Physiology of posture movementand equilibrium


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Physiology of posture movementand equilibrium

  2. 2. Control of Posture and Movement  Somatic motor activity depends on the pattern and rate of discharge of spinal motor neurons. These neurons, the finalcommon paths are bombarded from array of pathways.
  3. 3. The inputs converging on the motor neurons subserve three semi distinct functions through the: 1. Pyramidal System ( corticospinal pathways) = they bring about voluntary activity Fig. 12-1
  4. 4. 2. Extrapyramidal System - they adjust body posture to provide stable background for movement. Concerned with grosser movements and posture3.Cerebellum – coordinating and
  5. 5. Control of Axial and distal Muscles Medial or Ventral Pathways and neurons are concerned with control of muscle of the trunk and proximal portions of the limbs
  6. 6.  Lateral pathways are concerned with the control of muscles in the distal portions of the limbs Axial muscles are concerned with postural adjustment and gross movements Distal limb muscles are those that mediate fine, skilled movements
  8. 8. Anatomy and Function
  9. 9.  The fibers that cross the midline in the medullary pyramids and from the lateral corticospinal tract make up about 80% of the fibers in the corticospinal pathway. 20% of the fibers make up the anterior or ventral, corticospinal tract The lateral corticospinal tract is
  10. 10. Cortical Motor Areas
  11. 11.  30% of the fibers making up the corticospinal tracts come from the motor cortex 30% comes from the premotor cortex 40% from the parietal lobe especially the somatic sensory area
  12. 12. The cortical representation ofeach body part isproportionate in size to theskill with which the part isused for fine, voluntarymovement.
  13. 13. Effects of Section or Destruction of Pyramidal SystemA. Role in Movement Effects of Section or Destruction of the Lateral Corticospinal Tract loss of ability to grasp small objects between two fingers and to make isolated movements of the wrist can still use the hand in a gross
  14. 14. These deficits are consistent with loss ofcontrol of distal musculature of the limbs ,which is concerned with fine skilledmovements Lesions of Ventral Corticospinal Tract produce axial muscle deficits that cause difficulty with balance, walking and climbing
  15. 15. B. Effects on Stretch Reflexes prolonged hypotonia and flacidity rather than spasticity Damage of the lateral corticospinal tract produces Babinski sign: dorsiflexion of the great toe and fanning of the other toes when the lateral aspect of the sole of the foot is scratch
  16. 16. POSTURE-REGULATINGSYSTEMS ( Extrapyramidal Mechanisms)
  17. 17. When the neural axis istransected, the activities belowthe section are cut off orreleased from the “control ofhigher brain centers” and oftenappear to be accentuated
  18. 18. Levels of Integration
  19. 19. SPINAL INTEGRATION Spinal Shock – results from transection of the cervical spinal cord all spinal reflexes are depressed duration of the shock depends upon the degree of encephalization frogs and rats – lasts for minutes dogs and cats – lasts for 1-2 hours monkeys – lasts for days humans – minimum of 2 weeks
  20. 20. The recovery of the reflexexcitability may be due to:* development of denervationhypersensitivity to the mediatorsby the remaining spinalexcitatory endings* sprouting of collaterals fromexisting neurons
  21. 21. The first reflex response to appear as spinal shock wares off is slight contraction of the leg flexors and adductors in response to noxious stimulus Responses of Chronic Spinal Animal * Magnet reaction (positive supporting reaction) * Autonomic reflexes – reflex contraction of full bladder and rectum * Sexual reflexes * Mass reflex - evacuation of bladder
  23. 23.  Hindbrain and spinal cord are isolated from the rest of the brain by transection of the brainstem at the superior border of the pons. Procedure is called Decerebration Decerebrate rigidity develops as soon as the brainstem is transected It is found to be spastic due to
  24. 24. Facilitation is due to two factors: increased general excitability of the motor neuron pool increase in the rate of discharge in the gamma efferent neurons
  25. 25. Characteristics ofDecerebrate Rigidity
  26. 26. 1. Decerebrate Posture –“ Caricature of the normal standing position”– neck and limbs extended, back arched, tail elevated.
