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Thread: Lower Thoracic, Conus, and Cauda Equina Injuries: Diagnosis & Treatment

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    Lower Thoracic, Conus, and Cauda Equina Injuries: Diagnosis & Treatment

    Wise Young, Ph.D., M.D.
    W. M. Keck Center for Collaborative Neuroscience
    Rutgers University, Piscataway, New Jersey
    update: 13 May 2005

    Is it important to know whether you have a spinal cord injury, a conus injury, or a cauda equina injury? The three conditions have different prognoses and therapeutic implications. A spinal cord injury interrupts the spinal tracts that go from the brain and upper spinal cord to the lower spinal cord. Lower thoracic spinal cord injuries can damage not only the spinal cord but also spinal roots that run in the spinal canal in lower thoracic and lumbosacral spinal canal. A conus injury damages the sacral segments that are present at the tip of the spinal cord and, depending on the extension of the damage, may also damage spinal roots that are present in the spinal canal near the conus. Finally, a cauda equina injury damages only the spinal roots and not the spinal cord itself. Of course, one may have combination conus and cauda equina injuries but these are relatively rare.

    Injury Level

    Let me first review the anatomy of the spinal cord because people are always confusing spinal cord levels with bony vertebral levels. When a surgeon talks about levels, the surgeon is usually thinking about bony (vertebral) levels. During development and childhood, the spinal column grows more than the spinal cord and is much longer than the spinal cord. As figure 1 below shows, the spinal cord levels are defined by where the spinal roots enter the spinal cord. The vertebral levels are defined by where the spinal roots exit the vertebral column. The figure was relabeled from an article that I had posted earlier.

    In the cervical region, vertebral and spinal cord levels are similar. There are 8 cervical spinal cord segments and only 7 cervical vertebral segments. In the cervical spinal cord, the spinal roots exit the spinal column close to the spinal cord level. Also, in the cervical spine, the spinal roots exit just above the vertebral level. For example, C1 root exits above the C1 vertebra and the C7 root exits above the C7 vertebra. However, the C8 root exits above the T1 vertebra and the T1 root exits the spinal column above the T2 vertebra.

    Spinal cord levels and vertebral levels are not the same in the thoracic and lumbosacral segments. In the lower thoracic spinal cord, the spinal cord levels are progressively further away from the vertebral levels. So, for example, the T5 cord segment is located in the T4 vertebra. The L1 cord segment is located between T8 and T9 vertebral segments. The L5 cord segment is located in the T11 vertebral segment. The sacral spinal cord (S1-S5) is located between T11 to L1. The cauda equina is located from L2 vertebra to the coccyx (the tip the spinal column).

    An injury to C1 to L1 vertebral levels will damage the spinal cord. In the lower thoracic and lumbosacral spinal cord, trauma not only damages the spinal cord but also the spinal roots that exit the spinal column at the level of injury, as well as spinal roots that may be present in the spinal canal. So, for example, if you have a C5 vertebral injury, it should have damaged your C6 spinal cord and possibly the C5 spinal roots that exit the spinal column between the C4 and C5 vertebral bodies. Your neurological level should start out at C4 and may descend over time to C5 and possibly C6. If you have a T6 vertebral injury, it should have damaged your T8 spinal cord but also the T6 and T7 spinal roots that exist the spinal column above and below the T6 vertebrae.

    In summary, vertebral and spinal cord levels are not the same. In the cervical spinal cord, the vertebal and spinal cord levels are similar but there are 8 cervical spinal cord segments and only 7 cervical vertebrae. In the thoracic spinal cord, the spinal cord segmental level separates from the vertebral level progressively more as one gets lower down the spinal column. The lumbosacral spinal cord is located in vertebrae T8 to L1. Spinal roots run alongside the spinal cord from T8 to L1, where the conus is located. Beyond L1, the cauda equina occupies the spinal canal.

