Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0026838 (spasticity)
 6,471 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Heterotopic ossification (HO) is an important cause of restriction in range of movements and secondary motor disability following neurotrauma, orthopaedic interventions and burns. It has not received focussed attention in non-traumatic neurological disorders. In a prospective study of 377 patients, on medical problems in neurological rehabilitation setting, 15 subjects (3.97%) had neurogenic heterotopic ossification. Their clinical diagnosis was: transverse myelitis (7), neurotuberculosis (4), traumatic myelopathy (2) and stroke (2). Hip (10), knee (4) and elbow joints (1) were involved. The risk factors included urinary tract infection (15), spasticity (6), pressure sores (13) and deep venous thrombosis (DVT) (6). The initial diagnosis was often other than HO and included DVT (3), haematoma (2) and arthritis (2). ESR and serum alkaline phosphatase levels were elevated in all but one subject. The diagnosis of HO was established using X-rays, CT Scan and three-phase bone scan. Following treatment with non-steroidal anti-inflammatory drugs, the range of motion improved in only four patients. HO resulted in significant loss of therapy time during rehabilitation. High index of suspicion about this complication is necessary for early diagnosis and prompt intervention.
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PMID:Neurogenic heterotopic ossification : a diagnostic and therapeutic challenge in neurorehabilitation. 1130 39

We report a 48-year-old female with the history of Sjogren's syndrome who presented with 3-week history of tingling, numbness, and shooting back, waist, and bilateral leg pain and numbness in the pelvic region with urinary and bowel incontinence. Physical examination was remarkable for reduced motor power in both lower extremities with spasticity. Sensory deficit was noted at the T6 level. Laboratory investigation revealed elevated ESR and CRP and positive serum antiaquaporin-4 IgG. Thoracic and lumbar magnetic resonance imaging revealed abnormal patchy areas, leptomeningeal enhancement through the thoracic cord extending from T3 through T6 levels, without evidence of cord compression. Impression of neuromyelitis optica spectrum disorder was made and patient was treated with methylprednisolone intravenously followed by tapering oral prednisone. Neurological symptoms gradually improved with resolution of bowel and urinary incontinence. In a patient with Sjogren's syndrome who presents with neurological complaints, the possibility of neuromyelitis optica or neuromyelitis optica spectrum disorder should be considered. Awareness of the possibility of CNS disease is important due to the serious nature of CNS complications, some of which are treatable with immunosuppressants. Our patient with Sjogren's syndrome who presented with myelopathy benefited from early recognition and institution of appropriate therapy.
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PMID:A Rare Case of Neuromyelitis Optica Spectrum Disorder in Patient with Sjogren's Syndrome. 2550 22