eMedicine Specialties > Neurology > Introductory Topics
Cauda Equina and Conus Medullaris Syndromes: Treatment & Medication
Updated: Feb 10, 2009
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
- Multimedia
Treatment
Medical Care
Specific treatment is directed at the primary cause; these are discussed in other articles. As discussed below, the general treatment goals are to minimize the extent of injury and to treat ensuing general complications.- Acute care: In an acute setting, treatment options entail minimizing possible inflammation and preventing further trauma that might cause worsening of the injury. This is of even greater importance if the cause is trauma.
- Maintenance of adequate airway, cardiopulmonary resuscitation, fluid management, and initial immobilization (using a molded thoracolumbosacral orthosis) are necessary to limit further damage.
- Methylprednisolone should be administered as indicated in Medication. This 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 GM1 ganglioside 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.
- Any specific causal factor should be treated as soon as it has been identified.
- Treatment/prevention of possible complications should begin immediately, including the following:
- 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.
- Neurogenic bladder: Patients may require bladder catheterization.
- Pressure ulcers: These may be prevented by eliminating pressure, optimizing wound-healing environment, and debriding if necessary.
- Impotence: Use of sildenafil (Viagra) is becoming popular. Other drugs include yohimbine, papaverine, and alprostadil. Methods to promote coitus and/or ejaculation could also be used; these include implantable penile prostheses or vibrator stimulation.
- Fecal incontinence: Patients may require use of stool softener or manual evacuation.
- Heterotopic ossification: Heterotropic ossification (HO) can be confirmed by a triple-bone scan with associated elevated 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: 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.
- Spasticity: 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 Care
In acute compression of the conus medullaris or cauda equina, surgical decompression as soon as possible (preferably within 6 h of injury) becomes mandatory. 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 any of the following:
- Laminectomy and instrumentation/fusion for stabilization
- Discectomy
- Other surgical care may entail wound care, eg, debridement, skin graft, and skin flap/myocutaneous flap.
Consultations
Consultations to different specialties are needed for acute care and follow-up care.
- Urgent consults for follow-up and advice of the following specialists may be required:
- Neurosurgery/spinal orthopedics: This 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.1
- Plastic surgery: Plastic surgery may be needed if severe skin breakdowns occur.
- Rehabilitation: This 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).
- Dietitian: 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.
Diet
See Consultations.
Activity
The rehabilitation team, especially the spinal cord injury rehabilitation physician and occupational and physical therapists, should be involved as soon as possible.
- This entails setting 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. This involves the following rehabilitation modalities:
- Medical - Ensure adequate prevention and treatment of possible medical complications already discussed, especially deep venous thrombosis, bladder and bowel problems, and decubitus ulcers
- Physical therapy - 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 wheelchair propulsion training, standing table exercises, functional electrical stimulation for increased muscle tone, use of lower extremity orthoses to aid balance and walking, along with ambulation exercises, family training and community skills, and a home exercise program.
- Occupational therapy - 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; and a home exercise program.
- 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.
Medication
The rationale for the medications listed in this section was outlined in Medical Care.
Corticosteroids
These agents have anti-inflammatory properties and cause profound and varied metabolic effects. Corticosteroids modify the body's immune response to diverse stimuli.
Methylprednisolone sodium succinate (Adlone, Medrol, Solu-Medrol)
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; apparently has no benefit if started > 8 h after injury. Late treatment may have detrimental effects.
Adult
30 mg/kg IV over 15 min followed by a 45-min break, then restart IV infusion at 5.4 mg/kg/h for 23 h; medication must be started within 8 h after injury; starting after 8 h may have detrimental effect
Pediatric
0.5-1.7 mg/kg/d or 5-25 mg/m2/d PO/IV/IM divided q6-12h
Digoxin may increase digitalis toxicity secondary to hypokalemia; estrogens may increase levels; phenobarbital, phenytoin and rifampin may decrease levels (adjust dose); monitor patients for hypokalemia when taking concurrent diuretics
Documented hypersensitivity; viral, fungal or tubercular skin infections
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Hyperglycemia, edema, osteonecrosis, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, growth suppression, myopathy, and infections are possible complications of glucocorticoid use
Anticoagulants
These agents are taken as prophylaxis for deep venous thrombosis and/or pulmonary embolism.
