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)

Muscle hypertrophy in neurogenic disorders is an uncommon phenomenon which has been reported in various conditions: hereditary or acquired anterior horn cell diseases, essentially S1 radicular compressions, and polyneuritis generally of a demyelinating type. We report two cases of denervating disease with muscle hypertrophy. The first was an S1 radiculopathy, and the second a compression with ischemia of the spinal cord by herniation of the D11-D12 disc, and showing partial improvement after surgery. In both cases, electrophysiological examination of the hypertrophic muscles revealed abnormal activities identified as complex repetitive discharges. In the second case they were associated with a syndrome of continuous motor unit activity. Such activities are rare in peripheral nerve involvement. However they have quite often been recorded in cases of neurogenic muscle hypertrophy and may therefore be partly responsible for the development of the hypertrophy.
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PMID:[Neurogenic muscular hypertrophy. Association with abnormal electrophysiological activities]. 361 65

Exercise-induced weakness (fatiguing) is described in three patients with cervical compressive radiculopathy. In all three cases, the patients had symptoms only while at work, and in two cases, symptoms occurred in life-threatening situations. All patients had seen several physicians with a functional diagnosis being considered in all cases because of symptoms only at work and the absence of objective findings during examination. Precise history and examination techniques led to the correct diagnosis and treatment after appropriate investigation. The fatiguing weakness in our cases is thought to be a manifestation of early or mild neurologic involvement unmasked by exercise, rather than a manifestation of compression or ischemia.
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PMID:Fatiguing weakness: an initial symptom in cervical compressive radiculopathy. 683 95

Pathologic study of nerve tissue is especially useful for the recognition of interstitial events such as inflammation or vascular alterations that cannot be inferred from clinical or electrophysiologic findings and may provide insight into an underlying mechanism or cause. Considerable variation in the natural history and pathologic alterations among diabetic neuropathies suggests that they are heterogeneous. For diabetic polyneuropathy, two mechanisms need to be considered. The first assumes that hyperglycemia induces metabolic derangements that directly affect Schwann cells (or myelin), nodes of Ranvier, or axons. The second assumes that hyperglycemia and metabolic derangement affect the structure and function of endoneurial microvessels, which then induce fiber changes by altering the blood-nerve barrier, inducing hypoxia or ischemia, or by unknown mechanisms. In proximal diabetic neuropathy, there is increasing evidence that the characteristic lesion is an inflammatory (immune) vasculitis that induces ischemic nerve fiber degeneration. Truncal radiculopathy may be due to an inflammatory polyganglionopathy. In cranial nerve III neuropathy, the monophasic course and the pathologic alterations of ischemia suggest that localized vasculitis should be excluded in future cases. Many upper limb mononeuropathies in diabetes mellitus are from carpal tunnel syndrome. Repetitive shear forces, anatomic factors, and excessive stiffness of connective tissues may cause these mononeuropathies.
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PMID:Pathologic alterations in the diabetic neuropathies of humans: a review. 910 Jun 76

Three cases of extracranial vertebral artery dissections with upper limb peripheral motor deficit (C5-C6) are reported. Six similar cases were also found in the literature. Central neurological symptoms occurred in five of these nine cases, suggesting the diagnosis of dissection. The peripheral motor or sensorial deficit was strictly isolated in the four other cases, simulating radicular neuralgia due to discopathy or foraminal compression. In case of dissections, a precise analysis of pain is helpful to guide diagnosis; sharp, unbearable, continuous and extended neck pain without nocturnal paroxysms and posterior neck stiffness is typical. Analgesics or anti-inflammatory drugs are ineffective. Peripheral motor deficit is more common than sensory deficit. Recovery was complete in this series. In most cases, the radiculopathy appears to be due to cervical root compression in its extraforaminal course due to the dissection hematoma and rarely to radicular ischemia.
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PMID:[Cervical deficit radiculopathy in 3 cases of vertebral artery dissection]. 989 90

