Sd.cauda Equina Ingles

7/28/2019 Sd.cauda Equina Ingles

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The spinal cord tapers and ends at the level between the first and second lumbar vertebrae inan 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 acollection of nerve roots, which are horsetail-like in appearance and hence called the caudaequina (Latin for horse's tail). (See the image of cauda equina anatomy below.)

Illustration demonstrating the relevant anatomy of the cauda equina region

These nerve roots constitute the anatomic connection between the central nervous system(CNS) and the peripheral nervous system (PNS). They are arranged anatomically according tothe spinal segments from which they originated and are within the cerebrospinal fluid (CSF) inthe 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 urogenitalsymptoms resulting from the simultaneous compression of multiple lumbosacral nerve rootsbelow the level of the conus medullaris (see the image below). These symptoms include lowback pain, sciatica (unilateral or, usually, bilateral), saddle sensory disturbances, bladder andbowel dysfunction, and variable lower extremity motor and sensory loss (see Clinical).

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

Illustration demonstrating an example of cauda equina syndrome secondary to a spinalneoplasm Lesions involving the termination of the spinal cord (conus medullaris) are not discussed in thisarticle. Please see the article Spinal Cord Injuries.

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

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The white matter consists of various ascending and descending tracts of myelinated axonfibers, each with specific functions.

During development, the vertebral column grows more rapidly than the spinal cord. Spinalnerves exit the vertebral column at progressively more oblique angles because of the increasingdistance 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 asa tapered structure called the conus medullaris, consisting of sacral spinal cord segments. Theupper 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 thesubarachnoid 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 thedetrusor muscle of the urinary bladder. Conversely, somatic lower motor neurons from S2-S4innervate the voluntary muscles of the external anal sphincter and the urethral sphincter via theinferior rectal and the perineal branches of the pudendal nerve, respectively.

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

The conus medullaris obtains its blood supply primarily from 3 spinal arterial vessels: theanterior median longitudinal arterial trunk and 2 posterolateral trunks. Less prominent sourcesof blood supply include radicular arterial branches from the aorta, lateral sacral arteries, and thefifth 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, aproximal area of the nerve roots may have a zone of relative hypovascularity.

PathophysiologyIn understanding the pathological basis of any disease involving the conus medullaris, keep inmind that this structure constitutes part of the spinal cord (the distal part of the cord) and is inproximity 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 andmyotomes of the affected segments. On the other hand, a cauda equina lesion is an LMN lesionbecause the nerve roots are part of the PNS.

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

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

Several studies in different animal models have assessed the pathophysiology of cauda equinasyndrome.[2, 3] 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 Hgand the arterioles begin to occlude as the balloon pressure surpasses the mean arterial



pressure.[4, 5, 6, 2, 7] Despite this, even a pressure as high as 200 mm Hg failed to completely shutoff 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.[8] Similar results were reported inother 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.

[9]

Others have studied compound action potentials in afferent and efferent segments of nerves inthe CE region after application of balloon compression.[10, 11, 12] These researchers reported that0-50 mm Hg of pressure did not affect the action potentials (the threshold for disturbances inaction potentials was 50-75 mm Hg), and significant deficits were observed when pressure roseto 100-200 mm Hg.

EtiologyCauda equina syndrome is caused by any narrowing of the spinal canal that compresses thenerve roots below the level of the spinal cord.[13] Numerous causes of cauda equina syndromehave been reported, including disc herniation, intradural disc rupture, spinal stenosis secondaryto other spinal conditions, traumatic injury, primary tumors such as ependymomas and

schwannomas, metastatic tumors, infectious conditions, arteriovenous malformation or hemorrhage, and iatrogenic injury.[13, 14]

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

Lumbar stenosis (multilevel)

Spinal trauma including fractures[15]

Herniated nucleus pulposus (cause of 2-6% of cases of cauda equina syndrome)[16, 17, 18]

Neoplasm, including metastases, astrocytoma, neurofibroma, and meningioma; 20% of allspinal tumors affect this area

Spinal infection/abscess (eg, tuberculosis, herpes simplex virus, meningitis, meningovascular syphilis, cytomegalovirus, schistosomiasis)[19]

Idiopathic (eg, spinal anesthesia[20] ): these syndromes may occur as complications of the

procedure or of the anesthetic agent (eg, hyperbaric lidocaine, tetracaine) Spina bifida and subsequent tethered cord syndrome[21]

