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

An animal model of resting limb ischemia in the rabbit was developed and studied. Anesthetized rabbits underwent unilateral common iliac artery (CIA) division, allowing comparisons between an experimental (ischemic) and the contralateral control limb in the same animal. The time course and severity of the ischemic insult were measured by quantitating muscle blood flow in seven muscle groups using 57Co-radiolabeled microspheres, limb femoral arteriovenous oxygen differences (AVDO2), and limb arterial pressure. Nine of 20 animals had objective evidence of functional limb impairment judged by abnormal resting posture and/or abnormal gait. Muscle blood flow in the experimental limbs became significantly less than blood flows of corresponding contralateral muscle groups (P less than 0.05) when measured at 1 week after CIA division. By 17 days, mean muscle blood flow had returned to within 82.5% of that of the control limb. AVDO2 increased from 4.8 +/- 0.99 to 8.13 +/- 2.26 ml O2/dl blood following CIA division and remained persistently greater than the control limb value until Day 31. Limb arterial pressure decreased markedly after CIA division and remained significantly depressed beyond 6 weeks when the study was terminated. The reasons for the differential time courses of these parameters of blood flow are discussed. Common iliac artery division in the rabbit appears to produce persistent, partial ischemia at least 17 days in duration, allowing in-depth study of the effects of persistent limb ischemia on muscle cell function in the laboratory setting, as well as permitting the assessment of various therapeutic manipulations for the treatment of prolonged muscle ischemia.
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PMID:A model of persistent partial hindlimb ischemia in the rabbit. 224 91

Lower extremity symptoms are caused by lesions at any level of the neuraxis, from cortex to muscle. HIV affects virtually every level of the nervous system, either directly or indirectly. The presence of pathology at multiple levels and by multiple processes further complicates the bedside diagnosis of a patient with AIDS and neurologic symptoms. Many neuropathies and other conditions that affect the lower extremities can be identified with careful history and physical examination, confirmed with limited testing, and can be treated successfully. Distal symmetric polyneuropathy is the most common lower extremity disorder, but it must be distinguished from similar-appearing neuropathies caused by medications, B12 deficiency, or vasculitis. Diffuse infiltrative lymphocytosis syndrome also causes a painful peripheral neuropathy that must be distinguished from distal symmetric polyneuropathy. Inflammatory demyelinating polyneuropathies are characterized by muscle weakness. They occur in early, asymptomatic HIV infection and respond to plasmapheresis or steroids. Mononeuropathies in patients with CD4 counts more than 200 often resolve on their own. Multiple mononeuropathies, which occur in patients with CD4 counts less than 50, are often associated with cytomegalovirus infection and may follow a rapidly progressive course unless treated promptly and aggressively. Progressive polyradiculopathy occurs late in the course of AIDS, is often caused by cytomegalovirus, is rapidly progressive, and generally is fatal unless recognized and treated promptly. Muscle weakness, myalgia, and fatigue are common in HIV and have multiple causes. Lower extremity spasticity may be caused by treatable etiologies such as spinal cord abscess, tumor, disc compression, B12 deficiency, or ischemia. Gait disturbances are common but nonspecific and may be caused by treatable neurologic disorders at any level of the neuraxis.
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PMID:Neurologic problems of the lower extremity associated with HIV and AIDS. 957 54

Although vascular remodeling is important in preventing tissue damage and restoring muscle function, there is no evidence of a relationship between vascular remodeling and muscle function after peripheral vascular occlusion. Nitric oxide (NO) has been implicated in the process of vascular remodeling in hindlimb ischemia. Thus, development of alterations in hindlimb gait after ischemia may be associated with impaired nitric oxide-dependent, vascular blood flow recovery. We evaluated hindlimb gait as an index of ischemia-induced revascularization and tested the effects of NO synthase inhibition on both hindlimb blood flow and hindlimb gait locomotion. After 14 days of ischemia, the ischemic hindlimb showed no significant differences in gait locomotion compared to the sham-operated hindlimb. However, hindlimb ischemia drastically reduced hindlimb blood flow from 46+/-3 mL/min/100 g to 12+/-2 mL/min/100 g which reverted to 33+/-5 mL/min/100 g after 14 days of ischemia. eNOS mRNA expression levels at 3, 7, 14, and 28 days after initiation of ischemia, were increased by 50+/-5%, 100+/-10%, 140+/-8% and 270+/-12% respectively and eNOS protein expression levels at 7, 14, and 28 days, were increased by 28+/-3%, 62+/-6% and 80+/-16% respectively. However, eNOS inhibition caused by l-NAME treatment prevented blood flow recovery and correction of abnormal gait locomotion in rats. Thus, the duration of the stride-swing phase increased and the stride length decreased. The knee joint angle decreased during flexion and extension with eNOS inhibition. In conclusion, ischemia-induced revascularization is associated with recovery of both hindlimb blood flow and normal gait locomotion. Moreover, prevention of NO synthesis, a key messenger in ischemia-induced revascularization, is associated with impairment in hindlimb locomotion. Thus, gait locomotion represents a functional model that could be used to evaluate the degree of ischemia-induced revascularization.
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PMID:Hindlimb claudication reflects impaired nitric oxide-dependent revascularization after ischemia. 1701 Dec 43

