Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0152025 (polyneuropathy)
 7,862 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We investigated 103 consecutive patients primarily admitted to our Department of Neurosurgery (36 women, age: median 44, range 21-79; 67 men, age: 47, range 19-77) suffering from low back pain radiating into one or both legs. Neurological examination combined with computer tomography and lumbar myelography revealed lumbar-disc herniation in 74, vertebrostenosis in 10 and relapsed disc herniation in 9 patients. In 9 patients the diagnosis of pseudoradicular syndrome was established without definite neuroradiological morphological evidence. Two patients were diagnosed as having polyneuropathy, and 1 patient suffered from a nervus ischiadicus lesion due to a gluteal abscess. CSF of all patients was examined according to a fixed routine schedule (cells, protein, sugar, immunoglobulins, IgG index). Antibodies to Borrelia burgdorferi were found in the serum and CSF of 5.8%, and in the serum alone of 2% of patients. Intrathecally produced specific antibodies were detected in 3 patients (2.9%) with neuroradiological evidence of disc or spinal-canal disease, indicating the coexistence of previous CNS infection by B. burgdorferi with lumbar-disc herniation. None of the patients showed CSF pleocytosis; thus, in no case was acute radiculitis due to B. burgdorferi infection diagnosed.
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PMID:Incidence of nervous system Borrelia burgdorferi infection in patients with lumboradicular syndrome. 846 22

Attention has recently been drawn to chronic inflammatory demyelinating polyneuropathy (CIDP) with symptomatic nerve root hypertrophy. A 31-year-old woman had fluctuating and worsening low back pain. Absent tendon jerks and a slight weakness of the hand interossei muscles suggested a diffuse neuropathy. The electrophysiological and histological findings were diagnostic for CIDP. Lumbar spine MRI showed marked nerve root enlargement with gadolinium enhancement. This case widens the range of the clinical presentations of CIDP. Further studies are warranted to ascertain whether cauda equina gadolinium enhancement may be a useful tool in the diagnosis of CIDP and a marker of disease activity for monitoring response to therapy.
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PMID:Low back pain due to hypertrophic roots as presenting symptom of CIDP. 941 55

A purpose of the study was to develop the Stress Tolerance Scale (STS) and to assess its diagnostic efficacy in neurological clinical practice. The theoretical ground for stress tolerance measurement is the concept of personal environmental interaction as a process including phases of the subjective stress event appraisal, active reaction and subjective result appraisal. The STS encompasses the response items of the descriptions of the accomplished and unaccomplished person-environment and self-personal relations that result in stress overcoming or in stress maintenance, respectively. Within each group, the additional variants of the transactions were specified according to their space-temporal characteristics. Data sets from 112 healthy people and 247 patients (60 with chronic tension headache, 72 with chronic low back pain, 51 with myasthenia gravis, 14 with progressive muscular dystrophy, 27 with hereditary polyneuropathy and 23 with torticollis) have been analyzed. The validity and quiantitation of the STS were determined by Rasch analysis and comparison of the results with those of total STS score and subscale scores of the Hospital Anxiety and Depression Scale and Russian brief version of MMPI. All correlations were at a level of significance. A decrease of stress tolerance was found in patients with chronic pain syndromes and torticollis. The results indicate that the STS allows assessing stress tolerance and a structure of person-environment interactions used by a patient. It can be utilized for optimization of short-term psychotherapy of neurological patients.
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PMID:[Evaluation of stress tolerance in the neurological patients]. 1595 38

To present a case of cauda equina syndrome (CES) caused by chronic inflammatory demyelinating polyneuropathy (CIDP) which seemed clinically similar to Charcot-Marie-Tooth disease type1 (CMT1). CIDP is an immune-mediated polyneuropathy, either progressive or relapsing-remitting. It is a non-hereditary disorder characterized by symmetrical motor and sensory deficits. Rarely, spinal nerve roots can be involved, leading to CES by hypertrophic cauda equina. A 34-year-old man presented with low back pain, radicular pain, bilateral lower-extremity weakness, urinary incontinence, and constipation. He had had musculoskeletal deformities, such as hammertoes and pes cavus, since age 10. Lumbar spine magnetic resonance imaging showed diffuse thickening of the cauda equina. Electrophysiological testing showed increased distal latency, conduction blocks, temporal dispersion, and severe nerve conduction velocity slowing (3 m/s). We were not able to find genetic mutations at the PMP 22, MPZ, PRX, and EGR2 genes. The pathologic findings of the sural nerve biopsy revealed thinly myelinated nerve fibers with Schwann cells proliferation. We performed a decompressive laminectomy, intravenous IgG (IV-IgG) and oral steroid. At 1 week after surgery, most of his symptoms showed marked improvements except foot deformities. There was no relapse or aggravation of disease for 3 years. We diagnosed the case as an early-onset CIDP with cauda equine syndrome, whose initial clinical findings were similar to those of CMT1, and successfully managed with decompressive laminectomy, IV-IgG and oral steroid.
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PMID:A case of cauda equina syndrome in early-onset chronic inflammatory demyelinating polyneuropathy clinically similar to charcot-marie-tooth disease type 1. 2523 36

A 67-year-old male known to be hypertensive and diabetic had a sudden onset of severe low back pain and flaccid paraplegia with no sensory level or bladder affection and the distal pulsations were felt. Acute compressive myelopathy was excluded by MRI of the dorsal and lumbar spines. The nerve conduction study and CSF analysis was suggestive of acute demyelinating polyneuropathy. The patient developed ischemic changes of the lower limb and CT angiography revealed severe stenosis of the abdominal aorta and both common iliac arteries. We emphasize the importance of including acute aortic occlusion in the differential diagnosis of acute flaccid paraplegia especially in the presence of severe back pain even if the distal pulsations were felt.
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PMID:Acute aortic occlusion presenting as flaccid paraplegia. 2586 88