Other, rare causes include the following:

Spinal hemorrhage, especially subdural and epidural hemorrhage causing compression withinthe spinal canal

Intravascular lymphomatosis

Congenital anomalies of the spine/filum terminale, including tethered cord syndrome

Conus medullaris lipomas

Multiple sclerosis

Spinal arteriovenous malformations

Late-stage ankylosing spondylitis

Neurosarcoidosis

Deep venous thrombosis of the spinal veins (propagated)

Inferior vena cava thrombosis[22] A retrospective study of 66 consecutive cases of patients admitted to a neurosurgical unit withsuspected cauda equina syndrome found that almost half had no evidence of structuralpathology on MRI.[23] These researchers suggested that the symptoms have a functional origin insuch cases.

Trauma

Traumatic events leading to fracture or subluxation can lead to compression of the caudaequina.[15, 24, 25, 26, 27] Penetrating trauma can cause damage or compression of the cauda equina.Spinal manipulation resulting in subluxation has caused cauda equina syndrome.[28] Rare casesof sacral insufficiency fractures have been reported to cause cauda equina syndrome.[29] Acute

and delayed presentations of CES due to hematomas and posttraumatic arachnoid cysts havealso been reported.[30, 31, 32]



Herniated disk

The reported incidence of cauda equina syndrome resulting from herniated lumbar disk (see theimage below) varies from 1-15%.[33, 34, 18] Ninety percent of lumbar disk herniations occur either atL4-L5 or L5-S1.[35, 36]

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

Of cases of herniated disks leading to cauda equina syndrome, 70% occur in patients with ahistory of chronic low back pain; in 30%, cauda equina syndrome is the first symptom of lumbar disk herniation.[17] Men in the fourth and fifth decades of life are most prone to cauda equinasyndrome secondary to disk herniation.[37]

Most cases of cauda equina syndrome secondary to disk herniation involve either a largecentral disc or an extruded disc fragment that compromises a significant amount of the spinalcanal diameter .[38] The presentation may be acute or that of a more protracted course, with thelatter bearing a better prognosis.[34] Individuals with congenital stenosis who sustain a diskherniation are more likely to develop cauda equina syndrome because even a small herniationcan drastically limit the space available for the nerve roots.

Rare cases of intradural disk herniations have been reported to cause cauda equina

syndrome.[39]

Myelography in these instances typically demonstrates a complete block of thecontrast material. If an intradural disc fragment is identified, transdural removal of the extrudeddisc fragment may be helpful to prevent further stretching of the already compromised nerveroot.

Spinal stenosis

Narrowing of the spinal canal can be due to a developmental abnormality or degenerativeprocess. Although unusual, cauda equina syndrome from spinal stenosis secondary to spinaldisorders such as ankylosing spondylitis, spondylosis, and spondylolisthesis have all beenreported.[40, 41, 42, 43, 44, 45, 46]

Neoplasms

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

Myxopapillary ependymoma is the most common tumor of the filum. Recovery of the functionafter surgery depends on the duration of symptoms and the presence or absence of sphincter dysfunction[47] Paraganglioma of the filum, when present, needs to be differentiated from other tumors of this region.[48] Although rare, this entity may present as CES.

Schwannomas are benign encapsulated neoplasms that are structurally identical to a syncytiumof Schwann cells.[49] 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 thelevel of the conus or filum terminale. Primary tumors that affect the sacrum, such as chordomaand giant cell tumor of the bone, may produce similar symptoms as a result of bony destructionand collapse.[50]




Ependymomas are gliomas derived from relatively undifferentiated ependymal cells. They oftenoriginate from the central canal of the spinal cord and tend to be arranged radially around bloodvessels. Ependymomas are found most commonly in patients aged approximately 35 years.They can lead to increased intracranial pressure (ICP), and cerebrospinal fluid (CSF) has anincreased 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 metastasisaccounts for most tumors in the spine in general, metastatic tumors in the cauda equina arerelatively rare compared with primary tumors.

