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PubMed1989

[Study of conductivity of the motor fibers of the ulnar nerve with respect to intensity, localization and diagnosis of peripheral nerve disease. I. General and morphologic observations on the affected area of the ulnar nerve with emphasis on the elbow region and causes of the disease].

The introductory part deals with a great community impact of ulnar nerve damage and its high incidence. From peripheral nerves, this ulnar is the most frequently exposed to injuries and impresses. The impressory damage occurs mainly in elbow region. Anatomic peculiarities of ulnar nerve are scrutinized concerning with more connective tissue presence on its cutting section comparably to the other upper limb nerves. Frequent innervative deviations are referred to especially in ulnar and median nerve regions in the course of ulnar nerve branching. Also three types of anastomoses are listed between the both nerves which are important as to the clinical pattern in damages and for electrophysiologic diagnosing. From the clinical tests, those of rare use are emphasized (test of crossed fingers, palmaris brevis sign, Mumenthaler's sign, ulnar test). The last part deals in detail with anatomic, functional and clinical problems of ulnar nerve in elbow area. Its biomechanic relations in the cubital tunnel are elucidated as well as etiopathogenetic factors of neural damage in this area (traction and compressive theories and hypermobility of the nerve etc.). The most frequent causes of ulnar injuries are reviewed. The present work is of introductory value for those dealing mainly with electrophysiologic problems of both sensitive and motoric neural injuries varying in the intensity, location and diagnosis.

Humans↗
PubMed1996

Laboratory testing in peripheral nerve disease.

Selecting appropriate laboratory tests in diagnosing peripheral neuropathies is important because it increases the yield of correct diagnoses and is cost effective. A large number of tests are available. This article provides a guide to selecting appropriate tests and reviews the clinical situations that suggest specific tests. Electrodiagnostic testing is valuable in almost all patients with peripheral neuropathy. Quantitative sensory testing adds additional information and is especially useful in patients with small fiber neuropathy. On occasion, routine blood tests may discover metabolic disorders causing a patient's neurologic disorder. A number of antibody assays for neuropathies are available commercially, with the most useful being anti-MAG, anti-GM1, anti-GQ1b, anti-Hu, and anticalcium channel antibodies, but only in very select situations and not as "screening studies". The role of cutaneous nerve and skin biopsies in selected disorders is discussed.

Autoimmune Diseases↗
PubMed1992

Invited review: autonomic dysfunction in peripheral nerve disease.

The autonomic nervous system is affected in most peripheral neuropathies, but only in a small number of conditions, such as diabetes, amyloidosis, Guillain-Barré syndrome, porphyria, and familiar dysautonomia, is autonomic dysfunction of clinical importance. The pathological changes in the peripheral autonomic nervous system are similar to those in the peripheral somatic nerves. Autonomic disturbances are most likely to occur when there is acute demyelination or damage to small myelinated and unmyelinated fibers. Autonomic investigations should include tests of both sympathetic and parasympathetic function. Treatment consists of management of the underlying cause of peripheral neuropathy, physical and pharmacological measures.

Animals↗
PubMed1994

The triple cold syndrome. Cold hyperalgesia, cold hypoaesthesia and cold skin in peripheral nerve disease.

A syndrome of cold hyperalgesia associated with cold hypoaesthesia is described in 28 patients with peripheral polyneuropathy or mononeuropathy of various aetiologies. A mechanism of sensory disinhibition, where diminished cold-specific A delta input releases cold pain input carried by C nociceptors, is proposed to explain the hyperalgesia. In most patients, the symptomatic skin is abnormally cold. This is a likely consequence of vasospasm, due to sympathetic denervation supersensitivity, caused by dropout of sympathetic efferents as part of the small caliber nerve fibre insult. The term 'triple cold syndrome' is coined to describe this specific pathophysiological condition. Descriptively it is a mirror image of erythralgia, as described by Sir Thomas Lewis (1936) and updated by one of the present authors, a human condition also centred around anomalous primary nociceptor input, in which there is heat hyperalgesia and hot symptomatic skin due to C nociceptor sensitization and vasodilatation from antidromic discharge. Thus, like the latter condition, the triple cold syndrome emerges as an independent clinical entity with definable abnormal mechanisms which should be retrieved out of the all-embracing, descriptive, diagnostic category 'reflex sympathetic dystrophy--causalgia'.