Heparin
Augments activity of antithrombin III and prevents conversion of fibrinogen to fibrin. Does not actively lyse but is able to inhibit further thrombogenesis. Prevents re-accumulation of clot after spontaneous fibrinolysis. Administer low dose.
Adult
5000 U SC q8-12h
Pediatric
Not established
Digoxin, nicotine, tetracycline, and antihistamines may decrease effects; NSAIDs, aspirin, dextran, dipyridamole, and hydroxychloroquine may increase toxicity
Documented hypersensitivity; subacute bacterial endocarditis; active bleeding; history of heparin-induced thrombocytopenia
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
In neonates, preservative-free heparin recommended to avoid possible toxicity (gasping syndrome) by benzyl alcohol, which is used as preservative; caution in severe hypotension and shock
Skeletal muscle relaxants
These agents are thought to work centrally by suppressing conduction at the spinal level.
Baclofen (Lioresal)
May induce hyperpolarization of afferent terminals and inhibit both monosynaptic and polysynaptic reflexes at spinal level.
Adult
5 mg PO bid, with gradual increase q3d as tolerated to 30-80 mg qd in divided doses (tid/qid)
Intrathecal: Test dose 50-100 mcg, doses >50 mcg should be given in 25-mcg increments separated by 24h; maintenance: after positive response to test dose, initial dose (via intrathecal pump) is twice test dose, given over 24-h period
Pediatric
Generally not recommended for children <12 y for safety reasons
<12 years: 2.5 to 5 mg PO bid with gradual increase q3d as tolerated
<8 years: Not to exceed 30 mg/d
8-12 years: Not to exceed 60 mg/d
>12 years: Administer as in adults
Opiate analgesics, benzodiazepines, alcohol, TCAs, guanabenz, MAOIs, clindamycin, and hypertensive agents may increase effects
Documented hypersensitivity
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in patients with history of autonomic dysreflexia and when spasticity is utilized to obtain increased function; autonomic dysreflexia can result from withdrawal of this medication
Dantrolene (Dantrium)
Stimulates muscle relaxation by modulating skeletal muscle contractions at site beyond myoneural junction and acting directly on muscle itself. Prevents calcium release from sarcoplasmic reticulum.
Adult
Begin with 25 mg PO qd; increase to 25 mg bid/qid, then by 25-mg increments to as high as 100 mg, bid/qid prn
Pediatric
Start with 0.5 mg/kg PO bid, increase to 0.5 mg/kg bid/qid, then by increments of 0.5 mg/kg to 3 mg/kg bid/qid prn; not to exceed 100 mg qid
Toxicity may increase with coadministration of clofibrate and warfarin; coadministration with estrogen may increase hepatotoxicity in women older than 35 y
Documented hypersensitivity; active hepatic disease (hepatitis and cirrhosis)
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
May cause hepatotoxicity (use only for recommended indications); caution in impaired pulmonary function and severe cardiac insufficiency; may cause photosensitivity with exposure to sunlight
Benzodiazepines
These agents may act in the spinal cord to induce muscle relaxation.
Diazepam (Diastat, Diazemuls, Valium)
Depresses all levels of CNS (eg, limbic and reticular formation), possibly by increasing activity of GABA.
Individualize dosage and increase cautiously to avoid adverse effects.
Adult
Mild spasms: 5-10 mg PO q4-6h prn
Moderate spasms: 5-10 mg IV prn
Severe spasms: Mix 50-100 mg in 500 mL D5W and infuse at 40 mL/h
Pediatric
Mild spasms: 0.1-0.8 mg/kg/d PO divided tid/qid
Moderate or severe spasms: 0.1-0.3 mg/kg IV q4-8h
Phenothiazines, barbiturates, alcohols, and MAOIs increase CNS toxicity when administered concurrently
Documented hypersensitivity; narrow-angle glaucoma
Pregnancy
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Precautions
Caution with other CNS depressants, low albumin levels, or hepatic disease (may increase toxicity)
Alpha 2-adrenergic agonist agents
May reduce sympathetic outflow, which may produce a reduction in muscle tone.
Clonidine (Catapres)
Stimulates alpha2-adrenoreceptors in brain stem, activating an inhibitory neuron, which in turn results in reduced sympathetic outflow.