For the spine in general, sources of spinal metastases are as follows [51] :

Lung cancer (40-85%)

Breast cancer (11%)

Renal cell carcinoma (4%)

Lymphatic cancer (3%)

Colorectal cancer (3%) 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 themetastatic lesions were not at the level of the cauda equina.[51] Up to 8% of patients withprostate cancer experience malignant spinal cord compression; however, the percentage of cases involving cauda equina syndrome is unknown.[52]

The CE region is also a favored site for drop metastases from intracranial ependymoma,germinoma, and other tumors.[53] Other unusual metastatic spread from genitourinary andgynecologic cancer have also been reported at the conus region, causing neurologicalcompromise.[54, 55]

Inflammatory and infectious conditions

Long-lasting inflammatory conditions of the spine, including Paget disease and ankylosingspondylitis, 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 andspinal cord.[56] Symptoms generally include severe back pain and a rapidly progressing motor weakness.

Infectious causes for cauda equina syndrome may be pyogenic or nonpyogenic. Pyogenicabscesses are generally found in an immunocompromised or poorly nourishedhost. Staphylococcus aureus causes epidural abscesses in 25-60% of cases, but, recently, anincreasing incidence of infections with methicillin-resistantS aureus, Pseudomonas species,and Escherichia coli have been recorded. A high index of suspicion is helpful in correctdiagnosis and management.[56]

Nonpyogenic causes for abscess are rare and include tuberculosis. Resurgence of tuberculosissecondary to immunocompromise in individuals with HIV infection requires a high index of

suspicion, as the development of cauda equina syndrome may follow an indolentcourse.[57] Other uncommon organisms, such as Nocardia asteroides and Streptococcusmilleri, have also been reported as a cause of abscess that leads to the development of CES.[58,

59]

Iatrogenic causes

Complications of spinal instrumentation have been reported to cause cases of cauda equinasyndrome, including misplaced pedicle screws[60] and laminar hooks.[61, 62] Continuous spinalanesthesia also has been linked to cases of cauda equina syndrome.[63]

Rare cases of cauda equina syndrome caused by epidural steroid injections, fibrin glueinjection,[64] and placement of a free-fat graft have been reported.[65]



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.[66, 67]

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 spinalanesthesia have been related to the development of cauda equina syndrome –like syndromes.[34,

68, 69, 70, 71, 72]

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

Cauda equina syndrome is uncommon, both atraumatically as well as traumatically. It is oftenreported as a case report due to its rarity. Although infrequent, it is a diagnosis that must beconsidered 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 syndromeoccurs primarily in adults as a result of surgical morbidity, spinal disk disease, metastaticcancer, or epidural abscess.

PrognosisMorbidity and especially mortality rates are determined by the underlying etiology. Multipleconditions 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. Surgicaldecompression may be performed emergently, or, in some patients, delayed, depending on theetiology. Residual weakness, incontinence, impotence, and/or sensory abnormalities arepotential problems if therapy is delayed.

Investigators have attempted to identify specific criteria that can aid in predicting the prognosisof patients with cauda equina syndrome. Patients with bilateral sciatica have been reported tohave a less favorable prognosis than patients with unilateral pain. Patients with completeperineal anesthesia are more likely to have permanent paralysis of the bladder .[38]

The extent of perineal or saddle sensory deficit has been reported to be the most importantpredictor of recovery.[73] Patients with unilateral deficits have a better prognosis than patientswith bilateral deficits. Females and patients with bowel dysfunction have been reported to haveworse outcomes postoperatively.[74]

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

ASIA A: 90% of patients remain incapable of functional ambulation (reciprocal gait of 200 feetor more)

ASIA B: 72% of patients are unable to attain functional ambulation

ASIA C/D: 13% are unable to attain functional ambulation 1 year after injury Ambulatory motor index also is used to predict ambulatory capability. It is calculated by scoringhip flexion, hip abduction, hip extension, knee extension, and knee flexion on both sides, usinga 4-point scale (0=absent, 1=trace/poor, 2=fair, 3=good or normal); the score is expressed as apercentage of the maximum score of 30. Prognostic significance is as follows:

A patient with a score of 60% or more has a good chance for community ambulation with nomore than one knee-ankle-foot orthosis (KAFO)

A patient with a score of 79% or higher may not need an orthosis

A patient with a score of 40% or less may require 2 KAFOs for community ambulation

Patient Education



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

Training in self-catheterization and finger fecal disimpaction, if required

Use of measures to prevent pressure ulcers, such as skin inspection/care, positioning, turningand transferring tactics, use of skin protectors, or pressure-reducing support surfaces

Maintenance of endurance and strength-training exercises Regular follow-up by the consulting teams who treated the patient in the hospital

Instructions on how and when medications should be taken and when follow-up laboratorytests should be performed

