POSTURAL REFLEXES

Posture refers to the maintenance of upright position against gravity. The other function of postural reflex is to maintain balance and give background muscle tone during voluntary action.

The mechanism in the maintenance of muscle tone forms the static postural reflex and the mechanism, which maintains balance during voluntary action forms the phasic postural reflex.

These reflexes are integrated at various levels of nervous system starting from spinal cord to cerebral cortex, involving brain stem, basal ganglia, reticular formation and cerebellum. The importance of these regions in the regulation of posture can be known from the effects of experimental lesions in animals at various levels of nervous system.

Lesion of spinal cord and its effects on posture

The spinal shock that occurs in the complete section of spinal cord, results in total paralysis below the level of lesion and is due to the removal of higher center influence on the spinal cord.

During recovery, the flexor withdrawal reflex appears for noxious stimuli. The stretch reflex returns later. In both the cases the recovery is not complete and the reflexes are exaggerated. The experimental study, nevertheless, reveals the importance of spinal cord in the integration of reflexes such as stretch reflex, crossed extensor reflex, positive and negative supporting reactions.

Stretch reflex: It is a myotatic reflex responsible for maintaining muscle tone. The muscle tone forms the basis for posture regulation. Though the spinal cord integrates stretch reflex, the higher centers, such as reticular formation and vestibular nuclei regulate it.

Crossed extensor reflex: Flexion of one limb causes extension of opposite limb to maintain posture.

Positive supporting reaction: The standing posture is due to this mechanism. The dorsiflexion of toes forms the stimulus and the leg is converted into a rigid pillar by the contraction of both flexors and extensors.

Negative supporting reaction: The lifting of leg away from the ground is due to this reflex. The plantar flexion of toes forms the stimulus and the extensors are inhibited. The alternating positive and negative supporting reactions produce walking movement.

Lesion in the brainstem and its effects on postural reflexes

Decerebrate rigidity

Lesion at the upper border of pons (mid collicular section) results in decerebrate rigidity. The animal shows exaggerated extensor tone of all the four limbs and takes up a caricature of standing posture. It has no righting reflexes, but tonic labyrinthine and tonic neck reflexes are present.

The mechanism of decerebrate rigidity is due to the removal of inhibitory influences which go to medullary reticular formation. This causes the facilitatory region of reticular formation to become unopposed, resulting in increased firing of impulses in gamma motor neurons. The increased firing of γ motor neuron results in rigidity.

The medullary reticular formation receives three inhibitory inputs namely, cerebral cortex suppressor regions (2s, 4s, 8s 32), caudate nucleus of basal ganglia and anterior lobe of cerebellum (Fig. 4.61). When decerebration is done, two of the three inhibitory inputs are removed. The inhibitory influence coming from the anterior lobe of cerebellum will only be present. However, the

medullary reticular facilitatory region becomes unopposed and this causes increased firing of γ motor neurons to the muscle spindles and hence the rigidity occurs. The role of γ motor neuron’s increased discharge, as the cause for rigidity can be shown by sectioning the dorsal nerve and observing the absence of rigidity in the concerned spinal segments.

Decerebrate rigidity can also occur due to the removal of anterior lobe of cerebellum in animals.

In this case, the rigidity is caused by the increased discharge of α motor neuron. The vestibular nuclei receives inhibitory influence from two sources. One is cerebral cortex and the other is anterior lobe of cerebellum. The removal of anterior lobe of cerebellum inhibitory influence on the vestibular nuclei, results in increased discharge in the vestibulospinal tract and increases the firing of α motor neuron, giving rise to rigidity. The deafferentation in this case, does not abolish rigidity.

The decerebrate preparation gives us the understanding that the brainstem has centers, which influence the stretch reflex and also integrate righting reflexes.

Fig. 4.61: Diagram to explain the mechanism of decere-brate rigidity. The inhibitory region of reticular formation receives input from cortex, basal ganglia and cerebellum.

The activity of reticulospinal tract depends on the balance of activity between facilitatory and inhibitory regions of reticular formation. When decerebration is made, two of the three inhibitory inputs are removed and the facilitatory reticular formation will now become unopposed. Hence the rigidity of the muscle occurs

Decorticate preparation

Removal of cerebral cortex causes rigidity of the antigravity muscles, due to the removal of inhibitory influence from cortex to the medullary reticular formation. In this preparation, the righting reflexes are present, but the visual righting reflex, placing and hopping reactions are absent, as they are integrated in the cortex.

