All about Upper Motor Neuron Lesion.pptx

Upper Motor Neuron Lesion

1. Upper Motor Neuron Lesion . Paralysis that result from lesion of descending fiber between the origin of cortical motor areas and their termination on anterior horn cells in the spinal cord is called Upper Motor Neuron paralysis.

2. Features of UMN paralysis. Increase muscular tone (Spasticity) No muscular atrophy Muscle are affected in groups. Tendon reflexes are exaggerated. Superficial reflexes are lost. Extensor planter response ( Babinski’S sign positive) No fascicular twitches. No denervation potential in EMG. Normal nerve conduction studies. However, if pure corticospinal fibers are affected at medullary pyramid or experimentally produced lesion of medullary pyramid, the above mention feature are not observed. The most prominent feature of such lesion are paralysis or weakness of distal muscle of the limbs and Babinski’S sign positive. This indicate that descending fiber passing through pyramid are mostly of lateral corticospinal tract.

3. Physiological basis of features of UMN paralysis Spasticity - spasticity occurs due to increased discharge of motor neuron and increased excitability of the motor neuron pool. In UMN lesion , not only the corticospinal fibers are interrupted , but also the corticobulbar fibers are damaged. The corticobulbar fibers are inhibitory over reticulospinal and vestibulospinal tract. As the corticobulbar fibers are interrupted at internal capsule along with corticospinal tract, there is lose of inhibitory control over the reticulospinal and vestibulospinal tract, the reticulospinal and vestibulospinal tract are facilitatory to gamma motor neuron. There is increased discharged from gamma motor to muscle spindle, which may caused increased tone of extensor muscle of whole body. Hence, spascity and hypertonia are important feature of UMN paralysis. Exaggeration of deep tendon reflexes- usually UMN are inhibitory to lower motor neuron. UMN lesion , loss of inhibitory influences increases lower motor discharge i.c increased gamma motor discharged, increased sensitivity of muscle spindle to stretch. This result in increased deep tendon reflex. Absent of muscle atrophy- muscle atrophy occur either loss of blood supply or nerve supply to the muscle. In UMN lesion , the nerve supply is not interrupted. Therefore, atrophy Is not a feature of UMN paralysis.

4. Loss of superficial reflexes – the superficial reflex is a polysynaptic reflex that involved many parts of CNS. The afferent path of superficial reflex ascend up in the ascending sensory systems. The efferent path are the descending motor pathways that finally terminate in skeletal muscles. As the efferent pathway is disrupted in UMN paralysis, the superficial reflex es are abolished. Extersor Planter Response - the corticospinal tract excites the flexor motor neurons and inhibits the extensor motor neurons supplying the muscles of digits of the limbs. Therefore , normal stroking of the sole, the foot elicits planter flexion. In UMN paralysis ,disruption of corticospinal influence over the lumbosacral motor neurons causes dorsiflexion of big toe and fanning of other toes ,+ ve Babinski ‘s sign.

5. Rubrospinal Tract

6. Origin & course. Origin - Rubrospinal tract originate from red nucleus, located in the mid brain. Red nuclues receives strong excitatory input from motor cortex and cerebellum. Course - Immediately after originating from red nuclues , fiber cross over to the opposite side at the same level. After descending down through contralateral brain stem, fiber occupy the lateral column of the spinal cord. The fiber terminate on lateral group of motor neurons that innervate distal limb muscles. Rubrospinal tract excite flexor group of muscle and inhibits extensor muscles. Function - Rubrospinal tract control skilled voluntary movement. Applied - lesion of rubrospinal tract produce deficit in the distal limb muscles, especially in the flexor group of muscles. However if lateral corticospinal tract is intact, the deficit persists temporarily.