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

It is possible to learn more about peripheral nerve function in human subjects than is obtainable with routine nerve conduction studies, and thereby to study the basis of "positive" symptoms, such as paresthesias. Using microneurography, ectopic impulse activity in cutaneous afferents has been recorded in patients suffering from neurologic disorders and in normal subjects in whom paresthesias were provoked by hyperventilation, prolonged tetanization of cutaneous nerves and ischemia. Using relatively simple modifications of standard nerve conduction techniques, the increases in axonal excitability responsible for this ectopic activity have been documented in human volunteers. Hyperventilation increases axonal excitability but does not change supernormality, probably because Na+ channels are activated by the decrease in [Ca2+] on the axonal membrane. Prolonged tetanic stimulation and ischemia probably share similar mechanisms. At least in motor axons, postischemic ectopic activity occurs when the hyperpolarization that results from activation of the Na+/K+ pump lowers the membrane potential below the equilibrium potential for K+. A high extracellular [K+] can then result in an inward current producing depolarization and possibly triggering regenerative processes.
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PMID:Microneurography, impulse conduction, and paresthesias. 841 55

Acute arterial occlusions of the extremities present with the classical five P's: pain, pallor, pulselessness, paresthesia, paresis. Loss of sensitivity and motility are symptoms of the most severe grade of ischemia. The occlusions are due to embolism in about 70% of subjects and to local thrombosis in 30%. These patients have to be treated immediately with heparin. In the mildest forms, deobliteration is desirable, but in the more severe cases rapid restoration of flow not only saves limbs but also life. Deobliteration may be performed surgically or by means of catheters (local thrombolysis or thrombus aspiration) if available. Deep vein thrombosis, the other kind of emergency situation, requires immediate anticoagulation as soon as pulmonary embolism is suspected. It should be initiated by heparin and followed by oral anticoagulation. In patients presenting without pulmonary embolism but a swollen leg, ruptured Baker cysts or muscle hematomas should be ruled out before anticoagulation is started. Systemic thrombolysis or surgical thrombectomy is reserved for young patients with acute isolated thromboses. Thrombectomy must also be kept in reserve for the most severe form of deep venous thromboses, the phlegmasia cerulea dolens. In thrombophlebitis, no anticoagulation is indicated except in bedridden patients. The others must remain mobile and may be treated by systemic and local antiinflammatory drugs, incision of thrombosed varices, and bandages.
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PMID:[Emergencies in angiology]. 849 73

We reviewed 44 cases of ischemia and infarction of the spinal cord at two university hospitals. Three patients experienced transient ischemic attacks. Etiologies of completed strokes were diverse and included rupture and surgical repair of aortic aneurysms, aortic dissection, aortic rupture and thrombosis, global ischemia, anterior spinal artery embolism, repair and thrombosis of spinal arteriovenous malformations, hematomyelia, epidural hematoma, cervical osteophytosis, celiac plexus block, systemic lupus erythematosus, coagulopathy, and decompression sickness. Motor function improved in 12 patients, was substantial in only one, and occurred largely within the first 2 to 4 weeks. Favorable ambulatory outcome correlated with improving neurologic examinations and relatively preserved strength in hip abductors and knee extensors. More extensive deficits without initial improvement portended a more severe prognosis. Autonomic dysfunction, pain, paresthesia, and depression were common and impeded recovery in some patients. The mean level of deficit was at T-8 and in cases of global ischemia was at T-9, which leads us to dispute the classical view of a midthoracic watershed zone of ischemic vulnerability near T-4.
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PMID:Spinal cord infarction: etiology and outcome. 915 13

Proprioceptive loss, paresthesias, and atrophy of the hands can occur with disorders afflicting the upper cervical spinal cord. The diagnosis might be erroneous, because compression in this region might produce signs and symptoms that seem to originate in the lower cervical cord. This article reviews the clinical presentation and radiographic data of a consecutive series of 11 patients who presented between 1992 and 1994 with an extradural lesion above the C4 level. Each patient had a characteristic syndrome of finger and hand dysesthesia, hand atrophy, and occipital or cervical pain. These complaints usually preceded the development of spasticity and gait disturbance. Initial diagnoses included brachial plexopathy, shoulder dysfunction, viral syndrome, and cervical spondylosis at a lower segment. Cervical spondylosis or a herniated disc was the most common pathogenesis. The most commonly involved level was C3-C4. Nine patients underwent a surgical procedure; eight showed significant postoperative improvement (mean time of follow-up examination, 9.7 mo; follow-up range, 1-24 mo). One patient was lost to follow-up. Although the pathophysiology of these findings is unknown, theories include anterior spinal artery ischemia, venous obstruction, and differential decussation of the forelimb and hindlimb fibers of the corticospinal tract. Recognition of this syndrome might prevent inappropriate operative intervention in patients with coexisting pathological conditions of the lower cervical spinal cord.
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PMID:False localizing signs in upper cervical spinal cord compression. 897 49

