Cauda Equina and Conus Medullaris Syndromes

Back

Background

The spinal cord tapers and ends at the level between the first and second lumbar vertebrae in an average adult. The most distal bulbous part of the spinal cord is called the conus medullaris, and its tapering end continues as the filum terminale. Distal to this end of the spinal cord is a collection of nerve roots, which are horsetail-like in appearance and hence called the cauda equina (Latin for horse's tail). (See the image of cauda equina anatomy below.)



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Illustration demonstrating the relevant anatomy of the cauda equina region

See Back Pain: Find the Cause, Watch for the Comeback, a Critical Images slideshow, to help diagnose and manage this common problem.

These nerve roots constitute the anatomic connection between the central nervous system (CNS) and the peripheral nervous system (PNS). They are arranged anatomically according to the spinal segments from which they originated and are within the cerebrospinal fluid (CSF) in the subarachnoid space with the dural sac ending at the level of second sacral vertebra.

Cauda equina syndrome refers to a characteristic pattern of neuromuscular and urogenital symptoms resulting from the simultaneous compression of multiple lumbosacral nerve roots below the level of the conus medullaris (see the image below). These symptoms include low back pain, sciatica (unilateral or, usually, bilateral), saddle sensory disturbances, bladder and bowel dysfunction, and variable lower extremity motor and sensory loss (see Clinical).

Although the lesion is technically involves nerve roots and represents a "peripheral" nerve injury, damage may be irreversible and cauda equina syndrome may be a surgical emergency (see Treatment).[1]



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Illustration demonstrating an example of cauda equina syndrome secondary to a spinal neoplasm

Lesions involving the termination of the spinal cord (conus medullaris) are not discussed in this article. Please see the article Spinal Cord Injuries.

Anatomy

The spinal cord, which is the downward continuation of medulla that starts just below the foramen magnum, serves as a conduit for the ascending and descending fiber tracts that connect the peripheral and spinal nerves to the brain. The cord projects 31 pairs of spinal nerves on either side (8 cervical, 12 thoracic, 5 lumbar, 5 sacral, 1 coccygeal) that are connected to the peripheral nerves.

A cross-section of the spinal cord reveals butterfly-shaped gray matter in the middle, surrounded by white matter. As in the cerebrum, the gray matter is composed of cell bodies. The white matter consists of various ascending and descending tracts of myelinated axon fibers, each with specific functions.

During development, the vertebral column grows more rapidly than the spinal cord. Spinal nerves exit the vertebral column at progressively more oblique angles because of the increasing distance between the spinal cord segments and the corresponding vertebrae. Lumbar and sacral nerves travel nearly vertically down the spinal canal to reach their exiting foramen.

The spinal cord ends at the intervertebral disc between the first and second lumbar vertebrae as a tapered structure called the conus medullaris, consisting of sacral spinal cord segments. The upper border of the conus medullaris is often not well defined. The fibrous extension of the cord, the filum terminale, is a nonneural element that extends down to the coccyx.

The cauda equina (CE) is a bundle of intradural nerve roots at the end of the spinal cord, in the subarachnoid space distal to the conus medullaris. Cauda is Latin for tail, and equina is Latin for horse (ie, the "horse's tail"). The CE provides sensory innervation to the saddle area, motor innervation to the sphincters, and parasympathetic innervation to the bladder and lower bowel (ie, from the left splenic flexure to the rectum).[100]

The nerves in the CE region include lower lumbar and all of the sacral nerve roots. The pelvic splanchnic nerves carry preganglionic parasympathetic fibers from S2-S4 to innervate the detrusor muscle of the urinary bladder. Conversely, somatic lower motor neurons from S2-S4 innervate the voluntary muscles of the external anal sphincter and the urethral sphincter via the inferior rectal and the perineal branches of the pudendal nerve, respectively.

Hence, the nerve roots in the CE region carry sensations from the lower extremities, perineal dermatomes, and outgoing motor fibers to the lower extremity myotomes.

The conus medullaris obtains its blood supply primarily from 3 spinal arterial vessels: the anterior median longitudinal arterial trunk and 2 posterolateral trunks. Less prominent sources of blood supply include radicular arterial branches from the aorta, lateral sacral arteries, and the fifth lumbar, iliolumbar, and middle sacral arteries. The latter contribute more to the vascular supply of the cauda equina, although not in a segmental fashion, unlike the blood supply to the peripheral nerves.

The nerve roots may also be supplied by diffusion from the surrounding CSF. Moreover, a proximal area of the nerve roots may have a zone of relative hypovascularity.

Pathophysiology

In understanding the pathological basis of any disease involving the conus medullaris, keep in mind that this structure constitutes part of the spinal cord (the distal part of the cord) and is in proximity to the nerve roots. Thus, injuries to this area often yield a combination of upper motor neuron (UMN) and lower motor neuron (LMN) symptoms and signs in the dermatomes and myotomes of the affected segments. On the other hand, a cauda equina lesion is an LMN lesion because the nerve roots are part of the PNS.

Cauda equina syndrome may result from any lesion that compresses CE nerve roots. These nerve roots are particularly susceptible to injury, since they have a poorly developed epineurium. A well-developed epineurium, as peripheral nerves have, protects against compressive and tensile stresses.[2]

The microvascular systems of nerve roots have a region of relative hypovascularity in their proximal third. Increased vascular permeability and subsequent diffusion from the surrounding cerebral spinal fluid supplement the nutritional supply. This property of increased permeability may be related to the tendency toward edema formation of the nerve roots, which may result in edema compounding initial and sometimes seemingly slight injury.

Several studies in different animal models have assessed the pathophysiology of cauda equina syndrome.[3, 4] Olmarker et al, using a graded balloon pressure method in a porcine model, reported that the venules in the CE region begin to compress at a pressure as low as 5 mm Hg and the arterioles begin to occlude as the balloon pressure surpasses the mean arterial pressure.[5, 6, 7, 3, 8] Despite this, even a pressure as high as 200 mm Hg failed to completely shut off nutritional supply to the CE.

These studies showed that not only the magnitude but also the length and the speed of obstruction were also important in damaging the CE region.[9] Similar results were reported in other studies. Takahashi et al reported a reduction in blood flow to the intermediate nerve segment when 2 pressure points were applied along the path of the nerve in the CE.[10]

Others have studied compound action potentials in afferent and efferent segments of nerves in the CE region after application of balloon compression.[11, 12, 13] These researchers reported that 0-50 mm Hg of pressure did not affect the action potentials (the threshold for disturbances in action potentials was 50-75 mm Hg), and significant deficits were observed when pressure rose to 100-200 mm Hg.

Etiology

Cauda equina syndrome is caused by any narrowing of the spinal canal that compresses the nerve roots below the level of the spinal cord.[14] Numerous causes of cauda equina syndrome have been reported, including disc herniation, intradural disc rupture, spinal stenosis secondary to other spinal conditions, traumatic injury, primary tumors such as ependymomas and schwannomas, metastatic tumors, infectious conditions, arteriovenous malformation or hemorrhage, and iatrogenic injury.[14, 15]

The most common causes of cauda equina and conus medullaris syndromes are the following:

Other, rare causes include the following:

A retrospective study of 66 consecutive cases of patients admitted to a neurosurgical unit with suspected cauda equina syndrome found that almost half had no evidence of structural pathology on MRI.[24] These researchers suggested that the symptoms have a functional origin in such cases.

