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THE UPPER MOTOR NEURON

The upper motor neuron has its cell (Betz,s cell) in the area of the cerebrum. The axons pass

through the internal capsule, pons and medulla. In the spinal cord, they form the lateralcorticospinal tract of white matter and the fibers terminate in close association with the cells of

the lower motor neuron.

The axons of most upper motor neurons decussate (intersect) either in the medulla or in-the

spinal cord just before they terminate.

Upper motor neurons (UMN) are responsible for conveying impulses for voluntary motor

activity through descending motor pathways that make up the upper motor neurons.UMN send fibers to the LMN, and that exert direct or indirect supra nuclear control over the

LMN of the cranial and spinal nerves..

Axons from the cortical areas form the cortico spinal and corticobulbar tracts.

1/3 from primary motor cortex (Betzs cell axons -3-5%, and other 95% from smallneurons)

1/3 from the somatic sensory cortex (areas 1, 2, and 3), and

adjacent temporal lobe region.

Upper motor neuron control lower motor neuron through two different pathways Pyramidal tract Extra pyramidal tract

PYRAMIDAL TRACTS

corticospinal tract

EXTRAPYRAMIDAL TRACTS- Reticulospinal

Olivospinal

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Vestibulospinal Tectospinal

Rubrospinal tract Corticobulbar tract

Corticorubral tract

UMN

Maintenance of posture and balance, the co-ordination of muscle movement and the control of

muscle tone.

Spinal reflexes-- A reflex action is an immediate motor response to a sensory stimulus.

Many connector and motor neurons may be stimulated by afferent impulses from a small area of

skin, e.g., the pain impulses initiated by touching a very hot surface with the finger are

transmitted to the spinal cord by sensory nerves. These stimulate many connector and lowermotor neurons in the cord which results in the contraction of many skeletal.

Reflex Composed of three elements:

1. Sensory neurons

2. Connector neurons in the spinal cord and

3. Lower motor neuron

UPPER MOTOR NEURON LESION Loss of dexterity, voluntary skillful movements. (corticospinal)

Babinski sign(corticospinal) Loss of superficial reflex (corticospinal) weakness with no muscle atrophy

Spasticity is hallmark of the UMN disease. Spasticity is a state of sustained increase inmuscle tension in response to muscle lengthening, in particular, with passive movements.

Hyperreflexia. deep tendon reflex

Pseudobulbar palsy is feature of the UMN disorder

PSEUDOBULBAR PALSY Results from an upper motor neuron lesion to the corticobulbar pathways in the

pyramidal tract.

It results frombilateral lesion of UMNs

of the muscles of the tongue (XII), face (VII),speech and swallowing (IX,X).

Individuals with pseudo bulbar palsy also demonstrate inappropriate emotional suddenoccurrence.