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Query: UMLS:C0031117 (peripheral neuropathy)
 10,577 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report the clinical and pathologic features of a patient with peripheral neuropathy that was the first clinical expression of cholesterol emboli syndrome (CES). Biopsy of skeletal muscle and peripheral nerve revealed cholesterol clefts in lumens of small arteries, necrotizing arteritis, and severe degeneration of peripheral and intramuscular nerves. At autopsy, the peripheral nervous system was extensively affected by similar changes. We conclude that (1) peripheral neuropathy may be the initial manifestation of CES. Presumably, deposition of cholesterol leads to arteritis. (2) The underlying pathology of CES neuropathy is chronic axonal degeneration, possibly due to chronic ischemia of epineurial arteries. (3) Muscle biopsy is important in the antemortem diagnosis of CES. Nerve biopsy may show involvement of epineurial vessels. (4) CES may resemble polyarteritis nodosa clinically and pathologically. (5) CES may be under-recognized and should be included in the differential diagnosis of any neuropathy of uncertain cause, particularly when there is a history of vascular catheterization, or severe aortic atherosclerosis.
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PMID:Cholesterol emboli neuropathy. 131 May 30

A morphological study of a series of 100 human peroneal nerves proceeding from autopsies and amputations of patients hospitalized for different diseases was performed. A relation between the morphologic findings and the risk factors of neuropathy to which the patients may have been exposed is established. Following the analysis of their results the authors found that peripheral neuropathy is more frequent than suspected in clinical practice. The peripheral nerve is relatively resistant to regional ischemia. The risk factors considered in the casuist included diabetes as that which most influences in determining morphological alterations compatible with neuropathy.
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PMID:[Peripheral neuropathy and correlation with risk factors in material from autopsies and amputations]. 132 Sep 5

We examined 8 cases of allergic granulomatous angiitis (AGA). All cases showed peripheral nerve lesion, comprising damage of all myelinated fibers, which was more severe in larger ones. Immunofluorescent deposits of IgE were detected in the peripheral myelin. There was lymphocyte infiltration both around the endoneural capillaries and in the endoneurium, and an increase of endothelial cells. Nerve ischemia due to obstruction of the vasa nervorum, circulation insufficiency of the small vessels, or immunological abnormality through IgE may play a pathogenetic role in the peripheral neuropathy of AGA.
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PMID:Allergic granulomatous angiitis and peripheral nerve lesion. 133 6

Histological, immunohistochemical and ultrastructural sural nerve and skin biopsy findings in a case of cryoglobulinemia secondary to an IgM-kappa-producing non-Hodgkin lymphoma are described. The main finding was an occlusive microangiopathy present in both the sural nerve and the skin. Widespread cryoglobulin deposits of the proliferated vasa nervorum were associated with pronounced changes probably evoked by ischemia. Moderate perivascular inflammation, but no florid vasculitis was additionally present. Our observations indicate that occlusive microangiopathy by precipitated cryoglobulins may be a relevant pathogenetic factor in cryoglobulinemic peripheral neuropathy.
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PMID:Occlusive microangiopathy by immunoglobulin (IgM-kappa) precipitation: pathogenetic relevance in paraneoplastic cryoglobulinemic neuropathy. 157 20

The amplitudes of photo-electric-plethysmography (PPG) tracings were significantly increased by subcutaneous injections of methacholine (MC) and diminished by injections of atropine (AT) as compared with placebo injections of multi-electrolyte solution (MES) both in 8 normal subjects and 11 patients with diabetic peripheral neuropathy. AT-containing lotion delayed healing compared with placebo in the forearms of 6 normal subjects. MC-containing lotion sped healing compared with placebo in the forearms of 6 subjects with diabetic neuropathy. Thigh incisions in 6 neuropathic patients were shown to heal faster if soaked in MES rather than saline. Healing with the MES solution was shown to be further increased by the addition of MC to the solution and to be decreased by the addition of AT. The addition of MC produced erythema and an increase in the amplitude of PPG tracings. AT solutions produced blanching and a decrease in the PPG amplitude. It was concluded that (1) the slow healing characteristic of neuropathic ulcers is associated with a loss of cholinergic nerve function; (2) cholinergic stimulation will increase capillary blood flow and promote healing while cholinergic blockade has opposite effects; (3) secondary ischemia makes the ulcers susceptible to the deleterious effects of therapeutic agents such as saline; (4) the ischemic tissue will heal faster with a balanced MES than with saline; and (5) the benefits of MES on healing are augmented in patients with diabetic neuropathy by the addition of cholinergic agents to the solution.
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PMID:Role of cholinergic nervous system in healing neuropathic lesions: preliminary studies and prospective, double-blinded, placebo-controlled studies. 195 66