Bleeding and thrombosis are major causes of morbidity and mortality in patients with chronic myeloproliferative disorders. We retrospectively evaluated 101 consecutive patients affected by primary thrombocytosis (46 male, 55 female, aged 18-84 years; mean +/- SD 61 +/- 15) followed for a period ranging from 6 months up to 10 years (median 5 years) at our hematological unit. At the time of diagnosis 48 patients were asymptomatic; 26 had clinical evidence of atherothrombosis (cerebral ischemic attacks, ischemic heart disease, peripheral occlusive arterial disease), ten had venous thrombosis, four experienced major hemorrhages, 23 presented microvascular ischemic manifestations namely erythromelalgia, paresthesias, acrocyanosis and dizziness. At presentation 51.2% of the patients had elevated serum lactic dehydrogenase, 34.5% hyperuricemia, and 23.4% serum creatinine > 1.2 mg/dL. Color Doppler ultrasound provided evidence of vascular stenosis or medium-intimal hyperplasia of epiaortic vessels in 48.9% of patients studied, and similar alterations of lower limb arteries in 23.8% of cases. Therapy modality included an antiplatelet agent (picotamide 300 mg/bid); a cytoreductive agent (busulphan, hydroxyurea, pipobroman or melphalan) was used when platelet count was > 800000/microL. Symptoms due to microvascular ischemia promptly regressed after picotamide and cytoreductive therapy. During follow-up. nine patients suffered from atherothrombotic events (transient ischemic attacks, ischemic stroke, unstable angina pectoris) and five developed deep vein thrombosis or superficial thrombophlebitis. Five patients experienced major hemorrhages (two melena, two hematuria, one perioperative bleeding); the two gastrointestinal hemorrhages occurred in patients self-medicated with non steroidal anti-inflammatory drugs, and the two episodes of hematuria occurred on oral anticoagulant therapy and aspirin respectively. No major bleeding occurred in patients on continuative therapy with picotamide, even in the presence of upper digestive tract disorders. Seven patients died: mortality resulted from one sudden coronary death, three solid neoplasia, one blast crisis, one anile, and one massive hemorrhage due to abdominal aortic prosthesis tearing. Our study suggests that a long-term antithrombotic prophylaxis with picotamide may be of benefit in patients affected by primary thrombocytosis; a controlled clinical trial is warranted to assess whether picotamide can ameliorate the natural history of the disease.
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PMID:Thrombotic and hemorrhagic complications in chronic myeloproliferative disorders. 895 59

Paresthesia, pain and coldness of the upper limb strongly suggest ischemia. The questions raised concern the etiology and treatment. 1) Treatment is based on confirmation of the unilateral nature of the disorder requiring search for the a locoregional cause (examination of the subclavian outlet) and on elimination of a cardiac or general origin. Two noninvasive examinations are indicated. An X-ray examination of the upper chest bones is performed to search for an abnormal formation, usually a cervical rib. Presence of a cervical rib indicates a possible damage to the sub-clavian artery in the thoraco-brachial outlet and, inversely, absence of a cervical rib suggests either arterial damage or a fibromuscular cause. Ischemia of the upper limb results from repeated microtrauma to the sub-clavian artery due to a bone-ligament anomaly resulting in thickening and parietal ulceration, and sometimes post-stenosis embolism or in situ thrombosis. Duplex Doppler may be able to identify the nature of the cause without dynamic manoeuvres. An arteriography is essential to confirm the level of the obstacle, its nature, the status of the downstream bed and possible relationship between a bone anomaly and the sub-clavian artery. Several incidences may be required. 2) Therapeutic modalities must take into account the ischemia and its cause. Surgery is required to remove the obstacle and repair the arterial damage, and possibly to remove an embolus. It is relatively easy to remove a cervical rib or repair a bone muscle anomaly, allowing arterial repair with or without venous bypass. Embolectomy of an earlier embolus may require major reconstruction vascular surgery.
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PMID:[Paresthesia, pain, coldness of the arm and possible responsibility of the thoraco-brachial outlet syndrome]. 902 53

