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Results for “Spinal Cord Compression”

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At least 1,621 records · Page 90Linked to original sources
PubMed2006

Morphologic and morphometric magnetic resonance imaging features of Doberman Pinschers with and without clinical signs of cervical spondylomyelopathy.

OBJECTIVE: To compare morphologic and morphometric features of the cervical vertebral column and spinal cord of Doberman Pinschers with and without clinical signs of cervical spondylomyelopathy (CSM; wobbler syndrome) detected via magnetic resonance imaging (MRI). ANIMALS: 16 clinically normal and 16 CSM-affected Doberman Pinschers. PROCEDURES: For each dog, MRI of the cervical vertebral column (in neutral and traction positions) was performed. Morphologically, MRI abnormalities were classified according to a spinal cord compression scale. Foraminal stenosis and intervertebral disk degeneration and protrusion were also recorded. Morphometric measurements of the vertebral canal and spinal cord were obtained in sagittal and transverse MRI planes. RESULTS: 4 of 16 clinically normal and 15 of 16 CSM-affected dogs had spinal cord compression. Twelve clinically normal and all CSM-affected dogs had disk degeneration. Foraminal stenosis was detected in 11 clinically normal and 14 CSM-affected dogs. Vertebral canal and spinal cord areas were consistently smaller in CSM-affected dogs, compared with clinically normal dogs. In neutral and traction positions, the intervertebral disks of CSM-affected dogs were wider than those of clinically normal dogs but the amount of disk distraction was similar between groups. CONCLUSIONS AND CLINICAL RELEVANCE: The incidence of intervertebral disk degeneration and foraminal stenosis in clinically normal Doberman Pinschers was high; cervical spinal cord compression may be present without concurrent clinical signs. A combination of static factors (ie, a relatively stenotic vertebral canal and wider intervertebral disks) distinguished CSM-affected dogs from clinically normal dogs and appears to be a key feature in the pathogenesis of CSM.

Animals↗
PubMed2000

Malignant spinal neurofibrosarcoma.

STUDY DESIGN: A report of a case of metastatic spinal neurofibrosarcoma. OBJECTIVE: To document metastatic neurofibrosarcoma as a cause of spinal cord compression and to review the literature. SUMMARY OF BACKGROUND DATA: Three previously reported cases of metastatic neurofibrosarcoma of the spine were reviewed. METHODS: The patient's clinical record and radiologic investigations as well as the result of a search of the English literature are reported. Magnetic resonance images, computed tomographic scans, and histology photomicrographs are displayed. RESULTS: Paraparesis developed in this patient, due to a posterior extradural thoracic spinal cord compression by a neurofibrosarcoma believed to be metastatic from a neurofibrosarcoma of the femoral nerve. CONCLUSIONS: Malignant spinal metastasis remains a rare complication of neurofibromatosis, with a very poor prognosis.

Fatal Outcome↗
PubMed1996

Intraspinal extradural arachnoid cyst with spinal cord herniation.

A 17-year-old male presented with thoracic myelopathy 12 months after a stab injury to the thoracic spine. The patient reported that symptoms and signs had gradually worsened in the 3 months prior to his examination. Magnetic resonance imaging depicted not only an extradural arachnoid cyst but severe spinal cord compression. The cerebrospinal fluid pressure and dynamics associated with herniation of the spinal cord resulted in the formation and enlargement of an extradural arachnoid cyst. The pressure effect of the cyst accounted for the thoracic myelopathy.

Adolescent↗
PubMed1996

Spinal intermittent claudication due to cervical and thoracic degenerative spine disease.

STUDY DESIGN: Neurogenic intermittent claudication can be caused by spinal cord compression. In this study, 20 patients with spinal intermittent claudication due to degenerative spine diseases were evaluated. OBJECTIVES: This study clarified the clinical features and pathomechanism of spinal intermittent claudication due to degenerative spine diseases. SUMMARY OF BACKGROUND DATA: Spinal intermittent claudication may either be produced by intrinsic or extrinsic lesions. Little is known about spinal intermittent claudication due to extrinsic lesions such as spinal cord compression. Twenty patients with spinal intermittent claudication, caused by cervical or thoracic lesions, who were given surgical treatment except for one, were studied. Their main subjective symptoms were tightness, weakness, and numbness in the lower limbs and a strangulated sensation in the trunk to lower limbs. The objective findings were occurrence and/or aggravation of spinothalamic signs. METHODS: The gait loading test was performed on these 20 patients. Selective spinal angiography was performed on the patients with thoracic myelopathy and its therapeutic effects were evaluated. A radiographic assessment was made in all patients. RESULTS: The subjective symptoms and objective findings were reproduced by the gait loading test. Selective spinal angiography temporarily relieved or improved the spinal intermittent claudication due to the thoracic myelopathy. Spinal intermittent claudication disappeared immediately after surgical treatment. CONCLUSIONS: Circulatory impairment of the spinal cord seems to be closely related to the etiology of spinal intermittent claudication. Besides providing diagnostic information, selective spinal angiography may also have a temporary therapeutic effect.

