Intramedullary spinal cord abscesses are infrequently encountered in everyday neurosurgical practice. Hart reported the earliest documented spinal cord abscess in 1830. Since then, fewer than 100 cases have been reported in the medical literature. With modern antibiotics and neurosurgical techniques, even smaller numbers of these infections are expected to be encountered in the future. Since abscesses may occur anywhere along the spinal axis, anatomy varies with location involved. The most common location for an intramedullary abscess is the posterior thoracic spinal cord.
Since the original publication of this article, several other case reports have been published that discuss intramedullary spinal cord abscesses.[1, 2, 3, 4] These case reports, while detailing several unusual presentations of patients with intramedullary spinal cord abscesses, add little to the core concepts promulgated in the original article. Patients with intramedullary spinal cord abscesses present with neurological findings related to the level of spinal cord involvement; MRI with gadolinium is still the procedure of choice for early diagnosis; and successful outcomes depend upon early diagnosis, aggressive surgical treatment, and appropriate antibiotic treatment following surgery. Even when these guidelines are followed, 70% of patients are left with neurological sequelae.
The presumptive diagnosis of intramedullary abscess requires prompt definitive diagnosis. This of course necessitates demonstration of an infection with subsequent identification of that organism. Therefore, a laminectomy to diagnose and culture the organism is usually required.
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Abscess that compresses the spinal cord and its vasculature.
Spinal cord abscesses arise in spinal cord parenchyma and can be solitary or multiple, contiguous or isolated, and chronic or acute, depending upon the organism and individual patient. As may be expected, solitary lesions are more common and most likely appear in the thoracic cord. Holocord abscesses have been reported in approximately 5 patients. Some authors divide these abscesses into primary and secondary, depending on the source of infection. Abscesses are considered primary when no other infection source can be found. Secondary abscesses arise from another infection site, either distant from or contiguous to the spinal cord, most commonly from the lung, spine, heart valves, and genitourinary system. Intramedullary spinal cord abscesses most commonly arise from a secondary source such as the cardiopulmonary system or from a source in close proximity to the cord such as the mediastinum. These classifications rarely affect treatment or patient outcome.
Spinal cord abscesses occur more frequently in males than females with a peak incidence in the first and third decades of life. Too few cases have been reported to define any racial predilection. Patients with a history of intravenous drug abuse are at particularly high risk, as are other immunocompromised patients such as those with HIV, diabetes, or multiple organ failure.
The most common organisms cultured from spinal cord abscesses include Staphylococcus and Streptococcus species, followed by gram-negative organisms. Mixed flora abscesses are also encountered.
Other unusual organisms have been reported, including Actinomyces, Listeria, Proteus, Pseudomonas, Histoplasma capsulatum, and the tapeworm Sparganum.
In 1899, Hoche demonstrated that abscesses may occur in areas of infarction, thus explaining the common incidence of septic spread to the lower half of the thoracic cord.
The Batson plexus (the confluence of epidural veins in the spinal canal) may contribute to the origin of an abscess by allowing organisms to lodge and thus develop in the spinal cord and its surrounding parenchyma.
Postoperative intramedullary spinal cord abscess due to Mycoplasma hominis has been reported after a neurosurgical procedure.[5] Intramedullary Aspergillus abscess has also been reported.[6]
Spinal cord abscesses have many of the same characteristics of abscesses in other locations. Blood vessel involvement surrounded by an area of infection characterizes hematogenous spread. Areas of softening and early abscess formation characterize subacute infections (1-2 wk duration), whereas a classic abscess wall of fibrotic gliosis surrounding necrotic purulent material characterizes chronic infections. However, spinal cord abscesses do not destroy fiber tracts. Instead, the abscess displaces fiber tracts and spreads along axonal pathways.[7]
As with most neurological diseases, signs and symptoms depend upon the abscess location and duration. In an acute presentation, symptoms of infection (eg, fever, chills, back pain, malaise) are common. Neurological symptoms and signs include weakness, paresthesia, dysesthesia, bladder and bowel incontinence, and acute paraplegia. The neurological signs and symptoms are dependent upon the location in the spinal cord of the abscess with the most common location for an intramedullary abscess is the thoracic spinal cord. Clinical symptoms are similar to those of patients with epidural abscesses, but percussion tenderness is not noted.
In more chronic cases, signs and symptoms mimic those of an intramedullary tumor, and neurological symptoms predominate over those of a systemic infection. The neurological progression is gradual. A high degree of awareness is necessary to diagnose chronic spinal cord abscess; in contrast, acute abscesses are generally encountered in extremely ill patients presenting with acute onset of back pain.[8]
The outcome is generally good with appropriate use of antibiotics and surgical treatment. However, the abscess location determines the residual neurologic deficits. The patient's degree of sepsis ultimately establishes overall mortality. With the advent of modern antibiotics and lower surgical mortality, most abscesses are treated successfully. With steroids and more timely localization through MRI, neurologic deficits can be reduced.