Several aspects of tactile, thermal and pain perception were evaluated in an individual (R.S.) with a hemorrhagic lesion centered in her left lateral thalamus. Over a 4-year period, psychophysical evaluations were undertaken every 6-8 months, and five magnetic resonance (MR) studies were conducted. Early tests (1991-1992) revealed large contralateral deficits in R.S.'s perception of touch, innocuous temperature, and mechanically evoked cutaneous pain--more so for the upper versus the lower extremity. R.S. showed a similar pattern for heat pain sensitivity, but a more modest deficit than for mechanically evoked pain. She showed a deficit for cold pain sensitivity on her foot, but not for her hand. Thresholds for all types of stimuli ipsilateral to the lesion were within a normative range. Late in 1993, R.S. demonstrated improvements in sensory capacity for touch and mechanically evoked pain contralaterally, although deficits were still evident. During the same period, heat pain sensitivity improved contralaterally, and strikingly, a permanent, ipsilateral hypersensitivity to heat pain developed in her hand. Throughout the entire testing period, R.S.'s ratings of perceived unpleasantness matched the patterns of perceived pain intensity. Thus, the discriminative and the affective dimensions of her pain would change in tandem. However, perceptible innocuous thermal stimuli evoked no affective response when applied contralaterally, despite being described as pleasant when presented ipsilaterally. Throughout the testing period, R.S. reported a persistent numbness on her right hemi-body. Only during a 3-month period in 1995 did she experience spontaneous pain, which was referred to her right foot. The only change in psychophysical performance related to her right foot was a transient but intense thermal allodynia several months prior to her spontaneous pain. The MR studies over this 4-year period showed changes in the extent of edema, gliosis and/or ischemia that could be related to perceptual changes. Thus, the conspicuous observations in this thalamic lesion case were: (i) differential effects upon the various pain modalities (mechanical, heat and cold); (ii) development of thermal allodynia without mechanical allodynia, including an ipsilateral effect; (iii) a deficit in positive affective responses to temperature; and (iv) the different time courses for changes in evoked somesthetic capacity versus spontaneous paresthesias and pathological pain.
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PMID:A longitudinal study of somesthetic perceptual disorders in an individual with a unilateral thalamic lesion. 927 83

Paresthesias may be caused by central or peripheral nervous system abnormalities. Central nervous system-induced paresthesias are most commonly caused by ischemia, structural or compressive phenomena, infection, inflammation or degenerative conditions. Peripherally induced paresthesias can be caused by entrapment syndromes, metabolic disturbances, trauma, inflammation, connective tissue diseases, toxins, hereditary conditions, malignancies, nutritional deficiencies and miscellaneous conditions. Confirming the diagnosis and establishing an etiology may require appropriate laboratory and radiologic studies, or other studies. In most cases, the specific clinical syndromes associated with the paresthesias, coupled with the presenting neurologic findings, provide the physician with a framework for the diagnosis.
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PMID:Paresthesias: a practical diagnostic approach. 961 7

Upper extremity ischemia with finger necrosis: carpal-tunnel syndrome or thoracic outlet syndrome? A 26-year-old male patient complained of pain paraesthesia in the right upper extremity while working with the arm elevated. After electrophysiological diagnosis of a carpal-tunnel-syndrome the patient received surgical treatment. Following this treatment he developed acral necrosis at the fingers. Additional diagnostic effort let to the diagnosis of a thoracic-outlet-syndrome due to a cervical rib. This case report and a review of the literature show that electrophysiological investigations alone can not differentiate the carpal-tunnel-syndrome from the thoracic-outlet-syndrome. Thus an operative release of a carpal-tunnel should not be performed until the arterial perfusion of the upper extremity has been judged.
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PMID:[Ischemia of the arm with finger necroses: differential carpal tunnel syndrome and thoracic outlet syndrome diagnosis]. 945 58

Compared with control subjects, patients with amyotrophic lateral sclerosis (ALS) have been reported to experience less or no paresthesias during and after release of ischemic compression of the upper arm for 10 min. This is reminiscent of the resistance to ischemia of diabetic patients, in whom sensory and motor axons undergo less ischemic depolarization and less postischemic hyperpolarization than in control subjects. The present study compared the changes in axonal excitability produced by ischemia for 10 min in 21 patients with ALS and 14 age-matched control subjects. Fewer patients reported intraischemic or postischemic paresthesias and the intensity of paresthesias was less, but this was significant only for postischemic paresthesias. There were quantitatively similar changes in refractoriness, supernormality, and strength-duration time constant during ischemic compression, but the increase in excitability of motor axons was less during the second half of ischemia in the patients. After release of ischemia the postischemic hyperpolarization was greater in the ALS patients, the opposite of what occurs in diabetes. These changes could reflect reduced intraneural K+ accumulation due to loss of motor axons or an alteration in nerve metabolism or membrane properties. Either way, the present study has failed to confirm previous reports of "ischemic resistance" in ALS, and indicates that the changes in axonal properties in ALS are not analogous to those in diabetes mellitus.
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PMID:Ischemic resistance of cutaneous afferents and motor axons in patients with amyotrophic lateral sclerosis. 984 71


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