    Lower Thoracic Injury

    A lower thoracic injury, i.e. T8-T12, affects the lumbar cord and upper sacral spinal cord. As shown in figure 1, the lumbar cord is situated between T8 and T11 while the S1 and S2 segment is situated at T12. An injury to the lumbar and upper sacral spinal cord will cause damage to the motoneurons that innervate the pelvic and buttock muscles (L1-L3), the upper leg muscles (L2-4), and the lower leg muscles (L4-S1). In addition, injuries at these thoracic vertebral levels will interrupt descending tracts innervating the sacral spinal cord governing sexual, bladder, and bowel function (S2-S5). The injuries may also affect the spinal roots, firstly the spinal roots that are exiting at the level of the injury and secondly the spinal roots that are descending through the spinal canal at the injury site.

    A person with a T10 vertebral injury should have an injury to the L3 or L4 spinal cord, the T9 and T10 roots that exit above and below the T10 vertebra. In addition, the T10 to L4 spinal roots pass through the spinal canal at T10 may be affected. A person with a T11 vertebral injury should have an injury to the L5 spinal cord, as well as T11 and T12 spinal roots that exit the spinal cord and the spinal roots from L1 to L5 that pass through the spinal canal of the T11 vertebra. Likewise, a person with a T12 vertebral injury should have an injury to the S2 and S3 spinal segment, as well as the spinal roots of L1 to S2.

    Lower thoracic injuries are therefore combinations of spinal cord and spinal root injuries. They involve both upper and motoneuronal injuries. Upper motoneuronal injuries refer to loss of motor connection between the brain and the spinal cord. Lower motoneuronal injuries refer to damage of the motoneurons themselves or the axons that connect them to the muscles. They also cause loss of ascending spinal sensory tracts as well as sensory input to the spinal cord through the spinal roots. For that reason, their neurological presentation is complex. Careful and detailed neurological examinations are required to decipher the neurological losses.

    Because the thoracic cavity is strongly reinforced by the ribs, injuries to the thoracic spinal cord require massive accelerative forces and most injuries at lower thoracic levels tend to cause severe damage to the spinal cord. However, even the most severe injuries tend to spare some spinal roots passing through the canal at the injury site. So, one often sees a so-called "complete" spinal cord injury with a neurological level at L1-L5 but some sensory loss as high as T8 and involvement of abdominal muscles. In general, lower motoneuronal symptoms are restricted to the upper legs.

    The classic clinical presentation of a person with lower thoracic spinal injuries is paraplegia with some preservation of proximal (hip flexors and extension) muscles, flaccid paralysis of leg muscles depending on the precise level of injury, and spastic paralysis of muscles and bladder below that level. Depending on the severity of injury, there may be sparing of sexual, bladder, and bowel function. However, even in the case of severe injuries, the persons often have spastic bladders and bowel, and spasms, indicating that the spinal cord below the injury site is still alive and kicking.

    In summary, lower thoracic spinal injury usually damages a lower part of the spinal cord than indicated by the vertebral injury level. For example, a T10 vertebral injury damages the L3 and L4 spinal cord while a T12 vertebral injury damages the S2 and S3 spinal cord. The lumbosacral spinal cord is situated between T8 and L1. Injury damages not only the spinal cord but also the spinal roots that exit at the site of injury, as well as spinal roots running in the canal. Lower thoracic spinal cord injuries present with complex distributions of upper motoneuronal injuries, lower motor neuronal injuries at the site of injury, injuries to spinal roots that exit the vertebral level of injury, and damage to the spinal roots that are running in the spinal canal.

    Conus Injury

    A conus injury is damage to the tip of the spinal cord, involving S4/5 spinal cord segments located in the L1 vertebrae. Injury to the L1 vertebrae will also affect descending spinal roots from the L1-S3 spinal cord that exit from the L1-S5 vertebral bodies. So an L1 vertebral injury causes spinal cord gray matter damage in the S4 and S5 spinal cord segments but may also cause both motor and sensory loss due to damage to the L1-S3 spinal roots.

    The first clue to the diagnosis of conus injury is evidence of damage to the L1 vertebra. Although injuries to higher vertebra such as T12 can sometimes extend down into L1 and sometimes multiple level injuries can occur, the diagnosis of a conus injury requires evidence of damage to the conus itself. This should be looked for on MRI and CT scans of the lower spinal cord at the time of injury, for any evidence of compression of the conus at L1. There may be some MRI changes of the conus that may also reveal the presence of ischemic damage (i.e. increased signal).