Trauma

Traumatic events leading to fracture or subluxation can lead to compression of the cauda equina.[16, 25, 26, 27, 28] Penetrating trauma can cause damage or compression of the cauda equina. Spinal manipulation resulting in subluxation has caused cauda equina syndrome.[29] Rare cases of sacral insufficiency fractures have been reported to cause cauda equina syndrome.[30] Acute and delayed presentations of CES due to hematomas and posttraumatic arachnoid cysts have also been reported.[31, 32, 33]

Herniated disk

The reported incidence of cauda equina syndrome resulting from herniated lumbar disk (see the image below) varies from 1-15%.[34, 35, 19] Ninety percent of lumbar disk herniations occur either at L4-L5 or L5-S1.[36, 37]



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Sagittal MRI of a patient with cauda equina syndrome secondary to a large lumbar disk herniation

Of cases of herniated disks leading to cauda equina syndrome, 70% occur in patients with a history of chronic low back pain; in 30%, cauda equina syndrome is the first symptom of lumbar disk herniation.[18] Men in the fourth and fifth decades of life are most prone to cauda equina syndrome secondary to disk herniation.[38]

Most cases of cauda equina syndrome secondary to disk herniation involve either a large central disc or an extruded disc fragment that compromises a significant amount of the spinal canal diameter.[39] The presentation may be acute or that of a more protracted course, with the latter bearing a better prognosis.[35] Individuals with congenital stenosis who sustain a disk herniation are more likely to develop cauda equina syndrome because even a small herniation can drastically limit the space available for the nerve roots.

Rare cases of intradural disk herniations have been reported to cause cauda equina syndrome.[40] Myelography in these instances typically demonstrates a complete block of the contrast material. If an intradural disc fragment is identified, transdural removal of the extruded disc fragment may be helpful to prevent further stretching of the already compromised nerve root.

Spinal stenosis

Narrowing of the spinal canal can be due to a developmental abnormality or degenerative process. Although unusual, cauda equina syndrome from spinal stenosis secondary to spinal disorders such as ankylosing spondylitis, spondylosis, and spondylolisthesis have all been reported.[41, 42, 43, 44, 45, 46, 47]

Neoplasms

Cauda equina syndrome can be caused by primary or metastatic spinal neoplasms. Among the primary tumors able to cause CES include myxopapillary ependymoma, schwannoma, and paraganglioma.

Myxopapillary ependymoma is the most common tumor of the filum. Recovery of the function after surgery depends on the duration of symptoms and the presence or absence of sphincter dysfunction[48] Paraganglioma of the filum, when present, needs to be differentiated from other tumors of this region.[49] Although rare, this entity may present as CES.

Schwannomas are benign encapsulated neoplasms that are structurally identical to a syncytium of Schwann cells.[50] These growths may arise from peripheral or sympathetic nerves. Schwannomas, whether solitary or as a part of a syndrome, may cause CES if present at the level of the conus or filum terminale. Primary tumors that affect the sacrum, such as chordoma and giant cell tumor of the bone, may produce similar symptoms as a result of bony destruction and collapse.[51]

Ependymomas are gliomas derived from relatively undifferentiated ependymal cells. They often originate from the central canal of the spinal cord and tend to be arranged radially around blood vessels. Ependymomas are found most commonly in patients aged approximately 35 years. They can lead to increased intracranial pressure (ICP), and cerebrospinal fluid (CSF) has an increased protein level.

Metastatic lesions of the spine are being reported with increasing frequency because of earlier diagnosis, better imaging, and more effective treatment modalities. Although metastasis accounts for most tumors in the spine in general, metastatic tumors in the cauda equina are relatively rare compared with primary tumors.

For the spine in general, sources of spinal metastases are as follows[52] :

Although lung cancer is the most common source of spine metastases, in one study, only 0.7% of the lung cancer metastases to the spine produced cauda equina syndrome; most of the metastatic lesions were not at the level of the cauda equina.[52] Up to 8% of patients with prostate cancer experience malignant spinal cord compression; however, the percentage of cases involving cauda equina syndrome is unknown.[53]

The CE region is also a favored site for drop metastases from intracranial ependymoma, germinoma, and other tumors.[54] Other unusual metastatic spread from genitourinary and gynecologic cancer have also been reported at the conus region, causing neurological compromise.[55, 56]

Inflammatory and infectious conditions

Long-lasting inflammatory conditions of the spine, including Paget disease and ankylosing spondylitis, can lead to cauda equina syndrome secondary to spinal stenosis or fracture.

Infectious conditions, including epidural abscess, can lead to deformity of the nerve roots and spinal cord.[57] Symptoms generally include severe back pain and a rapidly progressing motor weakness.

Infectious causes for cauda equina syndrome may be pyogenic or nonpyogenic. Pyogenic abscesses are generally found in an immunocompromised or poorly nourished host. Staphylococcus aureus causes epidural abscesses in 25-60% of cases, but, recently, an increasing incidence of infections with methicillin-resistant S aureus, Pseudomonas species, and Escherichia coli have been recorded. A high index of suspicion is helpful in correct diagnosis and management.[57]

Nonpyogenic causes for abscess are rare and include tuberculosis. Resurgence of tuberculosis secondary to immunocompromise in individuals with HIV infection requires a high index of suspicion, as the development of cauda equina syndrome may follow an indolent course.[58] Other uncommon organisms, such as Nocardia asteroides and Streptococcus milleri, have also been reported as a cause of abscess that leads to the development of CES.[59, 60]

Iatrogenic causes

Complications of spinal instrumentation have been reported to cause cases of cauda equina syndrome, including misplaced pedicle screws[61] and laminar hooks.[62, 63] Continuous spinal anesthesia also has been linked to cases of cauda equina syndrome.[64]

Rare cases of cauda equina syndrome caused by epidural steroid injections, fibrin glue injection,[65] and placement of a free-fat graft have been reported.[66]

Several cases have involved the use of hyperbaric 5% lidocaine for spinal anesthesia. Recommendations are that hyperbaric lidocaine not be administered in concentrations greater than 2%, with a total dose not to exceed 60 mg.[67, 68]

Medical and surgical situations such as bone screw fixation, fat grafts, lumbar arthrodesis for spondylolisthesis, lumbar discectomy, intradiscal therapy, lumbar puncture forming an epidural hematoma, chiropractic manipulation, and a bolus injection of anesthetic during spinal anesthesia have been related to the development of cauda equina syndrome–like syndromes.[35, 69, 70, 71, 72, 73]

Epidemiology

Cauda equina and conus medullaris syndromes are classified as clinical syndromes of the spinal cord; epidemiological data on the 2 syndromes are often not available separately from the general data on spinal cord injury.

Cauda equina syndrome is uncommon, both atraumatically as well as traumatically. It is often reported as a case report due to its rarity. Although infrequent, it is a diagnosis that must be considered in patients who complain of low back pain coupled with neurologic complaints, especially urinary symptoms.

Age-related differences in incidence

Traumatic cauda equina syndrome is not age specific. Atraumatic cauda equina syndrome occurs primarily in adults as a result of surgical morbidity, spinal disk disease, metastatic cancer, or epidural abscess.

Prognosis

Morbidity and especially mortality rates are determined by the underlying etiology. Multiple conditions can result in cauda equina or conus medullaris syndrome. The prognosis improves if a definitive cause is identified and appropriate treatment occurs early in the course. Surgical decompression may be performed emergently, or, in some patients, delayed, depending on the etiology. Residual weakness, incontinence, impotence, and/or sensory abnormalities are potential problems if therapy is delayed.