Adult
1 mg PO bid; titrate to effect; not to exceed 2.4 mg/d
Pediatric
5-30 mcg/kg/d PO
Tricyclic antidepressants inhibit hypotensive effects of clonidine; coadministration of clonidine with beta-blockers may potentiate bradycardia; tricyclic antidepressants may enhance hypertensive response associated with abrupt clonidine withdrawal; hypotensive effects of clonidine are enhanced by narcotic analgesics
Documented hypersensitivity
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in cerebrovascular disease, coronary insufficiency, sinus node dysfunction, and renal impairment
Tizanidine (Zanaflex)
Centrally acting muscle relaxant metabolized in the liver and excreted in urine and feces.
Adult
4-8 mg PO q8h prn; not to exceed 36 mg/d
Pediatric
Not established
May interact with alcohol (increase somnolence, stupor) and oral contraceptives (which decrease its clearance), and can cause increased hypotensive effects when administered concurrently with diuretics
Documented hypersensitivity
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in renal impairment
Neuromuscular blocker agent, toxin
These agents inhibit transmission of impulses in neuromuscular tissue.
Botulinum Toxin Type A (BOTOX®)
Binds to receptor sites on motor nerve terminals and inhibits release of acetylcholine, which in turn inhibits transmission of impulses in neuromuscular tissue.
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. May be repeated q3-4mo.
Adult
1.25-2.5 U (0.05-0.1 mL) IM injection into most active muscles; give q3-4mo
Pediatric
<12 years: Not established
>12 years: Administer as in adults
Aminoglycosides or drugs that interfere with neuromuscular transmission may potentiate effects of botulinum toxin
Documented hypersensitivity
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Do not exceed recommended dosages and frequencies of administration; presence of antibodies to botulinum toxin type A may reduce effects of therapy; when used for cervical dystonia it may cause dysphagia, upper respiratory infection, neck pain, or headache; ptosis may occur when used for blepharism or strabismus
When used cosmetically for glabellar lines may cause headache, respiratory infection, flu syndrome, blepharoptosis, or nausea
Bisphosphonate derivatives
Analogs of pyrophosphate and act by binding to hydroxyapatite in bone-matrix, thereby inhibiting the dissolution of crystals. Prevent osteoclast attachment to the bone matrix and osteoclast recruitment and viability.
Etidronate disodium (Didronel)
Inhibits normal and abnormal bone resorption. Appears to inhibit bone resorption without inhibiting bone formation and mineralization.
Adult
20 mg/kg PO qd for 2 wk, then 10 mg/kg for as long as 12 wk
Pediatric
Not established
Coadministration with calcium containing products and other multivalent cations decrease absorption
Documented hypersensitivity; hypocalcemia, renal impairment
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Monitor hypercalcemia-related parameters (eg, serum levels of calcium, phosphate, magnesium and potassium); maintain adequate intake of calcium and vitamin D to prevent severe hypocalcemia; caution if active upper GI problems; do not administer with alendronate for osteoporosis in postmenopausal women
Phosphodiesterase (type 5) enzyme inhibitors
These agents increase vasodilatory effects of nitric oxide by inhibiting the enzyme phosphodiesterase type 5, which in tun increases sensitivity for erections.
Sildenafil (Viagra)
Phosphodiesterase type 5 (PDE5) selective inhibitor. Inhibition of PDE5 increases cGMP activity, which increases vasodilatory effects of nitric oxide. 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. The increased sensitivity for erections may last 24 h. Available as 25-, 50-, and 100-mg tabs.
Adult
25-100 mg PO 1 h before sexual activity
Pediatric
Not established
Potentiates vasodilatory effect of NO, resulting in potentially fatal drop in blood pressure; coadministration with ketoconazole, erythromycin, or cimetidine increases plasma sildenafil concentrations; coadministration with rifampin decreases plasma levels of sildenafil
Documented hypersensitivity; concurrent or intermittent using of organic nitrates in any form
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Adverse effects include headaches (16%), flushing (10%), upset stomach (7%), nasal congestion (4%), and a blue haze at the periphery of vision (3%); adverse effects occur more often in men taking the 100-mg dose; serious adverse effects occur in patients with severe heart disease and those who are taking nitrates; rates of MI were 1.7 and 1.4 per 100 man-years for sildenafil and placebo groups
Vardenafil (Levitra)
Phosphodiesterase type 5 (PDE5) selective inhibitor. Inhibition of PDE5 increases cGMP activity, which increases vasodilatory effects of nitric oxide. Effective in men with mild-to-moderate ED. Take on empty stomach about 1 h before sexual activity. Sexual stimulation is necessary to activate response. Increased sensitivity for erections may last 24 h. Available as 2.5-mg, 5-mg, 10-mg, and 20-mg tabs.
