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

Many arguments lead us to think that a possible etiologic factor in idiopathic Bell's palsy is the ischemia of the facial nerve and that angiography could help in diagnosis: (1) the rapid progress of the paralysis; (2) the correlation between Bell's palsy occurring after embolization of the internal maxillary artery, the middle meningeal artery, the occipital or posterior auricular artery, and their participation in the blood supply of the facial nerve; (3) the already known ischemic third nerve paralysis reported in diabetes and extending further to the facial nerve. Even if it is technically impossible to study Bell's palsy by angiography, it is interesting to understand and consider some complications of embolization and perhaps to envisage a new kind of treatment.
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PMID:[Angiographic study of facial paralyses (author's transl)]. 74 Feb 5

This report concerns itself with additional experimental evidence to support the immunologic concept for the pathogenesis of Bell's palsy, using the mast cell as an index of immunological activity. In a previous experimental study, we postulated that degranulation of mast cells activated by complement or specific allergens with release of histamine and other substances may be the mechanism leading to nerve edema, ischemia, and paralysis. In this study we observed a loss of granulated mast cells in the more severely damaged facial nerves of immunized dogs after the intrafallopian canal injection of various substances, in contrast with the relative abundance of these cells in nerves that showed little or no evidence of injury. In addition, we demonstrated that cromolyn sodium, a mast cell degranulation inhibitor, when infused intravenously at the time of the intrafacial canal injection of horse serum, very effectively lessened the degree of experimental paralysis and histologic nerve injury.
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PMID:Immunological concept for Bell's palsy: further experimental study. 86 31

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

Numerous causes of peripheral facial nerve paralyses have been described; however, none has satisfactorily explained the genesis of the most common type of paralysis, Bell's palsy. Two patients undergoing an experimental embolization of vascular intracranial tumors suffered a total peripheral facial nerve paralysis when occlusion of the middle meningeal artery had been accomplished. It is speculated that this paralysis resulted from ischemia of the horizontal portion of the facial nerve, an observation that has not previously been described and that might be applicable as well to the etiology of Bell's palsy.
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PMID:Ischemic paralysis of the facial nerve: a possible etiologic factor in Bell's palsy. 125 8

Based on the pathophysiology of Bell's palsy that edema as well as ischemia lead to both compression and hypoxia, Stennert employed high doses of cortisone and dextran and reported a high recovery rate. In the past 5 years, we have been treating patients with Bell's palsy and Hunt syndrome with a high dose of steroids or low-molecular dextran (SD therapy). SD therapy was administrated in 71 cases of Hunt syndrome, and the results were compared with those of a group of 36 patients who had been treated with orally administrated low-dose steroids. All patients with incomplete palsies recovered completely, regardless of the mode of treatment. In cases of complete palsy, 62% of patients recovered completely when treated with SD therapy. In contrast, 29% of the patients treated with orally administrated steroids recovered completely. These results indicate that for patients with complete palsy SD therapy is more effective than oral steroid therapy, while patients with incomplete palsy recover completely with oral steroids. On the basis of this study, oral steroids are best used in cases of incomplete palsy unless complete palsy develops. In these latter cases, we now believe that SD therapy should be started immediately.
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PMID:[Conservative treatment of Hunt syndrome]. 154 12

There is no consensus on the cause of Bell's palsy, just as there is no proven medical therapy. Disregarding the numerous theoretic causes, preponderant anatomic, electrophysiologic, radiologic, clinical, and pathologic evidence supports entrapment at the medical foramen of the fallopian canal as a final common pathway resulting in facial nerve ischemia and degeneration. Middle cranial fossa decompression of the meatal foramen may benefit those patients most severely affected with Bell's palsy.
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PMID:Surgical decompression of idiopathic facial palsy. 176 83

The etiology of Bell's palsy has not been as yet completely elucidated and the treatment is empirical and controversial. The two most common forms of treatment are steroid therapy and surgery. On the basis of the pathophysiology of Bell's palsy that edema as well as primary or secondary ischemia lead to both compression and hypoxia, Stennert employed high doses of cortisone for a strong antiphlogistic and anti-edematous effect, and dextran in combination with pentoxifylline to increase peripheral nerve perfusion and reported high recovery rate. Since the past 3 years, we have been treating patients with Bell's palsy with a high dose of steroid plus low-molecular dextran (SD therapy). Hydrocortisone was added directly to 500 ml of dextran solution with ATP and vitamins, starting with 500 mg and finally down with 100mg during 7 days. Before we had adopted this regimen, the patients with Bell's palsy were treated with orally-administrated steroid. A half dose of steroid was administrated in the latter regimen. SD therapy was employed in 120 cases of Bell's palsy, and its results were compared with those of 82 cases with orally-administrated steroid. In a total of 67 cases with incomplete palsy, all cases obtained complete recovery within one month after the onset regardless of the mode of treatment. Each patients with complete palsy was examined with a nerve excitability test (NET) at the first visit and one week later. According to the response of NET, the patients with complete palsy were divided into the following three groups; "good", "poor" and "absent". In "good" group, all cases with SD therapy had complete recovery, while the recovery rate of 31 cases with orally-administrated steroid therapy was 90%. This difference was statistically significant (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Conservative treatment of Bell's palsy--high dose steroid infusion with low-molecular dextran]. 248 43