    The second clue to the diagnosis of conus injury is the distribution of neurological deficits. These fall into three categories:
    • Loss of S4 and S5 function. The S4 and S5 dermatomes are located at and around the anus. There should be loss of sensation around the anus and absent anal sphincter tone. The anal sphincter should be flaccid if the conus injury is severe. If there is partial preservation of anal and sphincter function, there may be dissociation of pinprick and touch sensations and both should be tested.
    • Damage to T12 and L1 spinal roots. The T12 root exits the spinal column just above L1 vertebral body and the L1 spinal root exits just below the L1 vertebral body. Both of these roots may be affected by dislocation of the L1 vertebra. Therefore, there may be loss of sensation in the T12 dermatome situated just above the pelvic girdle and the L1 dermatome which covers most of the front of the groin and extends around the back. The T12 and L1 roots also innervate deep pelvic and hip flexion muscles and these may be affected.
    • Sensory loss from injury to descending L2-S3 spinal roots. The L2 through S3 spinal roots are present in the spinal canal of the L1 vertebral body. Depending on the severity of the injury, these roots may be affected as well but these should be variable. L2, L3, L4, and L5 dermatomes cover the front of the leg while the S1 and S2 dermatomes are located in the back of the leg. Please note that the S2 and S3 dermatomes innervate the penis and scrotal area and penile sensation may be spared in a conus injury. A careful and detailed examination of sensory dermatomes should be done to identify roots that have been damaged. Please note that because these are root injuries, both touch and pinprick sensations should be affected. Sometimes in incomplete spinal cord injuries, there is sparing of pinprick while touch is absent or vice-versa; however, this should be rare when the sensory loss is due to damage to the spinal roots.
    • Motor loss from injury to descending L2-S3 spinal roots. The L1 through S3 spinal roots of course innervate a great many muscles in the legs but there may be selective sparing of individual muscle groups. If the S1 root is involved, the ankle reflex should be absent. If the L3 and L4 roots are affected, the patellar (knee jerk) reflex should be absent. Severe injuries of the spinal roots may result in flaccid paralysis and atrophy of multiple leg muscles. However, there is often sparing of some muscle groups, particularly the muscles of the upper leg. Sexual and bladder function which is controlled by S2-3 may be spared or recover partly in people with conus injuries.

    The third clue is the clinical presentation of a conus injury. A conus injury usually presents with sudden onset of lower back pain, bilateral motor and sensory loss, particularly anal sensation and sphincter function. Fecal incontinence is common. Patients often complain of severe low back pain and occasionally radicular pain (shooting pain from the back into the leg). If the predominant pain complaint is radicular pain, cauda equina injury should be suspected. If there is damage to the sacral spinal roots, there may be early loss of erection and the bladder may be flaccid. Knee jerks are often preserved (L3/4) but ankle jerks (S1) may be diminished. A majority will eventually recover bladder reflexes (Beric, et al., 1992)). Patients are sometimes able to walk after conus injuries.

    In summary, a conus injury involves the S4/5 segment of the spinal cord situated in vertebral body L1. The injury may also involve the T12 and L1 spinal roots that exit respectfully above and below the L1 vertebral body. In addition, the spinal roots for L2 through S5 spinal roots pass through the spinal canal of the L1 vertebral body and severe occlusion of the spinal canal at L1 may result in damage to the spinal roots. The diagnosis of conus injury should include CT or MRI evidence of compression or other damage to the tip of the spinal cord at L1. Many patients may recover erection and bladder function, as well as walking, after conus injuries.

    Cauda Equina Injury

    The cauda equina consists of the spinal roots that descend from the spinal cord to end of the spinal column, exiting at each lumbar and sacral levels. Injury to L2 and any of the vertebral bodies below L2 may result in a cauda equina injury. The injury seldom damages all the spinal roots in the canal. The cauda equina syndrome frequently occurs as a result of disc herniation, stenosis (narrowing), or gradual dislocation of the spinal column and thus the onset of symptoms may be slow. Generally, cauda equina injury involves one side more than the other and is associated with radicular pain (shooting pain going into the affected limb). There is typically less back pain than in conus injuries.