  27. 27. 2. Tonic Labyrinthine Reflexes no righting reflexes are present, and the animal stays in position where they are put rigidity in the limbs varies with position if the animal is placed on its back extension of all 4 limbs is maximal as the animal is turned to either side, rigidity decreases
  28. 28. 3. Tonic Neck ReflexesRigidity changes with head movement head turned to one side limbs on that side (jaw limb) become more rigidly extended, while the contralateral limb become less flexion of the head causes flexion of the forelimbs and extension of the hindlimbs
  29. 29. III. MIDBRAIN COMPONENTS Midbrain Animal – produced by section of the neural axis at the superior border of the midbrain Chronic midbrain animal can rise to the standing position, walk, and right themselves
  30. 30. Manifestations:A. extensor rigidity – when animals lies quietly on its backB. Righting reflex – to maintain the normal standing position and keep head upright 1. head righting reflex 2. neck righting reflex 3. body righting reflexC. grasp reflex
  31. 31. IV. CORTICAL COMPONENTS Decortication (removal of the cerebral cortex) produces little motor deficit. Decorticate Animal
  32. 32. Effects of Decortication1. decorticate rigidity occurs only when animal is at rest2. Placing and Hopping reactions are disrupted Hopping movements – keep the limbs in position to support the body when animal standing is pushed laterally Placing reactions – place the foot firmly on the supporting surface
  33. 33. EQUILIBRIUM Brainstem structures, axial extensor tone, equilibrium Lesions of the medial brainstem interrupting decending reticulospinal vestibulospinal, and tectospinal systems that innervate proximal and axial muscles result in severe dysequilibrium. These brainstem efferents convey the output of networks involving the cerebellum (flocculonodular and anterior lobes), brainstem reticular and central vestibular pathways, and descending inputs from the basal ganglia, thalamus, and frontal and parietal lobes. The control of truncal posture in humans may be mediated by
  34. 34. HISTORY & COMMON SYMPTOMS OF GAIT DISTURBANCE A detailed account of the walking difficulty and its evolution provide the first clues to the underlying diagnosis. When evaluating the history it is helpful to note the particular circumstances in which the walking difficulty occurs, the leg movements most affected, and any associated symptoms. Because disorders at many levels of the peripheral and central nervous systems give rise to difficulty waling, it is necessary to consider whether the problem is caused by muscle weakness, a defect of higher motor control, or imbalance due to cerebellar disease or proprioceptive sensory loss. Walking over uneven ground exacerbates most walking difficulties, leading to tripping, stumbling, and falls. Aligamentous ankle strain or even a bony fracture may result form tripping and falling in this situation and may be presenting symptom of a gait disorder. Fear of falling may lead to a variety of voluntary protective measures to minimize the risk of injury. In some patients, particularly the elderly, compensatory strategies and a fear of falling lead to a “cautious” gait that dominates the clinical picture.
  35. 35. Weakness Weakness of the legs may be described in several ways. Complaints of stiffness, heaviness, or “legs that do not do what they are told” may be the presenting symptoms of a spastic paraparesis frequently report that they drag their legs to walk or that their legs suddenly give way, causing stumbling and falls. Weakness of certain muscle groups may be described as difficulty performing particular movements during the gait cycle,. Catching or Scraping the toe on the ground and a tendency to trip may be presenting symptom of hemiplegia (causing a spastic equinovarus foot posture) of footdrop caused by weakness of ankle dorsiflexion. Weakness of knee extension presents with a sensation that the legs will give way while standing or walking down stairs. Weakness of ankle plantar flexion intereres with the ability to stride forward, resulting in a shallow stepped gait. Weakness of certain movements may first become apparent in particular situations; for example, difficulty in climbing stairs or rising from a seated position is suggestive of proximal muscle weakness, which is most commonly caused by a myopathy.
  36. 36. CLINICAL EXAMINATION OF POSTURE AND GAIT POSTURE Trunk posture (upright or stooped) Postural reflexes (“pull test”) Stance (narrow or wide based) WALKINGInitiation (start hesitation shuffling, magnetic feet) Stepping Rhythm (regular, irregular Length (normal, short) Trajectory (shallow, high-setpping) SpeedAssociated trunk movement and arm swing.
  37. 37. Special maneuvers Heel-toe walking Romberg’s test Walking backward or running FORMAL MOTOR AND SENSORY EXAMINATION (SUPINE) Muscle bulk, tone, strength Voluntary movement Trunk movement (rolling over, standing or sitting up) leg movement when not standing or sitting up) Leg movement when not standing Tendon reflexes Sensation : Proprioception Heel-to-shin test
  38. 38. Musculoskeletal Examination Leg size and length Range of joint movement (especially hip)