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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Estimates of the number, density, and size distribution of myelinated fibers at selected levels of roots, spinal tracts, and sampled levels of peripheral nerves may be used in the detection and characterization of alterations of motor, sensory, and autonomic neurons and their axons with development, aging and disease. Use of imaging techniques, now available, increases the reliability, versatility, and speed of such analysis. In this study, the authors evaluated the spatial pattern of fibers in sampled frames and contour areas of transverse sections of nerve fascicles, utilizing, the coefficient of variation and index of dispersion (ID), the latter extensively employed by plant ecologists. The ID was used for recognization of increased, normal, or decreased variability of density within fascicles, between fascicles, and between nerves in health and in various experimental neuropathies. In addition, various morphometric measurements were made in transverse sections at defined levels along the hind limb nerves of rats in acute and chronic ischemia, after rhizotomy and in galactose neuropathy. These stereomorphometric studies, emphasizing the number, size, shape, and spatial pattern of fibers, revealed differences among experimental neuropathies and may be found to be helpful in the characterization and prediction of pathologic mechanisms in neuropathies of unknown cause. Specifically, these approaches could be used for study of whether fiber loss in human diabetic neuropathy is multifocal and determination of the levels of such losses.
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PMID:Spatial pattern of nerve fiber abnormality indicative of pathologic mechanism. 633 25

The role of ischemia in the pathophysiology of compression neuropathy is still a subject of debate. Nor is the effect on blood supply induced by neurolysis for this lesion so clearly elucidated. In order to shed some light on these problems, two series of experiments were undertaken. In the first series of experiments, the changes in intrafascicular blood flow and nerve function when acute, graded compression was applied to a dog's sciatic nerve by a specially designed compression device were investigated by means of the hydrogen washout technique, electrophysiological study and histological observation. In the second series, Type II injury according to the classification of Sunderland was experimentally caused by embedding a compression device for three weeks, and the intrafascicular blood flow of this model was measured by using the embedded electrode for the hydrogen clearance method. Furthermore, the blood flow before and after neurolysis for this lesion was compared, and cases in which internal neurolysis had been performed were observed after one and three weeks. The intrafascicular blood flow was decreased at 47.2 +/- 3.7 (mean +/- S.D.) mmHg, with increasing pressure, blood flow gradually declined and a statistically significant correlation was shown between the values (r=-0.77, p less than 0.01). This completely stopped at 118.6 +/- 5.9 mmHg (p less than 0.001). The effect of compression on intrafascicular blood flow was immediately observed and disappeared at once after release of the compression. An actual pressure of 118.6 mmHg maintained for 75 minutes produced complete conduction block, which was immediately recovered after release of the compression, though more slowly than the blood flow. When the compression device was applied, the intrafascicular blood flow was reduced to about 80% of the precompression level (p less than 0.05) and this reduction remained unchanged after three weeks (p less than 0.01), at which time the nerve had sustained the Type II injury. After the removal of the device, the blood flow was restored to more than the precompression level (p less than 0.01). Following this, when external neurolysis was performed, a slight reduction of blood flow was observed. After internal neurolysis, however, a remarkable reduction was noticed, the blood flow decreasing to about 20% of the precompression value (p less than 0.01). The blood flow after internal neurolysis was restored to about 70% of the precompression level after one week and, three weeks later, remained about the same.
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PMID:[Experimental study on compression neuropathy--determination of blood flow by a hydrogen washout technic]. 636 77

Sarcoidosis is an idiopathic systemic granulomatous disease which occasionally causes fluctuating auditory and vestibular dysfunction. The temporal bones from a 32-year-old man deaf for 5 years from CNS sarcoidosis were examined histologically and compared with other nervous system tissues. It was found that the acoustic, vestibular, and facial nerves were involved in a striking perivascular lymphocytic infiltration resulting in myelin and axonal degeneration. The cochlear and labyrinthine neuroepithelium and stria vascularis had degenerated. It is hypothesized that neurosensory deafness and vestibular dysfunction in sarcoidosis starts as a reversible neuropathy. In some patients, an ischemia secondary to the vasculitis results in irreversible damage to the inner ear neuroepithelium.
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PMID:Histopathology of neurosensory deafness in sarcoidosis. 646 82

