Descending Spinal Tracts Overview

Damage to the spinal cord at a specific level, resulting in loss of function in that segment.

Damage to the spinal cord that interrupts signals traveling up and down the spinal cord, affecting motor and sensory function below the lesion.

A type of spinal cord lesion that causes weakness, muscle wasting, and loss of reflexes in the lower limbs. It also causes loss of sensation and incontinence.

A syndrome characterized by weakness and paralysis on one side of the body and loss of pain and temperature sensation on the opposite side.

A lesion in the lower part of the neck affecting the spinal cord, resulting in weakness, muscle wasting, and loss of reflexes in the arms.

A lesion in the upper neck affecting the spinal cord, resulting in weakness and paralysis in all four limbs, with increased reflexes and exaggerated responses.

A condition characterized by loss of sensation and motor control below the level of the lesion.

An interruption of the spinal cord's blood supply, often caused by trauma or blood clots.

Descending pathways in the spinal cord that control voluntary movement, muscle tone, reflexes, and autonomic functions.

The major pathway for controlling precise, voluntary movements of the limbs, especially the fingers and toes.

Large nerve cells in the cerebral cortex, responsible for generating the largest corticospinal axons.

A massive bundle of white matter fibers that connect the cerebral cortex to the brainstem.

The point where the corticospinal tract fibers cross over to the opposite side of the body.

The portion of the corticospinal tract that travels down the opposite side of the spinal cord.

The portion of the corticospinal tract that travels down the same side of the spinal cord.

A genetic disorder that causes progressive weakness and stiffness, primarily affecting the legs.

The lateral corticospinal tract is the major pathway controlling voluntary movement. Damage to this pathway primarily affects the thoracic spinal cord, causing spastic paraparesis (weakness affecting both legs), hyperreflexia (increased reflexes), and extensor plantar responses (abnormal Babinski sign). However, sensation and bladder function are spared.

The rubrospinal tract originates from the red nucleus in the midbrain and crosses to the opposite side before descending to the spinal cord. This tract primarily influences the tone of limb flexor muscles, helping to control movement and posture.

The rubrospinal tract is a non-pyramidal pathway, meaning it doesn't directly originate from the motor cortex. It receives input from both the motor cortex and cerebellum, allowing for complex coordination of movement.

The tectospinal tract originates from the superior colliculus of the midbrain and crosses to the opposite side before descending to the spinal cord. It primarily terminates in cervical segments, influencing reflex movements in response to visual stimuli.

The superior colliculus plays a vital role in visual processing and reflex movements. It receives input from the visual system, allowing the tectospinal tract to mediate rapid responses to visual stimuli, such as turning the head to look at something that suddenly catches your eye.

The lateral vestibulospinal tract originates from Deiters' nucleus in the brainstem and descends ipsilaterally (on the same side) to the spinal cord. It primarily affects extensor motor neurons, influencing posture and balance.

The vestibular nuclei receive input from the labyrinthine system (inner ear) and from the cerebellum, allowing for integration of vestibular information (sense of balance and head position) with cerebellar feedback on movement.

The vestibular nuclei, through the vestibulospinal tracts, influence extensor motor neurons, helping us maintain an upright posture and making adjustments as necessary to keep our balance. Damage to this system can lead to problems with balance and coordination.