We reviewed the clinical and neuroradiological features in 16 patients with serious neurological complications of lumbar epidural anaesthesia. We observed acute, transient or permanent and delayed complications. Four patients had symptoms immediately after the procedure. One patient developed a subacute flaccid paraparesis. Two other patients had infectious spondylodiscitis at lumbar puncture level. Eight patients had a delayed progressive spastic paraparesis and were found to have subarachnoid cysts and irregularities of the surface of the spinal cord consistent with arachnoiditis; six of them had an extensive, complex syrinx within the cord. One patient had a severe lumbar polyradiculopathy, and MRI showed adhesive arachnoiditis involving the cauda equina. Although epidural anaesthesia is generally considered safe, rare but severe complications, such as radiculopathy, infectious disease, myelopathy from ischemia and arachnoiditis with a syrinx may occur. The patients with arachnoiditis had a relentless progression of the disease and a poor outcome: five are confined to a wheelchair, one is bedridden. Complications of epidural anaesthesia are easily recognised when they develop immediately; their relationship to the anaesthesia may be ignored or underestimated when they appear after a delay. Awareness of the possibility of delayed complications is important.
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PMID:Imaging and outcome in severe complications of lumbar epidural anaesthesia: report of 16 cases. 1099 61

Intermittent claudication (IC), the symptom of exercise-induced muscle ischemia of peripheral arterial disease (PAD), afflicts and limits the activities of a significant number of patients. Incidence and prevalence of IC depends on the population studied and the diagnostic instruments used. In large studies, prevalence has ranged from 3% to 10%, with a sharp increase in those aged > or =70 years. Over the next 20 years, the total number of patients affected is expected to increase significantly due to anticipated demographic changes. Analysis of the natural history of IC demonstrates that the risk of cardiovascular morbidity and mortality far exceeds that of severe limb ischemia or limb loss. In fact, only 2% to 4% of all patients with IC will require a major amputation in their lifetime. However, life expectancy is approximately 10 years less than that of an age-matched cohort. By now, PAD is well recognized as a marker of systemic atherosclerosis. The cornerstone of patient evaluation is a history and physical examination, including a detailed atherosclerotic risk-factor assessment. In the differential diagnosis of IC, clinicians should consider etiologies such as arthritis, spinal stenosis, radiculopathy, venous claudication, or inflammatory processes. In >80% of all patients, it is possible to locate the responsible arterial segment by combining the location and severity of pain with a pulse examination. Noninvasive diagnostic studies help determine the level of disease, may unmask a hemodynamically significant stenosis, and are useful in follow-up. Arteriography is reserved for patients in whom the decision for revascularization has been made. Knowing the anatomic detail of a lesion allows the clinician to determine whether and what type of intervention is feasible. Standard therapy for all patients should be directed at both peripheral and systemic atherosclerosis, beginning with risk-factor modification in the form of smoking cessation, optimal diabetes control, and lipid normalization. The benefits of supervised exercise rehabilitation include significantly increased walking distance and enhanced quality of life. Platelet inhibition has been shown to reduce the risk of ischemic stroke, myocardial infarction, and vascular death and should be prescribed for all but those in whom it is medically contraindicated. Symptom-specific pharmacotherapy with a broad range of medications has yielded disappointing results in the past. However, recent studies have demonstrated that patients receiving the novel agent cilostazol experienced increases in walking distance and improvements in quality of life.
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PMID:Intermittent claudication: magnitude of the problem, patient evaluation, and therapeutic strategies. 1143 94

Peripheral nerve involvement is a frequent complication of type 1 and type 2 diabetes, and can induce major disability. Almost all types of clinical or electrophysiological disturbances may be present: mononeuropathy involving cranial nerves or a limb; multiple mononeuropathy; proximal acute radiculopathy; distal, symmetric, sensory polyneuropathy; autonomic neuropathy. Physiopathology intricates probably several mechanisms but metabolic dysregulation and ischemia are mainly involved. Despite numerous controlled clinical trials no treatment has demonstrated efficacy for peripheral neuropathy, excepting the optimization of diabetes equilibrium. However, symptomatic treatments are available, particularly for the management of neuropathic pain.
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PMID:[Diabetic neuropathies]. 1179 22