The association between impaired circulation and peripheral nerve disorders has been recognized for many years. Although many experimental and clinical studies have been carried out on the "ischemic neuropathy", the routine examination to certify it may have not yet been established. Peripheral nerve evoked potential measurement has been used to evaluate the function of the peripheral nerve directly. Some electrophysiological findings concerning nerve ischemia were reported. Most authors reported decreased amplitude, slowed conduction rate, and increased refractory period. But a transient increase in amplitude during ischemia is a characteristic phenomenon in the peripheral nerve as well as in spinal cord evoked potential, as reported by the author previously. Since the purpose ot this study was whether this phenomenon could be a indicator of some kind of pathological condition of the peripheral nerve, experimental and clinical studies were designed to obtain the conditions required for the observation of this phenomenon and to establish a practical method for the differentiation of ischemic neuropathy from other ones. Twenty cats were used in the experimental study. The blood supply to the nerve was controlled by tightening a noose around the base of the ascending aorta. In the clinical studies, sixteen healthy subjects 11 diabetics, 3 patients with arteriosclerosis obliterans, and 3 patients with malignant RA were examined. Since a transient reduction in threshold was observed during ischemia simultaneously with a transient augmentation in amplitude, the latter was assumed to be due to the former. In the animal experiment, the amplitude did not increase further even during complete obstruction of the ascending aorta following a 10-minute partial obstruction of the blood supply. In the clinical studies, the augmentation of amplitude during ischemia was statistically higher in healthy persons than in the patients mentioned above. The requisites for observing the transient augmentation in amplitude were: (1) complete ischemia of the peripheral nerve; optimally ten minutes of ischemia, (2) submaximal stimulation; optimally the strength of stimulation with which the amplitude of the evoked potential became 1/3 of the maximum and (3) maintenance of the blood supply to the peripheral nerve before ischemia. The nerve should not be ischemic before complete ischemia or application of the tourniquet.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Effects of ischemia on peripheral nerve evoked potential. Experimental and clinical study]. 647 May 40

To investigate vascular responses in insulin-dependent diabetic patients both with and without retinopathy, we have assessed vasodilation by forearm transcutaneous pO2 measurement after 10 min of ischemia produced by a sphygmomanometer cuff. Diabetic patients with proliferative retinopathy had a delayed vasodilatory response at 60 s (mean +/- SD pO2 = 9 +/- 3 mm Hg) compared with those having diabetes without retinopathy (15 +/- 4 mm Hg, P less than 0.01) and matched normal subjects (14 +/- 4 mm Hg, P less than 0.01). Recently diagnosed insulin-dependent diabetic patients had a very similar response (15 +/- 5 mm Hg) to matched normal subjects (15 +/- 3 mm Hg). The diminished vascular reactivity may be a consequence of microangiopathy and neuropathy, although patients with an impaired vascular response might be particularly at risk from the development of capillary closure.
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PMID:Delayed vascular reactivity to ischemia in diabetic microangiopathy. 660 40

Ulcerative lesions of the foot are commonly due to ischemia, neuropathy or a combination of these factors. When these lesions fail to respond to conservative measures, they are usually treated by ablative or destructive procedures which often result in the loss of a portion of the foot or deformities, or both. These procedures or deformities may, themselves, lead to further problems as the weight is transferred to other areas not designed for this purpose. Reconstructive procedures may prevent these problems, as well as conserve the foot. Lesions of the heel, middle of the foot and forefoot were managed by excision and closure of the defects by the transposition of muscle or muscles into the area with or without subsequent skin grafts. A total of 31 patients were treated; in 22, muscles were transposed with primary healing of the lesion in 15, delayed healing in three, necrosis of the muscle in two and delayed healing of the incision in two. Ablative operations were required in nine patients, when 15 procedures were carried out, including below-knee amputations in two. In five patients, the peroneal tendons were explored behind the fibular malleoulus, and in two, unsuspected necrosis of a tendon was found. It is concluded that reconstructive rather than destructive surgical treatment be considered in ulcerative lesions of the foot. Spread of infection from foot to leg along the tendon sheaths should be suspected when supperative foot lesions persist despite apparently adequate treatment; small incisions over the suspected tendons may confirm this suspicion and allow timely surgical treatment which will prevent extensive surgical treatment on the leg, including amputation.
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PMID:Newer concepts in the surgical management of lesions of the foot in the patient with diabetes. 670 33

