Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

The aortic dissection is an expanding intramural hematoma in the aortic wall separating its layers. That is the most common catastrophic condition of the aorta. Its incidence in Hungary about 3.0%/000/year may be appreciated. The mortality rate of the untreated cases exceeds the 90 per cent. The dissection begins by an intimal tear or by a medial hemorrhage, seldom. The progressing hematoma results in a false lumen running parallel with the true aortic lumen. On the basis of the location of the primary intimal tear the dissection may be proximal or distal. The inherited or acquired medial weakness and the hypertension are the main etiologic factors. Some pathological findings refer to predisposing role of the atherosclerosis. The ischemia caused by the dissection may damage any organ. The clinical picture is characterized by the polymorphism and the migration of the clinical signs. The suspicion of the disease may be raised on the basis of the anamnesis and the clinical picture. The diagnosis may be confirmed by the rutin chest roentgenograms and by the angiography, CT, MRI and ultrasonic examinations. The transoesophageal echocardiography is the best diagnostic tool. The treatment is medical and/or surgical. Advances in the surgical treatment brought turn in the very poor prognosis.
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PMID:[Aortic dissection]. 916 92

Five patients with spinal cord infarction underwent electrophysiologic evaluation. Two subjects with complete paralysis had absent compound muscle action potentials (M-responses), suggesting complete loss of lower motoneurons (LMN). Three subjects with incomplete cord infarction had preserved M-responses, reduced voluntary recruitment and abnormally slow motor-unit firing rates during maximal effort, suggesting upper motoneuron (UMN) weakness. These five patients demonstrate a range of neuronal damage after cord ischemia. With severe cord infarction, there is LMN degeneration and paralysis. With partial cord infarction, there is selective interneuron loss, resulting in UMN weakness. Electrodiagnostic evaluation can help determine prognosis for motor recovery after spinal cord infarction.
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PMID:Spinal cord infarction: varying degrees of upper and lower motoneuron dysfunction. 923 91

The tethered spinal cord syndrome is more often encountered in children, but does also occur in adults. Its clinical spectrum comprises low back pain, neurological deficits such as distal motor weakness and trophic and sensory disturbances in the legs, urological symptoms and such musculoskeletal signs as scoliosis or foot deformities. In addition, cutaneous lesions or subcutaneous lipomas in the lumbosacral region may be indirect signs of an intraspinal pathology. This consists in a tight, thickened and sometimes shortened filum terminale, an intraspinal lipoma, intradural scar formation or other lesions that lead to conus fixation. The common mechanism of injury of these types of pathologies is an impairment of longitudinal movement of the spinal cord, especially the conus medullaris, which subsequently leads to chronic local ischemia. Diagnosis is most readily achieved by magnetic resonance imaging. Treatment is aimed at the restoration of cord mobility by means of microsurgical release of the conus, the cauda equina and the filum terminale with the aid of cauda equina neuromonitoring. Further progression can be effectively halted; in fact almost half of the patient actually improve. Therefore, every patients presenting with the clinical diagnosis of tethered cord syndrome should be offered specialized surgical treatment.
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PMID:[Tethered spinal cord syndrome in adults]. 927 57

[15O]-water PET was performed on 12 patients with structural lesions for localization of the motor (n = 5), language (receptive and expressive; n = 6), and visual cortex (n = 1). All these patients underwent interactive image-guided surgery using an infrared digitizer and intraoperative electrical stimulation mapping for motor, sensory, language, and visual cortex location. MRI-PET coregistration was performed using a surface matching approach that integrated functional information with interactive image guidance during the surgical procedure. An awake craniotomy with motor and sensory intraoperative stimulation was performed using a registered bipolar electrode that was tracked on real-time during the surgical procedure. Intraoperative functional findings were displayed and saved on the registered MRI images. The sites of functional PET activation during the performance of motor, visual and language tasks were then compared to the results of intraoperative cortical stimulation in 11 patients and visual evoked potentials in one. The results of the PET activation studies were concordant with the findings of intraoperative stimulation in all cases. During resection of the structural lesions, intraoperative stimulation was continued in the subcortical pathways, and five patients had positive responses on areas not identified by the functional PET. Furthermore, 3 patients showed transitory changes in function (speech arrest 1, naming difficulty 1, and motor weakness 1) that were reversible after changing the dissection technique or a brain retractor. [15O]-water PET was reliable in identifying the motor, visual, and language cortex. Language-related rCBF increases were highly distributive, although only part of these activations were subjected to intraoperative stimulation. We conclude that [15O]-water PET can be used for preoperative noninvasive identification of functional cortex and may be useful in neurosurgical preplanning. Intraoperative mapping still remains the main means to avoid neurological damage as it can be performed during the entire surgical procedure to avoid damage to cortex, pathways, and damage secondary to ischemia or edema (brain retraction).
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PMID:[15O]-water PET and intraoperative brain mapping: a comparison in the localization of eloquent cortex. 942 60

