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Results for “Spinal Cord Compression”

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At least 1,261 records · Page 70Linked to original sources
PubMed1989

[Spinal cord compression caused by Cladosporium trichoides. An anatomo-clinical case report].

The authors report a case concerning a 25-year-old man who presented a cervical cord compression. The pathologic examination of the mass disclosed a chronic granulomatous meningitis with dense fibrosis. Septate and pigmented hyphae of Cladosporium trichoides were present among the inflammatory infiltrate. A review of the literature concerning the involvement of the central nervous system by this agent is performed. This is the first case in which the disease started as a compressive cord syndrome.

Adult↗
PubMed1989

Symptomatic hydrocephalus and reversible spinal cord compression in Listeria monocytogenes meningitis. Case report.

Central nervous system infections with Listeria monocytogenes result in varied clinical syndromes ranging from meningitis to rhomboencephalitis. A case of Listeria meningitis complicated by symptomatic communicating hydrocephalus and hydrostatic cervical cord compression is presented which clinically and radiographically improved with aggressive ventricular drainage.

Brain↗
PubMedDate not supplied

Thymic lymphosarcoma with metastases causing spinal cord compression and pelvic limb paresis in a heifer.

Neurological examination of a heifer displaying pelvic limb ataxia and paresis progressing to a dog-sit position but with normal thoracic limb function indicated a spinal cord lesion in the low thoracic/high lumbar region. The progressive neurological deterioration despite normal radiological and cerebrospinal fluid findings were suggestive of a non-inflammatory, non-traumatic extradural compressive lesion; this was subsequently shown to be a lymphosarcoma.

Animals↗
PubMed2002

Development and characterization of a novel, graded model of clip compressive spinal cord injury in the mouse: Part 2. Quantitative neuroanatomical assessment and analysis of the relationships between axonal tracts, residual tissue, and locomotor recovery.

A detailed examination of the histopathological features of the clip compression injury in mice was performed to understand the relationships between neurological function and existing pathology of the spinal cord. Adult, female CD1 mice underwent three grades of extradural clip compression injury (3-g, 8-g, and 24-g FEJOTA mouse clips), transection, and sham injury at T3-4. Quantitative behavioural assessments were performed for 4 weeks following SCI. After 4 weeks, Fluoro-Gold was introduced caudal to the SCI site, at T9, and was retrogradely transported for 5 days to the origin of spared axons through the injury site. Counts of retrogradely labeled neurons in the brain-stem, midbrain, and sensory-motor cortex indicated that the number of intact descending axons that traversed the lesion decreased with increasing injury severity (F > 28; df = 4; p < 0.0001; one-way ANOVA). Independent linear correlation analyses were performed between indices of neurological recovery (BBB and IP test), counts of retrogradely labeled neurons and morphometric assessments of normal residual tissue at the injury epicenter. The BBB test correlated strongly with the amount of residual tissue at the injury epicenter (R = 0.945, df = 28, p < 0.0001). Counts of neurons retrogradely labeled with Fluoro-Gold were also strongly correlated with the BBB scores. The extrapyramidal (raphespinal, reticulospinal, vestibulospinal, and rubrospinal) tracts had Pearson correlation coefficients (R) of 0.814, 0.812, 0.813, and 0.747, respectively (df = 28, p < 0.0001). The pyramidal (corticospinal) tract had a correlation of R = 0.747, df = 28, p < 0.0001 with the BBB scores. The IP scores also correlated strongly with the persistence of extrapyramidal (raphespinal, reticulospinal, vestibulospinal and rubrospinal) tracts with correlation coefficients of 0.801, 0.782, 0.790, and 0.836, respectively (df = 28, p < 0.0001). These data indicate that the counts of retrogradely labeled neurons at the origin of distinct descending motor pathways are predictors of the variance of the functional recovery measured by the BBB and IP tests following spinal cord injury. In addition, we provide a detailed neuroanatomical study of clip compression injury in mice that can be used to study the molecular mechanisms of SCI in knockout and transgenic mice.

Animals↗
PubMed1990

Spinal cord compression due to ossification of ligaments: MR imaging.

A total of 108 patients with ossification of the posterior longitudinal ligament (OPLL) (n = 92), ossification of the yellow ligament (OYL) (n = 8), or both (n = 8) were examined with magnetic resonance (MR) imaging performed with 0.5-T superconductive and 0.22-T resistive units. OPLL was demonstrated as a low-signal-intensity band between the bone marrow of the vertebral body and the dural sac on T1- and T2-weighted images. Continuous cervical OPLL was easier to diagnose than segmental cervical OPLL. T2-weighted images were more useful for detection of ossification of the ligaments. OYL was recognized as an impression on the posterior dural sac. Formation of bone marrow within an area of ossification, shown as increased or intermediate signal intensity, was observed in 56% of the cases of continuous OPLL, 11% of the cases of segmental OPLL, and none of the cases of OYL. The degree of cord compression was more severe in continuous OPLL. Degeneration of the disk was frequently associated with both types of OPLL.

Adult↗
PubMed1999

Metastatic spinal cord compression. Influence of time between onset of motoric deficits and start of irradiation on therapeutic effect.

