Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0026838 (
spasticity
)
6,471
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
A 60-year-old female was admitted because of intermittent fever, arthralgia, itching of whole body, pretibial edema, urinary incontinence, pain of both legs and gait disturbance, after an insect bite. On admission, she had fever of 38 degrees C, and nuchal pain and stiffness. Neurological examination revealed
spasticity
of lower legs and increased deep tendon reflexes of all extremities. Hyperesthesia and hyperalgesia were noted on C2-4 and L5-S5 areas. Leukocyte count was 10,100/mm3 and
CRP
was 2+. CSF showed no pleocytosis (3/mm3, lymphocyte), but total protein (50 mg/dl) and IgG (10.5 mg/dl) were increased. On T2-weighted images of brain MRI, multiple small high signal areas were shown. The symptom improved markedly by prednisolone, but 3 months later left lateral gaze palsy appeared abruptly. A demyelinating lesion of the pons to the medulla oblongata including the left paramedian pontine reticular formation was suspected, and a corticosteroid pulse therapy was very effective. Serum titer of anti-Borrelia burgdorferi-IgG antibody by indirect immunoperoxidase method was 400 x at first and 1600 x after 3 months. Neuroborreliosis was diagnosed, but high doses of intravenous penicillin were not effective, and an immune-mediated demyelinating mechanism was probably thought to play a role in the pathogenesis of neuroborreliosis.
...
PMID:[Encephalomyelitis with elevated serum antibody against Borrelia burgdorferi]. 236 35
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.
...
PMID:A Rare Case of Neuromyelitis Optica Spectrum Disorder in Patient with Sjogren's Syndrome. 2550 22