Spinal CORD Syndrome

Spinal CORD Syndrome

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).

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 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.

Symptoms of cauda equina syndrome include the following:

• Low back pain 
• Unilateral or bilateral sciatica 
• Saddle and perineal hypoesthesia or anesthesia 
• Bowel and bladder disturbances 
• Lower extremity motor weakness and sensory deficits 
• Reduced or absent lower extremity reflexes 

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:

• Retention 
• Difficulty initiating micturition 
• Decreased urethral sensation 
• Typically, urinary manifestations begin with urinary retention and are later followed by an overflow urinary incontinence.

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.

Bowel disturbances may include the following:

• Incontinence 
• Constipation 
• Loss of anal tone and sensation

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).

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.

Treatment

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.

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.

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.

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