Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We elicited motor evoked potentials (MEPs) using transcortical magnetic stimulation in 150 control subjects aged 14 to 85 years and 275 patients with a variety of diseases. There were no significant side effects. Cortex-to-target muscle latencies measured 20.2 +/- 1.6 ms (thenar), 14.2 +/- 1.7 ms (extensor digitorum communis), 9.4 +/- 1.7 ms (biceps), and 27.2 +/- 2.9 ms (tibialis anterior). Central motor delay between the cortex and the C-7 and L-5 measured 6.7 +/- 1.2 ms and 13.1 +/- 3.8 ms, respectively. Mean spinal cord motor conduction velocity measured 65.4 m/s. MEP amplitude expressed as a percentage of the maximum M wave was never less than 20% of the M wave. A value of less than 10% is considered abnormal. MEP latency increases linearly with age and central motor delay is longer in older subjects. Compound muscle action potentials and absolute MEP amplitudes decreased linearly with age. In multiple sclerosis (MS), MEP latency and central delay were often very prolonged. The MEP was more sensitive than the SEP in MS. In amyotrophic lateral sclerosis, MEP latencies were only modestly prolonged; the characteristic abnormality was reduced amplitude. When pseudobulbar features predominated MEPs were often absent. The MEP was of normal latency in Parkinson's disease, but age-related amplitude was often increased. MEP latency and amplitude were normal in Huntington's disease. Abnormal MEPs persisted several months after stroke despite good functional recovery. The MEP could be used to advantage to demonstrate proximal conduction slowing and block in demyelinating neuropathies. In plexopathy, ability to elicit an MEP several days after onset of paresis was good evidence of neuronal continuity in motor fibers.
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PMID:AAEM minimonograph #35: Clinical experience with transcranial magnetic stimulation. 793 34

Twelve patients who developed radiation-induced brachial plexopathy (RIBP) after receiving radiation therapy for breast carcinoma (7 patients) or Hodgkin's lymphoma (5 patients) were followed for 12 or more years, with a mean follow-up time of 20 years. Tingling and numbness of the fingers as well as weakness of the hand or arm were the most prominent presenting symptoms of RIBP. Whereas pain in most patients evolved only later in the course, it became a predominant feature in only 2. In 8 of the 12 patients, the plexopathy was surgically treated, either by neurolysis only or by neurolysis plus omental grafting in order to stop progression or paresis and/or pain. In 8 patients, including 6 of the operated group, there was slow and steady progression of RIBP over time, with the final outcome being almost complete paralysis of the arm (2 patients) or severe sensorimotor paresis rendering the hand useless (6 patients). In only 4 patients, including 2 of the non-operated group, was there absence of progression and stabilization of the paresis with only slight functional loss of the affected arm in 3 patients and severe palsy in 1. None of the 12 patients had any clear long-lasting improvement of their sensorimotor impairment. It is concluded from this study that RIBP, irrespective of surgery (neurolysis and/or omentum transplant), left two-thirds of the patients with severe or total paresis of the arm. However, the almost complete relief of severe pain (6 of 8 patients), both immediately and in follow-up patients treated with neurolysis and/or omental transplant, indicates that surgical treatment has a beneficial effect on pain relief.
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PMID:Natural history of radiation-induced brachial plexopathy compared with surgically treated patients. 239 47

Irradiation neuropathy is a term for the damage to peripheral nerve tissue due to irradiation. Brachial irradiation plexopathy is irradiation neuropathy affecting the brachial plexus. This is most frequently a complication of irradiation therapy for cancer of the breast. The incidence varies considerably and is lowest with low total doses of irradiation and limited fractions. The latent period varies from months to several years. The neurological manifestations are paraesthesiae in the fingers, pain, hypaesthesia, hypalgesia, disaesthesia, paresis, hyporeflexia, muscular atrophy and possibly vegetative disturbances. Horner's syndrome may occur. Lymphoedema is observed in approximately on third of the patients. The course of brachial irradiation plexopathy is progressive. No specific treatment is available. The diagnosis is based on the case history, clinical picture, electrodiagnosis and CT of the brachial plexus region. The most important differential diagnosis is metastatic infiltration in the brachial plexus. These two conditions are differentiated best by means of CT guided surgical exploration and histological examination of the tissue. The irreversible nature of brachial irradiation plexopathy and its marked resistance to treatment are such that the optimal irradiation hygienic rules must be observed.
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PMID:[Brachial irradiation plexopathy]. 255 Oct 86