Investigators have attempted to identify specific criteria that can aid in predicting the prognosis of patients with cauda equina syndrome. Patients with bilateral sciatica have been reported to have a less favorable prognosis than patients with unilateral pain. Patients with complete perineal anesthesia are more likely to have permanent paralysis of the bladder.[39]

The extent of perineal or saddle sensory deficit has been reported to be the most important predictor of recovery.[74] Patients with unilateral deficits have a better prognosis than patients with bilateral deficits. Females and patients with bowel dysfunction have been reported to have worse outcomes postoperatively.[75]

Prognosis can be predicted with the American Spinal Injury Association (ASIA) impairment scale (see Physical Examination ), as follows:

Ambulatory motor index also is used to predict ambulatory capability. It is calculated by scoring hip flexion, hip abduction, hip extension, knee extension, and knee flexion on both sides, using a 4-point scale (0=absent, 1=trace/poor, 2=fair, 3=good or normal); the score is expressed as a percentage of the maximum score of 30. Prognostic significance is as follows:

Patient Education

Patient education needs will vary with the type and severity of persistent deficits, and may include the following:

For patient education information, see the Erectile Dysfunction Center and Brain and Nervous System Center, as well as Impotence/Erectile Dysfunction, Erectile Dysfunction FAQs, and Cauda Equina Syndrome.

History

Patients can present with symptoms of isolated cauda equina syndrome, isolated conus medullaris syndrome, or a combination. The symptoms and signs of cauda equina syndrome tend to be mostly lower motor neuron (LMN) in nature, while those of conus medullaris syndrome are a combination of LMN and upper motor neuron (UMN) effects (see Table 1, below). The history of onset, the duration of symptoms, and the presence of other features or symptoms could point to the possible causes.

Table 1. Symptoms and Signs of Conus Medullaris and Cauda Equina Syndromes



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Symptoms of cauda equina syndrome include the following:

Low back pain can be divided into local and radicular pain. Local pain is generally a deep, aching pain resulting from soft-tissue and vertebral body irritation. Radicular pain is generally a sharp, stabbing pain resulting from compression of the dorsal nerve roots. Radicular pain projects in dermatomal distributions. Low back pain in cauda equina syndrome may have some characteristic that suggests something different from the far more common lumbar strain. Patients may report severity or a trigger, such as head turning, that seems unusual.

Severe pain is an early finding in 96% of patients with cauda equina syndrome secondary to spinal neoplasm. Later findings include lower extremity weakness due to involvement of the ventral roots. Patients generally develop hypotonia and hyporeflexia. Sensory loss and sphincter dysfunction are also common.

Urinary manifestations of cauda equina syndrome include the following:

Bell et al demonstrated that the accuracy of urinary retention, urinary frequency, urinary incontinence, altered urinary sensation, and altered perineal sensation as indications of possible disk prolapse justified urgent MRI assessment.[76, 77]

Bowel disturbances may include the following:

The initial presentation of bladder/bowel dysfunction may be of difficulty starting or stopping a stream of urine. It may be followed by frank incontinence, first of urine then of stool. The urinary incontinence is on the basis of overflow. It is usually with associated saddle (perineal) anesthesia (the examiner can inquire if toilet paper feels different when the patient wipes).

Physical Examination

The symptoms of cauda equina syndrome are associated with corresponding signs pointing to an LMN or UMN lesion. Refer to the images and tables below for assistance in examining the patient and documenting examination findings. In addition to the signs listed below, signs of other possible causes should be sought (eg, examination of the peripheral pulses to rule out possible vascular cause or ischemia of the conus medullaris).



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Muscle groups, surface anatomy, peripheral sensory innervation, and dermatomes of the anterior lower limb. This image should be correlated with Tables....



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Muscle groups, surface anatomy, peripheral sensory innervation, and dermatomes of the posterior lower limb. This image should be correlated with Table....

Pain and deficits associated with nerve root involvement are shown in Table 2, below.

Table 2. Pain and Deficits Associated with Specific Nerve Roots



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Table 3. Root and Peripheral Nerve Innervation of the Lumbosacral Plexus



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Pain often is localized to the low back; local tenderness to palpation or percussion may be present. Pain in the legs (or radiating to the legs) is characteristic of cauda equina syndrome. Radicular pain is a common presentation in patients with cauda equina syndrome, usually in association with radicular sensory loss (saddle anesthesia), asymmetric paraplegia with loss of tendon reflexes, muscle atrophy, and bladder dysfunction. The presentation is somewhat similar to and is often confused with conus and epiconus lesions.

Reflex abnormalities may be present; they typically include loss or diminution of reflexes. Hyperactive reflexes may signal spinal cord involvement and exclude the diagnosis of cauda equina syndrome. Sensory abnormality may be present in the perineal area or lower extremities. Light touch in the perineal area should be tested. Anesthetic areas may show skin breakdown.

Muscle weakness may be present in muscles supplied by affected roots. Muscle wasting may occur in chronic cauda equina syndrome.

Poor anal sphincter tone is characteristic of cauda equina syndrome. Babinski sign or other signs of upper motor neuron involvement suggest a diagnosis other than cauda equina syndrome, possibly spinal cord compression.

In cauda equina syndrome, the peripheral nerve fibers from the sacral segments of the cord, as well as various lumbar dorsal and ventral nerve roots, may also be involved. This results in an asymmetric and higher distribution of motor and sensory symptoms and signs in the lower extremities. Incontinence of bowel and bladder is not severe and develops late for the same reason.

In conus and epiconus lesions, the sacral region neurons (S2-S4) are destroyed. The destruction of these neurons leads to an early and more severe involvement of bowel, urinary bladder, and sexual dysfunction than seen in those with CES. In contrast, for the same reason, the motor and sensory symptoms in the lower extremities are often not very severe and only the distal parts of the limb musculature are involved.

The anatomical proximity of the conus medullaris, the epiconus, and the cauda equina can lead to 2 of these anatomical structures being involved via a single lesion, resulting in an overlap of symptomatology.

The salient features and findings of cauda equina syndrome and conus medullaris syndrome are listed in Table 4, below.

Table 4. Cauda Equina Versus Conus Medullaris Syndrome



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Cauda equina syndrome

In cauda equina syndrome, muscle strength in the lower extremities is diminished. This may be specific to the involved nerve roots as listed below, with the lower lumbar and sacral roots more affected, leading to diminished strength in the glutei muscles, hamstring muscles (ie, semimembranosus, semitendinosus, biceps femoris), and the gastrocnemius and soleus muscles.

Sensation is decreased to pinprick and light touch in a dermatomal pattern corresponding to the affected nerve roots. This includes saddle anesthesia (sometimes including the glans penis or clitoris) and decreased sensation in the lower extremities in the distribution of lumbar and sacral nerves. Vibration sense may also be affected. Sensation of the glans penis or clitoris should be examined.

Muscle stretch reflexes may be absent or diminished in the corresponding nerve roots. Babinski reflex is diminished or absent.

Bulbocavernosus reflexes may be absent or diminished. This should always be tested.

Anal sphincter tone is patulous and should always be tested since it can define the completeness of the injury (with bulbocavernosus reflex); it is also useful in monitoring recovery from the injury.

Urinary incontinence could also occur secondary to loss of urinary sphincter tone; this may also present initially as urinary retention secondary to a flaccid bladder.

Muscle tone in the lower extremities is decreased, which is consistent with an LMN lesion.

Conus medullaris syndrome

Patients may exhibit hypertonicity, especially if the lesion is isolated and primarily UMN.

