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)

Of all patients presenting at our level 1 trauma center with multiorgan system injuries, 33 have been identified with acute lesions of the thoracic aorta. Mean severity injury score was 24 +/- 3. Four patients underwent resuscitative thoracotomy upon arrival in the emergency department. One survived and fully recovered. The rest underwent diagnostic procedures and repair of aortic lesions in conjunction with surgical treatment of other injured organ systems. The overall survival rate was 82 percent. Survivors arrived significantly faster to the ED and had lesser degree of multiorgan system injuries. There was no difference in the time spent to make the diagnosis of acute aortic disruption for survivors and nonsurvivors, nor was a difference in time to arrive in the operating room once the diagnosis of aortic injury has been established. Morbidity was related to ischemia to distal organs in four patients of whom two presented with multiple lesions of the thoracic aorta; two remained paralyzed and two had only lower limb spasticity. All discharged survivors were alive at 12 months' follow-up. The type of surgical repair did not influence the outcome of patients with single, typical aortic lesions; however, "clamp/sew" technique was not adequate when multiple aortic tears were found intraoperatively. The outcome of surgical treatment of the traumatic aortic lesions of patients with polytrauma may be influenced by the speed of arrival to the ED, the magnitude of multiorgan system involvement, and the application of appropriate surgical technique for repair according to the intrathoracic findings and the timing of aortic repair vis-a-vis other surgical treatment.
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PMID:Determinants of outcome in lesions of the thoracic aorta in patients with multiorgan system trauma. 173 50

Baclofen, the most effective drug for treating spasticity, is a specific agonist of gamma-aminobutyric acid-B receptors, and is very abundant in the superficial layers of the spinal cord. Given orally, baclofen does not easily penetrate the blood-brain barrier, and is distributed equally to the brain and spinal cord. Direct intrathecal administration was given in order to change the distribution of the drug by preferentially perfusing the spinal cord. Eighteen patients presenting a severe spastic syndrome were treated with chronic intrathecal infusion of baclofen in the lumbar cerebrospinal fluid. After clinical preselection, 38 patients were implanted with a lumbar access port allowing long-term trials in order to determine the efficacy of baclofen therapy and the effective 12-hour dose. The 18 patients selected for chronic administration were implanted with a programmable pump. The pathology in these cases was: multiple sclerosis (6 cases), posttrauma spastic syndrome (eight cases), and (one case each) cerebral palsy, ischemic cerebral lesion, spinal ischemia, and transverse myelitis. The mean follow-up period was 18 months (range 4 to 43 months). The clinical results were evaluated according to muscular hypertony on Ashworth's scale (changed for occurrence of painful spasms) and functional improvement. Results were better for spastic syndrome secondary to traumatic medullary lesion than for demyelinating disease. Hypertonia was improved in all cases as confirmed by the registration of the Hoffman (H) reflex. Painful muscular spasms disappeared in 14 of the 16 affected patients. Significant functional improvement was noted in nine patients and was considerable in three. The risk of side effects secondary to overdose (such as excessive hypotonia or central depression) and the absence of a specific baclofen antagonist stresses the necessity for accurate determination of the efficient dose. After an initial titration period and adjustment of the therapeutic dose, the individual doses were from 21 to 500 micrograms/24 hrs (mean 160 micrograms/24 hrs). This new conservative method is very effective, perfectly reversible, and safe when administered in conditions favorable to its use.
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PMID:Chronic intrathecal baclofen administration for control of severe spasticity. 230 74

Shoulder pain is a frequent and debilitating problem in hemiplegic patients, and its etiology remains poorly understood. The role played by hemineglect in the appearance of shoulder pain was studied. During two years, 94 hemiplegic subjects were involved in a rehabilitation program after cerebrovascular accidents. Their average age was 68 years; 45 (47.9%) subjects had shoulder pain, and 24 subjects (22.5%) had hemineglect. The subjects with shoulder pain were compared to those without pain (the control group) with respect to gender, age, diabetes, heart failure, cardiac ischemia, scapulohumeral arthritis, and calcified tendinitis of the rotator cuff. We were unable to demonstrate a relationship between hemineglect and shoulder pain in the hemiplegic (X2 (1) = 2.03, p = .15), although pain was significantly more frequent in subjects with right hemispheric cerebrovascular accident (X2 (1) = 5.0, p less than .025). The subjects with shoulder pain had significantly more spasticity of the affected limb (X2 (1) = 26.3, p less than .01), less sensitivity to pinprick of the upper paralyzed extremity (X2 (1) = 10.8, p less than .01), and a more severe subluxation of the affected shoulder (t(51) = 14.0, p less than .01).
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PMID:Painful shoulder in the hemiplegic and unilateral neglect. 237 73