The degree of participation and regional specificity of virus infection in relation to atraumatic acute peripheral facial palsy was studied, placing particular emphasis on change in the CF titre of varicella zoster virus (VZV), herpes simplex virus (HSV) and adenovirus (adeno). The subjects of the study were 91 patients with Hunt's syndrome and 396 patients with Bell's palsy treated at 17 institutions all over Japan in the period between April 1985 and November 1986. Among the cases of Hunt's syndrome, the positive conversion rate of CF antibody titre of VZV was 81%. In Bell's palsy cases, virus participation was detectable in 8% with VZV, 4% with HSV and 4% with adeno. With regard to the age distribution, Bell's palsy cases with possible virus involvement tended to be observed in younger patients than those without that possibility. As to regional specificity, the incidence of Bell's palsy with possible virus involvement tended to be higher in densely populated areas. With regard to the main cause of acute peripheral facial palsy, virus infection has been implicated, as well as insufficient blood circulation (ischemia). Even in cases of acute peripheral facial palsy, in which herpes zoster oticus is not observed, the participation of varicella zoster virus (VZV) as a cause of paralysis has been pointed out in some cases (zoster sine herpete). Furthermore, it is known that the serum antibody titres of various viruses such as herpes simplex virus (HSV) change significantly in some cases of Bell's palsy (2, 5-13).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Viral infections in acute peripheral facial paralysis. Nationwide analysis centering on CF. 284 57

At the present time there is no final explanation for the etiology of Bell's palsy. The theory of pathophysiology involving a combined primary and/or secondary ischemia is now well-accepted. As such, it is supposed that there is a dysfunction of the blood vessels which supply the nerve. This is followed by a hyperpermeability and transudation which lead to edema of the nerve and compression of the blood supply. The vicious circle starts and the final result is facial paralysis. The blood supply of the facial nerve has been described previously in the literature, although there have been no experimental investigations on in vivo perfusion of the nerve. In the present study we evaluated the percentage of those vessels perfused among the total blood vessels found in facial nerves of Wistar rats. Animals were examined after i.v.-injections of Evans blue dye, with perfused vessels demonstrable under a fluorescence microscope. Forty-eight hours later, the same tissue section was stained by indirect immunofluorescence and the primary antibody used was directed against myosin of non-muscle sources. This antibody cross-reacted with myosin of vascular endothelial cells and thus allowed identification of any existing blood vessels. More than 90% of the immunostained vessels were labeled with the dye, showing that almost all vessels were perfused.
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PMID:[Blood supply to the facial nerve]. 802 Nov 58

Ischemic lesions are presumed to be part of many facial nerve pathologies, such as Bell's palsy. The response of facial nerve to hypoxia has not been evaluated previously in an in vitro model. In the present study, the effects of transient anaerobic stress on functional parameters and their recovery were assessed. Extratemporal rat facial nerves were desheathed and incubated in an experimental chamber using solutions containing either low (5 mM) or high (25 mM) D-glucose. In some of the experiments, 40 microM phenytoin or lidocaine was added to observe the effects of membrane stabilizing drugs. Peak height of compound nerve action potential (CNAP), extracellular direct current (DC) potential and latency were measured simultaneously during and after a 40-min period of hypoxia, induced by bubbling the solutions with N2 or application of 3 mM cyanide. This resulted in a rapid decrease of CNAP and a depolarization of the DC potential with a fast and complete post hypoxic recovery. Elevated glucose concentrations led to a slower decline in CNAP and a smaller rise of membrane potential depolarization. This was accompanied by a slower change of latency. However, post-anaerobic recovery was always diminished in the high glucose solutions. In experiments with phenytoin or lidocaine longer impulse conduction during hypoxia was observed. These findings indicate that the availability of energy-rich components underlies the complex array of physiological derangements seen in ischemia. Membrane-stabilizing drugs show an effect on signal conduction during hypoxia and need further exploration.
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PMID:Susceptibility of isolated rat facial nerve to anaerobic stress. 906 31


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