Descending tracts of the spinal cord
Like a machine, the human body is a delicate balance of signal reception and output generation. The input signals are sensory experiences from the outside world which are detected by special receptors in the body. These receptors are connected to neurons which ascend and transmit signals to the brain for processing and interpretation, which become our sensory experiences.
Output comes in the form of movement: signals are initiated by specific neurons in the brain. The latter and other connecting neurons then transmit these signals to the rest of the body. This article will focus on the various descending tracts of the spinal cord or descending pathways—creating and transmitting the output—which are responsible for initiating both voluntary and involuntary motion, as well as regulating muscle tone, reflexes, and visceral functions.
- Corticospinal tract
- Corticobulbar tract
- Rubrospinal tract
- Tectospinal tract
- Reticulospinal tract
- Vestibulospinal tract
- Clinical notes
- Related diagrams and images
The corticospinal tract originates in the motor cortex, which is located in the precentral gyrus of the brain’s cerebral cortex. Depending on where the neurons originate within the gyrus, they will supply different regions of the body. For example, the foot and leg are controlled by neurons which originate in the inner, medial part of the gyrus; whereas the arms, hands, face, tongue, trunk, etc., are controlled by neurons which originate from the outer, lateral surface. This layout is often represented as a little cartoonish person with body parts proportional to the input they receive from their corresponding areas within the motor cortex. It is referred to as the homunculus. The sensory information received from the body by the somatosensory cortex is often depicted with a similar figure.
The corticospinal tract controls muscle movement within the trunk and extremities. It operates in a two-neuron sequence. The cell body of the first neuron is located in the motor cortex of the brain, and as such, is referred to as the upper motor neuron (UMN).
The motor fibers, or axons, of the UMNs first converge in a structure called the corona radiata and project ipsilaterally (on the same side) from the cortex through the anterior two-thirds of the posterior limb of a structure called the internal capsule. The internal capsule is a region of the brain which transmits signals to and from the cerebral cortex; it contains only axons and no cell bodies.
From the internal capsule, corticospinal fibers continue to descend ipsilaterally through the crus cerebri in the midbrain, the pons, and the medulla. Upon reaching the caudal medulla, the majority of the axonal fibers decussate (cross the midline) so as to continue their descent in the spinal cord contralaterally (on the opposite side of the body) from whence they originated. Like in the motor cortex, the axonal fibers in the corticospinal tract are arranged somatotopically – that is, they are arranged by the regions of the body they supply.
Each UMN eventually synapses with a second neuron, the lower motor neuron (LMN). The cell bodies of LMNs are located in the anterior (ventral) horn of the spinal cord. The axons of LMNs leave the spinal cord and synapse at the neuromuscular junction (NMJ), activating effector muscles and producing movement. In short, the corticospinal tract allows the left motor cortex to send signals and facilitate voluntary movement of the right-sided limbs; whereas the right motor cortex to sends signals and facilitates voluntary movement of the left-sided limbs.
- oculomotor (III)
- trochlear (IV)
- mandibular component of the trigeminal (V3)
- abducens (VI)
- facial (VII)
- glossopharyngeal (IX)
- vagus (X)
- spinal accessory (XI)
- hypoglossal (XII) nerves
UMNs descending from the cortex to the CN nuclei are considered part of the corticobulbar tract; whereas LMNs are considered as part of the CNs themselves, with their cell bodies in the CN nuclei and their axons projecting to the muscles of the face, head, and neck.
Corticobulbar motor fibers arise from the frontal eye fields (a region in the caudal portion of middle frontal gyrus), motor cortex (the precentral gyrus), and somatosensory cortex (the postcentral gyrus) where they travel from the cortex through the internal capsule and to the CN nuclei in the brainstem.
Fibers originating from the frontal eye fields project to two regions: the rostral interstitial nucleus of the MLF (riMLF), known as the vertical gaze center; and in the paramedian pontine reticular formation (PPRF), the horizontal gaze center. Fibers from these two gaze centers then project to CN III, CN IV, and CN VI motor nuclei.
The frontal eye fields and parietal eye field also provide cortical input to the superior colliculus, which also provides input to the riMLF and PPRF. The riMLF is part of the medial longitudinal fasciculus (MLF), a bundle of ascending and descending fibers (though mainly ascending) arising from the medial vestibular nucleus, reticular formation, and superior colliculus.
