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

The clinical course of six patients with isolated trochlear nerve palsy as the only ocular motor manifestation of herpes zoster ophthalmicus has been analyzed. Spontaneous recovery occurred in only three. Review of the literature does not clarify the mechanism of such palsies, which potentially may result from the following conditions: local orbital muscle inflammation and ischemia; contiguous intracavernous spread of inflammation from the trigeminal nerve; and a concurrent but independent motor neuropathy or ganglionitis.
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PMID:Isolated trochlear nerve palsies in herpes zoster ophthalmicus. 30 78

Eighteen patients with idiopathic optic neuropathy lacked symptoms and signs of cardiovascular and cerebrovascular disease, especially when compared to three groups of patients with sudden visual loss caused by retinal infarction, transient ischemia, and cerebral infarction. Many patients in the latter groups had hypertension, carotid bruits, heart disease, transient ischemic attack, and stroke. But among the patients with ischemic optic neuropathy, hypertension was the only evidence of cardiovascular disease, affecting 44% of the patients. We argue that, in many cases, ischemic optic neuropathy represents a direct and early complication of hypertension arterial disease affecting small arterioles supplying the anterior part of the optic nerve. The pathologic process may thus be similar or identical to lacunar infarction of the brain.
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PMID:Ischemic optic neuropathy as a possible early complication of vascular hypertension. 51 8

The pathogenesis of Bell's palsy is presented as retrograde epineurial compression edema with ischemia of the facial nerve. Although the etiology is unknown, an attractive theory is vasospasm, from any cause, along any facial nerve branch, with the chorda tympani, perhaps, the usual primary involvement. Retrograde vascular distension and edema, within the epineurium of the bony facial canal, compresses the nerve from outside its perineurial sheath. The compression force may be mild or severe, resulting in varying degrees of reversible or irreversible ischemic degeneration of myelin sheaths and axons, with varying degrees of cellular reaction to myelin breakdown. The edema may be resorbed, leaving reversible or irreversible nerve damage, or may stimulate collagen formation within the epineurium, with persisting fibrous compression (entrapment) neuropathy of the facial nerve. This concept is consistent with the varying results of Bell's palsy, and depends on the severity and duration of edema, and whether fibrosis occurs within the epineurium of the facial canal. Epineurial fibrosis also results in disturbance of metabolic exchange through the epineurial-perineurial-endoneurial tissues, and may ultimately result in obliteration of vascular drainage. Two temporal bone cases of Bell's palsy, one occurring ten years before death, with residual paralysis, and one two years before death, with clinical recovery, are added to the previously described four cases in the literature, three of early Bell's palsy, and one of remote palsy with almost complete recovery.
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PMID:Pathogenesis of Bell's palsy. Retrograde epineurial edema and postedematous fibrous compression neuropathy of the facial nerve. 88 28

We report the clinical and pathologic features of a patient with peripheral neuropathy that was the first clinical expression of cholesterol emboli syndrome (CES). Biopsy of skeletal muscle and peripheral nerve revealed cholesterol clefts in lumens of small arteries, necrotizing arteritis, and severe degeneration of peripheral and intramuscular nerves. At autopsy, the peripheral nervous system was extensively affected by similar changes. We conclude that (1) peripheral neuropathy may be the initial manifestation of CES. Presumably, deposition of cholesterol leads to arteritis. (2) The underlying pathology of CES neuropathy is chronic axonal degeneration, possibly due to chronic ischemia of epineurial arteries. (3) Muscle biopsy is important in the antemortem diagnosis of CES. Nerve biopsy may show involvement of epineurial vessels. (4) CES may resemble polyarteritis nodosa clinically and pathologically. (5) CES may be under-recognized and should be included in the differential diagnosis of any neuropathy of uncertain cause, particularly when there is a history of vascular catheterization, or severe aortic atherosclerosis.
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PMID:Cholesterol emboli neuropathy. 131 May 30

Postoperative femoral neuropathy is more common than it is generally appreciated. It can occur by a number of different mechanisms after a wide variety of operations as a result of either direct or indirect injury. Most instances occur after abdominopelvic operations and are associated with the placement of self-retaining retractors. A large body of evidence suggests that, in these patients, nerve compression by the lateral blades of the retractor is the cause. There is, however, evidence that the intrapelvic portion of the nerve is particularly susceptible to ischemia. Usually, there is a mild sensorimotor disturbance and the diagnosis is easily made by accurate physical examination during the early postoperative period. A diminished or absent knee jerk is the most reliable clinical sign. Recovery is the rule; it occurs usually from a few weeks to months. During this time, physiotherapy may be beneficial. Occasionally the lesion may be severe or prolonged, or both. In these instances, EMG studies are justified, not only to allay the fears of patients and physicians, but to evaluate the progress of the lesion over time. With the exception of certain unusual instances, this potentially debilitating postoperative complication can be avoided by careful placement of self-retaining retractors.
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PMID:Postoperative femoral neuropathy. 131 69

A morphological study of a series of 100 human peroneal nerves proceeding from autopsies and amputations of patients hospitalized for different diseases was performed. A relation between the morphologic findings and the risk factors of neuropathy to which the patients may have been exposed is established. Following the analysis of their results the authors found that peripheral neuropathy is more frequent than suspected in clinical practice. The peripheral nerve is relatively resistant to regional ischemia. The risk factors considered in the casuist included diabetes as that which most influences in determining morphological alterations compatible with neuropathy.
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PMID:[Peripheral neuropathy and correlation with risk factors in material from autopsies and amputations]. 132 Sep 5