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

HistoryPatients can present with symptoms of isolated cauda equina syndrome, isolated conusmedullaris syndrome, or a combination. The symptoms and signs of cauda equina syndrometend 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(Open Tablein a new window)

Conus Medullaris Syndrome Cauda Equina Syndrome

Presentation Sudden and bilateral Gradual and unilateral

Reflexes Knee jerks preserved but ankle jerks affected Both ankle and knee jerks affected

Radicular pain Less severe More severe

Low back pain More Less

Sensorysymptoms andsigns

Numbness tends to be more localized to perianal area; symmetrical and bilateral;sensory dissociation occurs

Numbness tends to be more localized to saddle area; asymmetrical, may beunilateral; no sensory dissociation; loss of sensation in specific dermatomes inlower extremities with numbness and paresthesia; possible numbness in pubicarea, including glans penis or c litoris

Motor strength Typically symmetric, hyperreflexic distal

paresis of lower limbs that is less marked;fasciculations may be present

Asymmetric areflexic paraplegia that is more marked; fasciculations rare;atrophy more common

Impotence Frequent Less 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 dysfunction

Urinary retention and atonic anal sphincter cause overflow urinary incontinence and fecalincontinence; tend to present early in course of disease

Urinary retention; tends to present late in course of disease

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 reflexesLow 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

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sharp, stabbing pain resulting from compression of the dorsal nerve roots. Radicular painprojects in dermatomal distributions. Low back pain in cauda equina syndrome may have somecharacteristic 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 theventral roots. Patients generally develop hypotonia and hyporeflexia. Sensory loss andsphincter 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 anoverflow urinary incontinence.

Bell et al demonstrated that the accuracy of urinary retention, urinary frequency, urinaryincontinence, altered urinary sensation, and altered perineal sensation as indications of possibledisk prolapse justified urgent MRI assessment.[75, 76]

Bowel disturbances may include the following:

Incontinence

Constipation

Loss of anal tone and sensationThe initial presentation of bladder/bowel dysfunction may be of difficulty starting or stopping astream of urine. It may be followed by frank incontinence, first of urine then of stool. The urinaryincontinence 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 toan LMN or UMN lesion. Refer to the images and tables below for assistance in examining thepatient 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 outpossible vascular cause or ischemia of the conus medullaris).

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.

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

Table 2. Pain and Deficits Associated with Specific Nerve Roots (Open Table in a new window)

NerveRoot

Pain SensoryDeficit

Motor Deficit Reflex Deficit

L2 Anterior medial thigh Upper thigh Slight quadriceps weakness; hip flexion; thigh

adduction

Slightly diminished

suprapatellar

L3 Anterior lateral thigh Lower thigh Quadriceps weakness; knee extension; thigh

adduction

Patellar or suprapatellar

L4 Posterolateral thigh, anterior

tibia

Medial leg Knee and foot extension Patellar

L5 Dorsum of foot Dorsum of

foot

Dorsiflexion of foot and toes Hamstrings

S1-2 Lateral foot Lateral foot Plantar flexion of foot and toes Achilles

S3-5 Perineum Saddle Sphincters Bulbocavernosus; anal

Table 3. Root and Peripheral Nerve Innervation of the Lumbosacral Plexus (Open Table in anew window)

Muscle Nerve Root

Iliopsoas Femoral L2, 3, 4

Adductor longus Obturator L2, 3, 4

Gracilis Obturator L2, 3, 4

Quadriceps femoris Femoral L2, 3, 4

Anterior tibial Deep peroneal L4, 5

Extensor hallucis longus Deep peroneal L4, 5




Extensor digitorum longus Deep peroneal L4,5

Extensor digitorum brevis Deep peroneal L4, 5, S1

Peroneus longus Superficial peroneal L5, S1

Internal hamstrings Sciatic L4, 5, S1

External hamstrings Sciatic L5, S1

Gluteus medius Superior gluteal L4, 5, S1

Gluteus maximus Inferior gluteal L5, S1, 2

Posterior tibial Tibial L5, S1

Flexor digitorum longus Tibial L5, S1

Abductor hallucis brevis Tibial (medial plantar) L5, S1, 2

Abductor digiti quinti pedis Tibial (lateral plantar) S1, 2

Gastrocnemius lateral Tibial L5, S1, 2

Gastrocnemius medial Tibial S1, 2

Soleus Tibial S1, 2

Pain often is localized to the low back; local tenderness to palpation or percussion may bepresent. 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 inassociation 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 caudaequina 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 skinbreakdown.

