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

Traumatic/ischemic events such as fractures, dislocations, lacerations, compression, vascular injuries, and embolus can result in several degrees of nerve injury with resultant sequelae of paralysis, sensory loss, and irritative phenomena (pain, hyperesthesia, and dysesthesia). Neuroma pain may prevent rehabilitation following amputation or nerve lacerations. Thirty-four patients with the late sequelae of traumatic/ischemic neuropathies underwent 36 neural operations using magnification techniques to define and repair neural lesions. Major bone and joint reconstruction could be performed at the same operation with protection of arterial and venous supply. A recovery score using defined criteria for motor, sensory, and irritative (pain) recovery has been developed to quantify the end results in compression/ischemia, contusion/stretch, laceration, idiopathic/irritative disorder, and painful neuroma. Excellent and good results were found in 39 of the 87 specific deficits analyzed (45%). Thus, there is the possibility of improved results in these late neuropathies with therapy before irrevocable muscle fibrosis occurs and intractable pain develops.
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PMID:Surgical management of late post-traumatic and ischemic neuropathies involving the lower extremities: classification and results of therapy. 377 May 97

Fibrotic contracture of skeletal muscle can follow weeks or months after the severe ischemic insult of compartment syndrome. Commonly known as Volkmann's ischemic contracture, the affected limb often becomes dysfunctional and painful, and may lose sensibility. The pathogenesis of the muscle contracture includes prolonged ischemia, myonecrosis, fibroblastic proliferation, contraction of the cicatrix, and myotendinous adhesion formation. Resultant shortening or overpull of involved muscles leads to stiffness and deformity. Simultaneously, nerve injury from initial ischemia or subsequent soft tissue fibrotic compression leads to muscle paresis or paralysis of the involved compartment and of those muscles more distally innervated. The resultant deformity is thus a combination of varying degrees of contracture and weakness depending on which muscles and nerves are affected. Deformity and functional impairment in the foot and ankle secondary to ischemia are determined by many factors, including: (1) which leg compartment, if any, has been affected and to what degree extrinsic flexor or extensor overpull is exhibited, (2) degree of nerve injury sustained causing weakness or paralysis of extrinsic or intrinsic foot and ankle muscles (3) which foot compartment, if any, has been affected and to what degree intrinsic overpull is exhibited, and (4) degree of sensory nerve injury leading to anesthesia, hypoesthesia, or hyperesthesia of the foot. Therefore, a variety of clinical presentations can be encountered following compartment syndrome of the leg and foot. Treatment is based on an appreciation of the pathoanatomy of the deformity. Nonoperative therapy is aimed at obtaining or preserving joint mobility, increasing strength, and providing corrective bracing and accommodative footwear. Operative management is usually reserved for treatment of residual nerve compression or severe and problematic deformities. Established surgical protocols are performed in a stepwise fashion, to include: (1) release of residual or secondary nerve compression, (2) release of fixed contractures, using infarct excision, myotendinous lengthening, muscle recession, or tenotomy, (3) tendon transfers or arthrodesis to increase function, and (4) ostectomy or amputation for severe, refractory deformities.
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PMID:Volkmann's ischemic contracture of the foot and ankle: evaluation and treatment of established deformity. 755 Sep 46

Nerve ischemia induces wallerian degeneration and peripheral neuropathy, the nerve constriction injury induces thermal hyperesthesia. Nerve ischemia is one possible mechanism in the development of thermal hyperesthesia in the nerve constriction injury model. Prostaglandin E1 increases tissue blood flow. In the present study, the authors examine the role of nerve ischemia in the maintenance of the thermal hyperesthesia induced by nerve constriction injury by orally administering OP-1206, a prostaglandin E1 derivative. A nerve constriction injury model was created by making four loose ligations around the rat sciatic nerve, which induces thermal hyperesthesia in the ligated paw in 2-5 days. OP-1206, was administered six times (Day 7, one time; Day 8, two times; Day 9, two times; Day 10, one time). A single administration of OP-1206 had no effect on the thermal hyperesthesia. Six hours after the sixth-administration of OP-1206, the level of the thermal hyperesthesia was attenuated in a dose-dependent manner, and this effect lasted more than 1 day after the last drug administration. These data indicate that nerve ischemia plays an important role in maintaining the thermal hyperesthesia induced by nerve constriction injury in the rat.
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PMID:OP-1206, a prostaglandin E1 derivative, attenuates the thermal hyperesthesia induced by constriction injury to the sciatic nerve in the rat. 786 17

