Reticulospinal Tract

Introduction[edit | edit source]

Reticulospinal tract: origin in the brainstem

Reticulospinal tract is a descending tract present in the white matter of the spinal cord, originating in the reticular formation (the archaic core of those pathways connecting the spinal cord and the brain). It consists of bundles of axons that carry information or orders from the reticular formation in the brainstem to the peripheral body parts.

The Reticulospinal tract is responsible primarily for locomotion and postural control. The Reticulospinal tract is comprised of the medial (pontine) tract and the lateral (medullary) tract.[1] It is part of the Extrapyramidal system.

Anatomy[edit | edit source]

Reticulospinal tract

Origin: The reticulospinal tract comprises of two parts:

  1. Medullary Reticulospinal Tract, arises from the nuclei of reticular formation located in the medulla of the brainstem.
  2. Pontine Reticulospinal Tract, arises from those nuclei of reticular formation which are present in pons.[2]

Course

  1. Medial Reticulospinal Tract (Pontine): Descends ipsilaterally in the anterior funiculus [1] Responsible for controlling axial and extensor motor neurons e.g enable extension of the legs to maintain postural support ; Stimulation of the midbrain locomotor centre can result patterned movements (e.g. stepping)[3]
  2. Lateral Reticulospinal tracts (Medullary): Descends bilaterally in the lateral funiculus [1] Responsible for flexor motor neurons [2]; Inhibits the medial reticulospinal tract and therefore extensor motor neurones enabling modulation of the stretch reflex [4]

Both the lateral and medial tracts act via interneurons shared with the corticospinal tract on proximal limb and axial muscle motor neurons.[1]

Function[edit | edit source]

Locomotion

Motor activity: The reticulospinal tract is one of the most important extra-pyramidal tracts for controlling the activity of lower motor neurons. It can influence the activities of the alpha and gamma motor neurons through interneurons neurons. The fibers of the reticulospinal tract can inhibit or stimulate motor activity.[5][2]

Posture Maintenance: The reticulospinal tract is essential for maintaining the posture of the body.

Control of Autonomic Functions: eg heart rate, circulation, breathing, respiratory rate[6]

Control of Sympathetic and Parasympathetic Outflow: The autonomic fibers in the reticulospinal tract also control the sympathetic outflow as well as the sacral parasympathetic outflow.[5]  

Locomotion: When generating movements in two sides of the body within humans, it results in reciprocal inhibition of the flexors and extensors. Primate studies have suggested that the  reticulospinal tract may facilitate flexors and suppress extensors ipsilaterally, and facilitate extensors and suppress flexors contralaterally[7]

  1. In animal studies, central pattern generators (CPGs) are found to be responsible for locomotion generation. As locomotion is generated by internuncial neurons in the cervical and lumbar regions, activating the flexors and extensors, the intermediate gray matter is able to initiate rhythmical movements.[1]
  2. In humans, locomotion is generated in the locomotion centre in the midbrain. The premotor cortex which is responsible for the overarching control of locomotion projects to the brainstem and therefore reticulospinal tract. As a consequence, the reticulospinal tract is able to modulate control of locomotion when working with the corticospinal tract.[1] [8]The reticular formation, due to its role in attention and conscious perception, can result in a specific reaction to sensory information. The cortico-reticulospinal tract is thereby responsible for transmitting excitatory and inhibitory information to be processed before being passed to the spinal cord.[3] The cerebellum however is thought to be responsible for error correction and motor learning in gait, and the lateral hypothalamus is responsible for goal direction for locomotion e.g. hunger. [3]

Pathology[edit | edit source]

Spastic paraplegia

Lesions to the cortico-reticulospinal system can result in decreased postural control and reduced selectivity of postural control.[3] If the excitatory fibres in the reticular formation have a leison this can result in hypotonia by the loss of descending excitatatory impulses to the spinal cord. Conversly in the inhibitory fibres are disrupted in the reticular formation this could result in hypertonia (spasticity) As the lateral reticulospinal's is involved in inhibition, if this pathway is disrupted it can result in spasticity [4]. In addition due to the lack of descending inhibition, the medial reticulospinal tract  would then maintain spasticity in the musculature.[4]

References[edit | edit source]

  1. 1.0 1.1 1.2 1.3 1.4 1.5 Fitzgerald MJT, Gruener G, Mtui E. Clinical neuroanatomy and neuroscience. Fifth Edition. Philadelphia: Elsevier Saunders, 2007
  2. 2.0 2.1 2.2 Crossman AR, Neary D. Neuroanatomy. An Illustrated colour text. Third Edition. Philadelphia: Churchill Livingstone, 2005
  3. 3.0 3.1 3.2 3.3 Gjelsvik BEB. The bobath concept in adult neurology. Stuttgart: Thieme, 2008
  4. 4.0 4.1 4.2 Trompetto C, Marinelli L, Mori L, Pelosin E, Currà A, Molfetta L, Abbruzzese G. Pathophysiology of spasticity: Implications for neurorehabilitation. BioMed research international. 2014 Oct 30;2014.
  5. 5.0 5.1 Brain made simple Reticulospinal tract Available;https://brainmadesimple.com/reticulospinal-tract/#Physiology (accessed 27.4.2022)
  6. Zaaimi B, Edgley SA & Baker SN( 2009 ). Reticulospinal and ipsilateral corticospinal tract contributions to functional recovery after unilateral corticospinal lesion. 2009 Abstract Viewer/Itinerary Planner , Programme No. 568.529 . Society for Neuroscience , Washington, DC .
  7. Davidson AG, Schieber MH, Buford JA. Bilateral spike-triggered average effects in arm and shoulder muscles from the monkey pontomedullary reticular formation. The Journal of neuroscience. 2007 Jul 25;27(30):8053-8.
  8. Drew T, Prentice S, Schepens B. Cortical and brainstem control of locomotion. Progress in brain research. 2004 Dec 31;143:251-61.