Thirteen patients with peripheral neuropathy caused by necrotizing vasculitis were clinico-pathologically analyzed. These patients consisted of nine classical periarteritis nodosa (PN), four allergic granulomatous angitis (Churg-Strauss syndrome, AGA). All of them were proven to have a necrotizing vasculitis by sural nerve biopsy. The characteristics of peripheral neuropathy of these patients were summarized as follows. 1) Mononeuritis multiplex was a principal features in all patients preferentially localized in common peroneal, sural, radial median and ulnar nerves, with all modality of sensory impairment. 2) Radiation or diffuse deep-pain was a major initial symptom. Since this pain occurs frequently in the manner of sudden onset, the patient can tell the day of onset. 3) Local edema on the skin of involved region was initially observed. 4) Muscular atrophy and weakness was distributed more widely than sensory impairment. 5) Morphometric and teased-fiber study of biopsied sural nerves revealed axonal degeneration as a major pathological process. As compared to myelinated fibers, unmyelinated fibers were likely to be well preserved in morphology and population, which suggests that unmyelinated fibers are relatively resistant to ischemia. 6) Motor and sensory conduction study showed greatly decreased sensory and motor action potentials frequently resulting in absent of recordings. Conduction velocity is almost within normal range or just below the normal. Routine EMG recordings showed active denervation potentials in the involved muscles. 7) Protein in CSF was rarely elevated which suggested involvement of the spinal roots is infrequent. 8) Hypereosinophilia, thrombocythemia, fever, increased erythrocyte sedimentation rate, positive CRP and RA, and polyclonal hypergammaglobulinemia (IgG, IgA) were observed in most cases.
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PMID:[Clinical features of the peripheral nerve involvement in necrotizing angitis--characteristics in polyarteritis nodosa and allergic granulomatous angitis]. 256 7

Patients with diabetes mellitus and coronary artery disease are thought to have painless myocardial ischemia more often than patients without diabetes. We studied 50 consecutive patients with diabetes and 50 consecutive patients without diabetes, all with ischemia, on exercise thallium scintigraphy to show the reliability of angina as a marker for exertional ischemia. The two groups had similar clinical characteristics, treadmill test results, and extent of infarction and ischemia, but only 14 [corrected] patients with diabetes compared with 34 [corrected] patients without diabetes had angina during exertional ischemia. In diabetic patients the extent of retinopathy, nephropathy, or peripheral neuropathy was similar in patients with and without angina. Angina is an unreliable index of myocardial ischemia in diabetic patients with coronary artery disease. Given the increased cardiac morbidity and mortality in such patients, periodic objective assessments of the extent of ischemia are warranted.
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PMID:Angina and exertional myocardial ischemia in diabetic and nondiabetic patients: assessment by exercise thallium scintigraphy. 334 50

The role of ischemia in the pathogenesis of diabetic peripheral neuropathy remains uncertain. We used the distribution of [14C]butanol to measure resting regional sciatic nerve blood flow in normal, anesthetized rats and in rats with acute experimental diabetes from streptozotocin administration. Regional flows in hind limb biceps femoris muscle and skin were simultaneously measured. In additional diabetic rats, these blood flows were compared in both limbs after proximal electrical stimulation of one sciatic trunk (10 shocks/s) for 15 min. One month after streptozotocin administration, 8 of 11 test rats were hyperglycemic. Resting nerve blood flow in the hyperglycemic rats--5.6 +/- 3.07 ml.min-1.100 g-1--was significantly less than that in the controls (9.4 +/- 3.9 ml.min-1.100 g-1, P = 0.002). Muscle blood flow was normal and skin blood flow decreased in these rats. Calculated tissue vascular resistances were elevated in all three tissues. Stimulation of one sciatic trunk in five other diabetic rats resulted in a stimulated nerve blood flow of 15.7 +/- 7.7 ml.min-1.100 g-1, and nerve blood flow in the resting control limb was 7.7 +/- 4.3 ml.min-1.100 g-1 (P = 0.009). Muscle blood flow increased approximately fourfold on the stimulated side but skin blood flow did not increase. Resting sciatic nerve blood flow is modestly decreased in acute streptozotocin-induced diabetes, but the neural blood vessels are still responsive to the increase in nerve metabolic activity associated with nerve stimulation.
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PMID:Regional blood flow in resting and stimulated sciatic nerve of diabetic rats. 334 43

Peripheral neuropathy induced by galactose feeding results in endoneurial edema with increased tissue pressure and ultimate demyelination of nerve fibers. To assess the role of ischemia in the pathogenesis of this neuropathy, nerve blood flow was measured 6 months after the start of galactose ingestion, between the onset of edema and nerve fiber changes. Measurement was carried out by a noninvasive technique involving the use of [14C]iodoantipyrine as a radioactive tracer of tissue perfusion. A significant decline in nerve blood flow was found, which correlated positively with increased nerve water content as quantified by a microgravimetric technique. We sought to establish the pathogenic role of nerve edema in the development of schwannopathy and demyelination by morphological examination. It was found that Schwann cells appeared normal in areas of the peripheral nervous system in which edema does not occur, such as spinal ganglia and roots, whereas in regions in which there was edema, massive glycogen accumulation in Schwann cells and demyelination occurred. These findings suggest that edema, rather than hyperactivity in the sorbitol pathway, is responsible for the pathological changes in galactosemic neuropathy and that ischemia resulting from edema and increased endoneurial fluid pressure is the mechanism responsible for fiber injury.
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PMID:Galactose neuropathy: impact of chronic endoneurial edema on nerve blood flow. 609 31

A histological, histochemical and ultrastructural study on muscle changes in chronic arterial insufficiency has been carried out in 40 patients. Muscle biopsy probes were taken in each patient either from the gastrocnemius or rectus femoris. In 7 patients submitted for amputation of a lower limb due to a more severe vascular disease, specimens were also obtained from both the sciatic and sural nerve for light and electron microscopic study. Our findings confirm the previous histological, histochemical and ultrastructural data on chronic ischemia of the skeletal muscle, suggesting that muscle damage is mainly based on a neurogenic noxa initiated by an ischemic peripheral neuropathy. In addition, many morphologic features also show the presence of a primary myopathic noxa, possibly depending on the direct damage of the mitochondrial respiratory chain by the deficit of the muscle blood supply.
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PMID:Skeletal muscle and peripheral nerve changes caused by chronic arterial insufficiency--significance and clinical correlations--histological, histochemical and ultrastructural study. 609 84


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