AUTHOR AND EDITOR INFORMATION

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INTRODUCTION

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Background

Occlusive vascular lesions affecting the spinal cord (spinal stroke) are diagnostic challenges. As is the case for the more common cerebrovascular accident affecting cerebral circulation, an acute onset and a requirement to exclude hemorrhage are paramount concerns. The circulation to the spinal cord has unique features related to the elongated and multimeric anatomy of the cord that affect both mechanism and clinical presentation (see Images 1-3).

Pathophysiology

The anterior spinal artery is a single long anastomotic channel that lies at the mouth of the anterior central sulcus and supplies the circulation to the anterior two thirds of the spinal cord (see Image 3). It gives origin to sulcal arteries that take an arching course to one or the other anterior gray horns. The posterior spinal arteries are smaller paired arteries lying just medial to the dorsal roots. The arterial supply of the spinal cord arises from the aorta and at its cephalad and caudal ends from tributaries of the subclavian and iliac arteries. Eight to ten unpaired anterior medullary arteries are branches of the larger afferent aorta and vertebral and iliac arteries. The largest anterior medullary artery, the great anterior medullary artery of Adamkiewicz, which is susceptible to occlusion with neurologic deficit, is located at the lumbar enlargement, usually at L2 on the left side (but may be at any point from T8 to L2).

Frequency

United States

Spinal cord infarction is not common, but only fragmentary or indirect data are available on incidence or prevalence. A large study showed that only 9 of 3784 autopsies revealed spinal cord infarction, with a rate of occurrence of 0.23% at death. Conversely, if spinal stroke is approximately 1.2% of strokes, an overall annual incidence of 12 in 100,000 can be estimated.

International

International incidence is similar to that in the United States. Recent reports that describe patients developing spinal cord infarction in an increasing number of situations and pathologies would influence this because procedures ranging from major surgery to injections for epidural anesthesia, infections and especially meningitis, and medications (eg, zolmitriptan for migraine) vary in different countries.

Mortality/Morbidity

The risk to life and its quality from spinal cord infarction is substantial because of the disability, which can be severe, with paraplegia, risk of pulmonary emboli, and risk of infection (eg, bladder, lungs, decubiti). However, no epidemiologic studies are available because of the relatively small number of patients affected.

Published series of reports of spinal cord infarction are relatively small ranging up to 36-44 patients. They find a mortality in the vicinity of 20-25% of patients admitted to hospital with spinal cord infarction (Cheshire, 1996; de la Barrera, 2001).

Race

No relationship to race is reported.

Sex

No relationship to sex is reported.

Age

No relationship to age is reported. However, the reported series do have a median age of 52 years.

CLINICAL

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History

Spinal cord infarction is marked by an acute onset, often heralded by sudden and severe spinal (back) pain, which may radiate caudad. This is associated with bilateral weakness, paresthesias, and sensory loss. Loss of sphincter control with hesitancy and inability to void or defecate becomes evident within a few hours.

• The spinal cord stroke, either ischemic or hemorrhagic, has an acute and often apoplectic onset evolving over minutes. This is emphasized because many of the confounding diagnoses, including acute transverse myelopathy, viral myelitis, Guillain-Barré syndrome, and mass lesions in the spinal canal, develop over 24-72 hours with an acute but discernibly slower evolution than the vascular lesions. Recent reports emphasize the occasional confusion of this diagnosis with angina pectoris or acute myocardial infarction (Chesire, 2000; Gross, 2001; Combarros, 2002).
• Neurologic deficit may occur without pain, but most (>80%) spinal infarcts are painful. This is an interesting and unexplained difference from cerebral infarction, which is usually not painful. However, it should be mentioned that closer scrutiny of this association in recent years has found a higher proportion of patients without pain (de la Barrera, 2002). In addition, the mimic of coronary ischemia is because of the occurrence of chest pain, which may be severe.
• Uncomplicated spinal cord infarction is most commonly thoracic (with peak at T8 in the series reported by Cheshire [1996]), and presents as acute paraparesis or paraplegia, numbness of the legs, and inability to void.
• The syndrome depends on the level of the cord lesion and may vary from mild or moderate and even reversible leg weakness to quadriplegia (see Image 4).
• Fever is a warning ("red flag"); heed this warning by considering infectious origins of a spinal cord syndrome, particularly acute bacterial meningitis, and focal extramedullary spinal lesions (eg, epidural and subdural abscess, granuloma) and viral myelitis due to herpes simplex, varicella-zoster, and other viruses.
• Many reports exist, and theses are usually of single or a few cases of spinal cord infarction occurring in context of and classed as complications of surgical procedures in which hypotension and prolonged positioning (eg, seated neurosurgical approaches, hyperlordosis) may be prominent factors. Also, injections for foraminal nerve block, for epidural anesthesia, or even self-injection by the addict seeking an intravenous access (Joseph, 2004) have been reported in association with and probably causative of spinal cord infarction.

