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)

The mechanism of nonhemorrhagic neurological deterioration from spinal arteriovenous malformation (AVM) and the role of acute surgical intervention in this setting are not well understood. The case is described of a 65-year-old man who presented with a 2-year history of mild gait spasticity and vague sensory complaints affecting both lower extremities. Following a diagnostic lumbar puncture, these symptoms progressed painlessly over a 4-day period to total motor paraplegia, urinary retention, and hypesthesia in all modalities with a midthoracic sensory level. Magnetic resonance imaging showed a probable spinal AVM but no evidence of hemorrhage or cord compression. Spinal angiography confirmed the diagnosis of spinal AVM fed by radicular branches of left T-7 and T-8 segmental intercostal arteries. Drainage was via long dorsal veins caudally. Emergency laminectomy with intradural exploration was performed. There was no evidence of prior hemorrhage or focal mass effect, although the cerebrospinal fluid pressure was elevated. The dural component of the spinal AVM was excised, and its communications with the spinal cord were disconnected intradurally. Neurological function started improving within 6 hours of the patient awakening from anesthesia. He had achieved antigravity strength in every muscle group of the lower extremities by the time of discharge to a rehabilitation center 10 days after surgery. Three months postoperatively, he was ambulating with a walker and was continent of urine and stool. Possible pathophysiological mechanisms are discussed in light of the favorable response to timely surgical intervention.
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PMID:Neurological deterioration in a patient with a spinal arteriovenous malformation following lumbar puncture. Case report. 201 87

We report on a stroke patient who showed delayed gait recovery between 8 and 11 months after the onset of intracerebral hemorrhage. This 32-year-old female patient underwent craniotomy and drainage for right intracerebral hemorrhage due to rupture of an arteriovenous malformation. Brain MR images revealed a large leukomalactic lesion in the right fronto-parietal cortex. Diffusion tensor tractography at 8 months after onset revealed that the right corticospinal tract was severely injured. At this time, the patient could not stand or walk despite undergoing rehabilitation from 2 months after onset. It was believed that severe spasticity of the left leg and right ankle was largely responsible, and thus, antispastic drugs, antispastic procedures (alcohol neurolysis of the motor branch of the tibial nerve and an intramuscular alcohol wash of both tibialis posterior muscles) and physical therapy were tried to control the spasticity. These measures relieved the severe spasticity, with the result that the patient was able to stand at 3 months. In addition, the improvements in sensorimotor function, visuospatial function, and cognition also seemed to contribute to gait recovery. As a result, she gained the ability to walk independently on even floor with a left ankle foot orthosis at 11 months after onset. This case illustrates that clinicians should attempt to find the cause of gait inability and to initiate intensive rehabilitation in stroke patients who cannot walk at 3-6 months after onset.
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PMID:Delayed gait recovery in a stroke patient. 2520 47