A 22-year-old male developed a tic of neck-flexion at the age of 14. The tic occurred 40 to 50 times per minute on its peak at age 16. Since then he noticed the atrophy and weakness of his both upper limbs. His right leg became weak at age 22. On admission, neurological examination revealed tic of lip and neck, severe muscle atrophy and weakness of bilateral upper limbs, mild muscle weakness and spasticity of right lower limb and hyperreflexia in four limbs. Needle EMG studies revealed fibrillation, positive sharp wave and giant MUP in the biceps, triceps and first interossei muscles. There were no abnormal findings suggesting cervical spondylosis or disc herniation on neck roentgenogram and neck MRI in neutral position. Neck MRI in the ventro-flexed position showed a flattening of the lower cervical cord and a band-like isointensity lesion in the posterior epidural space at C4-6. This isointensity lesion was considered to represent a congestion of the internal vertebral venous plexus. These findings suggest that frequent neck flexion by itself causes the injury of the lower cervical cord through (1) over-stretching of the cord, (2) compression of the cord by dural sac, (3) arterior ischemia, and/or (4) stagnant hypoxia due to venous congestion. Flexion myelopathy may represent one of the most important mechanisms of cervical cord injury accompanied with involuntary movement of neck.
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PMID:[Flexion myelopathy due to tic of neck]. 275 44

Ischemic spinal cord injury with resulting postoperative paraplegia is an inherent risk for operations on the thoracic aorta. The mechanism of injury is not clearly understood, and numerous adjuncts to avoid this complication have been suggested, with conflicting clinical results. A new technique of hypothermic regional perfusion of the spinal cord is described. Fifteen female pigs weighing 21 to 39 kg were used for the experiment. The control group consisted of 5 animals in which the thoracic aorta was clamped at the distal arch for 30 minutes. All of these animals sustained postoperative neurological damage. Eighty percent sustained postoperative paraplegia, and 20% had severe spasticity of the hind legs that precluded normal ambulation. The experimental group consisted of 10 animals in which hypothermic regional perfusion was performed for 30 minutes after cross-clamping of the distal arch. Perfusion cooling was followed by 30 minutes of ischemia in 5 animals and 45 minutes of ischemia in the remaining 5. All animals that underwent hypothermic regional perfusion were able to walk postoperatively, and no evidence of ischemic injury was found at postmortem examination of the spinal cords. This technique proved to be simple and effective in protecting the spinal cord for up to 45 minutes of ischemia in the experimental group. The clinical implications of this concept are promising for patients undergoing operations on the thoracic aorta.
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PMID:Hypothermic regional perfusion for protection of the spinal cord during periods of ischemia. 359 34

Two young patients are described who made good recoveries from a "locked-in" syndrome presumed to be due to ventral pontine ischemia. The first patient recovered completely from quadriplegia and mutism. In the second patient the only permanent sequellae were slight dysarthria and mild spasticity. Since patients may recover nearly completely from a "locked-in" syndrome, aggressive supportive therapy seems justified during the initial weeks or months.
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PMID:Reversible "locked-in" syndromes. 404 98

To characterize the behavioral and histopathological changes that occur in spinal cord after transient ischemia, reversible occlusion of the descending aorta was achieved in the halothane (1-1.5%)-anesthetized rat by the insertion and subsequent inflation of a 2F Fogarty catheter for 10, 15, 20, or 30 min. Neurological recovery was tested during 8 h of reperfusion. After reflow, animals undergoing 30 min of ischemia displayed an initial flaccidity at 1 h, spasticity at 4 h, and flaccidity at the end of 8 h. Following 20 min of ischemia the initial flaccidity was followed by hindlimb spasticity that persisted for 8 h. Shorter intervals of ischemia had minimal effects on motor function. After reflow, animals developed a prominent allodynea, the incidence of which was dependent on the duration of ischemia. A clear correlation of histopathological changes with the degree of neurological deficit was noted. In spastic animals, small and medium-sized interneurons localized in laminae III to VII were affected. Animals with flaccidity at 8 h additionally displayed a significant incidence of argyrophilic A motoneurons in the ventral horns. Corresponding to the frequent appearance of allodynea, these animals also showed a significant number of damaged neurons in lamina II.
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PMID:Transient spinal ischemia in the rat: characterization of behavioral and histopathological consequences as a function of the duration of aortic occlusion. 816 96