Physical

Neurologic dysfunction usually (ie, in approximately 95% of reported cases) stems from a lesion located in the anterior two thirds (or in the central "watershed") of the spinal cord and spares vibration and position sense perception, which are carried by the posterior columns and are relatively spared. See Image 2 for sensory pathways in the spinal cord and Image 3 for vascular anatomy of the spinal cord in the axial plane.

• In the acute stage (usually for several days),"spinal shock" with flaccid muscle tone and areflexia, including absent Babinski reflexes, is observed commonly.
• The classic presentation is a sensory pattern distal to the lesion, superficial pain and temperature discrimination are lost bilaterally with preservation of light touch, vibration, and position sense. See Image 4 for clinical determination of spinal level.
• Weakness and sensory loss (for all primary sensory modalities) are found at the spinal cord segmental levels of the spinal cord infarct.

Causes

Classifying the causes of spinal cord infarction according to the location of the vascular pathology is convenient and systematic. The pathology may involve the aorta or an intervening arterial feeder (eg, thoracic, intercostal, or cervical branch from subclavian or vertebral artery), or the radicular artery may affect the anterior spinal artery and intrinsic arterial vessels within the spinal cord. Spinal venous pathology may produce spinal infarction, although this is clinically rare.

• Involvement of intrinsic cord vessels has been reported with arteritis, both in systemic lupus erythematosus and granulomatous arteritis, and from emboli of atheroma or even from compression by or emboli of intervertebral disk fragments.
• Anterior spinal artery occlusion has been reported with arteritis, including that associated with syphilis and diabetes mellitus; after trauma; spontaneously or without recognized cause; and as a complication of spinal angiography, cervical spondylosis, spinal adhesive arachnoiditis, administration of intrathecal phenol, and spinal anesthesia.
• Aortic disease has produced spinal infarction in a variety of situations including dissecting aneurysm; aortic surgery, especially with aortic cross-clamping above the renal artery (below that level anastomotic flow via the artery of Adamkiewicz usually provides protective circulation); aortography; atherosclerotic embolization; and aortic thrombosis.
• Uncommon causes include decompression sickness, which has a predilection for spinal ischemic damage; complications of abdominal surgery, particularly sympathectomy; circulatory failure as a result of cardiac arrest or prolonged hypotension; and vascular steal in the presence of an arteriovenous malformation, or vascular compression by tumors in the spinal canal, vertebral fracture, or a herniated intervertebral disk. In 2000, Vijayan and Peacock reported a spinal cord infarct that occurred after treatment of a migraine headache with zolmitriptan.

DIFFERENTIALS

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Other Problems to be Considered

The top priority is to exclude spinal cord compression by a mass lesion. The pathologies associated with spinal cord infarction are numerous and include neoplasm, spinal epidural or subdural abscess, granuloma, spinal epidural or subdural hematoma, extramedullary spinal tumor (including meningioma, neurofibroma, extradural lymphoma, metastasis), and herniated intervertebral disk. These are "surgical" causes and reasons for prompt diagnosis because of the urgent clinical need for decompression.

Differentiate spinal cord infarction from acute inflammatory demyelinating polyradiculopathy (AIDP, Guillain-Barré syndrome) by following the diagnostic criteria for AIDP. The ADIP radiculopathy usually does not involve sphincter dysfunction and has a different pattern of sensory deficit (typical of peripheral neuropathy), with distal loss in the extremities and lacking a sensory level on the body.

Intraspinal hemorrhage (hematomyelia): Consider the possibility of an underlying arteriovenous malformation of the spinal cord. This is especially important because surgical extirpation may prevent recurrence of hemorrhage and/or progression to more severe disability such as complete paraplegia.