Adult↗
PubMed1982

Recurrent central cord injury: a case report.

A case of multiple episodes of central cord injury after minor trauma is reported. Cervical films showed a canal diameter of 11 mm at C-3, C-4 and minor instability with a canal diameter of 9 mm in extension. Anterior cervical fusion resulted in a stable spine and the prevention of further symptoms. The mechanism of central cord injury is reviewed, and it is suggested that in some cases careful evaluation will reveal remediable cord compression. Operative treatment may be indicated in central cord injury.

Cervical Vertebrae↗
PubMed1999

[Medullary compression in metastatic cancer].

Cancer patients with spinal cord compression may develop irreversible neurological deficit. The clinical picture implies back pain and subsequent neurological deficit. There is always a danger of rapid deterioration of the patient's condition. If spinal cord compression is suspected, the case is an emergency. MRI should be preferred in the diagnostic work-up, and corticosteroids be administered promptly. Radiation therapy or surgical treatment should be started as soon as possible. Patient outcome is related to the degree of neurological deficit at the start of treatment.

Combined Modality Therapy↗
PubMed1988

Comparison of MR and CT myelography in imaging the cervical and thoracic spine.

MR imaging and CT myelography were compared in a retrospective study of 38 patients with suspected lesions of the cervical and thoracic spinal canal and cord. Twenty-eight abnormal cases were found, including spondylosis (9), tumors (8), intramedullary cavities (3), arachnoiditis (3), disk-space-centered infection or osteomyelitis (2), nonneoplastic cord swelling (2), and CSF-borne metastasis (1). MR was equal or superior to CT myelography in depicting cases of cord enlargement, cord compression, and cord atrophy, providing better tissue characterization, no shoulder artifact, and no limitation caused by CSF block. CT myelography was superior to MR in depicting cases of spondylosis and arachnoiditis. It showed superior spatial resolution, which was most pronounced when comparing axial images and hence particularly superior in detecting the lateral extent of disk herniation. Use of surface coils and thin imaging sections is essential for accurate and complete MR evaluation of the cervical and thoracic spine.

Arachnoiditis↗
PubMed1999

Evidence for neurogenic transmission inducing degenerative cartilage damage distant from local inflammation.

OBJECTIVE: To investigate involvement of the nervous system in ipsilateral and contralateral joint inflammation. METHODS: Freund's complete adjuvant (CFA; 1 mg or 1 microg) was injected unilaterally and the messages (a) from the hind paw to the ipsilateral and contralateral knees and (b) from one knee to the contralateral knee were analyzed. The degenerative impact of the local injury on distant cartilage was assessed using patellar proteoglycan synthesis as an indicator. Neurogenic mechanisms were blocked either by spinal cord compression or by injection of neurokinin 1 (NK-1) antagonist, or they were mimicked by intraarticular injection of substance P. The data were compared with those gathered in a model of systemic inflammation, characterized by fever and serum interleukin-6 production. RESULTS: After unilateral subcutaneous injection of CFA, proteoglycan anabolism decreased bilaterally. Spinal cord compression and administration of the NK-1 antagonist inhibited the response in the contralateral limb. Following 1 mg CFA subcutaneous injection, the ipsilateral response implicated both neurogenic and systemic mechanisms, whereas the nervous system alone was implicated after 1 microg subcutaneous CFA injection. The 1 microg CFA intraarticular injection induced a degenerative contralateral signal, which was abolished by spinal cord compression and by pretreatment with the NK-1 antagonist. Intraarticular injection of 1 microg CFA also induced an ipsilateral increase of anabolism, which was enhanced by spinal cord compression. Similar results were obtained after intraarticular injections of substance P. These effects were not reproduced with turpentine treatment, a systemic model, in which spinal cord compression had no effect. CONCLUSION: A unilateral inflammation can induce, by neurogenic mechanisms, distal bilateral degeneration of articular cartilage, implicating involvement of neuropeptides.

Animals↗
PubMed2001

Juvenile asymmetric segmental spinal muscular atrophy (Hirayama's disease): three cases without evidence of "flexion myelopathy".

Compression of the cervical spinal cord during neck movements ("flexion myelopathy") was proposed to be the main pathomechanism of juvenile asymmetric spinal muscular atrophy (JASSMA). We present 3 patients with the clinical appearance of JASSMA and typical high-intensity signals in the anterior horn cell region of the lower cervical spinal cord (T2-weighted magnetic resonance images) but without evidence of dynamic spinal cord compression. In all these patients pathomechanism distinct from mechanical damage must be assumed.