Spinal cord stimulation is the most common mode of neuromodulation used in managing chronic low back pain. It is minimally invasive and reversible as opposed to nerve ablation. The basic scientific background of the initial spinal cord stimulation trials was based on the gate control theory of Melzack and Wall. It has been demonstrated in multiple studies that dorsal horn neuronal activity caused by peripheral noxious stimuli could be inhibited by concomitant stimulation of the dorsal columns. Various other mechanisms, which may play a significant role in the mechanism of action of spinal cord stimulation, include the suppressive effect of spinal cord stimulation on tactile allodynia, increased dorsal horn inhibitory action of gamma-aminobutyric acid (GABA), prevention or abolition of peripheral ischemia, and effects on human brain activity. Spinal cord stimulation is indicated in low back pain with radiculopathy, failed back surgery syndrome, complex regional pain syndrome, peripheral vascular disease, and ischemic heart disease. There is substantial scientific evidence on the efficacy of spinal cord stimulation for treatment of low back and lower extremity pain of neuropathic nature. Clinical studies revealed a success rate of from 50% to 70% with spinal cord stimulation, with decreased pain intensity scores, functional improvement and decreased medication usage. This review discusses multiple aspects of spinal cord stimulation, including pathophysiology and mechanism of action, rationale, indications, technique, clinical effectiveness, and controversial aspects.
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PMID:Spinal cord stimulation. 1690 66

The development of radiculopathy in patients with lumbar canal stenosis is thought to be closely related to intraradicular edema resulting from compression. However, there is little agreement as to question which is more essential for intermittent claudication: ischemia or congestion. The aim of the present experimental investigation was to examine the effect of ischemia and congestion on the nerve root using dogs. The aorta was clamped as an ischemia model of the nerve root and the inferior vena cava was clamped as a congestion model at the sixth costal level for 30 min using forceps transpleurally. Measurements of blood flow, partial oxygen pressure, and conduction velocity in the nerve root were repeated over a period of 1 h after release of clamping. Finally, we examined the status of intraradicular blood-nerve barrier under fluorescence and transmission electron microscope. Immediately after clamping of the inferior vena cava, the central venous pressure increased by about four times and marked extravasation of protein tracers was induced in the lumbar nerve root. Blood flow, partial oxygen pressure, and conduction velocity of the nerve root were more severely affected by aorta clamp, but this ischemia model did not show any intraradicular edema. The blood-nerve barrier in the nerve root was more easily broken by venous congestion than by arterial ishemia. In conclusion, venous congestion may be an essential factor precipitating circulatory disturbance in compressed nerve roots and inducing neurogenic intermittent claudication.
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PMID:Effects of arterial ischemia and venous congestion on the lumbar nerve root in dogs. 1853 56

It is generally believed that radiculopathy associated with the degenerative conditions of the spine may result from both mechanical compression and circulatory disturbance. However, the basic pathophysiology of circulatory disturbance induced by ischemia and congestion is not fully understood. This study investigated the effect of ischemia and congestion on the dorsal root ganglion (DRG) using an in vivo model. The sixth and seventh lumbar laminae were removed and the seventh lumbar DRG was exposed using adult dogs. The aorta was clamped as an ischemic model in the DRG, and the inferior vena cava was clamped as a congestion model at the sixth costal level for 30 min using forceps transpleurally. Measurements of blood flow, partial oxygen pressure, and action potentials in the DRG were recorded over a period of 1 h after clamp release. Finally, we examined the status of intraganglionic blood permeability under a fluorescence microscope following injection of Evans blue albumin into the cephalic vein to determine the type of circulatory disturbance occurring in the DRG. Immediately after inferior vena cava clamping, the central venous pressure increased approximately four times and marked extravasation of protein tracers was induced in the lumbar DRG. Blood flow, partial oxygen pressures, and action potentials within the DRG were more severely affected by the aorta clamping; however, this ischemic model did not reveal any permeability changes in the DRG. The permeability change in the DRG was more easily increased via venous congestion than by arterial ischemia. The intraganglionic venous flow was stopped with compression at much lower pressures than that needed to impact arterial flow. From a clinical perspective, intraganglionic edema formation, rather than arterial ischemia, may be an earlier phenomenon inducing DRG dysfunction.
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PMID:Changes in blood flow, oxygen tension, action potentials, and vascular permeability induced by arterial ischemia or venous congestion on the lumbar dorsal root ganglia in dogs. 1933 18


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