A 33 year old heroin addict developed a lumbosacral plexopathy which clinically and electrophysiologically resembled an "idiopathic lumbosacral plexus neuropathy". He complained of severe neuralgic pain, marked paresis, and distinct sensory loss in the right leg. The plexopathy was accompanied by rhabdomyolysis. He was treated with corticosteroids in high dosage. Within 3 days the disabling symptoms had almost completely disappeared. Clinical and electrophysiological findings are described in the course of the disease and are compared with the data in the literature.
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PMID:[Successful corticoid treatment of lumbosacral plexus neuropathy in heroin abuse. Clinical aspects, electrophysiology, therapy and follow-up]. 285 May 3

Radiation-induced brachial plexus lesions are progressive and irreversible complications. Until now, there is no way to successful prevention and treatment of this problem. In our series, relief of pain could be achieved by neurolysis in some cases, but there was no recovery of sensory and motor function. In order to improve the vascularity and nerve tissue regeneration, we performed muscle or gliding tissue flaps after neurolysis in our department. Since 1975, 25 patients who developed radiation-induced plexopathy were treated in our department. We followed 18 patients to evaluate the benefits of our surgical intervention. None of the patients had improvement of their sensory or motor impairment. Relief of severe pain was achieved in 83% either by neurolysis only with or without muscle or gliding tissue flap. In some cases, paresis worsened postoperatively. We also observed a return of severe pain after the operation.
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PMID:[Actinic brachial plexus lesion]. 974 78

Radiotherapy-induced lumbosacral plexopathy in cervical cancer treatment is a very rare, but extremely serious complication. The clinical course is associated with severe bilateral lower leg pain, reduced sensation, different degrees of weakness, paresis or paralysis, and sometimes also urinary or fecal incontinence. Patient quality of life becomes significantly deteriorated. Escalating neurological disorders may make self-sufficient functioning impossible. Neurological symptoms, most often irreversible, may develop at different times after irradiation, even after more than 30 years. We present a case of neurological toxicity in a patient successfully treated for cervical cancer with pelvis and para-aortic lymph node irradiation and weekly cisplatin. Neurological symptoms developed a few weeks after completion of external irradiation, were gradually escalating and resulted in complete immobilization of the woman. We underline the significance of long-term, systematic physiotherapy and pharmacological therapy which has resulted in significant improvement of motion efficiency. The literature review concerns the questions of frequency, clinical course and mechanisms of radiation-induced plexopathy.
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PMID:Radiotherapy-induced lumbosacral plexopathy in a patient with cervical cancer: a case report and literature review. 2378 77

Patients frequently suffer from lumbosacral plexus disorder. When conducting a neurological examination, it is essential to assess the extent of muscle paresis, sensory disorder distribution, pain occurrence, and blocked spine. An electromyography (EMG) can confirm axonal lesions and their severity and extent, root affliction (including dorsal branches), and disorders of motor and sensory fiber conduction. Imaging examination, particularly gadolinium magnetic resonance imaging (MRI) examination, ensues. Cerebrospinal fluid examination is of diagnostic importance with radiculopathy, neuroinfections, and for evidence of immunoglobulin synthesis. Differential diagnostics of lumbosacral plexopathy (LSP) include metabolic, oncological, inflammatory, ischemic, and autoimmune disorders.In the presented case study, a 64-year-old man developed an acute onset of painful LSP with a specific EMG finding, MRI showing evidence of plexus affliction but not in the proximal part of the roots. Painful plexopathy presented itself with severe muscle paresis in the femoral nerve and the obturator nerve innervation areas, and gradual remission occurred after 3 months. Autoimmune origin of painful LSP is presumed.We describe a rare case of patient with painful lumbar plexopathy, with EMG findings of axonal type, we suppose of autoimmune etiology.
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PMID:Painful lumbosacral plexopathy: a case report. 2592 15

Herpes zoster is a reactivation of the latent varicella zoster virus. Among the complications of herpes zoster is zoster-associated limb paresis. The clinical and imaging features of patients with zoster-associated limb paresis due to plexopathies (zoster-associated plexopathy) have had limited description in the literature. The Mayo Clinic patient data base was searched by diagnostic code for patients diagnosed with herpes zoster between January 1, 1996, and September 30, 2012. Patients who met the inclusion criteria for zoster-associated limb paresis or herpes zoster with MRIs obtained were reviewed. Ten patients with zoster-associated plexopathy were identified. Imaging abnormalities were found in 70% of patients. Secondary denervation changes in shoulder girdle muscles and nerve T2 signal hyperintensity were the most frequent abnormalities (50%), followed by nerve enlargement (20%). Enhancement was not evident in any cases despite early imaging in 80% of the cohort. These results demonstrate the clinical utility of MR imaging in confirming the diagnosis of zoster-associated plexopathy.
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PMID:Imaging Findings in Patients with Zoster-Associated Plexopathy. 2836 9