Signs are almost identical to those of the cauda equina syndrome, except that in conus medullaris syndrome signs are more likely to be bilateral; sacral segments occasionally show preserved bulbocavernosus reflexes and normal or increased anal sphincter tone; the muscle stretch reflex may be hyperreflexic, especially if the conus medullaris syndrome (ie, UMN lesion) is isolated; Babinski reflex may affect the extensors; and muscle tone might be increased (ie, spasticity).

Other signs include papilledema (rare, occurs in lower spinal cord tumors), cutaneous abnormalities (eg, cutaneous angioma, pilonidal sinus that may be present in dermoid or epidermoid tumors), distended bladder due to areflexia, and other spinal abnormalities (noted on lower back examination) predisposing the patient to the syndrome.

Muscle strength

Physical examination for cauda equina or conus medullaris syndromes would be incomplete without tests for sensation of the saddle and perineal areas, bulbocavernosus reflex, cremasteric reflex, and anal sphincter tone, findings for all of which are likely to be abnormal.

Muscle strength of the following muscles should be tested to determine the level of lesion:

ASIA impairment scale

In defining impairments associated with a spinal cord lesion, the American Spinal Cord Injury Association (ASIA) impairment scale is used in determining the level and extent of injury.

This scale should also be used in defining the extent of conus medullaris syndrome/cauda equina syndrome. The scale is as follows:

The injury should be described using this scale, for example, ASIA class A. Most patients with cauda equina/conus medullaris syndrome are in ASIA class A or B initially and gradually improve to class C, D, or E.

Complications

Complications include the following:

Approach Considerations

The diagnosis of cauda equina syndrome generally is possible on the basis of medical history and physical examination findings. Radiologic and laboratory studies are used to confirm the diagnosis and for localizing the site of the pathology and the underlying cause.

Myelography,[79] computed tomography,[80] and MRI are each used in specific cases with good degrees of accuracy. Each test can be used to determine the level of pathology and aid in the determination of the cause of the syndrome. Bone scan may detect malignant tumor or metastases and inflammatory conditions affecting the vertebrae.

Due to its ability to depict the soft tissues, MRI generally has been the favored imaging study for assisting the physician in the diagnosis of cauda equina syndrome.[81, 82, 83] Urgent MRI is recommended for all patients who have new-onset urinary symptoms with associated back pain or sciatica.

Nevertheless, the superiority of MRI over CT is only suggested by case reports. Early consultation with the appropriate subspecialty is encouraged to guide imaging studies.[24]

Depending on the findings from the history and physical examination, laboratory studies can include basic blood tests, chemistries, fasting blood sugar, sedimentation rate, and syphilis and Lyme serologies. CSF examination should also be included if signs of meningitis are present.[84]

Alteration in bladder function may be assessed empirically by obtaining urine via catheterization. A significant volume with little or no urge to void, or as a post-void residual, may indicate bladder dysfunction. Bedside ultrasonography may be also used to estimate or measure post-void residual bladder volume.

Urodynamic studies are useful to evaluate the degree and cause of sphincter dysfunction, as well as to monitor recovery of bladder function following decompression surgery. Intraoperative monitoring of somatosensory and motor evoked potentials allows for evaluation of radiculopathy and neuropathy.

Blood Studies

The following studies may help to define possible causes and any associated pathology, especially other causes of lesions in the lower spinal cord or cauda equina:

Radiography

Plain radiography is unlikely to be helpful in cauda equina syndrome but may be performed in cases of traumatic injury or in search of destructive changes, disk-space narrowing, or spondylolysis. For example, plain radiographs of the lumbosacral spine may depict early changes in vertebral erosions secondary to tumors and spina bifida.

Chest radiography is indicated to rule out a pulmonary source of pathology that could affect the lumbosacral spine (eg, malignant tumor, tuberculosis). Follow-up chest CT may be required.

Magnetic Resonance Imaging

MRI with gadolinium contrast of the lumbosacral area is the diagnostic test of choice to define pathology in the areas of the conus medullaris and cauda equina (see the images below). It provides a more complete radiographic assessment of the spine than other tests; plain x-rays and CT scan may be normal.[85, 82] . Gadolinium contrast MRI also may be able to rule out abdominal aneurysm, which could be the source of emboli causing conus medullaris infarction. See the following images for representative MRIs.



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Conus/epiconus infarction in the setting of sickle cell crisis. Image courtesy of Matthew J. Baker, MD.



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Conus/epiconus infarction in the setting of sickle cell crisis in the same patient shown in the above image. Image courtesy of Matthew J. Baker, MD.



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Conus/epiconus infarction in the setting of sickle cell crisis in the same patient shown in the images above. Image courtesy of Matthew J. Baker, MD.

Schwannomas are visible using myelography, but MRI is the criterion standard. Schwannomas are isointense on T1 images, hyperintense on T2 images, and enhanced with gadolinium contrast. With infectious conditions, MRI can display the abnormal appearance of the nerve roots being forced to one side of the dural sac.

Other Tests and Procedures

Needle electromyography (EMG)[86] may show evidence of acute denervation, especially in cauda equina lesions and multilevel lumbar spinal stenosis. EMG studies also could help in predicting prognosis and monitoring recovery. Performing needle EMG of the bilateral external anal sphincter muscles is recommended.

Nerve conduction studies,[12] especially of the pudendal nerve, may rule out more distal peripheral nerve lesions.

Somatosensory evoked potentials (SSEPs)[12] could be done as part of the workup to rule out multiple sclerosis, which could present initially as a lower spinal cord syndrome.

Duplex ultrasound of peripheral vessels may rule out compromised vasculature as a possible cause of associated claudication.

Lumbar puncture should be performed to examine the CSF to rule out inflammatory disease of the meninges or spinal cord.

Approach Considerations

Specific treatment is directed at the primary cause; these are discussed in other articles. The general treatment goals are to minimize the extent of injury and to treat ensuing general complications.[87]

Other medical treatment options are useful in certain patients, depending on the underlying cause of the cauda equina syndrome. Anti-inflammatory agents and steroids can be effective in patients with inflammatory processes, including ankylosing spondylitis.

Patients with cauda equina syndrome secondary to infectious causes should receive appropriate antibiotic therapy. Patients with spinal neoplasms should be evaluated for the suitability of chemotherapy and radiation therapy.

Methylprednisolone should be administered. It treatment must be started within 8 hours of injury. No evidence exists of any benefit if it is started more than 8 hours after injury; on the contrary, late treatment may have detrimental effects.

Administration of ganglioside GM1 sodium salt beginning within 72 hours of injury may be beneficial; the dose is 100 mg IV qd for 18-32 days.

Tirilazad mesylate (a nonglucocorticoid 21-aminosteroid) has been proven to be of benefit in animals and is currently under investigation. It inhibits lipid peroxidation and hydrolysis in the same manner as glucocorticoids.

Caution should be used in all forms of medical management for cauda equina syndrome. Any patient with true cauda equina syndrome with symptoms of saddle anesthesia and/or bilateral lower extremity weakness or loss of bowel or bladder control should undergo no more than 24 hours of initial medical management. If no relief of symptoms is achieved during this period, immediate surgical decompression is necessary to minimize the chances of permanent neurologic injury.

Emergency Department Care

No proven medical treatment exists, and therapy generally is directed at the underlying cause of cauda equina syndrome. For penetrating trauma, steroids have not shown significant benefit.

Surgery is controversial. The timing of decompression is controversial, with immediate, early, and late surgical decompression showing varying results.[15, 88, 89] For mechanical compression of the cauda due to disk herniation, surgical intervention may be indicated.