    The classic presentation of a cauda equina syndrome is saddle anesthesia, i.e. loss of sensation in the areas that innervated by the lower sacral segments (where one sits on a saddle). There is areflexic or flaccid paralysis of certain muscle groups innervated by affected spinal roots. Loss of erectile function is less common than in conus injuries (depends on whether the S2/3 roots are affected) but may happen. The bulbocavernosus reflex, penile or clitoral sensation may be absent or diminished, indicating damage to the S2/S3 roots. The cremasteric reflex (L2-L3), stroking the superior and medial part of thigh to elicit contraction of the scrotum and testes in the side of the stroked limb, should be preserved. Sensory loss should follow a dermatomal pattern. Urinary retention, if present, tends to present later or more rarely than in conus injuries.

    By definition, cauda equina injury is damage to the spinal roots. The distribution of neurological loss is variable, depending of the roots involved, and motor recovery frequently occurs but sensory recovery is limited. The reason is that some motor axons can regenerate in the peripheral nerve and reinnervate muscles. If the injury is very close to the spinal cord, motor regeneration is limited. Sensory axonal regeneration and recovery is rare because sensory axons that have been interrupted cannot re-enter the spinal cord (due to the CNS-PNS barrier stops growth of axons into the spinal cord). The spinal cord itself is not damaged in cauda equina injuries.

    In summary, cauda equina injuries produce saddle anesthesia, areflexic paralysis of selected lumbosacral segments, possible loss of erectile function and the bulbocavernosus reflex (S2/5) but intact cremasteric reflex (L2/3), and bowel/bladder dysfunction. Depending on the severity of injury, many people with cauda equina injuries end up with paralysis and sensory loss in certain muscle groups. Paralysis may reverse but sensory recovery is more rare. Patients often complain of radicular pain for one spinal cord segment that emanates into the affected limb. Bladder function is often affected but may be spared.

    Implications for Treatment

    Most of the therapeutic approaches to spinal cord injury have focused on damage to the spinal cord and regeneration of spinal tracts. People with lower thoracic spinal cord injury should benefit from such therapies. Thoracic and conus injuries would both benefit from neuronal replacement therapies. Cauda equina injuries will benefit from therapies that allow regrowth of sensory axons into the spinal cord and treatments that encourage peripheral axonal regeneration.

    There are several alternative therapies that can be used to restore function in people who have spinal root damage. One is to identify those roots that are not damaged and then do nerve bridging to connect those roots with muscles and sensory nerves supplied by damaged roots. In China, for example, Dr. Shaocheng Zhang at the Second Military Hospital in Shanghai has been doing nerve rerouting in hundreds of patients. He bridges the nerves from an intact root to the distal end of a damaged root. Although not quite like a tendon transfer, it allows a patient to move muscles and feel in areas of the body.

    Another approach is to stimulate regeneration in spinal roots that have been damaged. There is considerable research on methods to enhance peripheral nerve regeneration. In the case of spinal roots, there is an additional problem that must be solved: the regrowth of sensory axons into the spinal cord. Because the cell bodies of sensory axons are situated in the dorsal root ganglia just outside of the spinal cord, injury to nerve roots disrupts the sensory connections to the spinal cord. Sensory axons do not grow into the spinal cord. There are some animal studies that suggest that olfactory ensheathing glia may facilitate the entry of sensory axons into the spinal cord.

    It is likely that no single therapy will work for all people with lower thoracic, conus, or cauda equina injuries. The therapies must be specifically tailored for every person, depending on which and how many spinal roots are involved, and the extent to which the spinal cord is affected by the injury. Treaments must address both upper and lower motoneuronal deficits. We must also remember that motor function requires sensory input, i.e. reflexes, proprioceptive (position sensing), and muscle feedback, essential for coordinated motor control. Thus, a solution that restores muscle innervation is not likely to restore motor control without addressing the sensory component.

