Cauda equina syndrome

Cauda equina is the name given to the lumbar and sacral nerve roots within the dural sac caudal to the conus medullaris.

The conus medullaris is a concentrated region of cell bodies for existing lumbosacral nerve roots from L5 to S3.

The spinal cord terminates in adults between the lumbar 1 and lumbar 2 vertebrae, and caudal to this level individual nerve roots extend distally and appear like a horse’s tail or, cauda equina.

The cauda equine refers to the peripheral nerve roots that branch from the thecal sac at the terminal portion of the spinal cord, usually at L1.

The lower lumbar and sacral nerve roots distal to the  conus medullaris make up the cauda equina.

The dorsal nerve roots transmit sensory information, and the ventral roots provide motor and sympathetic output.

The anatomic levels of these nerve roots correspond with sensory motor functions of the distal limb, the peroneal and perianal sensations, and control of urinary and anal sphincters.

Cauda equina syndrome is usually the result of a ruptured, midline intervertebral disk, most commonly occurring at the L4 to L5 level.

CES results from processes that diminish the space available for the neurologic elements in the lumbosacral canal: compressive etiologies , inflammatory conditions and ischemia.

The most common cause for CES is a herniated lumbar disc, which generally occurs at the L4-5 or L5-S1 levels.

Other pathological events that can lead to the development of CES include: malignancy, infections, spinal stenosis, traumatic injuries, epidural hematoma‘s, and inflammatory diseases.

In pre-existing lumbar stenosis, lumbar sacral canal narrowing may be prone to develop CES with lesser degrees of mechanical compression.

CES may occur within 24 hours of spine surgery when the nerve roots are injured either directly or from aggressive retraction of the thecal sac.

CES can occur with direct injury from spinal epidural analgesia.

CES is minimalize postoperatively by withholding and a coagulation that can cause hematoma and by placing surgical drains.

CES is a potentially devastating spinal condition associated with significant morbidity.

Compression of the caudal nerve elements in the central spinal canal can produce a constellation of motor, sensory, and visceral symptoms known as the cauda equine syndrome.

CES ranges from mild peripheral nerve root irritation to catastrophic damage to neurologic and visceral structures.

Neurological dysfunction is a major component of CES with dysfunction of the parasympathetic, sympathetic, and somatic aspects of nerve root bladder function.

CES is associated with a patient’s loss of sense of bladder distention and cannot control the muscles that allow for micturition.

Urinary retention is the initial most common manifestation of bladder dysfunction, and it could also progress to overflow incontinence.

Saddle anesthesia can be a manifestation of CES with loss of sensation in the perineum and buttocks and portends a  poor prognosis.

Tumors and other masses may also cause the cauda equina syndrome.

Compression of the caudal nerve roots in the central spinal canal can occur secondary to: intervertebral disc herniation, traumatic fracture of the lumbar sacral vertebrae, epidural hematoma, neoplasm, epidural abscess, and progressive chronic lumbar stenosis.

Mechanical compression causes ischemia and venous congestion impairing the nutritional status of the cauda equina through diminished blood flow and nutrient diffusion from the spinal fluid.

Compression leads to swelling within the nerve roots.

When intra-neural pressure exceeds the perfusion pressure of the nerve roots, further ischemia occurs through a compartment syndrome like mechanism.

Acute or subacute intervertebral disc herniation is the most common cause of cauda equina syndrome.

The cauda equine syndrome, only occurs in approximately 2% of acute disc herniations.

Between two and 6% of all lumbar decompressions performed for disc herniation are associated with CES.

The majority of patients with CES also have a degree of low back pain, which can be subtle or delayed.

Other symptoms of CES include lower extremity sensory changes, weakness, diminished reflexes and radicular  pain.

Annual incidence of only 5 to 10 cases per million and a prevalence ranging between 1:100,000 to 1:33,000.

Cauda equina syndrome presents with symptoms of fecal or urinary incontinence, impotence, distal motor weakness, and sensory loss in a saddle distribution.

The two most common symptoms that patients with cauda equina syndrome present with include severe lower back pain in 83-100 percent of cases and unilateral or bilateral sciatica in 90-100% of cases.