Practice guidelines for the management of low back pain have been created.[90, 91, 92]

Admit patients to the appropriate service (usually neurology, neurosurgery, or orthopedic surgery) with frequent neurologic checks. Ideally, the admitting physician or service should examine the patient at the time of admission. Patients in whom acute cauda equina syndrome is being considered should not be treated or investigated on an outpatient basis without evaluation by a consultant and/or appropriate imaging.

Rehabilitation

The rehabilitation team, especially the spinal cord injury rehabilitation physician and occupational and physical therapists, should be involved as soon as possible. The team will set goals in the rehabilitation unit toward maintaining and improving endurance, with the ability to be independent in activities of daily living on discharge from the hospital or long-term care facility.

The rehabilitation goals are to maximize the medical, physical, psychological, educational, vocational, and social function of the patient. To maximize medical function, ensure adequate prevention and treatment of possible medical complications already discussed, especially deep venous thrombosis, bladder and bowel problems, and decubitus ulcers

Physical therapy

Perform range of motion and strengthening exercises, sitting balance, transfer training, and tilt table as tolerated (because of tendency to orthostatic hypotension). Tilt table should start at 15 degrees, progressing by 10 degrees every 15 minutes up to about 80 degrees with the necessary precautions.

Other activities include the following:

Occupational therapy

Conduct the following:

Orthotic/assistive devices may be needed for functional household ambulation and, if possible, community ambulation. This entails prescribing and training in proper use of knee-ankle-foot orthoses (KAFO) with forearm crutches for support; for lower lesions, KAFOs or AFOs with canes or crutches may be needed. In addition to the above, bathtub bench, transfer boards, pressure-relieving seats, and wheelchairs are devices that may be needed. The patient should be assessed for these needs prior to discharge from the acute rehabilitation setting.

Consultations

Consultations to different specialties are needed for acute care and follow-up care. Neurosurgery/spinal orthopedics consultation should assess the need for urgent surgical spinal decompression. Posterior decompression and stabilization offers at least equivalent neurologic outcomes as nonoperative or anterior approaches and has the additional benefits of surgeon familiarity, shorter hospital stays, earlier rehabilitation, and ease of nursing care.[16]

Plastic surgery may be needed if severe skin breakdowns occur.

For rehabilitation, the initial consultation may prevent possible complications, including contractures, and may offer the patient advice on bladder/bowel management, wound management, and the required physical therapy/occupational therapy and assistive devices; this would include follow-up, involvement of social workers, and vocational rehabilitation experts for home adaptation (needed on discharge).

A dietitian is needed to advise on optimizing the diet to ensure adequate caloric and protein intake. Patients with these syndromes often have an increase in metabolism associated with the healing process.

Long-Term Monitoring

Follow up with the rehabilitation team, including the spinal cord injury rehabilitation physician, physical therapist, and occupational therapist. These professionals are responsible for monitoring community and home integration and following improvements in the patient's strength, coordination, transfer, activities of daily living, and ambulation.

Follow up with a primary care physician to monitor posthospital medications and other laboratory tests.

Patients with any renal or bladder complications and impotence should undergo regular follow-up, because they have an increased tendency for recurrent urinary tract infection and calculi.[19] Yearly cystoscopy is recommended for patients with suprapubic catheters to help detect early bladder malignancies.

Regular follow-up urodynamic studies, renal ultrasound, and general cancer screening should be performed.

Prevention and Treatment of Complications

For deep venous thrombosis/pulmonary embolism, patients should use antiembolic compression stockings and subcutaneous heparin for 3 months as prophylaxis. Low-molecular-weight heparin also has been approved for prophylaxis. Ultrasound of the lower extremities may need to be done as an initial screening test with follow-up later. For neurogenic bladder, patients may require bladder catheterization.

In August 2011, onabotulinumtoxinA was approved by the US Food and Drug Administration for urinary incontinence in patients with neurologic conditions (eg, spinal cord injury, multiple sclerosis) who have overactive bladder. Therapy consists of 30 intradetrusor injections via cystoscopy. Trials have shown patients who received onabotulinumtoxinA had significant reduction in urinary incontinence episodes and improved urodynamics compared with placebo at 12 weeks.[93, 94, 95]

Pressure ulcers may be prevented by eliminating pressure, optimizing wound-healing environment, and debriding if necessary.

For impotence, use of a phosphodiesterase type 5 inhibitor (eg, sildenafil [Viagra]) is becoming popular. Other drugs for erectile dysfunction include yohimbine, papaverine, and alprostadil. Methods to promote coitus and/or ejaculation could also be used; these include implantable penile prostheses or vibrator stimulation.

Patients may require use of stool softener or manual evacuation for fecal incontinence.

Heterotopic ossification (HO) can be confirmed by a triple-phase bone scan with associated elevation in serum levels of alkaline phosphatase and phosphate, especially in the early stage. Treatment includes stretching exercises, disodium etidronate (20 mg/kg qd x 2 wk, then 10 mg/kg for as long as 12 wk), radiation, and surgical excision. Surgery is done only when the HO has matured or stabilized, which is evident by stable plain x-ray, normal alkaline phosphatase level, and decline in triple-phase bone scan activity.

Pain should be treated appropriately based on its origin; treatment may include narcotics in the acute setting and tricyclic antidepressants later. Patient education, biofeedback, and relaxation techniques may also be used.

Nerve root ischemia is partially responsible for the pain and decreased motor strength associated with cauda equina syndrome. As a result, vasodilatory treatment can be useful in some patients. Mean arterial blood pressure should be maintained above 90 mm Hg to maximize blood flow to the spinal cord and nerve roots.

Treatment with lipoprostaglandin E1 and its derivatives has been reported to be effective in increasing blood flow to the cauda equina region and reducing symptoms of pain and motor weakness. This treatment option should be reserved for patients with modest spinal stenosis with neurogenic claudication. No benefit has been reported in patients with more severe symptoms or patients with radicular symptoms.

Use of orthoses is advised to prevent contractures. Use of antispasticity medications also is encouraged. Other medications include dantrolene, diazepam, clonidine, and tizanidine. Nerve blocks also could be done to relieve spasticity; appropriate agents include phenol, botulinum toxin, or local anesthetics.

Surgical Decompression

In acute compression of the conus medullaris or cauda equina, surgical decompression as soon as possible becomes mandatory. The goal is to relieve the pressure on the nerves of the cauda equina by removing the compressing agent and increasing the space in the spinal canal. Traditionally, cauda equina syndrome has been considered a surgical emergency, with surgical decompression considered necessary within 48 hours after the onset of symptoms, and preferably performed within 6 h of injury.[61, 96, 97, 98]

For patients in whom a herniated disk is the cause of cauda equina syndrome, a laminotomy or laminectomy to allow for decompression of the canal is recommended, followed by gentle retraction and discectomy.

In a more chronic presentation with less severe symptoms, decompression could be performed when medically feasible and should be delayed to optimize the patient's medical condition; with this precaution, decompression is less likely to lead to irreversible neurological damage.

Surgical treatment may be necessary for decompression or tumor removal, especially if the patient presents with acute onset of symptoms. Surgical treatment may include laminectomy and instrumentation/fusion for stabilization or discectomy. Other surgical care may entail wound care (eg, debridement, skin graft, and skin flap/myocutaneous flap).

Many clinical and experimental reports have presented data on the functional outcome based on the timing of surgical decompression.[4] Several investigators have reported no significant differences in the degree of functional recovery as a function of the timing of surgical decompression.[96, 97, 99] Even with these findings, however, most investigators recommend surgical decompression as soon as possible after the onset of symptoms to offer the greatest chance of complete neurologic recovery.