Fibers originating from the somatosensory and motor cortices project to all other cranial nerve motor nuclei (except the aforementioned CN III, IV, and VI).
- CN III, CN IV, and CN VI - They provide motor innervation to the extraocular muscles. CN III innervates the superior, medial, and inferior recti, the inferior oblique, and levator palpebrae superioris. CN III also influences the sphincter pupillae and ciliary muscles of the eye via parasympathetic autonomic fibers originating from the Edinger-Westphal nucleus in the midbrain. This provides the efferent (motor) component of the pupillary light reflex. Of the remaining extraocular muscles, CN IV innervates the superior oblique, and CN VI innervates the lateral rectus.
- CN V3 - It provides motor input to the muscles of mastication. This includes the masseter, temporalis, and medial pterygoids, which act to close the jaw; and the lateral pterygoids, which acts to open the jaw. CN V3 also transmits sensory information from the lower third of the face to the brain. In fact, CN V3 is the only component of the trigeminal nerve (CN V) with a motor component: the ophthalmic (V1) and maxillary (V2) components of CN V transmit only sensory information from the upper and middle thirds of the face, respectively.
- CN VII - It innervates the muscles of facial expression via five branches: the temporal, zygomatic, buccal, marginal mandibular, and cervical. Examples of innervated muscles include the orbicularis oculi, risorius, and platysma, among many others. CN VII also plays a role in audition: by innervating the stapedius muscle in the ear, CN VII prevents the small stapes bone from moving too much, decreasing the amplitude of sound waves transmitted to the inner ear. CN VII is also responsible for transmitting taste sensation from the anterior two-thirds of the tongue.
- CN IX - It is primarily sensory, making up the afferent (sensory) component of the gag reflex. Motor fibers in this nerve innervate a single muscle in the pharynx, the stylopharyngeus. CN IX also transmits taste sensation from the posterior third of tongue.
- CN X - It has a number of functions. In terms of motor function, CN X innervates the majority of the pharyngeal and laryngeal muscles via the nucleus ambiguous, and as such is responsible for the efferent component of the gag reflex. Additionally, CN X transmits visceral sensory information to the brain, and provides parasympathetic autonomic nervous innervation to the heart, lungs, and upper gastrointestinal system.
- CN XI - It provides motor innervation to the sternocleidomastoid and trapezius muscles of the neck and shoulders
- CN XII - It innervates the majority of muscles making up the tongue.
The rubrospinal tract is primarily concerned with the control of the flexor muscles: the neurons in this tract function to facilitate flexion and inhibit extension.
The tract originates in the red nucleus of the midbrain. Its axons cross the midline within the midbrain at the ventral tegmental decussation and descend in the contralateral spinal cord in all levels. The dorsal part of red nucleus receives input from the region of the sensorimotor cortex dedicated to the upper limb, and supplies the cervical spinal segments; the ventral part of the red nucleus receives input from the region of the sensorimotor cortex dedicated to the lower limb, and supplies the lumbosacral spinal segments.
The axonal fibers of the rubrospinal tract terminate on interneurons which in turn project to neurons in the ventral horn of the spinal cord.
The tectospinal tract is believed to play a role in modulating head movements in response to visual and auditory stimuli. Originating from neurons deep within the superior colliculus, the axons in the tectospinal tract cross via the dorsal tegmental decussation, project to the spinal cord, and terminate in the upper cervical spinal levels. Although the tectum receives input from many cortical regions, the visual cortex provides the most highly organized input to the tectum.
The axons which form the reticulospinal tract arise from neurons in the pons and medulla. This tract has three different components.
The first component of the reticulospinal tract plays a role in motor functions. It has two components: the lateral bulboreticulospinal tract originating in the medulla, and the medial pontoreticulospinal tract originating in the pons. These components inhibit and facilitate extensor spinal reflexes respectively, ultimately assisting with posture and balance.
Fibers of the lateral reticulospinal pathway arise in the nucleus reticularis gigantocellularis of the medulla and project bilaterally along the full length of the spinal cord. The medial reticulospinal pathway arises from the nucleus pontis caudalis and the nucleus pontis oralis, two distinct clusters of nuclei in the medial pontine reticular formation. These fibers project ipsilaterally along the entire length of the spinal cord. Both the lateral and medial reticulospinal tracts receive input from several cortical areas in both hemispheres.