Subacute combined degeneration (posterolateral myelopathy of vitamin B-12 deficiency) is a treatable myelopathy with a different tempo; the symptoms develop more gradually over days to weeks or months.

Abducens (CN VI) nerve palsy
Acoustic neuroma
Back pain

Acute myelopathy
Acute transverse myelopathy
Viral myelitis
Demyelinating disease
Neurosarcoidosis
Tuberculosis
Neurosyphilis
Parasitic diseases (schistosomiasis, cysticercosis)

Other disorders with subacute onset
Focal spinal tumor, either intraaxial or extraaxial
Giant cell arteritis (occurs in the elderly and often with temporal artery and optic nerve involvement)
Meningeal carcinomatosis or lymphoma
Syringomyelia
Spinal arachnoiditis
Subacute necrotic myelitis (spinal thrombophlebitis)

WORKUP

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Lab Studies

• Routine CBC; fasting serum glucose; erythrocyte sedimentation rate; lipid panel for cholesterol, LDL-cholesterol, HDL-cholesterol, and triglycerides; serologic test for syphilis, and; electrolytes
• • Leukocytosis, including a left shift to polymorphonuclear WBCs, suggests an infectious myelitis or other infectious cause of spinal cord compromise.
  • Diabetes mellitus is present in approximately one half of patients with epidural abscess and is a vascular risk factor. Other risk factors including the metabolic syndrome with obesity and hypertension may also be relevant.
  • On rare occasions, hypokalemia or hyperkalemia presents with flaccid quadriparesis, which is in the differential diagnosis of myelopathy.
• Tests for vascular risk factors, especially diabetes mellitus, hypercholesterolemia, coagulopathies, and systemic lupus erythematosus and other forms of arteritis and vasculitis. The diagnosis of giant cell arteritis may be suspected by an elevated ESR but requires temporal artery biopsy for confirmation.
• • The search for vascular risk factors extends from diabetes mellitus (ie, fasting serum glucose), hypertension, and hypercholesterolemia (ie, lipid panel for low-density lipoprotein, very low-density lipoprotein, and high-density lipoprotein) to anticardiolipin or antiphospholipid syndromes (ie, activated partial thromboplastin time, antiphospholipid antibody titer) and other coagulation disorders, such as protein C and protein S deficiencies and thrombocytosis or thrombocytopenia (eg, thrombotic thrombocytopenic purpura [platelet count]).
  • The less common causes usually are sought only if no obvious vascular risk factor is found in a young patient with a spinal cord infarct.
• Infectious causes: Those that can be defined by examination of blood or cerebrospinal fluid (CSF). The infectious causes range from syphilis (eg, serum rapid plasma reagin [RPR], Venereal Disease Research Laboratory [VDRL] test, or Wasserman, CSF VDRL or Hinton) to viruses that can be identified specifically by polymerase chain reaction (PCR), such as herpes simplex type 1 and 2, varicella-zoster, Epstein-Barr, human T-cell leukemia type 1 (HTLV-1), HIV, and hepatitis B.
• Autoimmune assessment of blood and CSF: This assessment extends from screening by erythrocyte sedimentation rate (ESR), antinuclear antibody (ANA), and complement level assay to immunoassay determination of nuclear antibodies.

