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Query: UMLS:C0026838 (spasticity)
6,471 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Spasmodic dysphonia is a disturbance of phonation with laryngeal spasms. We report voice and neurologic examination findings in 45 subjects. Neurologic abnormalities were found in 32 subjects (71.1%). Rapid alternating movement abnormalities, weakness, and tremor were common. Incoordination and spasticity were rare. Lower extremity findings were frequent. Abnormalities were bilateral. Spasmodic dysphonia severity was related to age. Type, severity, and duration of vocal symptoms were not different for subjects with or without neurologic abnormalities. Vocal tremor was more frequent in neurologically abnormal subjects. Involvement of a pallidothalamic-supplementary motor area system could account for neurologic findings, brain imaging findings, and clinical heterogeneity. The view emerging is that spasmodic dysphonia is a manifestation of disordered motor control involving systems of neurons rather than single anatomical sites.
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PMID:Heterogeneity in spasmodic dysphonia. Neurologic and voice findings. 200 Nov 89

As mentioned previously, both MS and PML are demyelinating conditions of the CNS and pose diagnostic difficulties in their differentiation because of similarities in their clinical findings. However, certain features unique to each of these diseases are helpful in clinical diagnosis. MS, unlike PML, is a disease of unknown cause. Polygenetic influences in combination with exposure to an environmental agent and immune-mediated factors may be operative in the pathogenesis of MS. Age of onset peaks in the third to fourth decades with a predominance in women, as contrasted with PML, which peaks in the fifth to sixth decades in most non-AIDS-associated cases with a slight predominance in men. MS is more prevalent in areas farther from the equator: North America, Europe, Australia, and New Zealand. Common initial symptoms seen in MS include bilateral limb weakness (with the legs being affected twice as often as the arms), hyperreflexia, spasticity, optic neuritis, diplopia, incoordination, and paresthesias. (Paresthesias are typically found in the lower limbs in a symmetric pattern, but may follow no obvious anatomic distribution and often do not correspond to the distribution of sensory symptoms. Vibration and position sense are more frequently disturbed than pain and temperature.) Intellectual impairment and mental deterioration are uncommon early in MS, whereas they are a more frequent initial presentation in PML. In addition, the presence of speech impairment and monoparesis or hemiparesis with homonymous hemianopsia is more suggestive of PML. Brain stem involvement is infrequent.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Chronic encephalitis caused by leukoencephalopathy. 222 61

Cognitive impairments, often unrecognized in multiple sclerosis, include memory loss, new learning problems, denial and depression. Spasticity and incoordination of the oropharyngeal and respiratory muscles create functional problems with speech and swallowing. Genitourinary problems include sexual dysfunction and neurogenic bladder. Specific measures can be used to alleviate these problems.
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PMID:Multiple sclerosis: Part II. Common functional problems and rehabilitation. 406 Dec 42

The clinical, radiological, and neuropathological findings in early onset Cockayne syndrome are illustrated in identical twins and their brother. Their appearance of dwarfism with small head and prominent beaked nose strongly resembled that seen in the Seckel syndrome, but unlike patients with that syndrome they had a normal birth weight (for twins), thick cranial vaults, intracranial calcification, and a severe degree of mental retardation. The twins were deaf and blind, with optic atrophy and retinal pigmentation, while their brother had cataracts. Their hands and feet were large in proportion to their small trunk. They had cutaneous sensitivity to any slight exposure to ultraviolet light and severe neurologic problems with incoordination and spasticity. Radiologic findings included microcephaly, a thick cranial vault, a small pelvis, coxa valga, and "ivory epiphyses" in terminal phalanges of hands and feet. Pathologic findings included atrophy of white matter with widespread patchy demyelination, and massive siderocalcific deposits in the brain, particularly in the basal ganglia and cerebellum. While autosomal recessive inheritance is most likely, formally X-linked inheritance cannot be excluded.
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PMID:Identical male twins and brother with Cockayne syndrome. 689 Mar 11