Adult
10 mg PO 1 h before sexual activity; may increase to maximum recommended dose of 20 mg or decreased to 5 mg based on efficacy and side effects
Concurrent administration with ritonavir: Not to exceed 2.5 mg PO q72h
Concurrent administration with indinavir, ketoconazole (400 mg PO qd), or itraconazole (400 mg PO qd): Not to exceed 2.5 mg PO q24h
Concurrent administration with ketoconazole (200 mg PO qd), itraconazole (200 mg PO qd), or erythromycin: Not to exceed 5 mg PO q24h
Pediatric
Not established
CYP3A4 inhibitors (eg, erythromycin, ketoconazole, itraconazole, indinavir, ritonavir) may significantly increase levels of vardenafil; vardenafil potentiates hypotensive effect of nitrates or alpha-blockers; avoid coadministration with other drugs that prolong QT interval (eg, quinidine, procainamide, amiodarone, sotalol)
Documented hypersensitivity; concurrent or intermittent use of alpha-blockers or organic nitrates in any form
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Common adverse effects include headache, flushing, rhinitis, dyspepsia, or indigestion; assess cardiovascular status before use; caution with left ventricular outflow obstruction or conditions aggravated by hypotension or prolonged QT interval; caution with hepatic impairment (decrease dose); may cause prolonged or painful erection (<2%)
Tadalafil (Cialis)
Phosphodiesterase type 5 (PDE5) selective inhibitor. Inhibition of PDE5 increases cGMP activity, which increases vasodilatory effects of nitric oxide. Sexual stimulation is necessary to activate response. Increased sensitivity for erections may last 36 h. Available as 5-mg, 10-mg, and 20-mg tabs.
Adult
10 mg PO before sexual activity; may increase to maximum recommended dose of 20 mg or decreased to 5 mg based on efficacy and adverse effects; not to exceed 1 dose per day; may be taken without regard to food
Concurrent administration with potent CYP3A4 inhibitors (eg, ketoconazole, ritonavir): Not to exceed 10 mg PO q72h prn
Moderate renal impairment (CrCl 30-50 mL/min): 5 mg PO qd prn initially; may increase to 10 mg PO q48h prn
Severe renal impairment (CrCl <30 mL/min): Do not exceed 5 mg PO qd prn
Mild-to-moderate hepatic impairment: Do not exceed 10 mg PO qd prn
Pediatric
<18 years: Not established
CYP3A4 inhibitors (eg, erythromycin, ketoconazole, itraconazole, indinavir, ritonavir) may significantly increase levels of vardenafil; vardenafil potentiates hypotensive effect of nitrates or alpha-blockers; concurrent alcohol consumption may increase orthostatic hypotension risk
Documented hypersensitivity; concurrent or intermittent use of alpha-blockers (eg, doxazosin, terazosin, prazosin) or organic nitrates in any form
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Common adverse effects include headache, flushing, rhinitis, dyspepsia, or indigestion; assess cardiovascular status before use; caution with left ventricular outflow obstruction or conditions aggravated by hypotension; caution with hepatic or renal impairment (decrease dose); may cause prolonged or painful erection; may cause back pain or myalgias
More on Cauda Equina and Conus Medullaris Syndromes |
| Overview: Cauda Equina and Conus Medullaris Syndromes |
| Differential Diagnoses & Workup: Cauda Equina and Conus Medullaris Syndromes |
Treatment & Medication: Cauda Equina and Conus Medullaris Syndromes |
| Follow-up: Cauda Equina and Conus Medullaris Syndromes |
| Multimedia: Cauda Equina and Conus Medullaris Syndromes |
| References |
| « Previous Page | Next Page » |
References
Kingwell SP, Curt A, Dvorak MF. Factors affecting neurological outcome in traumatic conus medullaris and cauda equina injuries. Neurosurgical Focus. 2008;25(5):E7. [Medline].
Fujisawa H, Igarashi S, Koyama T. Acute cauda equina syndrome secondary to lumbar disc herniation mimicking pure conus medullaris syndrome--case report. Neurol Med Chir (Tokyo). Jul 1998;38(7):429-31. [Medline].
Raj D, Coleman N. Cauda equina syndrome secondary to lumbar disc herniation. Acta Orthop Belg. Aug 2008;74(4):522-7. [Medline].