The second component of the reticulospinal tract modulates autonomic functions. The fibers in this pathway originate from the ventrolateral medulla and project to the intermediolateral (IML) nucleus within the thoracolumbar spinal cord, where they excite sympathetic ganglionic neurons in the viscera.
The third component of the reticulospinal tract plays a role in modulating pain impulses. This pathway begins with enkephalinergic neurons in the midbrain periaqueductal gray (PAG). Their axons project to serotonergic neurons in the nucleus raphe magnus of the medulla, which project to the dorsal horn of the spinal cord. In the dorsal horn, they synapse with enkephalinergic interneurons, which act on primary afferent pain fibers to regulate pain impulses ascending the spinal cord via the spinothalamic tract.
The vestibulospinal tract has lateral and medial components.
Lateral vestibulospinal tract
The lateral vestibulospinal tract increases extensor muscle tone, mediating posture and balance. The lateral vestibular tract originates from neurons in the lateral vestibular nucleus located at the pontine-medullary border in the brainstem. The lateral vestibular nucleus receives inhibitory signals from the cerebellum and excitatory signals from the vestibular apparatus.
The fibers originating in the lateral vestibular nucleus span the entire length of the spinal cord, synapsing on interneurons within the cord. These interneurons activate motor neurons in the spinal cord, innervating extensor muscles of the trunk and ipsilateral limbs. Like many other nuclei and tracts, the lateral vestibular nucleus is arranged somatotopically: input to the lumbosacral cord originates in the dorsal and caudal regions of the lateral vestibular nucleus, whereas input to the cervical cord originates in the more rostral and ventral areas of the lateral vestibular nucleus.
Medial vestibulospinal tract
The medial vestibulospinal tract is considered a component of the MLF. As part of the MLF, the medial vestibulospinal tract originates from both the ipsilateral and contralateral medial vestibular nuclei in the pons and medulla.
The axonal fibers in this tract follow the ventral funiculus of the cervical spinal cord to synapse in the ipsilateral ventral horn; regulating the activity of motor neurons. The major role of this tract is to adjust the position and maintain stability of the head in response to changes in posture, such as those occurring during movement of the rest of the body.
A stroke occurs when there is an occlusion or rupture of a vessel in the brain leading to loss of oxygen to a region and subsequent neuronal damage and possible death. When a stroke occurs prior to the pyramidal decussation, interruption of descending motor fibers results in crossed hemiplegias, or loss of movement in the side of the body contralateral to the lesion. This could include the:
- motor cortex (via occlusion of a cerebral artery)
- medulla (Déjèrine syndrome)
- pons (Millard-Gubler or Foville syndromes)
- midbrain (Weber syndrome)
Lacunar strokes, which are lesions of the internal capsule, can also interrupt descending motor fibers and result in crossed hemiplegias.
Descending motor tracts can also be interrupted by occlusion of the anterior spinal artery (ASA). Although the dorsal columns and Lissauer’s tract are spared, ASA occlusion presents with UMN deficits below the level of the lesion due to interruption of the corticospinal tract, and LMN deficits at the level of the lesion due to damage to the cell bodies in the anterior horns. Pain and temperature sensation would also be lost below the lesion due to damage in the spinothalamic tract.
The tentorium cerebelli is a layer of the dura mater that covers the posterior cranial fossa. The occipital lobes rest above the tentorium, and the cerebellum lies just below. Brain lesions located above the tentorial notch are supratentorial, whereas lesions below the tentorial notch are infratentorial. Lesions that begin above the notch and extend downward, such as uncal herniation, can compress the brainstem and subsequently affect the rubrospinal, vestibulospinal, and reticulospinal tracts.
In a supratentorial lesion, the brainstem nuclei remain unaffected, presenting as decorticate posturing: the upper extremity is flexed at the elbow and wrist, the lower extremity is extended and internally rotated, and the feet and toes are plantar flexed. Once the lesion becomes infratentorial, the red nucleus becomes affected and loses its ability to influence the flexor muscles of the upper extremity. This results in decerebrate posturing, with the upper extremity extended and internally rotated.