Adult↗
PubMed2004

Lupus-like disease with anticardiolipin antibodies and lupus anticoagulant as a cause for atypical Eaton-Lambert syndrome and peripheral nerve disease: a case report.

In the practice of neurology, the type of clinical involvement suggests the site of the lesion and the mechanism beneath. Sometimes, the symptoms can be delusive, turning the diagnostic approach to a wrong path and raising the necessity of an algorithm considering the less probable entities. Dysimmunity as mechanism of neurological disease involving both the neuromuscular junction and peripheral nerves is frequently insidious and difficult to suspect on clinical basis alone. We report the case of a 67-year-old male with atypical Eaton-Lambert syndrome and mononeuropathy probably in relation with lupus-like entity. The patient has also high titers of anticardiolipin antibodies and lupus anticoagulant. We are considering the diagnostic algorithm before an isolated and atypical neurological presentation and reviewing the main neurological manifestations in lupus-like and autoimmune systemic disease. We raise the difficulty to classify an inflammatory connective tissue disease in the absence of other pathologic features than autoantibodies and isolated neurological symptoms and discussing the main therapeutic issues.

Aged↗
PubMed1976

[Peripheral nerve disease associated with acute renal failure due to bromate poisoning].

A case of 21 year old male with neuropathy caused by renal insufficiency was present. He had taken bromate (mixed powder of potassium bromate and sodium bromate) for the purpose of suicide and suffered from acute renal insufficiency and hard of hearing. Renal dysfunction improved gradually by peritoneal dialysis and hemodialysis. However, on the 32th day after the onset, burning pain appeared in the bilateral feets. Following this, he began to complain of the disturbances of superficial and deep sensory below the ankle jerks and the weakness of his toes. Considering the clinical features, we supposed that the disturbance of the peripheral nerve was caused by uremia due to taking bromate. N. suralis was biopsied on the 80th day after the onset and examined electron microscopically. Electroscopical findings was as follows. Degeneration of the Schwann cells and irregularity or destruction of the myelin sheaths were observed. The axoplasm of the myelinated nerve fiber were relatively preserved as compared with the changes of the myelin sheaths. In the unmyelinated nerve fibers, cavity formations were observed. The findings of regeneration were not observed. From the electron microscopical findings, we speculate that the changes of the Schwann cells and the myelin sheaths are primary resulting from the disturbance of the metabolism of the Schwann cells. We speculate that anemia and hypoproteinemia caused by bromate disturbed regeneration.

Acute Kidney Injury↗
PubMed1992

Wallerian degeneration in peripheral nerve disease.

This article first reviews the different classes of nerve injury. The temporal evolution of electrophysiologic changes occurring during Wallerian degeneration in humans is then described, followed by a description of sequential structural changes and cellular responses that occur after nerve transection. The final section focuses on the basis for resurgent research interest in Wallerian degeneration and the different research approaches being taken to answer basic science and clinical questions.

Animals↗
PubMed2000

[Peripheral nerve diseases and myopathies associated with HIV infection].

Diseases of the peripheral nervous system occur in up to 50% of persons infected with human immunodeficiency virus (HIV). In early stages of the infection, Guillain-Barré syndrome or a spontaneously remitting mononeuropathy can occur. The most frequent occurrence is distal symmetrical polyneuropathy associated with HIV, which can only be treated symptomatically. The most important differential diagnosis is a drug-induced polyneuropathy under antiretroviral therapy with the nucleoside analogues DDI, DDC, or D4T. Chronic inflammatory demyelinating polyneuropathy is less common and can be treated with immunoglobulins or corticosteroids. Very rare are steroid-responsive neuropathies with necrotizing vasculitis or in diffuse infiltrative lymphocytosis syndrome (DILS). In the AIDS stage, polyradiculitis can occur due to opportunistic infections--most often with cytomegalovirus (CMV) or M. tuberculosis--or polyradiculopathies due to lymphomatous meningiosis. Mononeuritis multiplex is rarely seen in disseminated CMV infection. Myopathies can occur in all stages of HIV infection; their frequency is about 1%. Primary polymyositis associated with HIV, which can be treated with corticosteroids or immunoglobulin, must be distinguished from myopathy induced by azidothymidine. Other forms of myopathy are very rare.

AIDS-Related Opportunistic Infections↗