Gleave JR, MacFarlane R. Prognosis for recovery of bladder function following lumbar central disc prolapse. Br J Neurosurg. 1990;4(3):205-9. [Medline].
Gellido CL, Onesti S, Llena J. Spinal schistosomiasis. Neurology. Jan 25 2000;54(2):527. [Medline].
Waters JH, Watson TB, Ward MG. Conus medullaris injury following both tetracaine and lidocaine spinal anesthesia. J Clin Anesth. Dec 1996;8(8):656-8. [Medline].
Kothbauer K, Seiler RW. [Tethered spinal cord syndrome in adults]. Nervenarzt. Apr 1997;68(4):285-91. [Medline].
Spencer TS, Campellone JV, Maldonado I, et al. Clinical and magnetic resonance imaging manifestations of neurosarcoidosis. Semin Arthritis Rheum. 2005;34(4):649-661. [Medline].
Coscia M, Leipzig T, Cooper D. Acute cauda equina syndrome. Diagnostic advantage of MRI. Spine. Feb 15 1994;19(4):475-8. [Medline].
Mathew P, Todd NV. Diagnosis of intradural conus and cauda equina tumours. Br J Hosp Med. Aug 18-31 1993;50(4):169-70, 172-4. [Medline].
Podnar S. Electromyography of the anal sphincter: which muscle to examine?. Muscle Nerve. Sep 2003;28(3):377-9. [Medline].
Rydevik B. Neurophysiology of cauda equina compression. Acta Orthop Scand Suppl. 1993;251:52-5. [Medline].
Biesek D, Ksiazkiewicz B, Wanat-Slupska E. [Conus medullaris and cauda equina infarct in the course of thrombosis of deep veins of lower extremities]. Pol Merkur Lekarski. Sep 2004;17(99):273-4. [Medline].
Butefisch C, Gutmann L, Gutmann L. Compression of spinal cord and cauda equina in Charcot-Marie-Tooth disease type 1A. Neurology. Mar 10 1999;52(4):890-1. [Medline].
Canale S. Circulation of spinal cord. In: Campbell's Operative Orthopaedics. Vol 9. St. Louis, Mo: Mosby; 1998:. 2683.
Delamarter RB, Sherman JE, Carr JB. 1991 Volvo Award in experimental studies. Cauda equina syndrome: neurologic recovery following immediate, early, or late decompression. Spine. Sep 1991;16(9):1022-9. [Medline].
Kaiboriboon K, Olsen TJ, Hayat GR. Cauda equina and conus medullaris syndrome in sarcoidosis. Case report and literature review. Neurology. 2005;11(3):179-183. [Medline].
Kostuik JP, Harrington I, Alexander D, et al. Cauda equina syndrome and lumbar disc herniation. J Bone Joint Surg Am. Mar 1986;68(3):386-91. [Medline].
Ku A, Lachmann E, Tunkel R. Neurosarcoidosis of the conus medullaris and cauda equina presenting as paraparesis: case report and literature review. Paraplegia. Feb 1996;34(2):116-20. [Medline].
Mascalchi M, Salvi F, Pirini MG. Transthyretin amyloidosis and superficial siderosis of the CNS. Neurology. Oct 22 1999;53(7):1498-503. [Medline].
Michelson DJ, Ashwal S. Tethered cord syndrome in childhood: diagnostic features and relationship to congenital anomalies. Neurol Res. 2004;26(7):745-753. [Medline].
Nascone JW, Lauerman WC, Wiesel SW. Cauda Equina Syndrome: Is it a surgical emergency?. Univ Pennsylvania Orthoped J. 1999;12:73-6.
Podnar S. Bilateral vs. unilateral electromyographic examination of the external anal sphincter muscle. Neurophysiol Clin. Oct 2004;34(3-4):153-7. [Medline].
Schizas C, Ballesteros C, Roy P. Cauda equina compression after trauma: an unusual presentation of spinal epidural lipoma. Spine. Apr 15 2003;28(8):E148-51. [Medline].
Further Reading
Keywords
lower spinal cord injury, compressive lumbosacral polyradiculopathy, cauda equina syndrome, conus medullaris syndrome, spinal cord compression, back pain, spinal cord injury, upper motor neuron symptoms, UMN symptoms, lower motor neuron symptoms, LMN symptoms, spinal cord syndromes
Treatment & Medication: Cauda Equina and Conus Medullaris Syndromes