Descending Spinal Tracts PDF

Descending spinal tracts Descending tracts of the spinal cord (see Fig. 8.15 ) originate from the cerebral cortex and brainstem. They are concerned with the control of movement, muscle tone, spinal reflexes, spinal autonomic functions and the modulation of sensory transmission to higher centres. Sa...

Descending spinal tracts Descending tracts of the spinal cord (see Fig. 8.15 ) originate from the cerebral cortex and brainstem. They are concerned with the control of movement, muscle tone, spinal reflexes, spinal autonomic functions and the modulation of sensory transmission to higher centres. Save to collection Share Corticospinal tracts The corticospinal tracts ( Figs. 8.20, 8.21 ) are particularly concerned with the control of voluntary, discrete, skilled movements, especially those of the distal parts of the limbs. Such movements are sometimes referred to as ‘fractionated’ movements. Corticospinal tract neurones arise from cell bodies in the cerebral cortex. The cells of origin are widely distributed in the motor and sensory cortices, including the precentral gyrus or primary motor cortex of the frontal lobe, where the large Betz cells give rise to the largest-diameter corticospinal axons. Corticospinal axons leave the cerebral hemispheres by passing through the massive subcortical fibre systems of the corona radiata and internal capsule to enter the crus cerebri of the midbrain ( Fig. 8.21 ). Fig. 8.21 The course of the corticospinal tract superimposed upon a coronal section of the brain. They then pass through the ventral portion of the pons to reach the medulla oblongata, where they form two prominent columns on its ventral surface. These are called the pyramids and, for this reason, the term pyramidal tract is used as an alternative name for the corticospinal tract. In the caudal medulla, the fibres within the pyramids undergo subtotal decussation. About 75% to 90% of fibres decussate and enter the contralateral lateral corticospinal tract , which is located in the lateral part of the spinal white matter, deep to the dorsal spinocerebellar tract; 10% to 25% of pyramidal fibres remain ipsilateral and enter the ventral corticospinal tract located lateral to the ventral median fissure. They also decussate near to their termination; as a result, the fibres of the pyramidal tract effectively innervate the contralateral side of the spinal cord and control movement of the contralateral side of the body. Hereditary spastic paraparesis Hereditary spastic paraparesis is an inherited degenerative disorder (autosomal dominant) in which progressive weakness affects the legs, leading to marked stiffness of gait. Degeneration of the lateral funiculi, including the lateral corticospinal tract, chiefly affects the thoracic spinal cord, causing a spastic paraparesis with hyperreflexia and extensor plantar responses, but with sparing of sensation and bladder function. Approximately 55% of corticospinal neurones terminate at cervical levels, 20% at thoracic and 25% at lumbosacral levels. Fibres terminate extensively in the spinal grey matter. Many of those fibres that originate from the motor cortex terminate in the ventral horn, some making monosynaptic contact with motor neurones. Save to collection Share Rubrospinal tract The rubrospinal tract originates from the red nucleus of the midbrain tegmentum ( Fig. 8.22 ). It exerts control over the tone of limb flexor muscles, being excitatory to the motor neurones of these muscles. Axons leaving the cells of the red nucleus course ventromedially and cross in the ventral tegmental decussation , after which they descend to the spinal cord where they lie ventrolateral to, and partly intermingled with, the lateral corticospinal tract. The red nucleus receives afferent fibres from the motor cortex and from the cerebellum. The rubrospinal tract, therefore, represents a non-pyramidal route by which the motor cortex and cerebellum can influence spinal motor activity. Save to collection Share Tectospinal tract Tectospinal tract fibres arise from the superior colliculus of the midbrain ( Fig. 8.23 ). Axons pass ventromedially around the periaqueductal grey matter and cross in the dorsal tegmental decussation. In the spinal cord, descending tectospinal fibres lie near the ventral median fissure and they terminate predominantly in cervical segments. The superior colliculus receives visual input and the tectospinal tract is thought to mediate reflex movements in response to visual stimuli. Save to collection Share Vestibulospinal tracts Vestibulospinal tract fibres arise from the vestibular nuclei situated in the pons and medulla, in and near the floor of the fourth ventricle ( Fig. 8.24 ). The vestibular nuclei receive input from the labyrinthine system by way of the vestibular nerve and also from the cerebellum. Axons from cells of the lateral vestibular nucleus ( Deiters’ nucleus ) descend ipsilaterally as the lateral