The decorticate animal shows tonic labyrinthine and tonic neck reflexes.

Tonic labyrinthine reflex is caused by the stimulation of utricle by gravity, due to the change in the position of head, which reflexly increases the tone of extensors of limbs.

Tonic neck reflex is caused by the stimula-tion of neck proprioceptors, due to the change in the position of the head and reflexly causes change in the tone of the limb muscles. If the animal is turned to one side, the extensor tone of the limbs on that side increases (jaw limbs) and in the opposite side the tone decreases. Bending the head forward, causes increase in the extensor tone in the hind limbs and decrease in the forelimbs, whereas, the bending of head backward, causes increase in the extensor tone of the fore limbs and decrease in hind limbs.

Midbrain preparation

Section at the superior border of the midbrain, results in midbrain animal. The animal shows rigidity only when placed on its back. Otherwise, it can do normal phasic postural reflexes, without any sign of rigidity. The righting reflexes are retained, barring visual righting reflex.

Righting reflexes

The righting reflexes are necessary to maintain balance and orient the head and body in relation to space.

There are five types of righting reflexes. The first four types are integrated in midbrain, while the fifth one (optical righting reflex) is integrated in the occipital cortex. The righting reflexes are:

1. Labyrinthine righting reflex 2. Neck righting reflex

3. Body righting reflex acting on the head 4. Body righting reflex acting on the body 5. Optical righting reflex.

Labyrinthine righting reflex: The stimulation of utricle by gravity due to movement of head results in reflex contraction of neck muscles and the head is held in position in relation to space.

Neck righting reflex acting on the body: The movement of head to a new position causes reflex contraction of muscles of the trunk and limbs to take up a position in relation to the change in position of head. These changes help the organism to orient itself and maintain balance.

Body righting reflex acting on the head: The movement of body also can cause reflex contraction of neck muscles, so that the head can be oriented to a new posture.

Body righting reflex acting on body: When one side of the body is stimulated by pressure and tactile receptors, the tone of the extensors on the opposite side is increased to maintain posture.

Optical righting reflex: Righting of the head also occurs, due to visual stimuli. The center which integrates this reflex is present in the occipital cortex. If labyrinthines are removed or diseased, underwater divers would find it difficult to orient themselves to reach the surface. This is especially significant when vision is impaired.

Placing and hopping reactions: A blindfolded animal which is suspended in air, when comes in contact with any hard surface, the extensor tone of limbs increases. This enables the animal to place itself on the surface. In hopping reaction, the maintenance of balance occurs, when the animal is laterally tilted. The placing and hopping reactions are integrated in the cerebral cortex.

The reflexes described above are seen, when the organism is in static position and during voluntary movement. They are grouped under static reflexes. The reflexes which occur to maintain balance during acceleration of the head are grouped under statokinetic reflexes.

Statokinetic reflexes

Posture maintenance becomes important when there is movement of head. When the head is turned to a new position in space, the tone of limb and body muscles are adjusted to maintain balance and also there is a reflex movement of eyes to fix objects in the visual field. There are two types of receptors responding to two types of acceleration. The vestibular apparatus which is also called labyrinthine apparatus consists of membranous labyrinth containing fluid filled semicircular canals and otolith organs. The semicircular canals respond to angular accele-ration (rotational movement of head) and otolith organs respond to linear acceleration of head such as forward and vertical movement of head.

Semicircular canals

They are enclosed in a bony canal in the inner ear. There are three pairs, comprising horizontal, superior and posterior canals (Fig. 4.62).These membranous canals are filled with a fluid called endolymph. It has the composition similar to ICF.

Each canal is at right angles to one another in each ear. The horizontal canal of one side is in the same plane to that of opposite side, whereas, the superior canal of one side is parallel to the posterior canal of opposite side. Each canal has a dilated part called ampulla which contains the receptors. The semicircular canals emerge from utricle which communicates with saccule. The saccule inturn is connected to cochlea.