    Lower thoracic, conus, or cauda equina injuries often result in flaccid paralysis and muscle atrophy. Can it be reversed or prevented? Most of the atrophy that occurs is very likely to be due to non-use. In people with cervical or upper thoracic spinal cord injuries, spasticity helps maintain the muscle. However, people who have conus or cauda injuries are less spastic. There is growing evidence that intense electrical stimulation with high electrical currents can build and maintain denervated muscles. On the other hand, it may be a number of years before we will be able to replace motoneurons in the spinal cord to reinnervate muscles.

    Recommended Web Reading

    Neurological Exams: Sensory Nerves and Deep Tendon Reflexes by Susan Spinasanta. This article from describes reflexes and sensory testing. Might be helpful for you to read if you are wondering what your doctor is doing when tapping your knee with a rubber hammer.

    Spinal Cord Hemorrhage by Richard M. Zweifler, M.D.. Hemorrhage or bleeding of the spinal cord often happens after trauma or vascular malformations. This article from discusses how the blood damages the spinal cord.

    Tumors of the Conus and Cauda Equina by Amiram Schneiderman, Joseph T. Alexander. Tumors are a major cause of conus and cauda equina injuries. This is a review in Emedicine both the diagnosis and treatment of this condition.

    Spinal Cord injury: Definition, Epidemiology, Pathophysiology by Segun T. Dawodu, M.D. This is a general article from Emedicine that provides definitions of the various ways of classifying spinal cord injury, conus medullaris syndrome, and cauda equina syndrome.

    Spinal Cord Injury: Anatomy and Physiology of the Spinal Cord by Fintan Sheerin. This article in Emergency Nurse Vol. 12 (8 December 2004) has some nice illustrations of spinal cord anatomy.

    Spinal Anatomy. This article of the Sofamordanek site has some nice pictures of spine anatomy.

    Thoracolumbar Vertebral Fractures: A Review of the Literature by V. M. Thomas, et al. A review of different thoracolumbar fractures published in the Journal of Orthopedics in 2004.

    Conus Medullaris and Cauda Equina Syndrome as a Result of Traumatic Injuries: Management Principles by James S. Harrop, Gabriel E. Hunt, Jr., and Alexander R. Vaccaro in Medscape. This 2004 article includes MRI and CT images of L1 burst fractures and other injuries that lead to conus or cauda equina injuries.

    Neurogenic Bladder, Neurogenic Bowel, and Sexual Dysfunction in People with Spinal Cord Injury by Barbara T. Benevento and Marca L. Sipski. This review article in Physical Therapy Volume 82, June 2002 summarizes some of the bladder, bowel, and sexual changes that occur with lower spinal cord injury.

    Cauda Equina Syndrome by Michael S. Beeson, M.D. This review article in eMedicine was last updated on 7 April 2005. It provides a good review of the cauda equina syndrome.

    Cauda equina syndrome cased by lumbar disc herniation: Commentary by John P. Kostuik. This comment in Neurosurgery Focus, Volume 16, June 2004, states that cauda equina syndrome is frequently misdiagnosed or unrecognized but can have a relatively good outcome if rapidly decompressed. Delaying surgery by more than 48 hours produces significantly worse recovery.

    Cauda Equina Syndrome: Is it a Surgical Emergency? by Jason W. Nascone, William C. Lauerman, and Sam W. Wiesel of Georgetown University in 1999. This review suggests that decompression should be performed when medically feasible in patients with chronic cauda equina compression but that early decompression is important for acute cauda equina syndrome.

    Non-painful sensory phenomena after spinal cord injury by Phillip J. Siddal and Joan McClelland (1999), Journal of Neurology, Neurosurgery, Psychiatry, Volume 66: 612-622. According to this article from Sydney, Australia, 83% "non-painful" phantom sensations in spinal cord injury,

    [This message was edited by Wise Young on 05-19-05 at 10:23 AM.]
    Last edited by Wise Young; 09-28-2006 at 04:18 AM.

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