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)

Outcomes in self-care following rehabilitation in 226 patients were correlated with 11 stroke syndromes, reflecting several pathophysiologic disturbances subsequent to either infarction or hemorrhage in cerebral or vertebro-basilar vessels. Self-care was scored on a 20-point scale for bed movements, transfers, feeding, dressing, personal hygiene, and bathing. Interjudge error among therapists did not exceed 2.5%. Mean score in left cerebral infarction without aphasia was used as a referent value. Scores in left cerebral infarction with aphasia and right parietal lobe syndrome with and without spatial agnosia were similar to the referent. Brain stem dysfunction with spasticity and right cerebral infarction with paresis and spatial agnosia fell below the referent value (Pless than 0.05). Higher levels were achieved in the syndromes of left and right anterior cerebral artery territories, brain stem dysfunction with ataxia, and left parietal lobe syndrome with comprehension aphasia, although t-values were not significant. Length of stay among the 11 groups was fairly uniform except for the group with brain stem dysfunction with spasticity and the group with left hemiplegia with spatial agnosia. These groups indicated rather severe disabilities. Aside from neurologic dysfunction the range of scores was influenced by associated cardiopulmonary involvement.
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PMID:Neurophysiologic syndromes in stroke as predictors of outcome. 68 54

Twenty-six patients presented with slowly progressive focal neurologic symptoms that conformed clinically to one of three categories: asphasia, perceptuomotor dysfunction, or neuropsychiatric dysfunction. Of 12 patients with progressive aphasia, seven were dysfluent and five were fluent. Nine patients had progressive perceptuomotor impairment due to bilateral parietal lobe atrophy, which also included frontal lobe signs in seven patients and occipital lobe signs in three patients. The right hemisphere was more severely involved in five patients and the left hemisphere in four. Five patients had a progressive neuropsychiatric syndrome, and there was also generalized spasticity in three patients due to frontal lobe atrophy. The clinically suspected anatomic localization of cortical atrophy or hypoperfusion in all three categories was confirmed with neuroimaging techniques. A brain biopsy specimen from one patient showed mild, nonspecific degenerative changes. A clinical classification scheme incorporating our observations as well as the observations of others is presented to aid in the recognition of these syndromes.
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PMID:Asymmetric cortical degeneration syndromes. A proposed clinical classification. 149 6

We report a patient with herpes simplex virus encephalitis who presented with left hemiparesis and progressed to aphasia and generalized spasticity. Computerized axial brain tomography with and without infusion of contrast medium was normal, as were the cerebrospinal fluid findings. However, magnetic resonance imaging scan and brain biopsy, were diagnostic of herpes simplex encephalitis.
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PMID:Magnetic resonance imaging in an unusual presentation of herpes encephalitis. 336 12

We report a 73-year-old woman who presented progressive motor clumsiness, cortical sensory loss, and focal parietal lobe atrophy. She was well until one year prior to the present admission when she suffered from what appeared to be mild Fisher syndrome from which she showed excellent recovery. However, soon she noted a gradual onset of difficulty in hand movements and in the recognition of objects by hands. Neurologic examination revealed an alert and well oriented Japanese woman without dementia. Cranial nerves were unremarkable. Although, she did not have aphasia, apraxia, or agnosia, she showed marked clumsiness in skilled hand movements such as using chopsticks, hand writing, and buttoning. She had no motor weakness, ataxia, rigidity, or spasticity. Deep tendon reflexes were symmetrically diminished. Sensory examination revealed cortical sensory loss such as disturbances of two point discrimination, weight sensation, and stereotactic sensations. Her motor clumsiness appeared to be caused by her cortical sensory loss. MRI revealed marked focal atrophy in the bilateral parietal lobe, particularly in the postcentral gyrus and the adjacent association areas. Recently, neurodegenerative disorders with focal brain atrophy such as corticobasal degeneration, Pick's disease, and dementia of frontal lobe type have been reported, however, our patient does not fit to any of these known disorders nor clinical features are distinctly different from Alzheimer's disease. Our patient may be another example of progressive cerebral degeneration with emphasis on the parietal cortex.
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PMID:[A patient with focal bi-parietal atrophy presenting motor clumsiness and cortical sensory loss]. 971 Nov 23