Imaging Studies

• A crucial examination is the imaging that can identify (or exclude) a mass or space-occupying lesion that is compressing or compromising the circulation of the spinal cord (extraaxial) or is within the cord tissue (intraaxial). The easiest and safest procedure for this is spinal MRI. Take care to avoid the pitfall of limiting the spinal region studied by failing to appreciate that high cervical regions have little local symptomatology or signs. Another diagnostic pitfall is failing to appreciate that a sensory level may be caudad to the lesion because of the topographic lamination with superficial location of the ascending sensory pathways (lateral spinothalamic tracts) from the lower spinal segments; this also may limit the spinal region studied.
• Delineation of the spinal cord infarct has been the greatest advance in recent years. Numerous reports (Weidauuer, 2002; Luo, 2003; Kuker, 2004; Shinoyama, 2005; Zhang, 2005) of central high-intensity lesion delineation appropriate to the cord lesion are available. Diffusion weighted imaging (DWI) is particularly sensitive to the ischemic change and may become standard at least in the specialized treatment centers that are best for these patients.
• Myelography, especially with the greater sensitivity of the enhanced CT myelography, is satisfactory for definition of mass lesions and can be used if MRI is unavailable or for any reason unsatisfactory (eg, a very obese patient). Parenthetically, the latest of the open-frame MRI equipment appears to be satisfactory for spinal diagnosis. A diagnostic pearl is to use cranial MRI. It is valuable in the patient with multiple sclerosis because the abnormalities found provide confirmatory evidence.
• • This principle is also true for other multifocal CNS diseases such as systemic lupus erythematosus, infectious disorders, and sarcoid.
  • A diagnostic pitfall to remember is the "cerebral" paraparesis that can occur in such parasagittal disorders as parasagittal meningioma or epidural empyema/abscess. Bilateral anterior cerebral artery ischemia also can occur in the anomalous common stem of these arteries.
• Spinal CT scan has little application to the diagnosis of spinal ischemia. It lacks the sensitivity, especially in the cervical region, to be adequate for reliable exclusion of several of the mass lesions in the differential diagnosis. Likewise, little value is found in plain radiography of the spine for the diagnoses considered here.
• Spinal angiography (arteriography) is indicated occasionally, usually for diagnosis and treatment of a spinal arteriovenous malformation. The procedure is technically difficult and somewhat risky and usually is performed only at tertiary care medical facilities. Spinal MRI has achieved a level of sensitivity and reliability that it may suffice although for the definitive diagnosis of spinal AVM, spinal angiography is often indicated.

Other Tests

• Electromyography (EMG) and nerve conduction velocity (NCV) determination will reveal deficits in H and F waves early after the onset of ischemia and subsequent loss of motor action potentials and changes of denervation. These occur because of the loss of anterior horn and other cells in the spinal cord.
• For differentiating spinal cord infarction from polyneuropathy: EMG and NCV findings are usually (approximately 75%) abnormal in AIDP and can be of value in this differential consideration. Enhancement of the nerve roots after gadolinium administration appears to be specific and useful in making the diagnosis of AIDP.

Procedures

• CT-guided biopsy or culture may be diagnostic in some of the diagnostic differential pathologies. It is not indicated for the diagnosis of spinal ischemia.
• Surgical biopsy sometimes is indicated for diagnosis of differential possibilities including neoplasm, meningeal tumor or sarcoidosis, granuloma, and focal indolent infections.
• Temporal artery biopsy can confirm the diagnosis of giant cell arteritis that can underlay spinal cord infarction.
• CSF examination is useful for determining any abnormality that is not fully specific but suggests inflammatory (including neurosarcoidosis) or neoplastic causation. This is typically increased cell counts and pleocytosis, increased CSF protein, and occasionally decreased CSF glucose.
• • An increase in CSF immunoglobulin G (IgG index) or an oligoclonal heterogeneity of immunoglobulins suggests multiple sclerosis, although oligoclonal banding can also be found in other inflammatory disorders including sarcoidosis, viral pathologies, and autoimmune diseases.
  • Specific diagnoses of the viral myelitides are now possible by PCR. This promises to revolutionize the specific diagnosis of the intraaxial myelopathies.
  • Confirming diagnosis of a focal spinal lesion of bacterial, mycobacterial, fungal, or parasitic origin by culture is rare, but still worth pursuing in the patient whose disorder is worrying.

Histologic Findings

Histologic findings are appropriate to the pathologies outlined in the preceding section (see Image 5).

TREATMENT

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Medical Care

The standard drug therapy is aspirin. This is based upon the consensus recommendation for acute treatment of ischemic stroke at any site. Clopidogrel and a combination of aspirin and controlled-release dipyridamole also may be of benefit in reducing the risk of myocardial infarction, recurrent stroke, and death. No direct studies have examined efficacy of drug therapy in spinal cord infarction. This is because of the uncommon nature of the disorder and frequent delay in diagnosis. However, a multicenter study of these therapies would be possible and may yet be done.

• The standard measures for management of the complications of acute paraplegia, directed at prevention of peripheral thrombophlebitis and pulmonary embolism, are recommended. These include pulsatile leg wraps, low-dose heparin administered subcutaneously, and physiotherapy.
• Neuroprotective strategies, including antioxidant, antiglutamatergic, and protease inhibition, improve outcome in animal experimentation with models of acute ischemia but have not yet been reported effective in human cord ischemia. One would hope that these approaches are more vigorously pursued as research into modes of preventing cell death progresses.
• Anticoagulation is considered at 2 dosage levels with different rationales (see above). It is considered at low dosage with the goals of preventing peripheral venous thrombosis and reducing the risk of pulmonary embolism, and it is considered at higher dosage with the goals of preventing extension of the acute ischemic injury and, over the longer term, of reducing recurrent morbidity and mortality rates. However, as stated previously, no definitive studies define the use of anticoagulation in spinal cord infarction.