Muscle weakness may be present in muscles supplied by affected roots. Muscle wasting mayoccur 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 equinasyndrome, possibly spinal cord compression.

In cauda equina syndrome, the peripheral nerve fibers from the sacral segments of the cord, aswell as various lumbar dorsal and ventral nerve roots, may also be involved. This results in anasymmetric 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 samereason.



In conus and epiconus lesions, the sacral region neurons (S2-S4) are destroyed. Thedestruction of these neurons leads to an early and more severe involvement of bowel, urinarybladder, 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 thedistal parts of the limb musculature are involved.

The anatomical proximity of the conus medullaris, the epiconus, and the cauda equina can leadto 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 syndromeare listed in Table 4, below.

Table 4. Cauda Equina Versus Conus Medullaris Syndrome (Open Table in a new window)

Features Cauda Equina Syndrome Conus Medullaris

Vertebral level L2-sacrum L1-L2

Spinal level Injury to the lumbosacral nerve roots Injury of the sacral cord segment (conus and epiconus) and roots

Severity of symptoms

and signs

Usually severe Usually not severe

Symmetry of

symptoms and signs

Usually asymmetric Usually symmetric

Pain Prominent, asymmetric, and radicular Usually bilateral and in the perineal area

Motor Weakness to flaccid paralysis Normal motor function to mild or moderate weakness

Sensory Saddle anesthesia, may be asymmetric Symmetric saddle distribution, sensory loss of pin prick, and

temperature sensations (Tactile sensation is spared.)

Reflexes Areflexic lower extremities; bulbocavernosus

reflex is absent in low CE (sacral) lesions

Areflexic lower extremities

(If the epiconus is involved, patellar reflex may be absent, whereas

bulbocavernosus reflex may be spared.)

Sphincter and sexual

function

Usually 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

EMG Multiple root level involvement; sphincters may

also be involved

Mostly normal lower extremity with external anal sphincter

involvement

Outcome May be favorable compared with conus

medullaris syndrome

The outcome may be less favorable than in patients with CES



Cauda equina syndrome

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

Sensation is decreased to pinprick and light touch in a dermatomal pattern corresponding to theaffected 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 sacralnerves. Vibration sense may also be affected. Sensation of the glans penis or clitoris should beexamined.

Muscle stretch reflexes may be absent or diminished in the corresponding nerve roots. Babinskireflex 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 recoveryfrom the injury.

Urinary incontinence could also occur secondary to loss of urinary sphincter tone; this may alsopresent 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 conusmedullaris syndrome signs are more likely to be bilateral; sacral segments occasionally show

preserved bulbocavernosus reflexes and normal or increased anal sphincter tone; the musclestretch 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), cutaneousabnormalities (eg, cutaneous angioma, pilonidal sinus that may be present in dermoid or epidermoid tumors), distended bladder due to areflexia, and other spinal abnormalities (notedon lower back examination) predisposing the patient to the syndrome.

Muscle strength

Physical examination for cauda equina or conus medullaris syndromes would be incompletewithout 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:

L2 - Hip flexors (iliopsoas)

L3 - Knee extensors (quadriceps)

L4 - Ankle dorsiflexors (tibialis anterior)

L5 - Big toe extensors (extensor hallucis longus)

S1 - Ankle plantar flexors (gastrocnemius/soleus)

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/caudaequina syndrome. The scale is as follows:



A - Complete; no sensory or motor function preserved in sacral segments S4-S5

B - Incomplete; sensory, but not motor, function preserved below the neurologic level andextends through sacral segments S4-S5

C - Incomplete; motor function preserved below the neurologic level, and the majority of keymuscles below the neurologic level have a muscle grade less than 3

D - Incomplete; motor function preserved below the neurologic level, and the majority of key

muscles below the neurologic level have a muscle grade greater than or equal to 3 E - Normal; sensory and motor function normal

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

Complications

Complications include the following:

Thromboembolic phenomena

Neurogenic bladder/bowel

Erectile dysfunction

Pressure ulcers Heterotopic ossification

Osteoporosis

Chronic neuropathic pain

Spasticity/contractures

Recurrent urinary tract infections

Urethral stricture

Bladder calculi

Depression

Diagnostic ConsiderationsConus medullaris infarction should be considered in the differential diagnosis, and a source of emboli should be sought by ultrasound to rule out an abdominal aortic aneurysm. Heterotopic

ossification should be ruled out by triple-bone scan in a patient with pain and swelling of thelower extremity in whom deep venous thrombosis (DVT) has been ruled out. In other words,heterotopic ossification should always be considered as a differential diagnosis of DVT in thesepatients.

