on cortex; upside down
21Primary 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.
22Supplementary Motor Area (M-II) Location:Found in lateral and medial aspect of theFrontal lobe.Function:It works together with premotor cortex.Involved in programming of motor sequences.Lesions:Reduces ability in performing complex activity.
23Premotor Cortex (PMC) Location: Functions: Broadmann’s area 6. It lies immediately anterior toprimary motor cortex. It is more extensive than primarymotor cortex (about 6 times)Functions:It works with the help of basal ganglia, thalamus,primary motor cortex, posterior parietal cortex. It playsrole in planning and anticipation of a specific motoract.
24Lesion: Its lesion do not cause paralysis but only Slowing of the complex limb movement.Lesion may result in loss of short-term orWorking memory.
26White matter of the spinal cord Ascending pathways:Sensory information by multi-neuron chains from body up to more rostral regions of CNSDorsal columnSpinothalamic tractsSpinocerebellar tractsDescending pathways:Motor instructions from brain to more caudal regions of the CNS.Pyramidal (corticospinal) most important to know.All others (“extrapyramidal”).
27Functions 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 oppositeside.Pure corticospinal tract lesion cause hypotonia insteadof spasticity.The reason is that pure pyramidal tract lesion isvery rare, and spasticity is due to loss of inhibitorycontrol of extrapyramidal tract.
28Some Descending Pathways Synapse with ventral (anterior) horn interneuronsPyramidal tracts:Lateral corticospinal – cross in pyramids of medulla; voluntary motor to limb musclesVentral (anterior) corticospinal – cross at spinal cord; voluntary to axial muscles (Trunk and upper leg muscles).“Extrapyramidal” tracts: one example
29Somatic Motor Clinical signs Position sense testClonusBabinski signEnhanced deep tendon responsesSpasticityClasp knife response
30Position senseWith 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.
31ClonusA series of fast, involuntary contractions symptomatic of damage to upper motor neurons.
32Babinski reflexAn 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.
33Enhanced 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.
34-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.
35SpasticityThe man exhibits spasticity of the right side, while the woman exhibits spasticity of the left side.
36Clasp knife responseInitially there is great resistance to extension of the joint, followed by a gradual “melting” of the resistance as continued, steady pressure is applied.
37Features of upper motor neurone disease 1) Paralysis affect movement rather than muscles.2) No remarkable muscle wasting, but disuse atrophy3) Spasticity ( hypertonia ) , frequently called“ clasp-knife spasticity ”4) Clonus Repetitive jerky motions (clonus), especially when limb moved & stretched suddenly5) exaggerated tendon jerks6) Extensor plantar reflex = Babinski sign ( dorsiflexion of the big toe and fanning out of the other toes )7) Absent abdominal reflexes
38Features 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.