In syringomyelia, a fluid-filled cavity called a syrinx forms within the center of the spinal cord. As the cavity expands, it can damage a number of spinal tracts; although it is most commonly associated with damage to the anterior white commissure of spinothalamic tract. This leads to bilateral loss of pain and temperature sensation in what is referred to as a “cape-like” distribution. Additional sensory and motor symptoms in a patient with syringomyelia suggest increased severity of the condition.
Corticobulbar tract and cranial nerve lesions
Lesions affecting the cranial nerves and parts of the corticobulbar tract have their own tell-tale signs.
- Damage to CN III interrupts motor input to the majority of extraocular muscles, leading to a “down-and-out” shifted eye and eyelid ptosis (drooping); and lesion of the parasympathetic fibers within this CN results in mydriasis (pupil dilation)
- CN IV palsy results in the eye pointing upward and inward due to loss of motor innervation to the superior oblique muscle; and CN VI palsy results in an adducted eye due to loss of motor innervation to the lateral rectus.
- Depending on the location of the lesion, damage to CN V can result in paralysis of the muscles of mastication on the ipsilateral side of the lesion with deviation of the jaw to the contralateral side, and loss of sensation of the ipsilateral face and/or mouth.
- The presentation of a facial nerve lesion depends on whether UMNs or LMNs are damaged. Destruction of UMNs in the motor cortex or damage to their axons (i.e. as they travel through the internal capsule) connecting their cell bodies to the facial nucleus in the pons can result in contralateral paralysis of the lower muscles of facial expression. The forehead muscles are not paralyzed because, unlike the lower muscles, they receive innervation from UMNs in both cerebral hemispheres. As such, loss of forehead movement distinguishes a UMN facial nerve lesion from a LMN facial nerve lesion: when the facial nucleus or the facial nerve (CN VII) is damaged, forehead muscles are paralyzed along with the lower muscles of facial expression. Patients with LMN lesions also experience hyperacusis due to paralysis of the stapedius muscle, and loss of taste sensation to the anterior tongue. If facial paralysis is idiopathic, it is referred to as Bell’s palsy; however, it can also be caused by Lyme disease, herpes simplex virus (HSV), varicella zoster virus (VZV), sarcoidosis, and tumors (i.e. of the parotid gland), among others. Most patients gradually recover function.
- Damage to CN IX and X can result in loss of the afferent portion of the gag reflex (via loss of sensation in the tonsillar region and posterior pharynx); dysphagia (difficulty eating); dysarthria (difficulty with speech articulation); and hoarseness. During attempts to speak, the uvula will deviate to the contralateral side of the lesion.
- Damage to CN XI causes weakness in the shoulder on the lesioned side (loss of motor innervation to the trapezius) and difficulty turning the head to the opposite side (loss of motor innervation to the sternocleidomastoid).
- Damage to CN XII causes the tongue to deviate towards the side of the lesion.
- If the midbrain is affected, lesions affecting the corticobulbar tract can present with either vertical gaze palsies or upward gaze paralysis, otherwise known as Parinaud syndrome.
- If the MLF is lesioned between the motor nuclei of CN III and VI, internuclear opthalmoplegia—the inability to adduct the medial rectus muscle of one eye when the lateral rectus of the other eye is abducted for lateral gaze—can occur. This occurs due to the intricacies of connectivity between the nuclei for CN III and VI. For example: the right CN VI innervates the right lateral rectus muscle. When the right CN VI is activated, the right lateral rectus contracts and pulls the eye so that it is abducted, with the pupil facing laterally (to the right). Via the MLF, right-side abducens neurons cross the midline and project to left oculomotor neurons, which innervate the medial rectus muscle in the left eye, facilitating synchronous movement of these muscles for rightward gaze. As such, an interruption in the MLF between the right CN VI nucleus and the left CN III nucleus will block signals to the left eye to look right when the right eye looks right: in a patient with this lesion, the right eye will abduct to the right, but the left eye will be stationary, continuing to gaze forward.
- Lesions to the nucleus of CN VI and the PPRF can result in either horizontal gaze palsies or a condition called one-and-a-half syndrome. One-and-a-half syndrome is a combination of internuclear ophthalmoplegia with CN VI palsy: the result is an inability to abduct (lateral rectus palsy) and adduct (medial rectus palsy) the ipsilateral eye (the “one”), and an inability to adduct the contralateral eye (the “half”).