A variety of clinical presentations can be encountered following compartment syndrome of the leg and foot. Deformity and functional impairment in the foot and ankle secondary to ischemia are determined by: 1) which leg compartments have been affected and to what degree extrinsic flexor or extensor "overpull" is exhibited, 2) degree of nerve injury sustained causing weakness or paralysis of extrinsic or intrinsic foot and ankle muscles, 3) which foot compartments have been affected and to what degree intrinsic "overpull" is exhibited, and 4) degree of sensory nerve injury leading to anesthesia, hypoesthesia, or hyperesthesia of the foot. Nonoperative therapy attempts to obtain or preserve joint mobility, increase strength, and provide corrective bracing and accommodative foot wear. Operative management is undertaken for treatment of residual nerve compression or refractory problematic deformities. Established surgical protocols are performed in a stepwise fashion, and include: 1) release of residual or secondary nerve compression; 2) release of fixed contractures, using infarct excision, myotendinous lengthening, muscle recession, or tenotomy; 3) tendon transfers or arthrodesis to increase function; and 4) osteotomy or amputation for severe, non-salvageable deformities.
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PMID:Ischemic contracture of the foot and ankle: principles of management and prevention. 886 51

PURPOSE: Patients with ischemic neuropathy always have a progressive reduction in nerve conduction resulting in a transient increase in sensation, such as pain or hyperesthesia. We examined the effect of acute complete ischemia on neurophysiological functions in rat and related electrophysiological changes in ischemic nerve with adenosine 5'-triphosphate (ATP) administration. METHODS: The sciatic nerve of rat was placed directly on 16 parallel 0.5 mm diameter platinum electrodes (5 mm interelectrode distance) in a Perspex chamber bathed in Ringer's solution. The stimulus was applied through the electrode at the rostral end of the nerve, and the action potential recorded along different recording electrodes towards the caudal end of the nerve. Measurements were recorded immediately upon initial nerve placing and then 5, 10, 15, 30, 60, 90 and 120 min after nerve placing. RESULTS: We observed two major components in the monophasic compound action potential of the sciatic nerve of rats (A and B waves). Nerve conduction and amplitude of A and B waves underwent an initial increase followed by a reduction and after ATP administration, the transient augmentation of conduction velocity and amplitude in A and B waves disappeared. The median survival time of peripheral nerve was 60 min. CONCLUSION: At the onset of ischemia, the membrane Na-K pump does not work resulting in an increase of threshold potential in nerve membrane. When ATP levels further decrease, nerve function progressively fails.
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PMID:Ischemic neurophysiological changes of rat sciatic nerve in vitro. 1238 59

The prevalence of diabetes and resultant complications continues to increase in many countries, including Brazil. A 1-day, multicenter descriptive study involving people with type 2 diabetes was conducted 1) to identify and describe indicators of foot neuropathy and ischemia and examine their relationship, and 2) to examine the relationship between existing risk factors and patient demographic and clinical variables. Seventy-nine (79) patients with an average age of 60.9 years (SD = 13.28) participated in the study. After obtaining a history, the feet of all participants were examined (assessment, palpation, and sensitivity tests using a 128-Hz tuning fork and a 10-g Semmes-Weinstein monofilament). The majority of study participants were women (57%) and the average length of time since diagnosis of diabetes for all participants was 7.76 years (SD = 6.69). The majority of participants were found to have neuropathic and ischemic changes, risk factors for the development of ulcers, or both. Thirty-one patients (42.47%) had cramps, 29 reported numbness (39.73%), 31 (39.24%) lacked sensory perception to the monofilament, 26 (35.62%) experienced tingling, 16 had paresthesia (22.86%), 15 (19.99%) lacked vibratory perception to the tuning fork, 14 felt burning (19.44%), and six had hyperesthesia (10.34%). Certain neuropathic and ischemic changes, as well as some risk factors, were observed more often in male and aged patients, respectively. Men were significantly more likely than women to lack vibratory perception or posterior tibial pulse and to have calluses and an ingrown toenail. Claw toe, lack of sensory perception to the monofilament, lack of posterior tibial pulse, lack of hair, reduced capillary filling, onychomycosis, ingrown toenail, and varices were significantly more common in older than in younger study participants. These results reinforce the importance of regular preventive foot examinations of patients with type 2 diabetes mellitus and confirm that nursing foot care can easily be expanded to include these much-needed assessments.
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PMID:Neuropathic and ischemic changes of the foot in Brazilian patients with diabetes. 1463 64

Surfer's myelopathy is a rare, nontraumatic spinal cord injury that typically occurs in beginner surfers. The condition was first described in 2004 by Thompson et al and usually presents in thin young men. We present a 19-year-old man who developed lower back pain, profound bilateral lower limb paraparesis, and hyperesthesia during his first learn to surf class. The event was not associated with trauma. Subsequent magnetic resonance imaging demonstrated features consistent with spinal cord ischemia. The motor recovery due to surfer's myelopathy is variable; our case remained a paraplegic with a T10 sensory level.
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PMID:An Australian case of surfer's myelopathy. 2254 59