After reviewing the size of the problem of multiple sclerosis, and the likely case-load for doctors in different settings, this paper than proceeds to consider the major challenges in management and rehabilitation for this disease. The latter resolve themselves into what to discuss with the patient; relapses and their prevention, including general advice on such matters as stress, pregnancy, and infection; major problems including bladder and bowel dysfunction, sexual difficulties, spasticity, ataxia and incoordination, vision, and intellectual and psychological manifestations, and other problems, such as menstruation, obesity, and pressure sores. The paper concludes with a discussion of the role of specialist physicians.
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PMID:Multiple sclerosis--management and rehabilitation. 720 3

Two cases of alcoholic cerebellar degeneration with pyramidal sign were reported. Patient 1 with alcohol dependence syndrome was a 46-year-old woman. After the alcohol abuse of about eight years, she complained of gait disturbance. The gait disturbance progressively worsened in about two months and she could not ambulate freely by herself. Neurological examination revealed nystagmus, ataxic and spastic gait, slight weakness and spasticity of the lower extremities, hyperreflexia of the extremities, bilateral Babinski's signs, and incoordination of the lower extremities. Examination of liver function and serum B12 was normal. Cranial CT scan and MRI revealed atrophy of the cerebellar vermis and dorsal part of the cerebellum. Though neurological signs slightly improved after the admission to our hospital and the abstinence from alcohol abuse, ataxic gait and hyperreflexia of the extremities have continued. Patient 2 was a 58-year-old man. He was a heavy drinker, but was not a patient with alcohol dependence syndrome. After the heavy drinking of about 40 years, he complained of gait disturbance. The gait disturbance had progressively worsened in about four months. Neurological examination revealed ataxic gait, hyperreflexia of the lower extremities, and bilateral Babinski's signs. Laboratory examination revealed slight liver dysfunction with minimal GPT and moderate gamma-GTP elevation. Examination of serum B12 was normal. Cranial CT scan and MRI revealed atrophy of the cerebellar vermis. Though bilateral Babinski's signs disappeared after the abstinence from heavy drinking, ataxic gait and hyperreflexia of the lower extremities have continued. Alcoholic myelopathy without hepatic cirrhosis was rarely reported. In the relation of alcoholic cerebellar degeneration to alcoholic myelopathy, our cases are interesting and important.
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PMID:[Alcoholic cerebellar degeneration with pyramidal sign--in relation to alcoholic myelopathy]. 847 68

Patients with developmental disorders, including adolescents, comprise a large and heterogeneous group of individuals who vary in underlying diagnosis and degree of disability. The largest numbers of patients are those with cerebral palsy and with traumatic brain injury. While these conditions themselves do not directly cause airway or parenchymal lung dysfunction, consequences of neuromuscular dysfunction, especially aspiration and ineffective cough, may lead to lung damage. Poor nutritional status, impairment of airway clearance by muscular weakness or incoordination and poor pulmonary reserve (due to chest wall or spine deformity) increase the risk of significant morbidity and mortality from respiratory infections. Individuals who were premature infants or who had prolonged neonatal courses may also have residual chronic lung disease (bronchopulmonary dysplasia) contributing to their pulmonary problems. This review discusses conditions that have adverse effects on the airway and lung (drooling, feeding problems, gastroesophageal reflux, aspiration, spasticity, scoliosis) and some of the consequences of these insults (disordered airway clearance, pneumonia, sleep apnea). Also discussed are issues important to the prevention or amelioration of respiratory difficulties, including preventive care, the effects of exercise, dental hygiene, and surgical intervention.
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PMID:Respiratory problems in the adolescent with developmental delay. 1106 May 58