Metastatic malignant neoplasms of the spine should be ruled out and the primary source soughtas part of the workup in any patient presenting with any of the symptoms listed in Clinical.

Other problems to be considered include the following:

Amyloidosis with deposits in the spinal cord

Ankylosing spondylitis and other spondyloarthropathy

Charcot-Marie-Tooth disease (types 1 and 3)

Intravascular lymphomatosis Lipomas within the spine

Lumbar stenosis (multilevel)

Paget disease of the spine

Spinal infection/abscess and meningitis

Tethered cord syndrome/short filum terminale

Vascular intermittent claudication

Differential Diagnoses Acute Inflammatory Demyelinating Polyradiculoneuropathy

Amyotrophic Lateral Sclerosis

Diabetic Neuropathy

Guillain-Barré Syndrome

HIV-1 Associated Neuromuscular Complications (Overview)

Multiple Sclerosis















Neoplasms, Spinal Cord

Neurosarcoidosis

Spinal Cord Infections

Traumatic Peripheral Nerve Lesions

Approach Considerations

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

Myelography,[77] computed tomography,[78] and MRI are each used in specific cases with gooddegrees of accuracy. Each test can be used to determine the level of pathology and aid in thedetermination 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.[79, 80, 81] Urgent MRI isrecommended for all patients who have new-onset urinary symptoms with associated back painor sciatica.

Nevertheless, the superiority of MRI over CT is only suggested by case reports. Earlyconsultation with the appropriate subspecialty is encouraged to guide imaging studies.[23]

Depending on the findings from the history and physical examination, laboratory studies caninclude basic blood tests, chemistries, fasting blood sugar, sedimentation rate, and syphilis andLyme serologies. CSF examination should also be included if signs of meningitis are present.[82]

Alteration in bladder function may be assessed empirically by obtaining urine viacatheterization. A significant volume with little or no urge to void, or as a post-void residual, mayindicate 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. Intraoperativemonitoring of somatosensory and motor evoked potentials allows for evaluation of radiculopathyand neuropathy

Blood StudiesThe 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:

CBC count, blood glucose, electrolytes, blood urea nitrogen (BUN), and creatinine - As part of the workup to rule out associated anemia, infection, and renal dysfunction, especially inassociated retroperitoneal mass

Erythrocyte sedimentation rate (ESR) – Elevation may point to an inflammatory pathology

Syphilis serology to rule out meningovascular syphilis

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

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

Magnetic Resonance ImagingMRI 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). Itprovides a more complete radiographic assessment of the spine than other tests; plain x-raysand CT scan may be normal.[83, 80] . 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.

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.

Schwannomas are visible using myelography, but MRI is the criterion standard. Schwannomasare isointense on T1 images, hyperintense on T2 images, and enhanced with gadoliniumcontrast. 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 ProceduresNeedle electromyography (EMG)[84] may show evidence of acute denervation, especially incauda equina lesions and multilevel lumbar spinal stenosis. EMG studies also could help inpredicting prognosis and monitoring recovery. Performing needle EMG of the bilateral externalanal sphincter muscles is recommended.

Nerve conduction studies,[11] especially of the pudendal nerve, may rule out more distalperipheral nerve lesions.

Somatosensory evoked potentials (SSEPs)[11] could be done as part of the workup to rule outmultiple sclerosis, which could present initially as a lower spinal cord syndrome.












Upper extremities training to increase strength for the increased demands of wheelchair propulsion and walking with assistive devices

Home evaluation

Family training

A home exercise programOrthotic/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-footorthoses (KAFO) with forearm crutches for support; for lower lesions, KAFOs or AFOs withcanes 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 shouldbe assessed for these needs prior to discharge from the acute rehabilitation setting.

ConsultationsConsultations to different specialties are needed for acute care and follow-up care.Neurosurgery/spinal orthopedics consultation should assess the need for urgent surgical spinaldecompression. Posterior decompression and stabilization offers at least equivalent neurologicoutcomes as nonoperative or anterior approaches and has the additional benefits of surgeonfamiliarity, shorter hospital stays, earlier rehabilitation, and ease of nursing care.[15]

Plastic surgery may be needed if severe skin breakdowns occur.