On discharge from the surgical ward, patients often are transferred to an acute rehabilitation unit, from which they may be discharged, transferred to a subacute unit, or transferred to long-term care, depending on the level of long-term disability.

Medication Summary

Appropriate analgesia should be provided for a patient with cauda equina syndrome. Anti-inflammatory medication may prevent worsening of injury. Anticoagulants provide prophylaxis against thrombotic complications. Use of antispasticity medications to reduce muscle tone is encouraged. Bisphosphonates may be beneficial in patients with bony lesions. Phosphodiesterase type 5 inhibitors treat erectile dysfunction (ED).

Methylprednisolone (DepoMedrol, Medrol, Medrol Dosepak)

Clinical Context:  This agent decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing increased capillary permeability. This prevents further worsening of injury.

Treatment must be started within 8 h of injury; treatment apparently has no benefit if started later than 8 h after injury. Late treatment may have detrimental effects.

Class Summary

These agents have anti-inflammatory properties and cause profound and varied metabolic effects. Corticosteroids modify the body's immune response to diverse stimuli.

Heparin

Clinical Context:  Heparin augments the activity of antithrombin III and prevents conversion of fibrinogen to fibrin. It does not actively lyse clot but is able to inhibit further thrombogenesis. It prevents re-accumulation of clot after spontaneous fibrinolysis. Administer low dose.

Class Summary

These agents are taken as prophylaxis for deep venous thrombosis and/or pulmonary embolism.

Baclofen (Lioresal, Gablofen)

Clinical Context:  Baclofen may induce hyperpolarization of afferent terminals and inhibit both monosynaptic and polysynaptic reflexes at the spinal level.

Dantrolene (Dantrium, Revonto)

Clinical Context:  Dantrolene stimulates muscle relaxation by modulating skeletal muscle contractions at sites beyond the myoneural junction and acting directly on muscle itself. It prevents calcium release from sarcoplasmic reticulum.

Class Summary

These agents are thought to work centrally by suppressing conduction at the spinal level.

Diazepam (Diastat, Valium)

Clinical Context:  Diazepam depresses all levels of the CNS (eg, limbic and reticular formation), possibly by increasing activity of gamma-aminobutyric acid (GABA). Individualize dosage and increase cautiously to avoid adverse effects.

Class Summary

These agents may act in the spinal cord to induce muscle relaxation.

Clonidine (Catapres)

Clinical Context:  Clonidine stimulates alpha2-adrenoreceptors in the brain stem, activating an inhibitory neuron, which in turn results in reduced sympathetic outflow.

Tizanidine (Zanaflex)

Clinical Context:  Tizanidine is a centrally acting muscle relaxant that is metabolized in the liver and excreted in urine and feces.

Class Summary

These agents may reduce sympathetic outflow, which may produce a reduction in muscle tone.

OnabotulinumtoxinA (BOTOX)

Clinical Context:  This agent binds to receptor sites on motor nerve terminals and inhibits release of acetylcholine, which in turn inhibits transmission of impulses in neuromuscular tissue.

It is most useful for treating spasticity in the gastrocnemius and soleus muscles; less effective in larger muscles such as quadriceps. Re-examine patients 7-14 d after initial dose, to assess for response. It may be repeated q3-4mo.

Also indicated for urinary incontinence in patients with neurologic conditions (eg, spinal cord injury, multiple sclerosis) in adults who have an inadequate response to or are intolerant of an anticholinergic medication. Intradetrusor injections are administered about every 9 months.

Class Summary

These agents inhibit transmission of impulses in neuromuscular tissue.

Etidronate disodium

Clinical Context:  Etidronate inhibits normal and abnormal bone resorption. It appears to inhibit bone resorption without inhibiting bone formation and mineralization.

Alendronate (Fosamax, Binosto)

Clinical Context:  Alendronate inhibits bone resorption via actions on osteoclasts or osteoclast precursors. It is used to treat osteoporosis in both men and women and it may reduce bone resorption and incidence of fracture at spine, hip, and wrist by approximately 50%. Alendronate should be taken with a large glass of water, at least 30 min before eating and drinking, to maximize absorption. Because of possible esophageal irritation, patients must remain upright after taking the medication. Since it is renally excreted, it is not recommended in patients with moderate-to-severe renal insufficiency (ie, CrCl < 30 mL/min or CrCl >3.0 mg/dL), thus its use in perirenal transplantation is limited.

Ibandronate (Boniva)

Clinical Context:  Ibandronate inhibits osteoclast-mediated bone resorption. In postmenopausal women, it reduces bone turnover rate, leading to a net gain in bone mass.

Class Summary

These agents are analogs of pyrophosphate. They act by binding to hydroxyapatite in bone-matrix, thereby inhibiting the dissolution of crystals. They prevent osteoclast attachment to the bone matrix and osteoclast recruitment and viability.

Sildenafil (Viagra)

Clinical Context:  Sildenafil is a phosphodiesterase type 5 (PDE5) selective inhibitor. Inhibition of PDE5 increases the activity of cyclic guanosine monophosphate (cGMP), which increases the vasodilatory effects of nitric oxide. This agent is effective in men with mild-to-moderate ED.

Vardenafil (Levitra, Staxyn)

Clinical Context:  Vardenafil is a PDE5 selective inhibitor. Inhibition of PDE5 increases cGMP activity, which increases the vasodilatory effects of nitric oxide. It is effective in men with mild-to-moderate ED.

Take on an empty stomach about 1 h before sexual activity. Sexual stimulation is necessary to activate response. Increased sensitivity for erections may last 24 h. Vardenafil is available as 2.5-mg, 5-mg, 10-mg, and 20-mg tabs.

Tadalafil (Cialis)

Clinical Context:  Tadalafil is a PDE5 selective inhibitor. Inhibition of PDE5 increases cGMP activity, which increases the vasodilatory effects of nitric oxide. Sexual stimulation is necessary to activate response. Increased sensitivity for erections may last 36 h. Tadalafil is available as 2.5-mg, 5-mg, 10-mg, and 20-mg tabs.

Class Summary

These agents increase the vasodilatory effects of nitric oxide by inhibiting the enzyme phosphodiesterase type 5, which in turn increases sensitivity for erections.