Large vessel disease, small vessel disease, and neuropathy leave the diabetic foot especially vulnerable to ulceration. The degree of vascular impairment of diabetic feet can vary, and such, patients with ulcers can be separated into ischemic and nonischemic groups. The degree of ischemia, and not necessarily the extent of the lesion, is the most significant factor in evaluating the potential outcome of treatment. Forty-eight cases of diabetic ulceration treated with local surgical intervention in an effort to avoid higher amputation were classified as ischemic and nonischemic, based on Doppler studies and physical examination. The success rate in the ischemic group was 25%. The success rate of the nonischemic group was 83%. It is concluded that local surgical management of diabetic ulceration can be a successful alternative to radical amputation in the diabetic patient, especially when adequate blood flow can be verified. Various surgical and nonsurgical approaches to all grades of diabetic feet are also discussed.
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PMID:Surgical treatment of diabetic foot ulcers: a review of forty-eight cases. 672 55

We have described a patient who had an acutely ischemic hand after brachial artery puncture in the antecubital fossa. Because of the anatomy of the forearm, hematoma formation and compression of the brachial artery and median nerve are poorly tolerated and predispose to irreversible ischemia or neuropathy. We recommend that brachial artery puncture in the antecubital fossa be avoided.
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PMID:Brachial artery puncture: a definite risk to the hand. 672 63

Iatrogenic pathology of the optic nerve is examined according to a framework which distinguishes direct and indirect effects on the optic nerve. Direct effects due to toxic drugs should be suspected when unexplained, usually bilateral loss of visual acuity occurs. The 3 clinical stages of classical optic toxic neuropathy are 1) anomalies of color vision, 2) loss of visual acuity and narrowing field of vision, and 3) papillary palor corresponding to irreversible optic atrophy. Usually only the 1st stages are reversible, but the reversibility may be incomplete. The list of drugs which can cause such effects is lengthy and includes antiinfectious drugs such as sulfamides and derivatives of hydroxyquinoleins, chloramphenicol especially when used to treat cystic fibrosis of the pancreas in children, the antituberculins ethambutol in high doses and isoniazide, which occasion particular risks when combined; antiparasitics such as quinine and its derivatives chloroquine and hydroxychloroquine, which cause optic neuropathy through their effect on the retina; arsenic pentavalents such as tryparsamide, quinacrine, trecator and mystatin; drugs affecting the central nervous system such as monoamineoxydase inhibitors, laroxyl, phenothiazine and the barbituates; anticonvulsants such as phenytoin; antimitotics such as vincristine; digitalics, disulfiram; penicillamines, and pexid. The action of lasers on the optic nerve can have a similar effect. The optic nerve may be indirectly damaged during surgical procedures leading to hypotonia, acute ischemia of the head of the optic nerve or embolic accident after a local or regional injection. Damage may also be caused by radiotherapy of intracranial tumors and certain drugs which cause isolated papillary edema or edema associated with headaches, such as Tetracycline, large doses of vitamin A or D, corticoids, and oral contraceptive (OC) pills, which may cause papillary edema through cerebral pseudo-tumors that regress with discontinuation of treatment. This condition has been observed in women with uncontrolled hyperlipidemia. It is probable that an alteration ofaxonal transport is at the basis of the neuropathic mechanisms. The 1st step in therapy is the suppression of the toxin, or at least its discontinuation. Some success has been obtained with vitamin B therapy, corticotherapy, zinc, or isaxonine, depending on the specific condition.
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PMID:[Iatrogenic pathology of the optic nerve]. 676 92

Despite the clinical importance of ischemia in the pathogenesis of many human neuropathies, little is known about the effect of circulatory compromise on the structure of peripheral nerves. This results in part from the lack of an entirely satisfactory model in which to study ischemic neuropathy. We therefore injected arachidonic acid, a potent stimulus to platelet aggregation and vasoconstriction, into the femoral artery of normal rats. This resulted in the rapid onset of focal infarction of the proximal posterior tibial nerve in all animals. Distally there was evidence of Wallerian degeneration but not of primary ischemic damage. The site and nature of the infarct and the temporal sequence of the pathological changes were highly consistent. This new method is a simple and highly reproducible means of producing experimental nerve infarction.
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PMID:Arachidonate-induced experimental nerve infarction. 722 55


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