Muscle stretch reflexes may be reduced in cauda equina syndrome.

Urinary retention is the single most consistent finding in cauda equina syndrome.

In acute cauda equine syndrome, immediate surgical decompression is recommended.

In a more chronic presentation, decompression is performed when medically feasible.

A serious neurologic condition in which damage to the cauda equina causes loss of function of the lumbar plexus nerve roots of the spinal canal below the termination of the. conus medullaris of the spinal cord.

Cauda equina syndrome is a lower motor neuron lesion.

Results in saddle anesthesia, which is anesthesia or paraesthesia involving S3 to S5 dermatomes.

CES is slightly more common in men than women.

Symptoms involve the perineum, external genitalia and anus.

Manifests as numbness or pins-and-needle sensations of the groin and inner thighs.

Results in bladder and bowel dysfunction, caused by decreased tone of the urinary and anal sphincters.

Sciatica-type pain on one side or both sides may occur, although pain may be wholly absent.

Weakness of the muscles of the lower legs may occur.

Bilateral absent Achilles reflex.

Sexual dysfunction

Absent anal reflex and bulbocavernosus reflex

The presence of severe back pain, saddle-like anesthesia, incontinence and sexual dysfunction require urgent investigation.

After the conus medullaris, the canal contains the mass of nerves, the cauda equina, that branches off the lower end of the spinal cord and contains the nerve roots from L1-5 and S1-5.

The nerve roots from L4-S4 join in the sacral plexus which affects the sciatic nerve, which travels caudally.

Compression, trauma or other damage to this region of the spinal canal can result in cauda equina syndrome.

The cauda equine syndrome may be a temporary side-effect of a sacral extra-dural injection.

Any lesion which compresses or disturbs the function of the cauda equina may impair the nerves, although the most common is a central disc prolapse.

Metastatic disease may also be a cause of the cauda equina syndrome, as can direct trauma.

Common causes include: iatrogenic lumbar punctures, burst fractures resulting in posterior migration of fragments of the vertebral body, severe disc herniations, spinal anaesthesia involving trauma from catheters and high local anaesthetic concentrations around the cauda equina, penetrating trauma such as knife wounds or ballistic trauma, lumbar spinal stenosis from a degenerative process of the spine or a developmental defect which is present at birth, and In the most severe cases of spondylolisthesis.

Less commonly chronic spinal inflammatory conditions such as Paget disease, neurosarcoidosis, chronic inflammatory demyelinating polyneuropathy, ankylosing spondylitis and chronic tuberculosis can cause cauda equine syndrome.

Patients most at risk for disc herniation are the most likely to develop the process.

African Americans appear slightly less likely to develop it than other groups.

Men are slightly more likely to develop it than women.

Middle age is a notable risk factor.

Heavy lifting can also be inferred as a risk factor.

Pain prick examination, shows leg analgesia with maintenance of perineal sensation.

The triad of paraplegia with lumbar loss of pain sensation and presence of perineal altered sensation help confirm the diagnosis.

CES can present with  either sudden onset or in a delayed fashion.

Insidious onset CES can be associated with delay in diagnosis and treatment:average time to surgery in a kilo and say it is 1.1 days and 3.3 days in insidious onset.

Diagnosis is usually confirmed by an MRI scan or CT scan.

Early surgery in acute onset of symptoms is important.

Early diagnosis can allow for preventive treatment.

Early diagnosis include changes in bowel and bladder function and loss of feeling in groin.

Management frequently involves surgical decompression.

When caused by a herniated disk early surgical decompression is recommended.

When of sudden onset is regarded as a medical/surgical emergency.

Surgical decompression is by means of laminectomy or other approaches may be undertaken within 6, or 48 hours of symptoms developing if a compressive lesion, is demonstrated.

Early treatment may significantly improve the long-term neurological damage.

Surgery may be required to remove blood, bone fragments, a tumor or tumors, a herniated disc or an abnormal bone growth.

If a malignant tumor cannot be removed surgically then radiotherapy or chemotherapy may be used as an alternative.

If the syndrome is due to an inflammatory condition, , anti-inflammatory agents including steroids can be used.

