1. PHYSIOLOGY OF POSTURE,MOVEMENTAND
EQUILIBRIUM
PROF.A.V.SRINIVASAN, MD, DM, PhD, F.A.A.N, F.I.A.N,
I
Emeritus Professor, The
Tamilnadu Dr.M.G.R. University,
Former HOD
INSTITUTE OF NEUROLOGY
MADRAS MEDICAL
COLLEGE,CHENNAI

2. Control of Posture
and Movement
 Somatic motor activity
depends on the pattern and
rate of discharge of spinal
motor neurons.
These neurons, the final
common paths are bombarded
from array of pathways.

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. 2. Extrapyramidal System - they
adjust
body posture to provide stable
background for movement.
Concerned
with grosser movements and
posture
3.Cerebellum – coordinating and

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.  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

7. CORTICOSPINAL
TRACT

8. Anatomy and Function

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. Cortical Motor Areas

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

13. The cortical representation of
each body part is
proportionate in size to the
skill with which the part is
used for fine, voluntary
movement.

14. Effects of Section or Destruction
of Pyramidal System
A. 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

15. These deficits are consistent with loss of
control of distal musculature of the limbs ,
which is concerned with fine skilled
movements
 Lesions of Ventral Corticospinal
Tract
 produce axial muscle deficits
that cause difficulty with
balance, walking and climbing

16. 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

17. POSTURE-REGULATING
SYSTEMS ( Extrapyramidal
Mechanisms)

18. When the neural axis is
transected, the activities below
the section are cut off or
released from the “control of
higher brain centers” and often
appear to be accentuated

19. Levels of Integration

20. 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

21. The recovery of the reflex
excitability may be due to:
* development of denervation
hypersensitivity to the mediators
by the remaining spinal
excitatory endings
* sprouting of collaterals from
existing neurons

22. 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. II. MEDULLARY COMPONENTS

24.  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

25. 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

27. Characteristics of
Decerebrate Rigidity

28. 1. Decerebrate Posture –
“ Caricature of the normal standing position”
– neck and limbs extended, back arched,
tail elevated.

29. 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

30. 3. Tonic Neck Reflexes
Rigidity 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

31. 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

32. Manifestations:
A. extensor rigidity – when
animals lies quietly on its back
B. Righting reflex – to maintain
the normal standing position
and keep head upright
1. head righting reflex
2. neck righting reflex
3. body righting reflex
C. grasp reflex

33. IV. CORTICAL COMPONENTS
 Decortication (removal of
the cerebral cortex) produces
little motor deficit.
Decorticate Animal

34. Effects of Decortication
1. decorticate rigidity occurs only when
animal is at rest
2. 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

35. 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

36. 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.

37. 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.

38. CLINICAL EXAMINATION OF
POSTURE AND GAIT
POSTURE
 Trunk posture (upright or stooped)
 Postural reflexes (“pull test”)
 Stance (narrow or wide based)
WALKING
Initiation (start hesitation shuffling, magnetic feet)
Stepping
 Rhythm (regular, irregular
 Length (normal, short)
 Trajectory (shallow, high-setpping)
 Speed
Associated trunk movement and arm swing.

39. 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

40. Musculoskeletal Examination
 Leg size and length
 Range of joint movement (especially
hip)