vestibulospinal tract , which is located in the ventral funiculus. Lateral vestibulospinal tract fibres mediate powerful excitatory effects upon extensor motor neurones. They serve to control extensor muscle tone in the anti-gravity maintenance of posture. The medial vestibular nucleus contributes descending fibres to the ipsilateral medial longitudinal fasciculus , also known as the medial vestibulospinal tract , which is located adjacent to the ventral median fissure and descends as far as cervical levels. The medial longitudinal fasciculus contains fibres that link the vestibular nuclei with the nuclei innervating the extraocular muscles (oculomotor, trochlear and abducens nuclei) and is, thus, important in coordinating head and eye movements ( Chapter 9 , p 93 ; Chapter 10 , pp 103–104 ). Save to collection Share Reticulospinal tracts The reticular formation of the pons and medulla gives rise to reticulospinal fibres. Axons arising from the pontine reticular formation descend ipsilaterally as the medial (or pontine ) reticulospinal tract. Axons from the medulla descend bilaterally in the lateral (or medullary ) reticulospinal tracts. Both tracts are located in the ventral funiculus. Reticulospinal fibres influence voluntary movement, reflex activity and muscle tone by controlling the activity of both alpha and gamma motor neurones. They also mediate pressor and depressor effects upon the circulatory system and are involved in the control of breathing. White matter of the spinal cord: principal descending tracts ​ Corticospinal tract controls discrete, skilled movements, particularly of the distal extremities. It originates from motor and sensory cortices. Fibres descend through the internal capsule, crus cerebri and ventral pons to reach the medullary pyramid. Most fibres (75%–90%) decussate to form the lateral corticospinal tract, the remainder forming the ipsilateral ventral corticospinal tract. ​ Rubrospinal tract controls limb flexor muscles and originates from the red nucleus of the midbrain. Fibres cross in the ventral tegmental decussation. ​ Tectospinal tract is involved in reflex responses to visual input. It originates from the contralateral superior colliculus and fibres cross in the dorsal tegmental decussation. ​ Vestibulospinal tracts descend from the vestibular nuclei. The lateral vestibulospinal tract originates from the ipsilateral lateral vestibular nucleus and mediates excitation of limb extensor muscles. ​ Reticulospinal tracts descend from the pons and medulla. They are involved in the control of reflex activities, muscle tone and vital functions. Lesions of the spinal cord Focal lesions of the spinal cord and the nerve roots produce clinical manifestations in 2 ways: ​ 1 The lesion destroys function at the segmental level. ​ 2 The lesion interrupts descending motor and ascending sensory tracts. Damage to different parts of the spinal cord, therefore, is accompanied by distinctive clinical syndromes ( Fig. 8.25 ). Acute lesions of the spinal cord follow occlusion of the anterior spinal artery and trauma, causing fractures of the spine. Chronic compression of the spinal cord and emerging nerve roots is caused by infection and tumours of the spine, meninges and nerve roots and by prolapsed intervertebral discs. Subacute and chronic lesions of the spinal cord are commonly due to the immune disorder of multiple sclerosis. Fig. 8.25 (A) Lumbosacral spinal cord lesion. A lumbosacral cord lesion causes weakness, wasting and fasciculation of muscles, areflexia of the lower limbs (lower motor neurone lesion), incontinence, sensory loss below the level of the lesion and ‘sensory’ ataxia. Refer also to Fig. 1.48. (A) Lumbosacral spinal cord lesion. A lumbosacral cord lesion causes weakness, wasting and fasciculation of muscles, areflexia of the lower limbs (lower motor neurone lesion), incontinence, sensory loss below the level of the lesion and ‘sensory’ ataxia. Refer also to Fig. 1.48. (C) Hemilesion of the thoracic spinal cord gives rise to the Brown–Séquard syndrome. This is characterised by ipsilateral loss of proprioception and upper motor neurone signs (hemiplegia/monoplegia) plus contralateral loss of pain and temperature sensation. Refer also to Fig. 1.48. (D) Lower cervical spinal cord lesion. A lower cervical cord lesion causes weakness, wasting and fasciculation of muscles, and areflexia of the upper limbs (lower motor neurone lesion). In addition, there is spastic paraparesis, hyperreflexia and extensor plantar responses (upper motor neurone lesion) in the lower limbs, incontinence, sensory loss below the level of the lesion and ‘sensory’ ataxia. Refer also to Fig. 1.48. (E) Upper cervical spinal cord lesion. A high cervical cord lesion causes spastic tetraplegia with hyperreflexia, extensor plantar responses (upper motor neurone lesion), incontinence, sensory loss below the level of the lesion and ‘sensory’ ataxia. Refer also to Fig. 1.48.