If a bacterial infection is the cause then an appropriate course of antibiotics can be used.

Physical therapy and rehabilitation is centered on controlling the bladder and bowel functions and decreasing muscle weakness in the lower extremities.

Rehabilitation depends on the severity of the injury.

If permanent damage occurs, bladder and bowel control may be lost or impaired.

Once surgery is performed, full recovery of bowel and bladder control can take as long as two years.

Physical therapy can assist in sitting stability, transf2242ing, balance, gait, since muscle weakness or paralysis may occur in the lower extremities.

Electrical stimulation therapy enhance muscle tone.

The prognosis is dependent on the severity and duration of compression upon the damaged nerve.

Surgical intervention with decompression of the cauda equina can assist recovery, but delay or severe nerve damage can take several years to recover due time slow nerve growth

About 50-70% of patients have urinary retention on presentation with 30-50% having an incomplete syndrome.

The latter group, especially if the history is less than a few days, usually requires emergency MRI to confirm the diagnosis followed by prompt decompression.

The nerve roots extending from the lumbar spine are susceptible to compression, leading to cauda equina syndrome.

Intervertebral discs dislocation can contribute to such compression.

Various causes include; fractures, abscesses, hematomas, and any compression of the relevant nerve roots.

In all cases of thoracolumbar spine injury in a clinical diagnosis of cauda equine syndrome must be considered.

Traumatic spinal cord injuries occur in approximately 40 people per million annually in the United States.

Traumatic spinal cord injuries can result from motor vehicle accidents, sporting injuries, falls, and other factors.

The most frequent injuries of the thoracolumbar region are to the conus medullaris and the cauda equina.

The most frequent injuries of the thoracolumbar region occur between T12 and L2.

CES mainly affects middle-aged individuals, particularly those in their forties and fifties.

CES presents more often in men.

CES develops in only 4 to 7 out of every 10,000 to 100,000 patients, and is more likely to occur proximally.

Disc herniation is reportedly the most common cause of CES.

1 to 2% of all surgical disc herniation cases result in CES.

Considered an emergent condition.

CES is a clinical diagnosis, imaging helps confirm the diagnosis and facilitates surgical planning.

MRI is the preferred imaging study as it allows for depiction of soft tissues and neural elements and confirms diagnosis in 20% of suspected cases and helps to localize the areas of compression.

CT tomography myelogram is an alternative imaging study in patients who cannot undergo MRI.

Evaluation includes sensory testing for diminished or absent sensation in the dermatomal distribution of the lumbar sacral nerve roots.

CES produces  lower motor neuron symptoms with innervated muscle dysfunction resulting in decreased tone and weakness.

Motor testing of the lower extremities: hip flexors, knee extensors, ankle dorsiflexors and plantarflexors and great toe extensor  evaluates the lumbar and upper  sacral nerve roots.

The lower sacral nerve roots can be tested by evaluating rectal tone anal sphincter contraction.

Lower motor neuron symptoms may produce decreased or absent reflexes and can be noted by testing the patella tendon and Achilles tendon reflex arcs.

CES requires emergent spine surgery.

Additional measures such as antibiotics for infection or reversal agents for a hypocoagulable state may be required.

Surgery is focused on decompressing the area of mechanical compression and may require adjuvant surgical stabilization with hardware.

Patients treated within 48 hours have adequate outcomes.

Generally, patients retain neurologic functions that were intact at the time of decompression, and the level of neurologic dysfunction at the time of surgery is the most important prognostic determinant.

Overall patients with CES have 85% chance of improvement in radicular symptoms with surgery.

improvements in back pain after surgery is less predictable.

The majority of patients will have some degree of pain and neurologic dysfunction that prevents a complete return to their preoperative baseline.

Factors associated with a poor prognosis following surgery include multilevel involvement, bilateral radiculopathy, the presence of saddle anesthesia.

There is a high prevalence of urinary, bowel, and sexual dysfunction that persists for years.

Approximately 20% of patients with CES require long-term care involving catheterization, colostomy, sexual dysfunction, physical rehabilitation, and psychological ailments such as depression and unemployment.



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