Adolescent↗
PubMed1997

Coexisting peripheral nerve and cervical cord compression.

STUDY DESIGN: The authors investigated the clinical usefulness of recording motor evoked potentials after transcranial magnetic stimulation in coexisting peripheral nerve and cervical cord lesions. OBJECTIVE: To show that the measurement of central motor conduction time from the abductor policis brevis and the abductor digiti minimi can be used as a good screening method for double lesions involving peripheral nerves and the cervical cord. SUMMARY OF BACKGROUND DATA: Transcranial magnetic stimulation has been used in the diagnosis of compressive cervical myelopathy. This technique could be useful in the assessment of patients with an entrapment neuropathy and cervical myelopathy. METHODS: Motor evoked potentials after transcranial magnetic stimulation, compound muscle action potentials, and F waves after supramaximal peripheral nerve stimulation were recorded from the abductor policis brevis and the abductor digiti minimi. The central motor conduction time was calculated by subtracting the peripheral conduction time from the motor evoked potentials latency. RESULTS: Ten patients with coexisting peripheral nerve and cervical cord lesions were evaluated. Two patients did not show satisfactory improvement after the decompression of the entrapment lesions, and six patients had hyperreflexia of lower limbs. In seven of these patients, the central motor conduction time was prolonged an average of 2.5 standard deviation of the normal value. The remaining two patients had spinal cord compression due to the ossification of the posterior longitudinal ligament. The spinal cord compression was demonstrated by magnetic resonance imaging, but the central motor conduction time was normal. Subjective symptoms improved in these two patients after decompressive surgery at the entrapment site alone. CONCLUSIONS: Measurement of the central motor conduction time using motor evoked potentials is an ideal diagnostic approach for patients with coexisting entrapment neuropathy and cervical cord compression.

Carpal Tunnel Syndrome↗
PubMed2006

Type I congenital multiple intraspinal extradural cysts associated with distichiasis and lymphedema syndrome.

OBJECTIVE: The hereditary syndrome of multiple congenital intraspinal cysts associated with distichiasis, lymphedema and other congenital deformities is extremely rare. Modern imaging techniques have promoted the non-invasive diagnosis of spinal pathology and paved the way for better surgical planning. We reviewed the clinical data, imaging studies and treatment outcomes of a 12-year-old boy with this syndrome. CLINICAL PRESENTATION: Progressive spastic paraparesis with signs of spinal cord compression leading to frequent falls. This was associated with bilateral double row of eyelashes and pretibial edema. The MRI of thoracic spine depicted two large elongated extradural lesions extending from D5-D10 with signal intensity compatible with cerebrospinal fluid leading to severe compression of the spinal cord dorsally. TREATMENT: Laminotomy and complete microsurgical excision of the cysts resulted in a fast and full clinical recovery of his neurological deficit. CONCLUSION: Type I congenital intraspinal cysts is a rare etiology of cord compression syndrome and may be associated with distichiasis, lymphedema and other congenital deformaties. It has several characteristics, which include the higher incidence in thoracic spine and younger age group, disproportional sever motor deficit as compared with sensory disturbances and the excellent clinical recovery following successful surgical treatment.

Child↗
PubMed1982

Anterior decompression of the spine for metastatic epidural cord compression: a promising avenue of therapy?

Most metastatic epidural tumors arise in a vertebral body and invade the anterior epidural space. Therefore, it is logical to decompress the spine anteriorly and not by traditional laminectomy. Surgical decompression is indicated if relapse occurs after radiotherapy and further radiation cannot be administered, if there is neurological deterioration during radiotherapy, and when histological diagnosis of the primary tumor is lacking. This pilot study consists of eleven consecutive anterior decompressions of the spine performed in nine patients. In seven instances other treatment modalities had been exhausted, and in four patients a tissue diagnosis was lacking. Before operation eight of the patients were nonambulatory, four of them paraplegic. Following decompression all but one patient became ambulatory. At operation the main bulk of the compressing tumor was found anterior or anterolateral to the cord. Spine stabilization was done when stability was a problem. Wound infection in one patient was the only postoperative complication. The encouraging outcome of our management prompts us to suggest that anterior decompression of the spine should be considered more often in metastatic compression of the cord and cauda equina.

Cauda Equina↗
PubMed1995

Paraparesis after rib penetration of the spinal canal in neurofibromatous scoliosis.

Paraplegia or paraparesis is uncommon in patients with neurofibromatous scoliosis. The main causes of spinal cord compression in neurofibromatosis are vertebral angulation, vertebral subluxation, and tumorous lesions around the spinal cord. We report a rare case of paraparesis due to spinal cord compression by a rib penetrating the spinal canal in a patient with neurofibromatous scoliosis. There was complete recovery after laminectomy and proximal resection of the compressing rib along with combined anterior and posterior spinal fusion.

Child↗