There is nothing more discouraging than for a patient to be given a specific diagnosis, then to be told that there is nothing that can be done. Physicians are equally disheartened to see exponential progress being made in the understanding of the pathophysiology of a complex disorder but few direct benefits resulting for their patients. Over the past 5 years, molecular genetic research has completely revolutionized the way in which the progressive cerebellar ataxias are classified and diagnosed, but it has yet to produce effective gene-based, neuroprotective, or neurorestorative therapies. The treatment of cerebellar ataxia remains primarily a neurorehabilitation challenge, employing physical, occupational, speech, and swallowing therapy; adaptive equipment; driver safety training; and nutritional counseling. Modest additional gains are seen with the use of medications that can improve imbalance, incoordination, or dysarthria (amantadine, buspirone, acetazolamide); cerebellar tremor (clonazepam, propranolol); and cerebellar or central vestibular nystagmus (gabapentin, baclofen, clonazepam). Many of the progressive cerebellar syndromes have associated features involving other neurologic systems (eg, spasticity, dystonia or rigidity, resting or rubral tremor, chorea, motor unit weakness or fatigue, autonomic dysfunction, peripheral or posterior column sensory loss, neuropathic pain or cramping, double vision, vision and hearing loss, dementia, and bowel, bladder, and sexual dysfunction), which can impede the treatment of the ataxic symptoms or can worsen with the use of certain drugs. Treatment of the associated features themselves may in turn worsen the ataxia either directly (as side effects of medication) or indirectly (eg, relaxation of lower limb spasticity that was acting as a stabilizer for an ataxic gait). Secondary complications of progressive ataxia can include deconditioning or immobility, weight loss or gain, skin breakdown, recurrent pulmonary and urinary tract infections, aspiration, occult respiratory failure, and obstructive sleep apnea, all of which can be life threatening. Depression in the patient and family members is common. Although no cures exist for most of the causes of cerebellar ataxia and there are as yet no proven ways to protect neurons from premature cell death or to restore neuronal populations that have been lost, symptomatic treatment can greatly improve the quality of life of these patients and prevent complications that could hasten death. Supportive interventions should always be offered-- education about the disease itself, genetic counseling, individual and family counseling, referral to support groups and advocacy groups, and guidance to online resources. Misinformation, fear, depression, hopelessness, isolation, and financial and interpersonal stress can often cause more harm to the patient and caregiver than the ataxia itself.
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PMID:Cerebellar Ataxia. 1109 49

The prevalence of bowel dysfunction in multiple sclerosis (MS) patients is higher than in the general population. Up to 70% of patients complain of constipation or faecal incontinence, which may also coexist. This overlap can relate to neurological disease affecting both the bowel and the pelvic floor muscles, or to treatments given. Bowel dysfunction is a source of considerable ongoing psychosocial disability in many patients with MS. Symptoms related to the bladder and the bowel are rated by patients as the third most important, limiting their ability to work, after spasticity and incoordination. Bowel management in patients with MS is currently empirical. Although general recommendations include maintaining a high fibre diet, high fluid intake, regular bowel routine, and the use of enemas or laxatives, the evidence to support the efficacy of these recommendations is scant. This review will examine the current state of knowledge regarding the pathophysiological mechanisms underlying bowel dysfunction in MS, outline the importance of proper clinical assessment of constipation and faecal incontinence during the diagnostic work-up, and propose various management possibilities. In the absence of clinical trial data on bowel management in MS, these should be considered as a consensus on clinical practice from a team specialized in bowel dysfunction.
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PMID:Pathophysiology and management of bowel dysfunction in multiple sclerosis. 1133 78

Questions persist about adverse effects such as impaired cognition and attention, incoordination, spasticity, or parkinsonism from chronic, low-level exposures to organophosphate (OP) compounds. In a prospective cohort study, we evaluated chlorpyrifos-manufacturing workers and a referent group on 2 occasions, 1 year apart, to determine whether occupational exposure to chlorpyrifos produced clinically evident central nervous system (CNS) dysfunction. Chlorpyrifos subjects had significantly higher TCP excretion and lower average BuChE activity than referents in a range in which physiological effects on B-esterases exist. Few subjects had neurologic symptoms or signs, and there were no significant group differences in terms of signs at baseline or second examinations. Chronic chlorpyrifos exposure produced no clinical evidence of cortical, pyramidal tract, extrapyramidal, or other CNS dysfunction among chlorpyrifos subjects compared with referents, either at baseline or after 1 year of additional chlorpyrifos exposure.
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PMID:The effects of occupational exposure to chlorpyrifos on the neurologic examination of central nervous system function: a prospective cohort study. 1507 55


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