What is the anatomy of cauda equina?What is cauda equina syndrome (CES)?Which spinal cord anatomical features are useful in understanding cauda equina and conus medullaris syndrome?What is the anatomy of the cauda equina (CE) and conus medullaris?What type of symptoms accompany conus medullaris injuries?What is the pathogenesis of cauda equina syndrome (CES)?What is the role of compression in the pathophysiology of cauda equina syndrome (CES)?What causes cauda equina syndrome (CES)?What are the most common causes of cauda equina and conus medullaris syndromes?What are less common causes of cauda equina and conus medullaris syndromes?What does the lack of structural pathology indicate in cauda equina syndrome (CES)?What is the role of trauma in the etiology of cauda equina syndrome (CES)?What is the frequency of cauda equina syndrome (CES) caused by a herniated lumbar disk?In what conditions is cauda equina syndrome (CES) secondary to spinal stenosis?Which primary malignancies cause cauda equina syndrome (CES)?Which metastatic cancers may cause cauda equina syndrome (CES)?Which inflammatory conditions may lead to cauda equina syndrome (CES)?What are infectious causes of cauda equina syndrome (CES)?What are uncommon causes of cauda equina syndrome (CES)?What are possible iatrogenic causes of cauda equina syndrome (CES)?How are cauda equina and conus medullaris syndromes classified?How common is cauda equina syndrome (CES)?Does the incidence of cauda equina syndrome (CES) vary by age?How are morbidity and mortality rates of cauda equina and conus medullaris syndromes determined?Which factors are prognostic indicators in cauda equina syndrome (CES)?How is the ASIA) impairment scale used to predict prognosis in cauda equina and conus medullaris syndromes be predicted by?How is ambulatory capability predicted in cauda equina and conus medullaris syndromes?What information about cauda equina and conus medullaris syndromes should patients receive?What are the signs and symptoms of cauda equina and conus medullaris?What are the most common symptoms of cauda equina syndrome (CES)?How is back pain characterized in cauda equina syndrome (CES)?What are the urinary symptoms of cauda equina syndrome?What bowel dysfunction may be present in cauda equina and conus medullaris syndromes?What types of lesions are associated with cauda equina syndrome (CES)?Which pain and deficits of nerve roots suggest cauda equina syndrome (CES)?Where is pain located in cauda equina and conus medullaris syndromes?What reflex abnormalities may be present in cauda equina and conus medullaris syndrome?When is a finding of muscle weakness suggestive of cauda equina syndrome (CES)?Which findings of upper motor neuron involvement help to differentiate cauda equina syndrome from spinal cord compression?How do motor and sensory symptoms differ between cauda equina syndrome (CES) and conus medullaris?What cause overlapping symptomology between cauda equina and conus medullaris syndrome?What are the physical findings characteristic of cauda equina and conus medullaris syndrome?What are the motor and sensory findings characteristic of cauda equina syndrome?What are the motor and sensory findings characteristic of conus medullaris syndrome?Which tests should be performed during the physical exam of cauda equina and conus medullaris syndrome?Which muscles should be assessed during a physical exam of suspected cauda equina and conus medullaris syndrome?Which is the role of the ASIA impairment scale in the evaluation of cauda equina and conus medullaris syndromes?What are possible complications of cauda equina and conus medullaris syndromes?What conditions should be included in the differential diagnoses of conus medullaris syndrome?What conditions should be included in the differential diagnosis of cauda equina syndrome (CES)?What are the differential diagnoses for Cauda Equina and Conus Medullaris Syndromes?How is cauda equina syndrome (CES) diagnosed?What tests are performed in the workup of cauda equina and conus medullaris syndrome?What is the role of imaging studies in the diagnosis of cauda equina and conus medullaris syndrome?What is the role of lab studies in the diagnosis of cauda equina and conus medullaris syndrome?How is bladder function assessed during the evaluation of cauda equina and conus medullaris syndrome?How is sphincter dysfunction assessed during the evaluation of cauda equina and conus medullaris syndrome?Which studies are performed to identify the underlying cause of cauda equina syndrome (CES)?What is the role of radiography in the evaluation of cauda equina and conus medullaris syndrome?What is the role of MRI in the evaluation of conus medullaris and cauda equina syndrome?What is the role of needle EMG in the evaluation of cauda equina and conus medullaris syndrome?Which tests are performed to rule out differential diagnoses of cauda equina and conus medullaris syndrome?What are treatment options for cauda equina and conus medullaris syndrome?When should medication be initiated for the treatment of cauda equina and conus medullaris syndrome?What is the role of tirilazad mesylate in the treatment of cauda equina and conus medullaris syndrome?When is surgical intervention indicated in the treatment of cauda equina and conus medullaris syndrome?What is the focus of ED treatment of cauda equina and conus medullaris syndrome?When is hospitalization indicated for the treatment of cauda equina or conus medullaris?What is the role of rehabilitation therapy in the treatment of cauda equina and conus medullaris syndrome?What are goals for rehabilitation therapy of cauda equina and conus medullaris syndrome?Which exercises should be included in the physical therapy for cauda equina and conus medullaris syndrome?What should be included in the rehabilitation therapy for cauda equina and conus medullaris syndrome?What should be included in occupational therapy for cauda equina and conus medullaris syndrome?Which specialist consultations are needed for the treatment of cauda equina and conus medullaris syndrome?What monitoring should be provided by the rehabilitation team of patients with cauda equina and conus medullaris syndrome?When is follow-up with a physician indicated for patients with cauda equina and conus medullaris syndrome?How are the complications of cauda equina and conus medullaris syndrome managed?What is the role of onabotulinumtoxinA (Botox) in the treatment of cauda equina and conus medullaris syndrome?How are pressure ulcers prevented in patients with cauda equina and conus medullaris syndrome?How is erectile dysfunction managed in cauda equina and conus medullaris syndrome?When are stool softeners indicated in the treatment of cauda equina and conus medullaris syndrome?What are the treatment options for heterotopic ossification (HO) in cauda equina and conus medullaris syndrome?How is pain associated with cauda equina and conus medullaris syndrome treated?What is the role of lipo prostaglandin E1 in the treatment of cauda equina syndrome?How are contractures prevented in cauda equina and conus medullaris syndrome?When is surgical decompression indicated in the treatment of cauda equina and conus medullaris syndrome?How does the timing of surgical intervention for cauda equina and conus medullaris syndrome affect functional outcome?Where should patients be transferred following surgery for cauda equina and conus medullaris syndrome?What medications are used in the treatment of cauda equina and conus medullaris syndrome?Which medications in the drug class Phosphodiesterase (type 5) Enzyme Inhibitors are used in the treatment of Cauda Equina and Conus Medullaris Syndromes?Which medications in the drug class Bisphosphonate Derivatives are used in the treatment of Cauda Equina and Conus Medullaris Syndromes?Which medications in the drug class Neuromuscular Blocker Agent, Toxin are used in the treatment of Cauda Equina and Conus Medullaris Syndromes?Which medications in the drug class Alpha 2-adrenergic Agonist Agents are used in the treatment of Cauda Equina and Conus Medullaris Syndromes?Which medications in the drug class Benzodiazepines are used in the treatment of Cauda Equina and Conus Medullaris Syndromes?Which medications in the drug class Skeletal Muscle Relaxants are used in the treatment of Cauda Equina and Conus Medullaris Syndromes?Which medications in the drug class Anticoagulants are used in the treatment of Cauda Equina and Conus Medullaris Syndromes?Which medications in the drug class Corticosteroids are used in the treatment of Cauda Equina and Conus Medullaris Syndromes?

Author

Segun Toyin Dawodu, JD, MD, MS, MBA, LLM, FAAPMR, FAANEM, Attending Interventional Physiatrist, Wellspan Health

Disclosure: Nothing to disclose.

Coauthor(s)

James F Kellam, MD, FRCSC, FACS, FRCS(Ire), Professor, Department of Orthopedic Surgery, University of Texas Medical School at Houston

Disclosure: Nothing to disclose.

Kirsten A Bechtel, MD, Associate Professor of Pediatrics, Section of Pediatric Emergency Medicine, Yale University School of Medicine; Co-Director, Injury Free Coalition for Kids, Yale-New Haven Children's Hospital

Disclosure: Nothing to disclose.

Michael S Beeson, MD, MBA, FACEP, Professor of Emergency Medicine, Northeastern Ohio Universities College of Medicine and Pharmacy; Attending Faculty, Akron General Medical Center

Disclosure: Nothing to disclose.

Scott D Hodges, DO, Consulting Surgeon, Department of Orthopedic Surgery, Center for Sports Medicine and Orthopedics

Disclosure: Received royalty from Medtronic for consulting; Received royalty from Biomet Spine for consulting.

S Craig Humphreys, MD, Orthopedic Spine Surgeon, Department of Orthopedic Surgery, Center for Sports Medicine and Orthopedics

Disclosure: Nothing to disclose.