In the ampulla, there is a mass of tissue called cristae in which the hair cells are present. The

hair cells are the receptors and the hairs are embedded in a gelatinous substance called cupula, which completely blocks the roof of ampulla (Fig. 4.63).The base of hair cells are supplied by the axons of vestibular division of VIII cranial nerve. There is a single tallest hair called kinocilium at one end of the cell. The remaining hairs show a progressive decrease in height and these are called stereocilia (Fig. 4.64).

The hairs are in a polarised state when not stimulated. The bending of stereocilia towards kinocilium causes depolarization of hair cells and

Fig. 4.62: Semicircular canals

Fig. 4.63: Diagram of cristae present in the ampulla of semicircular canal

Fig. 4.64: Hair cells in cristae

Fig. 4.66: Mechanism of stimulation of hair cells. In horizontal canals, the bending of stereocilia towards kinocilium will produce depolarization, while stereocilia bending away from kinocilium will cause hyperpolarization

stereocilia bending away from kinocilium leads to hyperpolarization (Fig. 4.66). The horizontal canal shows stimulation of hair cells as described above. The vertical canals show exactly the opposite mechanism. That is, the bending of stereocilia away from kinocilium causes depolarization of hair cells.

The otolith organs are stimulated by gravita-tional pull. The utricle responds to horizontal linear movement of head and the saccule is stimulated by vertical linear acceleration of head.

They convey information about the static position of head and also changes in its position during linear acceleration. The hair cells are present in the macula and the hairs are covered by calcium carbonate crystals called otokinia (Fig. 4.65).

Since the specific gravity of otokinia is higher than endolymph, the hairs sink within the otokinia and gravitational pull causes bending of hairs resulting in depolarization of hair cells.

Lateral tilting of head would stimulate utricle, whereas, the saccule is stimulated by the linear acceleration of the head, such as, jumping, walking and forward movement of head. The otolith organs stimulation can be noticed during travel in train,car, bus and ship. The symptoms of motion sickness are due to the excessive stimulation of otolith organs.

Stimulation of semicircular canals: There is a tonic basal discharge of impulses from these canals even during absence of rotational movement. The stimulation of the canal will occur, when the rotation is in the same plane as that of the canal. For example, rotation of the head with forward bending of head at 30^o would

stimulate the horizontal canal. The rotation of head causes movement of endolymph within the canal. Because of the inertia of the fluid, it lags behind rotational movement and when it starts moving, it will be in the opposite direction of rotational movement (Figs 4.66 and 4.67). For example, if rotation of head from right to left occurs, the endolymph in the left canal would move in the opposite direction, but it causes the bending of cupula backward and the hair cells are stimulated in the left canal. This forms the leading canal. In the right canal, the movement of endolymph causes the bending of cupula forward and the hair cells are hyperpolarised.

This canal is the trailing canal. When the speed of rotation of head is uniform, then the speed of fluid movement becomes identical to it, the cupula comes back to its normal position and stimulation stops. However, if the speed of head rotation is changed, the rate of change of speed is sensed by the stimulation of hair cells again. When rotation stops (deceleration), the endolymph moves in

Fig. 4.67: Mechanism of stimulation in horizontal canal. The left canal is the leading canal and the right canal is the trailing canal

Fig. 4.65: Otolith organs

opposite direction in the canal, causing the stimulation in the trailing canal and inhibition in the leading canal. At the end of rotation, there is a feeling to fall towards the opposite direction of rotation. This is due to the changes described in the canal at the cessation of rotation. Thus, we observe that the semicircular canals send information to the brainstem about the beginning of rotation, rate of change of speed of rotation and end of rotation.

In the case of vertical canals, the stimulation of superior canal of one side will cause the inhibition of posterior canal of opposite side and vice versa.

Vestibulo ocular reflex

During rotational movement, the eyes move in the opposite direction for visual fixation of objects.

This reflex occurs due to the stimulation of semicircular canals. The connection from vestibular nuclei in the medulla, to the III, IV and VI cranial nerve nuclei through medial longi-tudinal bundle is responsible for the reflex response.

Nystagmus

The jerky movement of the eye at the beginning and end of rotation is known as nystagmus. It is a reflex,which helps in the visual fixation of stationary objects when the body rotates At the start of rotation, the eyes move slowly in a direction opposite to the direction of rotation.

