PHYSIOLOGY OF POSTURE,MOVEMENT

Dr kamplo D
I

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

3.Cerebellum – coordinating and smoothing

movements
 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
• 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
CORTICOSPINAL

TRACT
Anatomy and Function
• 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 concerned

with skilled movements
Cortical Motor Areas
• 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
The cortical representation of
each body part is
proportionate in size to the
skill with which the part is
used for fine, voluntary
movement.
 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 fashion and
can stand and walk
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
 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
POSTURE-REGULATING SYSTEMS
( Extrapyramidal Mechanisms)
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
Levels of Integration
 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
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
 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 and
rectum, sweating, pallor
II. MEDULLARY COMPONENTS
 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 diffuse

facilitation of stretch reflexes
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
Characteristics of Decerebrate
Rigidity
1. Decerebrate Posture –
“ Caricature of the normal standing position”
– neck and limbs extended, back arched,
tail elevated.
 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
 when prone, the rigidity is minimal
 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

 extension of the head causes flexion of the

hindlimbs and extension of the forelimbs
 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
 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
 IV. CORTICAL COMPONENTS

• Decortication (removal of the cerebral

cortex) produces little motor deficit.
Decorticate Animal
 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
 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 similar networks.
 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.
 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.
 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.
 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
 Musculoskeletal Examination

• Leg size and length

• Range of joint movement (especially hip)