Consultations

• Neurosurgeon - If compressive lesions are observed
• Physiatry or neurorehabilitation specialist - To implement rehabilitation measures, including prevention of decubiti and spasticity

Diet

Diet is not directly relevant. A diet with a high fiber content prevents constipation.

Activity

Early in the course, transfer to chair and ambulation as possible adjuncts to rehabilitation and to prevent thrombophlebitis and pulmonary embolization.

MEDICATION

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In general, the prophylaxis of stroke by inhibition of platelet aggregation is prudent and recommended. If an unusual cause for the spinal thrombosis is suggested, such as vasculitis or infection, one must consider drugs effective in that disorder including steroids and antibiotics, respectively.

Inhibition of platelet aggregation should be implemented with the goals of limiting extension of the acute ischemic lesion and reducing the longer-range risks of recurrent stroke, myocardial infarction, and death.

To this point, there have been no reports of the use of thrombolytic agents such as tissue thromboplastin activator in spinal cord infarction.

Drug Category: Antiplatelet agents

These agents inhibit platelet function by blocking cyclooxygenase and subsequent aggregation. Antiplatelet therapy has been shown to reduce mortality rate by reducing the risk of fatal strokes, fatal myocardial infarctions, and vascular death in patients with a history of transient ischemic attacks.

FOLLOW-UP

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Further Inpatient Care

• The patient is evaluated by the rehabilitation or physiatry service. Episodes of infarction are usually single or monophasic with a low frequency of recurrence, although this can depend on the etiology of the ischemic cord lesion. The prognosis for functional recovery should be guarded in light of the series in the medical literature. A minority of patients improve and rarely ( <10%) there is a remarkable recovery of function particularly of motor control and ability to walk.

Further Outpatient Care

• Treat persisting spasticity, which may be manifest by painful cramps and/or spasms, with oral baclofen, tizanidine, or occasionally diazepam. If the spasticity is unrelieved and remains symptomatic with manifestations such as stiffness, limited gait, spasms, cramps, and pain, proceed to interventional measures; the most successful are intramuscular injection of botulinum toxin and intrathecal baclofen by subarachnoid pump.
• Impotence may respond to oral sildenafil (or related phosphodiesterase-5 inhibitors). The dose of sildenafil is 50 mg (not to exceed 100 mg) taken 30-45 minutes before sexual activity. Intervention by intraurethral alprostadil or intracavernous injection of alprostadil also may be effective.
• One can manage urinary incontinence and urgency with oral oxybutynin. It is also available as a slow-release capsule (Ditropan XL). Detrol (tolterodine) or Detrol LA is a newer drug effective in the treatment of overactive bladder.

In/Out Patient Meds

• Persisting spasticity can be alleviated with conventional measures beginning with oral baclofen, tizanidine, and occasionally diazepam. If these measures are ineffectual, intramuscular botulinum toxin or intrathecal baclofen by subarachnoid pump can be recommended.

Transfer

• The acute stage involves an urgency for diagnosis and the necessity for excluding emergency spinal decompressive surgery that mandates admission to a major center or hospital facility with the requisite imaging, neurosurgical, and related capabilities.
• Neurologic and other disability is usually either permanent or slowly resolving. Hence, long-term care in a rehabilitation hospital or equivalent facility is the best setting once the acute phase is complete and the patient is medically stable. Transfer to this service should be a goal established early in the planning. The optimum setting for maximal and efficient recovery is the clinical unit devoted to spinal cord disorder or injury.

Deterrence/Prevention

• Spinal cord ischemia and infarction are determined by vascular risk. Diabetes mellitus is common in this disorder, affecting approximately 50% of patients. As is generally the case for the tertiary complications of diabetes, strict control of blood glucose to minimize the resultant arteriolosclerosis reduces the risk of spinal cord infarction. Giant cell arteritis should be considered particularly in elderly persons and if headache, elevated ESR, or concurrent visual symptoms is present.
• Other vascular risk factors including hyperlipidemia, hypertension, and arteritis of numerous types, including dysimmune, syphilis, and "vascular fungi" such as mucormycosis, may predispose patients to spinal cord infarction. Appropriate management of these risk factors is recommended for prophylaxis for future vascular complications.