Then the eyes quickly move to a new fixation point. This is followed by slow movement in the opposite direction. The quick component of eye movement during nystagmus gives the direction of rotation. When rotation stops, the quick component will be in the opposite direction of rotation (post-rotatory nystagmus). The slow component is due to the impulses coming from labyrinths and the quick component occurs due to the activity of brain stem. Lesion of labyrinths or cerebellum results in spontaneous nystagmus.

That is, without any rotational movement the nystagmus occurs and is abnormal.

Central vestibular connections

The axons (vestibular division of VIII cranial nerve) coming from hair cells of membranous labyrinths and otolith organs, reach the brain stem and end in four groups of vestibular nuclei (superior, inferior, medial and lateral). The lateral nucleus (Deiter’s nucleus) sends descending fibers to the spinal cord forming vestibulospinal tract (Fig. 4.68). The vestibular nuclei receive connections (inhibitory) from cortex and cerebellum. It also sends connections to vestibulo cerebellum. The medial longitudinal bundle from vestibular nuclei sends connections to 3rd, 4 th and 6 th cranial nerve nuclei. The vestibulo spinal tract activity helps to change the tone of extensors of limbs and body during change in position of head. The connections from vestibular nuclei to cranial nerve nuclei supplying ocular muscles help to give visual fixation of objects during movement of head.

Effects of excessive stimulation of vestibular apparatus

During motion in train, bus, ship, car, elevators, etc. the labyrinths are under constant stimulation and this leads to autonomic disturbances like headache, vertigo, nausea, vomiting, sweating and changes in blood pressure. These symptoms are called motion sickness.

Fig. 4.68: Connections of vestibular nuclei

Vertigo: It is false sense of rotation when actual rotation is not present. This occurs in motion sickness, and clinical stimulation of semicircular canals.

Clinical stimulation of semicircular canals is done by irrigating the ear with cold or warm saline with the help of a syringe. The temperature difference between the saline and endolymph will cause convection currents, resulting in stimulation of the canal and symptoms of nystagmus, vertigo, nausea, etc, will occur. The canal is also stimulated clinically by using Barany chair and subjecting the individual for rotation in the horizontal direction. This stimulates the horizontal canal and the symptoms described above can be noticed.

THALAMUS

It is a mass of grey matter consisting of two thalami. The two thalami are connected by massa intermedia, which contain midline group of intrinsic nuclei.In each thalamus, there is a intralaminar group, which also contain intrinsic nuclei.

There are specific and nonspecific nuclei which are concerned with the regulation of cortical activity, visceral functions, emotion, sensory and motor functions.

The specific nuclei of thalamus are divided as follows (Fig. 4.69):

Anterior nucleus Dorsal

Dorsomedial Dorsolateral Ventral

Anterior lateral Posterior lateral Medial

Pulvinar

Lateral geniculate body Medial geniculate body Reticular nucleus

Connections of thalamic nuclei Thalamo-cortical-thalamic circuit

The thalamic nuclei, especially the midline group, intralaminar group, dorsomedial and lateral groups send projections to neocortex and from neocortex, there are connections coming back to thalamus forming a circuit (thalamo-cortical-thalamic circuit). This is responsible for both cortical and thalamic activity. The electrical activity (EEG)of cortical neurons is due to the activity of thalamocortical projections.

Anterior nucleus

The afferents come from the mammillary body of hypothalamus and the efferents go to cingulate gyrus. This forms part of the circuit for emotion.

Dorsomedial

It receives connections from striatum and hypo-thalamus and sends efferents to cortex.

Ventral anterior

Afferents from globus pallidus and substantia nigra go to this nucleus. The efferents are projected to the frontal cortex.

Ventrolateral

Fibers from dentate nucleus of cerebellum go to this nucleus directly or through red nucleus.

Efferent connections from here go to frontal lobe.

Fig. 4.69: Nuclei of thalamus VA ventral anterior; VL ventrolateral;

PVM posteroventromedial; PVL posteroventrolateral;

LGB lateral geniculate body; MGB medial geniculate body

Ventral posterior lateral (VPL)

It receives sensory projections from spinal and medial lemnisci, which carry protopathic and

It receives sensory projections from spinal and medial lemnisci, which carry protopathic and