A 57-year-old woman presented with a slowly progressive gait disturbance in 1992 (53 years of age). Over the next year, she gradually began to talk less, but her speech itself became more rapid than before. He speech was frequently too fast even for family members to understand. In 1997, she was admitted to our hospital. On admission, the patient was disoriented but able to follow simple verbal commands, to name things, and to write simple words. Neither apraxia, aphasia, hemispatial neglect, nor a corpus callosum disconnection syndrome was observed. There was no muscle weakness or atrophy. She showed a positive Babinski sign with mild spasticity in the legs and Gegenhalten, but no rigidity. Her speech was monotonous and abnormally fast (cluttering-like speech). Her speech became faster and faster toward the end of sentences, skipping several syllables or even words. She was unable to speak slowly and clearly, even when efforts were made to pace her speech to the speed set by the examiner. She was able to stand only with a wide base of support and body flexion. When standing, she was unable to place one foot directly beside the other; as she tried to have one foot near the other, the former repelled the latter. She had great difficulties in taking her first step forward, and showed rapid freezing of gait even when she managed to succeed in starting. She was able to imitate walking or bicycling with her legs unloaded, indicating that her gait disturbance was a kind of apraxia of gait. Her intelligence was somehow difficult to assess because of her peculiar speech disturbance. However, her family members had noticed her memory disturbance and personality change (offensiveness) since 3 to 4 years before the admission. Moreover, she was defective not only on Hasegawa Damentia Scale-Revised but also on Raven's Colored Progressive Matrices which estimates non-verbal intelligence. It was also noted that she was inattentive and lazy in thinking on questionnaires. Thus we considered that she was at least mildly demented and the type of dementia was of frontal pathology. Laboratory data were all normal except for the head MRI, which demonstrated prominent and thinness of the corpus callosum from the anterior part of the body to splenium without any other brain lesions that could cause the thinness secondarily. Our case resembles two cases reported by Sunohara et al in 1985, together comprising a unique clinical feature. Although Sunohara et al did not refer to the thinness of the corpus callosum in their cases, the clinical profiles in our case and theirs raise the possibility that they form a new disease entity. A further study in a large number of similar cases, including autopsies will provide a conclusion.
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PMID:[A case report of dementia with cluttering-like speech disorder and apraxia of gait]. 1042 42

A case of a 37-year-old man with urinary retention secondary to aseptic meningitis is described. He was admitted to our hospital with complaints of fever, nausea, headache, and gait disturbance. He had begun treatment 1 week previously for high fever, headache and joint pain at an outpatient department. On admission, neurological examination revealed neck stiffness, spasticity and hyperreflexia of the extremities, hypesthesia of the lower extremities, and ataxic gait. A spinal fluid examination revealed aseptic meningitis. Disturbed consciousness, diplopia, aphasia, tetraparesis, and urinary retention appeared after admission. Computed tomography and magnetic resonance imaging (MRI) of the head revealed no abnormal lesions. On the 2nd day of hospitalization, a Foley catheter was inserted for urinary retention. The patient was treated with conservative therapy, and his symptoms gradually resolved. The Foley catheter was removed on hospital day 13, but bladder dysfunction was persisted. MRI of the lumbar spine revealed herniated lumbar discs at level L3-4, L4-5, and L5-S1, but the nerve roots were not compressed. The patient was managed with clean intermittent catheterization for more than two weeks. Cystometry revealed atonic bladder. Nineteen cases of urinary retention secondary to aseptic meningitis have been reported in the previous literature. We reviewed their clinical presentation and treatment.
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PMID:[A case of urinary retention secondary to aseptic meningitis]. 1157 16