Complications

• Immobility stemming from the paresis and paralysis has a host of medical consequences of which the more common and serious are venous stasis, thrombosis and pulmonary embolus, pneumonia, and decubitus ulcer.

Prognosis

• Spinal cord ischemia (and its irreversible tissue injury of infarction) is a myelopathy, generally associated with substantial motor, sensory, and bladder and/or bowel dysfunction. The short-term mortality rate is 20-25% over the first month following onset of symptoms. The overall life expectancy is diminished because of the vascular, infectious, and other medical complications. The striking improvement in medical care and rehabilitation has led to an improvement in quality of life for patients with spinal cord strokes since World War II.
• Because the extent of damage is less than that sustained in most traumatic cord injuries, and the potential for recovery is greater because ischemia is reversible in part, these patients may have better function than patients with traumatic cord injuries though the prognosis for substantial motor recovery should be guarded.

Patient Education

• Those at risk of spinal ischemia cannot be differentiated readily from those at risk of more common disorders of the circulation such as cerebrovascular stroke, myocardial infarction, and renal failure. The measures recommended to reduce these vascular disorders also reduce the incidence and occurrence of myelomalacia. Hence, education of those bearing a treatable vascular risk in regard to diabetic treatment, aspirin prophylaxis, antihypertensive agents, and immunomodulatory therapy logically can be expected to be of benefit and reduce the incidence of spinal thrombosis.
• For excellent patient education resources, visit eMedicine's Stroke Center. Also, see eMedicine's patient education article Stroke.

MISCELLANEOUS

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Medical/Legal Pitfalls

• The short period (<24 h) during which reversible spinal insult can recover poses a legal hazard that cannot be overemphasized. Any acute spinal dysfunction should be evaluated and managed on an urgent basis.
• It is crucial that compression due to mass lesions is corrected surgically as quickly as possible. Failure to recognize, diagnose, and intervene in these patients can be catastrophic with permanent severe disability. Hence, proper assessment of the patient with acute paraparesis or paraplegia to diagnose accurately and to facilitate a rapid treatment response is essential. Appropriate spinal MRI or spinal myelography must be performed.
• In the patient with ischemia of the spinal cord, less can be done during the acute period to reverse the disability. Consequently, less diagnostic or management vulnerability is present than in clinically similar syndromes of cord compression caused by hematoma, herniated intervertebral disk, spinal epidural metastasis or lymphoma, spinal intradural meningioma or neurofibroma, spinal epidural or subdural abscess, or treatable spinal or "transverse myelitis" due to herpes simplex or varicella-zoster infection. Differentiation of these causes of myelopathy is very important in directing optimum patient care and treatment. This approach reduces exposure to criticism of the urgent diagnosis and care of the patient with acute paraparesis and related disorders.

MULTIMEDIA

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Media file 1:  Transverse section of spinal cord showing location of main pathways. The lamination of fibers in posterior columns and in lateral spinothalamic and lateral corticospinal tracts is indicated (C, cervical; T, thoracic; L, lumbar; S, sacral).
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Media file 2:  Simplified representation of course of major sensory pathways in the spinal cord. Decussation of the spinothalamic tracts occurs within one or two segments of their entry.
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Media file 3:  Pattern of arterial supply to spinal cord and (left) territories of the anterior and posterior spinal arteries.
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Media file 4:  Guide to clinical determination of the segmental spinal cord level.
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Media file 5:  Transverse section of spinal cord at T12-L1 showing infarction of central cord. The patient became paraplegic following resection of a ruptured abdominal aortic aneurysm. During surgery, prolonged occlusion of the abdominal aorta and great anterior radicular artery was necessary.
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Media type:  Image

REFERENCES

Section 11 of 11

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• Follow-up
• Miscellaneous
• Multimedia
• References

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• Vijayan N, Peacock JH. Spinal cord infarction during use of zolmitriptan: a case report. Headache. Jan 2000;40(1):57-60. [Medline].
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Article Last Updated: Mar 29, 2006