However, patients may be affected by devastating neurologic sequelae and may succumb to this disease. Overall mortality rates vary from 10-20%. Moreover, approximately 70% of patients demonstrate residual neurological sequelae following appropriate treatment. Importantly, a significant percentage of patients have recurrence of the abscess. Consequently, repeat MRIs are essential in patients' long-term and follow-up care.
For excellent patient education resources, visit eMedicineHealth's Infections Center and Brain and Nervous System Center. Also, see eMedicineHealth's patient education articles Brain Infection and Antibiotics.
Neurologic deficits such as paraplegia may occur, depending upon the rapidity with which the abscess is diagnosed and treated and the spinal cord level. Since the abscess and inflammatory process involve the surrounding vasculature, spine cord infarction may lead to irreversible paraplegia.
Cerebrospinal fluid (CSF) examination may show elevated protein and leukocyte levels but can be within reference ranges.
Cultures with sensitivities from abscess aspirate are needed to identify infective organisms. Cultures should include tests for aerobic and anaerobic bacteria, fungi, and tuberculosis. Slides should also be taken to look for parasites. Even with appropriate culture techniques, 25-40% of abscesses are microbiologically sterile.
The procedure of choice for diagnosing a possible intramedullary spinal cord abscess is gadolinium-enhanced MRI.[9, 10, 11, 12, 13] If a high probability of spinal abnormality is present, an MRI of the area will demonstrate the mass. MRI is also valuable in demonstrating any associated disease process (eg, epidural or subdural infection, bone involvement, dermal sinus).[14]
MRI does not differentiate among the types of masses (ie, between tumor and abscess), although an abscess generally demonstrates ring-enhancement, while a metastatic lesion generally demonstrates a nodular pattern of enhancement.
Spinal cord abscesses produce homogeneous spinal cord enlargement on T1-weighted images but produce high signal intensity on T2-weighted images. The abscess margin enhances brightly with gadolinium.
Diffusion-weighted imaging (DWI) with a b-value of 1000 and apparent diffusion coefficient (ADC) maps provide early and accurate detection of abscess and pus collection. DWI is useful not only for the diagnosis but also for the treatment planning of pyogenic and non-pyogenic spinal infections[13]
Most other diagnostic modalities are ineffectual in showing an abscess. Plain radiographs show only bony changes (if present). Myelography usually shows only widening of the spinal cord.
Treatment involves a combination of 3 modalities: surgical drainage of the abscess cavity, identification of the infecting organism, and administration of appropriate antibiotics for a proper length of time.
During the entire course of treatment, steroids are used to reduce spinal cord swelling and edema associated with the abscess.
As mentioned in Lab Studies, cultures of the abscess cavity should include tests for aerobic and anaerobic bacteria, fungi, and tuberculosis. Slides looking for parasites are also recommended.
Prior to identifying the organism, administer a broad-spectrum antipenicillinase penicillin.
Once the organisms are identified and sensitivities established, the appropriate antibiotics can be administered.
Once MRI has localized the abscess, laminectomy is performed to expose the lesion and surrounding cord.[10] Laminectomy is usually performed one level above and below the abscess edges for complete abscess visualization. The dura is opened and the area of spinal cord involvement, as indicated by swelling, hemorrhage, and distended veins, is identified.
At this point, aspiration of the lesion is performed for culture of both aerobic and anaerobic organisms, as well as for fungal infection and tuberculosis. Additionally, complete Gram stain and India ink preparation should be analyzed. A myelotomy over the length of the abscess is next performed, with complete drainage of the abscess cavity. Lastly, the wound and abscess cavity should be irrigated with an antibiotic solution, following by closure in anatomic layers. A drain is optional.[5]
During the preoperative phases, dexamethasone is used to reduce cord swelling. The usual dosage is 4-10 mg every 6 hours.
Intravenous antibiotic therapy is continued for a minimum of 6 weeks following surgery. Similar to the preoperative period, dexamethasone can be used during the postoperative phase to reduce cord swelling. The usual dosage is 4-10 mg every 6 hours. Steroids are tapered on a delayed basis (eg, after 2 wk of treatment).
Obtain a follow-up MRI to detect recurrence of the abscess. However, enhancement of the cavity will likely continue for several weeks.
Rod J Oskouian, Jr, MD, Consulting Physician, Swedish Neuroscience Specialists, Swedish Neuroscience Institute, Seattle
Disclosure: Nothing to disclose.
Coauthor(s)
Charles E Rawlings III, MD, Consulting Surgeon, Department of Neurosurgery, Rawlings Neurosurgical Consulting
Disclosure: Nothing to disclose.
Specialty Editors
Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Received salary from Medscape for employment. for: Medscape.
Chief Editor
Brian H Kopell, MD, Associate Professor, Department of Neurosurgery, Icahn School of Medicine at Mount Sinai
Disclosure: Received consulting fee from Medtronic for consulting; Received consulting fee from Abbott Neuromodulation for consulting.
Additional Contributors
Paul L Penar, MD, FACS, Professor, Department of Surgery, Division of Neurosurgery, Director, Functional Neurosurgery and Radiosurgery Programs, University of Vermont College of Medicine
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