We report a 47-year-old woman with progressive multifocal leukoencephalopathy (PML). She was a carrier of HTLV-I virus, and developed subacute right hemiparesis and marked motor aphasia. She had a malignant lymphoma in the left neck and basal cell carcinoma in the right inguinal region. Three months after the onset, she became unable to walk because of the right leg weakness or to speak because of motor aphasia. Magnetic resonance imaging (MRI) revealed multifocal T2-high lesions in the white matter of the left frontal lobe, and a brain biopsy revealed demyelinating pathology. A biopsy of the left parotid gland revealed a diffuse pleomorphic type large B cell lymphoma. Although anti-HTLV-I antibody was positive in the serum and cerebrospinal fluid (CSF), no adult T-cell leukemia (ATL) cells were found in the blood or CSF. The patient was then admitted to our hospital. Neurological examinations revealed severe motor aphasia, mild sensory aphasia/cognitive impairment, right hemiplegia, mild right hemihypesthesia, limb-kinetic apraxia in the left hand, idiomotor apraxia, agraphia, perseveration, marked spasticity and brisk tendon reflex in four extremities, and positive bilateral pathological reflexes. MRI showed multifocal T2-high lesions mainly in the cerebral white matter, predominantly in the left hemisphere, and partly in the cerebral cortex. No gadolinium enhancement was found. In addition, 99mTcECD-SPECT showed a broad decrease in cerebral blood flow (CBF) in the cortex. Anti-HTLV-I antibody was positive but anti-HIV antibody was negative in serum. ATL cells were found in 1-3% of the peripheral white blood cells after admission. CSF examination revealed that the cell count (1/microl), protein level (24 mg/dl), and IgG index (0.4) were all normal. However, the myelin basic protein level (321 pg/ml; normal < 102) was increased, JC virus DNA was detected by PCR, and anti-HTLV-I antibody (x 8) was detected in CSF. The regulatory region of the JC virus DNA in the CSF was partly deleted; immunostaining with anti-JC virus protein antibodies revealed the existence of JC virus in biopsied brain specimens, and these findings were consistent with PML. Her symptoms such as motor aphasia, cognitive dysfunction and left hemiparesis were subacutely progressive, and she developed akinetic mutism two weeks after admission. Since the efficacy of cytosine arabinoside for PML has been reported, she was administered 80 mg/day of the drug for five days. After treatment, her communication function was mildly improved but the efficacy was transient. Since it has been reported that HTLV-I, as well as HIV, activates the JC virus promoter and its proliferation, the latent infection of HTLV-I in the central nervous system (CNS) in this case might have stimulated the JC virus proliferation, promoting lesion extension over the cerebral cortex. There have been only a few reports of broad decreases in CBF by SPECT in PML patients. Further MRI and SPECT studies on PML patients are therefore necessary to evaluate the significance of HTLV-I in promoting the JC virus infiltration into the CNS.
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PMID:[A case of progressive multifocal leukoencephalopathy presenting white matter MRI lesions extending over the cerebral cortex and a marked decrease in cerebral blood flow on SPECT, and associated with HTLV-I infection]. 1602 67

An 11-year old girl suffered a diffuse axonal injury after car accident. On admission, she was unconscious (GCS 4) and presented with brain contusion, pulmonary contusion, severe tetraparesis, spasticity and seizures. She did not respond to sedatives and anti-epileptic drugs. After 18 days at Intensive Care Unit, she was selected to baclofen screening. She received 100 microg of baclofen and her spasticity decreased and motor and sensor aphasia resolved.
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PMID:[Sudden improvement of all neurological functions after general anesthesia and two-day intrathecal infusion of baclofen in a child with primary brain-stem injury]. 1795 72

