Descending tracts

At the end of the class, Student should be able to:• Classify descending tracts. a) Pyramidal tract b) extrapyramidal tract• Describe origin, course termination of the descending

tracts.• Functions of the descending tracts.• Differences between pyramidal & extrapyramidal tract• Differences between lower & upper neuron lesion

Functions of pyramidal tracts

Tracts : Lateral corticospinal tractsFunction: Controlling the voluntary movements- fine,

precise movements of the fingers and hands to carry out skilled work.

Tracts : Anterior corticospinal tracts Function: Control of muscles of trunk & proximal

portions of the limbs to carry postrual adjustments and gross movements

• They form a part of the pathways for superficial reflexes such as cremasteric, abdominal and plantar reflexes.

• Some corticospinal fibers end at excitatory synapses on α and γ-motor neurons, whereas other end on interneurons that may excite or inhibit the α-motor neurons. Thus the effect of the corticospinal pathway on the α-motor neurons may be excitatory or inhibitory.

• Some fibers transmit information from the brain to ‘afferent’ neurons and so can effect afferent system, they do this by ending either:

(a) Presynaptically on the axon terminals of afferent neurons as these fibers enter the CNS; or (b) directly on the dendrites or cell bodies of neurons in the ascending pathways

• Corticospinal fibers arising from the somatic sensory area (I and II) and parietal lobe association cortex are concerned with sensory-motor coordination. For example, aiming the hands towards it, hand-eye coordination etc. lesion of these areas causes defects in motor performance that are characterized inability to execute learned sequences f movements such as eating with a knife and fork.

Functions of corticobulbar (corticonuclear) tracts

• These are responsible for voluntary control of muscles of larynx, pharynx, palate, upper and lower face, jaw, eye etc. Pseudobulbar Palsy is a condition resulting in paralysis or weakness of the muscles which control swallowing, talking, tongue and lip movements due to bilateral lesion of these tracts.

EXTRAPYRAMIDAL TRACTS

• Extrapyramidal system is made up of those areas the CNS (other than the pyramidal and cerebellar system) that are concerned with muscular movements and posture. Its fibers have many synapses in their descending path with cells of the nuclear masses on the way which include: nuclei of the cerebral cortex, basal ganglia, hupothalamus and nuclei of the reticular formation in the brain stem. In the spinal cord the fibers form separate groups according to their site of origin.

FUNCTIONS OF EXTRAPYRAMIDAL TRACTS• Corticobulbar (corticonuclear) fibers control the movements

of the eye balls.• They are responsible for control of tone, posture and

equilibrium (rubrospinal- for tone and posture; tectospinal- for visuospinal reflex; vestibulospinal -for the equilibrium).

• They control complex movements of the body and limb such as coordinated movements of arms and legs during walking.

• They exert tonic inhibitory control over the lower centres. Their damage increases rigidity of the muscles, called release phenomenon.

• If the pyramidal tracts are damaged, they can carry out voluntary movement to some extent.

Descending pathways that contribute to the extrapyramidal system

TRACTS DESCRIPTION(ORIGIN AND COURSE) Main function

1. Rubrospinal tract

It originates from the Red nucleus (nucleus Magnocellularis i.e. large nucleus ) located in the mid brain; crosses immediately to the opposite side, some fibers end in the cerebellum. The tract does not extend below the thoracic region.

Facilitatory influence over flexor muscle tone.

2. Tectospinal and tectobulbar tract

It originates from the superior colliculus (which is an optic centre); crosses at once to the opposite side. The tract descends upto the lower cervical region.

Mediate reflex postural movements in response to visual and auditory stimuli.

3. Reticulospinal tract

Origin from neurons of the reticular formation in pons and medulla.(i)Medial division i.e. fibers from the pontine reticular formation are mainly crossed (ii)Lateral division i.e. medullary reticular fibers descend uncrossed.

(i) Facilitate or inhibit voluntary movements, mainly influence γ–motor neurons.

(ii) Alteration in muscle tone, respiration and blood pressure

4. Vestibulospinal tract

Origin: from lateral vestibular nucleus located at the junction of pons and medulla. It receives fibers from the vestibular division of VIII nerve. Both lateral and medial division descend uncrossed throughout the entire length of the spinal cord

Facilitatory influence upon reflex activity in the spinal cord and upon the mechanism which control muscle tone (mainly extensor group i.e. antigravity group of muscles).

5. Medial longitudinal fasiculus (orbundle)

Origin: from the medial vestibular nucleus, reticular formation, superior colliculus and interstitial nucleus of Cajal; the tract descend uncrossed upto upper cervical region

Coordinator of reflex ocular movements and integration of eye and neck movements.

Major differences between pyramidal exrapyramidal tracts

Pyramidal tracts Extrapyramidal tracts

1. Origin Origin

2. Its axons pass without relay to the spinal segmental levels where they form synapses with either interneurons in the dorsal horn or directly with the motor neurons themselves.

They have many synapses in their descending path with cells of nuclei of the striatum (caudate and putamen), the globus pallidus, the hypothalamus and the nuclei of the reticular formation.

3. They have grater influence over motor neurons that control muscles involved in the fine movements, particularly those of the fingers and hand.

They are more involved with coordination of the large muscle groups used in the maintenance of upright posture, in locomotion, and in head and body movements when turning towards a specific stimulus.

4. Lesion of this tract produces ‘spasticity’ in the muscles involved.

Its lesion produces ’rigidity’ of the involved muscles.

Differences between lower and upper motor neuron lesion

Lower motor neuron lesion(LMNL) Upper motor neuron lesion(UMNL)

1. It is due to lesion of the lower neurons (LMNs) i.e. the spinal and cranial motor neurons that directly innervate the muscles

It is due to lesion of the upper motor neurons (UMNs) i.e. the neurons in the brain and spinal cord that can influence the activity of LMNs; major cause being lesion of pyramidal tracts.

2. Here usually single or individual muscle is affected.

It involves a group of muscles.

3. Muscle becomes completely paralysed (flaccid paralysis). This is due to complete loss of muscle tone which depends on integrity of the reflex arc.`

Affected muscles due to pyramidal tract lesion become hypertonic (spastic paralysis). This is due to:(i)Release phenomenon i.e. loss of higher inhibitory control; and (ii)Denervation hypersensitivity of centres below the transection.

4. Disuse atrophy of the muscle occurs i.e. shrinkage of muscle fiber which is finally replaced by fibrous tissue(fibrous muscle).

The Muscle atrophy is not severe (if present, very mild) because muscles though not used in the voluntary movements are continuously in action to maintain posture by ‘reflexes’.

5. All reflexes (superficial or deep) are absent (lost) as the motor pathway is damaged

(i) Deep reflexes are hyperactive (accentuated) because of increased γ-motor discharge; and ii) Superficial reflexes; only abdominal, cremastric and anal reflexes are lost.

6. Babinski plantar response: Babinski sign not elicited.

Babinski sign: positive (abnormal). In UMNL, stroking outer edge the sole of the foot with firm tactile stimulus produces first an upward movements (dorsiflexion) of the great toe and fanning out (abduction) of the small toes. This is due to contraction of extensor hallucis longus (Anatomists misleadingly call it an ‘extensor response’), physiologically a ‘flexor’ (withdrawal response. (note: All the muscles which contract during a flexor response are called physiological flexors.)