CSF middle ear effusion/otorrhea can develop in adults without a prior history of meningitis or head trauma or any apparent proximate cause. Although presenting symptoms can be subtle, early suspicion and confirmatory imaging aid in establishing the diagnosis. Because surgical repair by way of a mastoid approach alone can be inadequate if there are multiple tegmen defects, a middle fossa approach alone, or in combination with a transmastoid approach, should be considered in most cases.

Prostaglandin E2 (PGE2) has been shown to dilate and constrict the systemic vascular beds, including cerebral vessels. The exact mechanism of PGE2-induced cerebral vasoconstriction, however, is less clarified. The authors' preliminary studies showed that PGE2 exclusively constricted the adult porcine basilar arteries. The present study, therefore, was designed to examine the receptor mechanisms involved in PGE2-induced constriction of large cerebral arteries in the adult pig. Results from an in vitro tissue-bath study indicated that PGE2 and its agonists 17-phenyl trinor PGE2 (17-PGE2), sulprostone (EP1/EP3 receptor agonists), and 11-deoxy-16,16-dimethyl PGE2 (11-PGE2, an EP2/EP3-receptor agonist) induced exclusive constriction, which was not affected by endothelium denudation or cold-storage denervation of perivascular nerves. The constriction induced by PGE2, 17-PGE2, and sulprostone, but not by potassium chloride, was blocked by SC-19220 (a selective EP1-receptor antagonist), AH-6809 (an EP1/EP2-receptor antagonist), and U-73122 and neomycin (phospholipase C inhibitors). AH-6809, however, did not affect 11-PGE2-induced contraction. These results suggest that the contraction was not mediated by the EP2-receptor, but was mediated by EP1- and EP3-receptors. Furthermore, EP1-receptor immunoreactivities were found across the entire medial smooth muscle layers, whereas EP3-receptor immunoreactivities were limited to the outer smooth muscle layer toward the adventitia. Western blotting also showed the presence of EP1- and EP3-receptor proteins in cultured primary cerebral vascular smooth muscle cells. In conclusion, PGE2 exclusively constricts the adult porcine large cerebral arteries. This constriction is mediated by phosphatidyl-inositol pathway via activation of EP1- and EP3-receptors located on the smooth muscle cells. These two receptor subtypes may play important roles in physiologic and pathophysiologic control of cerebral vascular tone.

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A case of acute posttraumatic myelopathy resulting from hemorrhage into synovial cysts bilaterally at the C-6, C-7 facet joints is presented. The pathogenesis of synovial cysts remains unclear, although reports in the literature have implicated trauma leading to cyst enlargement. Hemorrhage into the cavity of the synovial cysts resulted in epidural compression of the spinal cord in this patient. Because spinal synovial cysts cannot be unequivocally diagnosed preoperatively, other more common conditions must be considered in the differential diagnosis. Radiographic analysis including plain films, computed axial tomography, and metrizamide myelography are of value in establishing a neurological diagnosis. Surgical decompression and excision of the lesion may result in significant neurological improvement.

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Background and Purpose-Prostaglandin E 2 (PGE 2 ) modulates autonomic transmission in the peripheral circulation. We investigated the role of endogenous PGE 2 and its presynaptic EP 1 receptor subtype in modulating the autonomic neurotransmission in cerebral vasculature. Methods-The standard in vitro tissue-bath technique was used for measuring changes in isolated porcine basilar arterial tone. Calcium imaging and nitric oxide estimation along with immunohistochemical analysis for cyclo-oxygenase-1, cyclo-oxygenase-2, EP 1 receptor, PGE synthase, and neuronal nitric oxide synthase were done in cultured sphenopalatine ganglia and basilar artery. Results-Selective EP 1 receptor antagonists (SC-19220 and SC-51322) inhibited relaxation of endothelium-denuded basilar arterial rings elicited by transmural nerve stimulation (2 and 8 Hz) without affecting that induced by nicotine or sodium nitroprusside (a nitric oxide donor). The SC-19220 inhibition of transmural nerve stimulation-elicited relaxation was blocked by cyclo-oxygenase inhibitors (salicylic acid and naproxen) but was not affected by guanethidine (a sympathetic neuronal blocker) or atropine. Perivascular cyclo-oxygenase-1-and cyclo-oxygenase-2-immunoreactive fibers were observed in basilar arteries. PGE synthase and EP 1 receptor immunoreactivities were coincident with neuronal nitric oxide synthase immunoreactivities in perivascular nerves of the basilar arteries and the sphenopalatine ganglia.

Summary:Prostaglandin E 2 (PGE 2 ) has been shown to dilate and constrict the systemic vascular beds, including cerebral vessels. The exact mechanism of PGE 2 -induced cerebral vasoconstriction, however, is less clarified. The authors' preliminary studies showed that PGE 2 exclusively constricted the adult porcine basilar arteries. The present study, therefore, was designed to examine the receptor mechanisms involved in PGE 2 -induced constriction of large cerebral arteries in the adult pig. Results from an in vitro tissue-bath study indicated that PGE 2 and its agonists 17-phenyl trinor PGE 2 (17-PGE 2 ), sulprostone (EP 1 /EP 3 receptor agonists), and 11-deoxy-16,16-dimethyl PGE 2 (11-PGE 2 , an EP 2 /EP 3 -receptor agonist) induced exclusive constriction, which was not affected by endothelium denudation or cold-storage denervation of perivascular nerves. The constriction induced by PGE 2 , 17-PGE 2 , and sulprostone, but not by potassium chloride, was blocked by SC-19220 (a selective EP 1 -receptor antagonist), AH-6809 (an EP 1 /EP 2 -receptor antagonist), and U-73122 and neomycin (phospholipase C inhibitors). AH-6809, however, did not affect 11-PGE 2 -induced contraction. These results suggest that the contraction was not mediated by the EP 2 -receptor, but was mediated by EP 1 -and EP 3 -receptors. Furthermore, EP 1 -receptor immunoreactivities were found across the entire medial smooth muscle layers, whereas EP 3 -receptor immunoreactivities were limited to the outer smooth muscle layer toward the adventitia. Western blotting also showed the presence of EP 1 -and EP 3 -receptor proteins in cultured primary cerebral vascular smooth muscle cells. In conclusion, PGE 2 exclusively constricts the adult porcine large cerebral arteries. This constriction is mediated by phosphatidyl-inositol pathway via activation of EP 1 -and EP 3 -receptors located on the smooth muscle cells. These two receptor subtypes may play important roles in physiologic and pathophysiologic control of cerebral vascular tone.

No abstract