Stroke, Multiple Sclerosis (MS), traumatic brain injuries (TBI) and neuropathies are the most important diseases in neurological rehabilitation financed by the German Pension Insurance. The primary goal is vocational (re)integration. Driven by multiple findings of neuroscience research the traditional holistic approach with mainly empirically derived strategies was developed further and improved by new evidence-based interventions. This process had been, and continues to be, necessary to meet the health-economic pressures for ever shorter and more efficient rehab measures. Evidence-based interventions refer to symptom-oriented measures, to team-management concepts, as well as to education and psychosocial interventions. Drug therapy and/or neurophysiological measures can be added to increase neuroregeneration and neuroplasticity. Evidence-based aftercare concepts support sustainability and steadiness of rehab results.Mirror therapy, robot-assisted training, mental training, task-specific training, and above all constraint-induced movement therapy (CIMT) can restore motor arm and hand functions. Treadmill training and robot-assisted training improve stance and gait. Botulinum toxine injections in combination with physical and redressing methods are superior in managing spasticity. Guideline-oriented management of associated pain syndromes (myofascial, neuropathic, complex-regional=dystrophic) improve primary outcome and quality of life. Drug therapy with so-called co-analgetics and physical therapy play an important role in pain management. Swallowing disorders lead to higher mortality and morbidity in the acute phase; stepwise diagnostics (screening, endoscopy, radiology) and specific swallowing therapy can reduce these risks and frequently can restore normal eating und drinking.In our modern industrial societies communicative and cognitive disturbances are more impairing than the above mentioned disorders. Speech and language therapy (SLT) is dominant in communicative disorders; the therapists use communicative and/or linguistics-oriented strategies. SLT must begin early after disease onset and with high frequency to elicit good results. PC-assisted (self-)training, possibly telemedically applied, can increase training frequency and time and, hence, improve outcome in aphasia. High-frequency and task-specific training, often PC-assisted, were found to be relevant for improving cognitive functions in all dimensions. Several strategies seem to be efficient in neglect. Visual field deficits can be treated restitutively and compensatingly by PC-assisted training. Attention, memory and executive dysfunctions each require multimodal specific treatment strategies, performed in single and group therapy and in PC-assisted training. Also, education of patients to cope with their impairments and disabilities is another important part. Combined medically and vocationally oriented rehabilitation settings are necessary for raising the rate of return-to-work, especially in patients with motor hand impairments or cognitive disorders. Education of patients and relatives to cope with the chronic neurological diseases and disablements highly improve the sustainability of rehab results and can, in the long run, also reduce mortality and admission to nursing homes. Appropriate physical activity and sports are relevant in the phase of aftercare, by stabilizing both motor coordination and cognitive factors; in MS patients fatigue can be diminished effectively.The main mental comorbidities are anxiety and depression. Pharmacological and psychological treatments have been found to be equally important in this context. Frequently, these mental disorders appear in the phase of aftercare and long-term course only, then worsening outcome sustainability. Efficient concepts to deal with this aspect are still missing. The ambulatory health care system can not cope with it until now.The multitude of evidence-based interventions have over the last 20 years after the Rehab Commission of the Federation of the German Pension Insurance Institutes contributed decisively to even improving primary outcomes and quality of life of neurological patients in spite of shortened length of stay and other restrictions. Neurorehabilitative research, especially the clinically oriented part, had a major influence on the process of professionalization of all members in the neurorehabilitative team. This fact enables new and more efficient organizational structures and working processes within the team; the discussion on this topic has however only just started.
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PMID:[DGRW-update: neurology--from empirical strategies towards evidence based interventions]. 2213 65

We describe the case of a man who presented with spasticity and aphasia related to continuous electroencephalographic epileptic activity in the left frontal-temporal regions. Magnetic resonance imaging (MRI) documented in diffusion-weighted images (DWI) two areas of restricted diffusion in the left frontal and temporal cortex. After starting treatment with levetiracetam 3000 mg/day there was progressive recovery of the clinical picture as well as the gradual disappearance of the electroencephalographic seizure activity and the vanishing of areas of restricted diffusion in brain MRI. Based on the clinical, EEG and MRI data, we hypothesized that both aphasia and spasticity represented ictal signs. To our knowledge, this is the first case report of ictal spasticity.
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PMID:Spasticity as an ictal pattern due to excitotoxic upper motor neuron damage. 2310 17


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