Hemiballism and hemichorea following anesthesia-induced hypotension has rarely been described, but a recent case suggests an association. After experiencing marked hypotension during spinal anesthesia, a 70-year-old woman developed hemiballism and hemichorea. Involuntary ballistic movements with writhing, consisting of repetitive rotation and flexion-extension without apparent muscle weakness, affected her left limbs proximally. Low-amplitude, involuntary, choreiform movements involved the distal portions of these limbs. Magnetic resonance imaging demonstrated an area of high signal intensity in the contralateral subthalamic nucleus, suggestive of a focal ischemic lesion. Although such occurrences are rare, anesthesiologists should be aware of the risk of subthalamic nucleus ischemia following marked hypotension.
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PMID:Hemiballism-hemichorea from marked hypotension during spinal anesthesia. 952 38

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

We describe the clinical and neurophysiologic findings in a group of diabetic patients with a severe ulnar neuropathy. All patients attending a large inner-city diabetes center were prospectively screening for hand wasting and weakness due to ulnar nerve disease. Twenty diabetic patients fulfilling the clinical criteria underwent nerve conduction studies and electromyography. All but one patient with a motor ulnar neuropathy had systemic complications, mostly severe: ten were amputees, four had had a renal transplant, and two were blind. The onset of hand weakness was sudden in five. All patients had a classical "ulnar hand" (bilateral in five) but forearm muscles were little affected. Sensory loss was prominent in only one-half. Nerve conduction studies showed markedly reduced ulnar motor responses (mean, 1.2 mV versus 7.4 mV in controls) and ulnar/median motor ratios. Motor conduction was disproportionately slowed across the elbows, with or without conduction block, in only eight of 34 affected ulnar nerves. Five of these patients had a habit of leaning on their elbows and/or a Tinel's sign. Median sensory action potentials (SAPs) were recordable in 12 patients but ulnar SAPs were absent in 30 of 34 affected nerves. Electromyography revealed advanced denervation of ulnar supplied hand muscles. We conclude that motor ulnar neuropathy is not uncommon in patients with diabetes of long standing, especially in those with severe systemic complications. Nerve entrapment at the elbows occurs in some, but in many the lesion is axonal, and damage may occur through ischemia.
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PMID:Observations on severe ulnar neuropathy in diabetes. 961 67

Although hypercalcemia may cause drowsiness, lethargy, weakness, confusion and coma it rarely causes seizures or cerebral infarction. The patient presented had a clinical evolution from hallucinosis to a generalized tonic-clonic seizure, and subsequent cortical blindness with occipital cerebral ischemia as evidenced by SPECT and MRI scans. EEG revealed occipital PLEDs. With reversal of hypercalcemia, there was a return of vision, resolution of EEG epileptiform activity, although with some residual occipital infarction. This case, in concert with a literature review of hypercalcemia, reveals examples of occipital and watershed ischemia, blindness, seizures and hypertension, a pattern markedly similar to that of eclampsia. Furthermore, medications such as magnesium sulfate, believed to reverse cerebrovasospasm responsible for the eclamptic neurologic findings, may counter the effects of hypercalcemia at a cellular level, lending support to a calcium-mediated injury in eclampsia.
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PMID:Reversible hypercalcemic cerebral vasoconstriction with seizures and blindness: a paradigm for eclampsia? 966 11

Exertional compartment syndrome is characterized by intracompartmental pressures that rise transiently following repetitive motion or exercise, thereby producing temporary, reversible ischemia, pain, weakness, and, occasionally, neurologic deficits. The exact cause or pathogenesis remains unclear; a disturbance of microvascular flow caused by elevated intramuscular pressure leads to tissue ischemia, depletion of high-energy phosphate stores, and cellular acidosis. Anatomic contributing factors may include a limited compartment size, increased intracompartmental volume, constricted fascia, loss of compartment elasticity, poor venous return, or increased muscle bulk. The diagnosis is suspected based on history and confirmed with physical examination and intramuscular pressure evaluation before and after exercise (stress test). Differential diagnosis includes claudication or other vascular abnormalities, myositis, tendinitis, periostitis, chronic strains or sprains, stress fracture, other compression or systemic neuropathies, and cardiac abnormalities with angina or referred extremity pain. Initial treatment includes activity modification; refractory symptoms can be managed with elective fasciotomy.
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PMID:Exertional compartment syndrome of the upper extremity. 974 26


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