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Physiology of posture movementand equilibrium
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
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
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.
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
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
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
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
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