The lower extremity complications of 100 consecutive patients who required the placement of an intra-aortic balloon pump (IABP) during a 3-year period were studied. Indications for the IABP included hypotension during cardiac catheterization (33%) or coronary angioplasty (13%), hemodynamic instability after open heart surgery (35%), unstable angina (5%), and cardiac arrest (14%). The incidence of IABP morbidity was 29%. Complications included ischemia (25%), bleeding (2%), lymph fistula (1%), and femoral neuropathy (1%). Twenty patients required 1 or more surgical interventions for lower extremity vascular complications. The majority of patients who underwent operation (70%) had significant pre-existing arterial occlusive disease. Local femoral artery reconstruction or repair was performed in 18 patients. Two patients had adjunctive bypasses. Continued IABP support was required in four patients after treatment of complications. One patient (1%) had an above-knee amputation. Limb ischemia was treated nonoperatively by removal of the IABP in five patients. Color-flow duplex scans were useful in distinguishing hematomas from pseudoaneurysms as well as for assessing femoral artery flow. We conclude that: (1) limb ischemia remains the primary complication of the IABP; (2) pre-insertion documentation of the severity of existing peripheral arterial disease by noninvasive studies may aid in the management of subsequent acute limb ischemia; (3) femoral artery thrombectomy or endarterectomy is usually sufficient for revascularization; and (4) noninvasive color flow studies are an important diagnostic tool in the nonoperative management of limb complications.
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PMID:Vascular complications of the intra-aortic balloon pump. 144 80

There are several anecdotal reports of improvement in diabetic sensory neuropathy following a course of pentoxifylline therapy. Pentoxifylline theoretically could improve skin blood flow, thus reducing ischemia at axonal endings. The authors used laser Doppler techniques to measure skin blood flow and measured sine wave current perception thresholds (CPTs) in pentoxifylline-treated diabetic patients with sensory neuropathy. Twenty-four patients completed a six-month course of treatment. These patients had a predominantly "stocking" neuropathy; all the major abnormalities on clinical, laser Doppler, and current perception testing were found on the lower extremity. Seventeen of the 24 patients reported symptomatic improvement. A careful, graded neurologic examination confirmed that improvement, with a decrease in symptom score on the lower extremity (SSDW) from a baseline of 5.0 +/- 0.7 to 3.5 +/- 0.7 (p < 0.01) and of physical score (PSDW) from baseline 22.0 +/- 2.0 to 16.0 +/- 1.9 (p < 0.01) after six months. On the lower extremity, there was an increase in laser Doppler measured flow score (FS) both at 35 degrees and at 44 degrees C. FSDW (35 degrees) increased from 10 +/- 2 to 14 +/- 3 at six months (p < 0.05). FSDW (44 degrees) increased from 58 +/- 5 to 77 +/- 7 at six months (p < 0.01). There was an improvement in sine wave current perception measured by current perception threshold score (TS). TSDW dropped from 150 +/- 32 to 84 +/- 28 at six months (p < 0.03). In patients with diabetic sensory neuropathy, pentoxifylline appears to improve skin blood flow. Current perception thresholds improve in tandem, corroborating improvement in clinical neurologic findings.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Skin blood flow and current perception in pentoxifylline-treated diabetic neuropathy. 147 72

Transperineurial and epineurial vessels are innervated by plexuses of unmyelinated axons. Human sural nerve biopsies were examined ultrastructurally and immunocytochemically with an antibody which recognizes a neuronal and neuroendocrine protein, PGP 9.5, to characterize perivascular axons of these plexuses. Diabetics exhibited a greater degree of abnormal innervation of the vasa nervorum than nondiabetics with and without neuropathy. Abnormal innervation included: a reduction in the percentage of vessels exhibiting perivascular axons and a concomitant increase in the percentage of vessels having denervated Schwann cell units, particularly around vessels confined to perineurial compartments, and remaining axons in nerves from diabetics exhibited fewer varicosities. Denervated arterioles of diabetics also displayed structural changes indicating injury. The arteriolar structural defects and loss of neurogenic control of neural blood flow may lead to or aggravate endoneurial ischemia or hypoxia. The patchy, focal endoneurial fiber loss that is prominent in proximal nerves and associated with the distal myelinated fiber loss of some diabetic patients may be due in part to perivascular denervation of the vasa nervorum.
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PMID:Innervation of the vasa nervorum: changes in human diabetics. 148 91

Gluteal compartment syndromes are rare. The pathophysiology and the principles of diagnosis and treatment, however, are the same as those for leg and forearm compartment syndromes. Trauma may not be a salient feature of gluteal compartment syndromes where substance abuse and a prolonged period of unconsciousness, recumbency, or both are more typical. Because of this and the large muscle mass involved, systemic manifestations of a crush syndrome are usually present. Altered mental status and metabolic abnormalities may distract from the primary problem, resulting in delayed diagnosis and treatment. The proximity of the sciatic nerve can result in compression induced neuropathy. Measurement of an elevated compartment pressure confirms the diagnosis. In three patients, aged 37, 31, and 37 years, prompt fasciotomy relieved muscle ischemia, preserved neurologic function, and produced a satisfactory functional result.
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PMID:Gluteal compartment and crush syndromes. Report of three cases and review of the literature. 155 37


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