Neurology: Corticospinal Tracts Overview

A tract in the brainstem that originates from the vestibular nuclei and controls extensor muscle tone for maintaining posture.

A tract in the brainstem that originates from the reticular formation in the pons and medulla, influencing voluntary movement, muscle tone, and reflex activity. It also plays a role in controlling breathing and blood pressure.

The descending tract from the motor and sensory cortices that controls precise, skilled movements, especially in the hands and feet.

The descending tract from the red nucleus in the midbrain that primarily controls limb flexor muscles.

A descending tract from the superior colliculus that controls reflex responses to visual stimuli, particularly rapid head movements.

The part of the vestibulospinal tract that originates from the lateral vestibular nucleus and primarily excites extensor muscles.

The part of the vestibulospinal tract that originates from the medial vestibular nucleus and is involved in coordinating head and eye movements. It is located in the medial longitudinal fasciculus.

A bundle of fibers that connects the brainstem with the spinal cord, carrying information for various motor functions, including the medial vestibulospinal tract.

Descending tracts of the spinal cord that originate from the cerebral cortex and brainstem, controlling various functions like movement, muscle tone, reflexes, and sensory modulation.

Large nerve cells in the cerebral cortex that are the origin of the corticospinal tracts. They play a crucial role in initiating voluntary movements.

A collection of nerve fibers that connect the cerebral cortex to the spinal cord, transmitting information from the brain to lower regions.

A prominent structure visible on the ventral surface of the medulla oblongata, formed by corticospinal fibers before they cross over.

The process by which a significant portion of the corticospinal fibers cross over to the opposite side of the spinal cord.

A tract located in the lateral part of the spinal cord, containing fibers that have crossed over from the opposite side of the brain.

A tract located on the same side of the brain and spinal cord as its origin, containing a smaller percentage of corticospinal fibers.

A condition characterized by spasticity, increased reflexes, and extensor plantar responses, often caused by damage to the lateral corticospinal tract in the spinal cord, typically affecting the thoracic region.

A part of the central nervous system that primarily coordinates motor functions, including muscle control and movement coordination.

A group of nerve cells located in the ventral horn of the spinal cord that directly innervate and control skeletal muscles.

The movement of a limb, controlled by the nervous system, in response to a stimulus, often visual or auditory.

A lesion in the spinal cord can interrupt descending motor and ascending sensory tracts, leading to specific clinical syndromes based on the affected area.

Damage at the level of the spinal cord segment directly affects the muscles and sensory function in that specific segment.

An acute spinal cord injury, often caused by trauma or a stroke, damages the spinal cord quickly.

Chronic spinal cord damage develops gradually over time, often due to conditions like tumors, infections, or disk herniation.

Multiple sclerosis, an autoimmune disorder, can cause gradual damage to the spinal cord, often leading to subacute or chronic lesions.

A lesion in the lumbosacral spinal cord causes weakness, wasting, and fasciculations in the lower limbs. The lower limbs are also areflexic, meaning reflexes are absent. Additionally, incontinence, sensory loss below the lesion, and sensory ataxia (impaired coordination) are present.

A lesion in the lower cervical spinal cord leads to weakness, wasting, and fasciculations in the upper limbs, along with areflexia. The lower limbs exhibit spastic paraparesis, hyperreflexia, and extensor plantar responses. Additionally, incontinence, sensory loss below the lesion, and sensory ataxia are present.

A Brown-Séquard syndrome is characterized by an ipsilateral loss of proprioception and upper motor neuron signs, such as hemiplegia or monoplegia. Contralaterally, there is a loss of pain and temperature sensation.