Poliomyelitis and Werdnig-Hoffman disease
Both poliomyelitis and Werdnig-Hoffman disease are the result of degeneration of the LMN cell bodies in the anterior horns of the spinal cord. Poliomyelitis results from a poliovirus infection, but has been largely eliminated in developed countries due to vaccination practices. Werdnig-Hoffman disease is a congenital disorder which is inherited in an autosomal recessive manner; in severe cases infants may be described as “floppy.”
In both diseases, damage to LMNs results in flaccid paralysis. In poliomyelitis, weakness and paralysis tend to be asymmetrical; whereas infants with Werdnig-Hoffman present with a symmetrical weakness and paralysis.
Amyotrophic lateral sclerosis
In amyotrophic lateral sclerosis (ALS, or Lou Gehrig disease), loss of neurons in the cerebral cortex and the anterior horns of the spinal cord results in a combination of UMN and LMN deficits. ALS can be caused by a defect in the enzyme superoxide dismutase-1 (SOD1), and commonly presents with asymmetric limb weakness, fasciculations, and atrophy. It is eventually fatal.
Subacute combined degeneration of the spinal cord
Prolonged vitamin B12 deficiency leads to subacute combined degeneration of the spinal cord. This results in demyelination of axons in the spinocerebellar and lateral corticospinal tracts, as well as in the dorsal columns. Patients present with ataxic gait, paresthesia (the “funny tingling”), and impaired position and vibration senses.
B12 deficiency can be associated with a strict vegetarian or vegan diet (B12 is acquired from consumption of meat and other animal-based foods), autoimmune gastritis (destruction of parietal cells in the stomach leads to loss of production of intrinsic factor, which is required for B12 absorption), and malabsorption syndromes and inflammatory conditions preventing B12 absorption in the ileum.
Myasthenia gravis is an autoimmune disorder of the NMJ. Normally, the neurotransmitter acetylcholine (Ach) is released by neuronal axons at the NMJ and binds to receptors on the muscle, triggering movement. In patients with myasthenia gravis, antibodies against the Ach receptor destroy the receptors. This inhibits the final step in the pathway, the activation of motor fibers to facilitate movement. Patients present with muscle weakness that becomes more severe with continued use throughout the day.
The Tensilon test can confirm this diagnosis: giving a short-acting acetylcholinesterase inhibitor like edrophonium (which prevents acetylcholinesterase, the enzyme responsible for breaking down Ach at the NMJ after it is released, from doing its job) will temporarily relieve the patient’s symptoms.
This condition can be associated with tumors or general over-activity of the thymus, the organ responsible for the production and maturation of T-cells. If this is the case, removal of the implicated tissue will eliminate the disease. Otherwise, myasthenia gravis can be managed with a longer-acting acetylcholinesterase inhibitor.
You’re working the overnight shift in the ER of a hospital in a rough part of town. Around 1 am, a victim who was stabbed during a bar fight is wheeled in. Though clearly intoxicated, he’s conscious and able to communicate; and at the first opportunity apprehensively slurs that he cannot move his right leg. Upon further investigation, you note that his right leg not only retains no motor function, but also lacks light touch, proprioception, and vibration sense. On a hunch, you check the left leg: although motor function, vibration sense, light touch, and proprioception are present, pinprick elicits no reaction. What is your diagnosis?
Brown-Séquard syndrome occurs due to hemi-section of the spinal cord. When the spinal cord is cut, the cell bodies at that level are damaged and the axons at that level are cut, preventing them from transmitting information from the body up to the brain, and from the brain to the body below the injured level of the spinal cord. This affects the descending motor tracts in characteristic ways.
Damage to the anterior horn cells (LMNs) in the spinal cord results in loss of muscle tone, muscle atrophy, loss of reflexes, and loss of voluntary movement in the form of ipsilateral flaccid paralysis at the level of the lesion.
The result of damage to axons of UMNs descending in corticospinal tract in the spinal cord is ipsilateral hyper-reflexivity, abnormal extensor plantar reflex (the “Babinski sign”), and loss of voluntary movement in the form of spastic paralysis.
Spinal cord hemi-section, however, affects more than just the descending motor pathways: note that sensation in this patient is also affected, and damage to sensory tracts and cells results in ipsilateral loss of all sensation at the level of the lesion; ipsilateral loss of proprioception, vibration, light touch, and tactile sense below the level of the lesion; and contralateral loss of pain and temperature sensation and crude touch below the level of the lesion.