Specialty Editors

Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

J Stephen Huff, MD, FACEP, Professor of Emergency Medicine and Neurology, Department of Emergency Medicine, University of Virginia School of Medicine

Disclosure: Nothing to disclose.

Chief Editor

Nicholas Lorenzo, MD, MHA, CPE, Co-Founder and Former Chief Publishing Officer, eMedicine and eMedicine Health, Founding Editor-in-Chief, eMedicine Neurology; Founder and Former Chairman and CEO, Pearlsreview; Founder and CEO/CMO, PHLT Consultants; Chief Medical Officer, MeMD Inc; Chief Strategy Officer, Discourse LLC

Disclosure: Nothing to disclose.

Additional Contributors

Milind J Kothari, DO, Professor, Department of Neurology, Pennsylvania State University College of Medicine; Consulting Staff, Department of Neurology, Penn State Milton S Hershey Medical Center

Disclosure: Nothing to disclose.

Acknowledgements

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous author Jason C Eck, DO, MS,to the development and writing of a source article.

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Illustration demonstrating the relevant anatomy of the cauda equina region

Illustration demonstrating an example of cauda equina syndrome secondary to a spinal neoplasm

Sagittal MRI of a patient with cauda equina syndrome secondary to a large lumbar disk herniation

Muscle groups, surface anatomy, peripheral sensory innervation, and dermatomes of the anterior lower limb. This image should be correlated with Tables 1 and 2 in the text. Image courtesy of Nicholas Y. Lorenzo, MD.

Muscle groups, surface anatomy, peripheral sensory innervation, and dermatomes of the posterior lower limb. This image should be correlated with Tables 1 and 2 in the text. Image courtesy of Nicholas Y. Lorenzo, MD.

Conus/epiconus infarction in the setting of sickle cell crisis. Image courtesy of Matthew J. Baker, MD.

Conus/epiconus infarction in the setting of sickle cell crisis in the same patient shown in the above image. Image courtesy of Matthew J. Baker, MD.

Conus/epiconus infarction in the setting of sickle cell crisis in the same patient shown in the images above. Image courtesy of Matthew J. Baker, MD.

Muscle groups, surface anatomy, peripheral sensory innervation, and dermatomes of the anterior lower limb. This image should be correlated with Tables 1 and 2 in the text. Image courtesy of Nicholas Y. Lorenzo, MD.

Muscle groups, surface anatomy, peripheral sensory innervation, and dermatomes of the posterior lower limb. This image should be correlated with Tables 1 and 2 in the text. Image courtesy of Nicholas Y. Lorenzo, MD.

Conus/epiconus infarction in the setting of sickle cell crisis. Image courtesy of Matthew J. Baker, MD.

Conus/epiconus infarction in the setting of sickle cell crisis in the same patient shown in the above image. Image courtesy of Matthew J. Baker, MD.

Conus/epiconus infarction in the setting of sickle cell crisis in the same patient shown in the images above. Image courtesy of Matthew J. Baker, MD.

Illustration demonstrating the relevant anatomy of the cauda equina region

Illustration demonstrating an example of cauda equina syndrome secondary to a spinal neoplasm

Sagittal MRI of a patient with cauda equina syndrome secondary to a large lumbar disk herniation

Epidural abscess with effacement of thecal sac in a 56-year-old man.

  Conus Medullaris Syndrome Cauda Equina Syndrome
PresentationSudden and bilateralGradual and unilateral
ReflexesKnee jerks preserved but ankle jerks affectedBoth ankle and knee jerks affected
Radicular painLess severeMore severe
Low back painMoreLess
Sensory symptoms and signsNumbness tends to be more localized to perianal area; symmetrical and bilateral; sensory dissociation occursNumbness tends to be more localized to saddle area; asymmetrical, may be unilateral; no sensory dissociation; loss of sensation in specific dermatomes in lower extremities with numbness and paresthesia; possible numbness in pubic area, including glans penis or clitoris
Motor strengthTypically symmetric, hyperreflexic distal paresis of lower limbs that is less marked; fasciculations may be presentAsymmetric areflexic paraplegia that is more marked; fasciculations rare; atrophy more common
ImpotenceFrequentLess frequent; erectile dysfunction that includes inability to have erection, inability to maintain erection, lack of sensation in pubic area (including glans penis or clitoris), and inability to ejaculate
Sphincter dysfunctionUrinary retention and atonic anal sphincter cause overflow urinary incontinence and fecal incontinence; tend to present early in course of diseaseUrinary retention; tends to present late in course of disease
Nerve Root Pain Sensory Deficit Motor Deficit Reflex Deficit
L2Anterior medial thighUpper thighSlight quadriceps weakness; hip flexion; thigh adductionSlightly diminished suprapatellar
L3Anterior lateral thighLower thighQuadriceps weakness; knee extension; thigh adductionPatellar or suprapatellar
L4Posterolateral thigh, anterior tibiaMedial legKnee and foot extensionPatellar
L5Dorsum of footDorsum of footDorsiflexion of foot and toesHamstrings
S1-2Lateral footLateral footPlantar flexion of foot and toesAchilles
S3-5PerineumSaddleSphinctersBulbocavernosus; anal
Muscle Nerve Root
IliopsoasFemoralL2, 3, 4
Adductor longusObturatorL2, 3, 4
GracilisObturatorL2, 3, 4
Quadriceps femorisFemoralL2, 3, 4
Anterior tibialDeep peronealL4, 5
Extensor hallucis longusDeep peronealL4, 5
Extensor digitorum longusDeep peronealL4,5
Extensor digitorum brevisDeep peronealL4, 5, S1
Peroneus longusSuperficial peronealL5, S1
Internal hamstringsSciaticL4, 5, S1
External hamstringsSciaticL5, S1
Gluteus mediusSuperior glutealL4, 5, S1
Gluteus maximusInferior glutealL5, S1, 2
Posterior tibialTibialL5, S1
Flexor digitorum longusTibialL5, S1
Abductor hallucis brevisTibial (medial plantar)L5, S1, 2
Abductor digiti quinti pedisTibial (lateral plantar)S1, 2
Gastrocnemius lateralTibialL5, S1, 2
Gastrocnemius medialTibialS1, 2
SoleusTibialS1, 2
Features Cauda Equina Syndrome Conus Medullaris
Vertebral levelL2-sacrumL1-L2
Spinal levelInjury to the lumbosacral nerve rootsInjury of the sacral cord segment (conus and epiconus) and roots
Severity of symptoms and signsUsually severeUsually not severe
Symmetry of symptoms and signsUsually asymmetricUsually symmetric
PainProminent, asymmetric, and radicularUsually bilateral and in the perineal area
MotorWeakness to flaccid paralysisNormal motor function to mild or moderate weakness
SensorySaddle anesthesia, may be asymmetricSymmetric saddle distribution, sensory loss of pin prick, and temperature sensations (Tactile sensation is spared.)
ReflexesAreflexic lower extremities; bulbocavernosus reflex is absent in low CE (sacral) lesionsAreflexic lower extremities



(If the epiconus is involved, patellar reflex may be absent, whereas bulbocavernosus reflex may be spared.)



Sphincter and sexual functionUsually late and of lesser magnitude;



lower sacral roots involvement can cause bladder, bowel, and sexual dysfunction



Early and severe bowel, bladder, and sexual dysfunction that results in a reflexic bowel and bladder with impaired erection in males
EMGMultiple root level involvement; sphincters may also be involvedMostly normal lower extremity with external anal sphincter involvement
OutcomeMay be favorable compared with conus medullaris syndromeThe outcome may be less favorable than in patients with CES