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

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

Long-Term MonitoringFollow 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'sstrength, 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 andcalculi.[18] Yearly cystoscopy is recommended for patients with suprapubic catheters to helpdetect early bladder malignancies.

Regular follow-up urodynamic studies, renal ultrasound, and general cancer screening shouldbe performed

Approach ConsiderationsSpecific treatment is directed at the primary cause; these are discussed in other articles. Thegeneral treatment goals are to minimize the extent of injury and to treat ensuing generalcomplications.

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

Patients with cauda equina syndrome secondary to infectious causes should receiveappropriate antibiotic therapy. Patients with spinal neoplasms should be evaluated for thesuitability 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 thecontrary, late treatment may have detrimental effects.

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

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

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

Prevention and Treatment of Complications

For deep venous thrombosis/pulmonary embolism, patients should use antiemboliccompression stockings and subcutaneous heparin for 3 months as prophylaxis. Low-molecular-weight heparin also has been approved for prophylaxis. Ultrasound of the lower extremities mayneed 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, multiplesclerosis) who have overactive bladder. Therapy consists of 30 intradetrusor injections viacystoscopy. Trials have shown patients who received onabotulinumtoxinA had significantreduction in urinary incontinence episodes and improved urodynamics compared with placeboat 12 weeks.[90, 91, 92]

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

For impotence, use of a phosphodiesterase type 5 inhibitor (eg, sildenafil [Viagra]) is becomingpopular. Other drugs for erectile dysfunction include yohimbine, papaverine, and alprostadil.Methods to promote coitus and/or ejaculation could also be used; these include implantablepenile 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 associatedelevation 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 10mg/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 phosphataselevel, and decline in triple-phase bone scan activity.

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

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

Treatment with lipoprostaglandin E1 and its derivatives has been reported to be effective inincreasing 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 severesymptoms or patients with radicular symptoms.

Use of orthoses is advised to prevent contractures. Use of antispasticity medications also isencouraged. Other medications include dantrolene, diazepam, clonidine, and tizanidine. Nerveblocks also could be done to relieve spasticity; appropriate agents include phenol, botulinum

toxin, or local anesthetics.

Surgical DecompressionIn acute compression of the conus medullaris or cauda equina, surgical decompression as soonas possible becomes mandatory. The goal is to relieve the pressure on the nerves of the caudaequina by removing the compressing agent and increasing the space in the spinal canal.Traditionally, cauda equina syndrome has been considered a surgical emergency, with surgicaldecompression considered necessary within 48 hours after the onset of symptoms, andpreferably performed within 6 h of injury.[60, 93, 94, 95]

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 gentleretraction and discectomy.

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

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

Many clinical and experimental reports have presented data on the functional outcome basedon the timing of surgical decompression.[3] Several investigators have reported no significantdifferences in the degree of functional recovery as a function of the timing of surgicaldecompression.[93, 94, 96] Even with these findings, however, most investigators recommendsurgical decompression as soon as possible after the onset of symptoms to offer the greatestchance of complete neurologic recovery.

On discharge from the surgical ward, patients often are transferred to an acute rehabilitationunit, 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

RehabilitationThe rehabilitation team, especially the spinal cord injury rehabilitation physician andoccupational and physical therapists, should be involved as soon as possible. The team will setgoals in the rehabilitation unit toward maintaining and improving endurance, with the ability tobe 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 adequateprevention and treatment of possible medical complications already discussed, especially deepvenous thrombosis, bladder and bowel problems, and decubitus ulcers

Physical therapy

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

Other activities include the following:







Wheelchair propulsion training

Standing table exercises

Functional electrical stimulation for increased muscle tone

Lower extremity orthoses to aid balance and walking

Ambulation exercises

Family training and community skills

A home exercise programOccupational therapy

Conduct the following:

Wheelchair training, especially for advanced wheelchair activities

Transfer training

Activities of daily living program with assistive devices for dressing, feeding, grooming,bathing, and toileting

Motor coordination skills training

Shower program

Upper extremities training to increase strength for the increased demands of wheelchair propulsion and walking with assistive devices

Home evaluation Family training

A home exercise programOrthotic/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-footorthoses (KAFO) with forearm crutches for support; for lower lesions, KAFOs or AFOs withcanes 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 shouldbe assessed for these needs prior to discharge from the acute rehabilitation setting.

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