Cortical laminar necrosis is a histopathological entity, related to conditions of cerebral energy depletion. Clinical correlates are supposed to be spastic motor deficits, decreased intellectual capacity and epilepsy. A study was performed in 45 children with cortical laminar abnormalities in signal intensity on MRI. The purpose of the study was to evaluate causes and clinical consequences of these cortical abnormalities on MRI in order to find indirect evidence for the hypothesis that they may represent cortical laminar necrosis. In view of the frequently present concomitant white matter damage, two contrast groups were formed: one group of 40 children with periventricular white matter abnormalities, part of them with subcortical extensions of the white matter damage; and another group of 53 children without abnormalities on MRI. Data concerning history, present clinical condition and final diagnosis were collected. The presence of cortical laminar abnormalities on MRI was found to be strongly associated with a history of cerebral energy depletion, especially hypoxia-ischemia, either in the perinatal period or later in life. Whereas white matter abnormalities tended to be more frequent in premature children, cortical laminar abnormalities tended to occur more frequently in term neonates and older children. The presence of cortical laminar abnormalities on MRI was correlated with an increased risk of spasticity in children without concomitant white matter abnormalities. In children with white matter lesions, cortical laminar abnormalities did not contribute to the risk of spasticity, which was already highly increased by the presence of white matter damage. No association was found between cortical abnormalities on MRI and epilepsy or psychomotor retardation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cortical laminar abnormalities--occurrence and clinical significance. 835 19

Proprioceptive loss, paresthesias, and atrophy of the hands can occur with disorders afflicting the upper cervical spinal cord. The diagnosis might be erroneous, because compression in this region might produce signs and symptoms that seem to originate in the lower cervical cord. This article reviews the clinical presentation and radiographic data of a consecutive series of 11 patients who presented between 1992 and 1994 with an extradural lesion above the C4 level. Each patient had a characteristic syndrome of finger and hand dysesthesia, hand atrophy, and occipital or cervical pain. These complaints usually preceded the development of spasticity and gait disturbance. Initial diagnoses included brachial plexopathy, shoulder dysfunction, viral syndrome, and cervical spondylosis at a lower segment. Cervical spondylosis or a herniated disc was the most common pathogenesis. The most commonly involved level was C3-C4. Nine patients underwent a surgical procedure; eight showed significant postoperative improvement (mean time of follow-up examination, 9.7 mo; follow-up range, 1-24 mo). One patient was lost to follow-up. Although the pathophysiology of these findings is unknown, theories include anterior spinal artery ischemia, venous obstruction, and differential decussation of the forelimb and hindlimb fibers of the corticospinal tract. Recognition of this syndrome might prevent inappropriate operative intervention in patients with coexisting pathological conditions of the lower cervical spinal cord.
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PMID:False localizing signs in upper cervical spinal cord compression. 897 49

Lower extremity symptoms are caused by lesions at any level of the neuraxis, from cortex to muscle. HIV affects virtually every level of the nervous system, either directly or indirectly. The presence of pathology at multiple levels and by multiple processes further complicates the bedside diagnosis of a patient with AIDS and neurologic symptoms. Many neuropathies and other conditions that affect the lower extremities can be identified with careful history and physical examination, confirmed with limited testing, and can be treated successfully. Distal symmetric polyneuropathy is the most common lower extremity disorder, but it must be distinguished from similar-appearing neuropathies caused by medications, B12 deficiency, or vasculitis. Diffuse infiltrative lymphocytosis syndrome also causes a painful peripheral neuropathy that must be distinguished from distal symmetric polyneuropathy. Inflammatory demyelinating polyneuropathies are characterized by muscle weakness. They occur in early, asymptomatic HIV infection and respond to plasmapheresis or steroids. Mononeuropathies in patients with CD4 counts more than 200 often resolve on their own. Multiple mononeuropathies, which occur in patients with CD4 counts less than 50, are often associated with cytomegalovirus infection and may follow a rapidly progressive course unless treated promptly and aggressively. Progressive polyradiculopathy occurs late in the course of AIDS, is often caused by cytomegalovirus, is rapidly progressive, and generally is fatal unless recognized and treated promptly. Muscle weakness, myalgia, and fatigue are common in HIV and have multiple causes. Lower extremity spasticity may be caused by treatable etiologies such as spinal cord abscess, tumor, disc compression, B12 deficiency, or ischemia. Gait disturbances are common but nonspecific and may be caused by treatable neurologic disorders at any level of the neuraxis.
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PMID:Neurologic problems of the lower extremity associated with HIV and AIDS. 957 54


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