Cerebellar infarctions often go unrecognized and misdiagnosed. Easily confused with peripheral vestibular system dysfunction, physicians often miss the cardinal symptoms of dizziness and an abnormal gait. If not treated appropriately and quickly, cerebellar infarcts can lead to coma and death. This review discusses the key features of cerebellar infarction, including the anatomical origination and clinical symptomology of the infarcts. Evaluation recommendations include neuroimaging analysis, which can help clarify the etiology and aid in making therapeutic decisions. Management of patients with cerebellar infarcts is similar to that of patients with posterior circulation ischemia. Antithrombotic drugs, thrombolytics, surgery, and angioplasty/stenting are options.
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PMID:Cerebellar infarcts: key features. 1981 98

The study used a focal ischemia rat hindlimb model to investigate muscle activity changes during a 10-day body weight support (BWS) treadmill training program. The changes being studied included fatigue effects, EMG burst duration in the gait cycle, and the symmetry of muscle activation between affected and unaffected sides. Intramuscular EMG of medial gastrocnemius (MG) and tibialis anterior (TA) muscles in male Sprague Dawley rats at affected side (n=10) and unaffected side (n=10) were recorded during the treadmill running before a middle cerebral artery occlusion/reperfusion (MCAo/r) surgery and poststroke recovery stage. Behavioral test score and bodyweight were recorded at a daily basis after stroke. The mean power frequency (MPF) of the EMG, EMG burst duration in the gait cycle, and symmetry index between two sides were used for analysis. The drop rate of MPF of MG at the unaffected side increased (P<0.05) at poststroke day 2 and it generally decreased along the poststroke training days and almost returned to baseline value at poststroke day 6. Symmetry index of MG and TA showed a large imbalance right after stroke and tended to return to normal. Our findings of the MPF drop after stroke might indicate fatigue effects due to the compensation loading share of the ipsilateral side muscle and the increase of the symmetry index reflects abnormal gait pattern after the onset of stroke. The recovery rate after stroke could be investigated with EMG parameters together with the behavioral score, and both were improved during and after the BWS treadmill training.
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PMID:Muscle activation changes during body weight support treadmill training after focal cortical ischemia: A rat hindlimb model. 2096 73

OBJECTIVE Spinal dural arteriovenous fistulas (dAVFs) are rare vascular abnormalities caused by arteriovenous shunting. They often form at the dural root sleeve between a radicular feeding artery and draining medullary vein causing venous congestion and edema, decreased perfusion, and ischemia of the spinal cord. Treatment consists of either surgical ligation of the draining vein or selective embolization via an endovascular approach. There is a paucity of data on which modality provides more durable and effective outcomes. METHODS The authors performed a retrospective review of a prospectively maintained database by the senior author to assess clinical outcomes in patients undergoing surgical treatment of spinal dAVFs. Preoperative and postoperative motor and Aminoff-Logue Scale (ALS) scores were collected. RESULTS A total of 41 patients with 44 spinal dAVFs were identified, with a mean patient age of 64 years. The mean symptom duration was 14 months, with weakness (82%), urinary symptoms (47%), and sensory symptoms (29%) at presentation. The fistula locations were as follows: 30 thoracic, 9 lumbar, 3 sacral, and 2 cervical. Five patients had normal motor and ALS scores at presentation. Among the remaining 36 patients with motor deficits or abnormal gait and micturition at presentation, 78% experienced an improvement while the remaining 22% continued to be stable. There was a trend toward improved outcomes in patients with shorter symptom duration; mean symptom duration among patients with clinical improvement was 13 months compared with 22 months among those without improvement. Additionally, rates of improvement were higher for lower thoracic and lumbosacral dAVFs (85% and 83%) compared with those in the upper thoracic spine (57%). No patient developed recurrent fistulas or worsening neurological deficits. CONCLUSIONS Surgery is associated with excellent outcomes in the treatment of spinal dAVFs. Early diagnosis and treatment are critical, with a trend toward improved outcomes. No patient in this study had fistula recurrence or worsening of symptoms. Among patients with abnormal motor or ALS scores, 78% improved after surgery. Therapeutic embolization is an option for some lesions, but for cases with unfavorable anatomy where embolization is not feasible, surgery is a safe option associated with high success.
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PMID:Timing, severity of deficits, and clinical improvement after surgery for spinal dural arteriovenous fistulas. 2967 70