BACKGROUND: In a retrospective analysis we investigated the prognostic significance of the interval between first appearance of motoric deficits and the beginning of radiation therapy (RT) with regard to posttreatment motoric function. MATERIAL AND METHODS: Data of more than 400 consecutive patients being irradiated at our department between 1994 and 1997 because of vertebral metastases were reviewed. Ninety-six patients fulfilled selection criteria including motoric deficits, no preceding surgical or radiotherapeutic treatment of the spine, minimum total dose of 24 Gy referred to spinal cord, and additional treatment with dexamethasone. Two subgroups with a similar number of patients for better comparability were formed according to the time of developing motoric deficits: 1 to 13 days (49 patients) and > or = 14 days (47 patients). Effect of irradiation on motoric function was evaluated 2 weeks and about 3 months after radiotherapy. Patients with severe deterioration of motoric function within 48 hours before radiation therapy (31 patients) were looked at separately. RESULTS: Two weeks after radiotherapy 42/47 patients (89%) developing motoric deficits > or = 14 days showed improvement of motoric function in comparison to 6/49 patients (12%) of the other group. Deterioration occurred in 1/47 patients (2%) of the first and in 24/49 patients (49%) of the latter group. In case of severe deterioration of motoric function within 48 hours before radiation therapy only 2/31 patients (6%) showed improvement, but 20/31 (65%) deterioration. About 3 months after radiotherapy comparable results were observed. Median survival time was 4 months. CONCLUSION: A slower development of motoric deficits before beginning of radiotherapy means a better therapeutic effect and a more favorable functional outcome after treatment. The prognosis is extraordinarily poor if severe deterioration of motoric function occurs within 48 hours before radiotherapy.

Humans↗
PubMed2005

Extranodal Rosai-Dorfman disease with multifocal bone and epidural involvement causing recurrent spinal cord compression.

Sinus histocytosis with massive lymphadenopathy, or Rosai-Dorfman disease, is a rare histiocytic disorder that typically presents with chronic, self-limiting, cervical lymphadenopathy. We present a case, a diagnostic dilemma for multiple consultation services, of an otherwise well 17-year-old boy without lymphadenopathy who, 8 months after excision of a T9 lytic vertebral lesion and epidural mass that caused cord compression, again presented with cord compression from progressive vertebral disease, recurrent epidural mass, and development of a paraspinal mass and tibial lesion. The excised vertebral and epidural lesions, 2 paraspinal biopsies, and tibial biopsy were interpreted as chronic inflammation until large histiocytes were noted, which were positive for CD68, S100 protein, fascin, and MAC387, and demonstrated characteristic emperipolesis (lymphophagocytosis) that was diagnostic of Rosai-Dorfman disease. This atypical clinical behavior and sites of involvement of multiple bones but not of lymph nodes is unusual and constitutes the aggressive end of the clinical spectrum and a rare cause for cord compression.

Adolescent↗
PubMed1989

Actinomycosis as a cause of spinal cord compression: a case report and review.

A case is presented of a 40-year-old man with rapidly progressing symptoms of thoracic medullary compression, initially thought to be caused by metastatic pulmonary malignancy. Further investigations, however, revealed thoracic actinomycosis spreading to the vertebral column and an actinomycotic epidural granuloma was causing medullary compression. After decompression by laminectomy and antibiotic treatment with penicillin there was some neurological improvement. The condition is rare, and some of the diagnostic difficulties are discussed.

Actinomycosis↗
PubMedDate not supplied

Back pain and epidural spinal cord compression.

The physician must have a high index of suspicion to detect SCC early in patients with malignancy. Back pain is the first symptom in almost all patients, and the diagnosis should be considered for all older patients with back pain. Asking about back pain should be a routine part of the review of systems, especially for patients with known malignancies. Clinically, it is impossible to tell whether or not a patient who has back pain and cancer has epidural SCC. Patients may be stratified as to the likelihood of SCC using the history and physical examination, but the diagnosis relies on radiographic visualization of the spinal cord. It may be acceptable to closely follow patients with normal neurologic examinations and normal plain films, but even this is controversial and includes only a minority of patients. Myelography remains the test of choice. MRI will play an increasingly important role in the future, but has not yet been systematically evaluated. The best therapeutic approach is not clear, but standard treatment is only about 50% effective in all cases. At present, radiation therapy is the treatment of choice for many patients, in particular those who are ambulatory at diagnosis. Anterior resection with vertebral body reconstruction is an exciting approach and may substantially improve the prognosis for patients who are paraparetic or paraplegic. It is important to attempt to choose for each patient the diagnostic and therapeutic options offering the best chance for comfort and preservation of function. The decision of how or even whether to treat is multifactorial and is more complicated than the determination of simply whether or not compression is present.(ABSTRACT TRUNCATED AT 250 WORDS)

Back Pain↗
PubMed1997

A new model of acute compressive spinal cord injury in vitro.

A novel in vitro method of spinal cord injury was developed to facilitate the study of cellular and molecular mechanisms underlying neural trauma. A 3-cm length of thoracic spinal cord was removed from the adult Wistar rat. A strip of dorsal column and its associated dorsal horn gray matter was excised and pinned in an in vitro recording chamber where it was constantly perfused with oxygenated Ringer's solution at either 25 degrees C or 33 degrees C. Injury was performed by compressing the dorsal column segment in vitro with a modified aneurysm clip (closing force 2.0 g) for 15 s. Microelectrode and sucrose gap recordings were generated to characterize the physiological effects of compressive injury. Longitudinal thin sections of control and injured dorsal column segments were examined by electron microscopy. At 25 degrees C, injured axons were characterized by a significant reduction in amplitude of the compound action potential (CAP) to 76.9 +/- 2.4% (P < 0.0005) and an increase in response latency to 112.5 +/- 2.5% (P <0.005). At 33 degrees C, the effects of injury on the CAP amplitude were accentuated (P< 0.0001). With the K+ channel blocker, 4-AP (1 mM), there was broadening of the CAP of injured axons and a delay in repolarization of the axonal resting membrane potential, suggesting myelin disruption with exposure of paranodal K+ channels. Ultrastructurally, injured dorsal column segments showed considerable axonal and myelin pathology including splaying of the myelin sheath and vesicular degeneration.

4-Aminopyridine↗