Spontaneous resolution of cerebrospinal fluid otorrhoea in a patient with a Hyrtl's fissure.

OBJECTIVE: This paper reports a rare case of cerebrospinal fluid leak due to a Hyrtl's fissure and discusses the non-operative management of the case. Background and case report: Cerebrospinal fluid otorrhoea is a rare phenomenon arising from an abnormal communicating tract between the subarachnoid space and middle ear. Affected patients are at a higher risk of developing meningitis and other neuro-otological complications. There are four common congenital causes of cerebrospinal fluid otorrhoea in the region of a normal labyrinth. This paper describes a case of cerebrospinal fluid in the middle ear resulting from a Hyrtl's fissure, which resolved spontaneously. CONCLUSION: A literature search indicated this to be the first case with such a resolution without the need for any intervention.

Case report: the pulmonary lesions of chickenpox pneumonia--revisited.

Infection with the varicella zoster virus can include pulmonary complications. These may cause such minor symptomatology as to go unrecognized and unimaged. We describe a case of active chickenpox pneumonia that mimicked pulmonary metastases and was detected incidentally by means of computed tomography in a man with a past history of testicular teratoma.

Effects of blockade of extraneuronal uptake on responses to isoprenaline in perfused rat heart.

1. Isolated rat hearts accumulated 102 pmol/g wet wt/min of isoprenaline when perfused for 5 min with 0-6 muM (+/-)-3H-isoprenaline. 2. The 3-methoxy derivative of isoprenaline ('methoxy isoprenaline') (10 muM) significantly inhibited this uptake by 57%, metanephrine (10 muM) by 29% and normetanephrine (10 muM) by 21%. 3. (+/-)-Isoprenaline (0-6 muM) infused into isolated perfused rat hearts for 5 min activated glycogen phosphorylase 2-4-fold. Normetanephrine (10 muM) or metanephrine (10 muM included in the perfusate significantly potentiated this activation, but 3-0-methyl isoprenaline (10 muM significantly reduced it. However, 3-0-methyl isoprenaline potentiated the ability of 4-8 muM isoprenaline to stimulate phosphorylase. 4. Neither metanephrine (10 muM) nor normetanephrine (10 muM) altered peak inotropic responses to injections of (+/-)-isoprenaline into the solution perfusing isolated rat hearts. 3-0-methyl isoprenaline (10 muM) shifted the isoprenaline dose-response curve to the right, but did not affect the inotropic responses to CaCl2, confirming that 3-0-methyl isoprenaline possess beta-adrenoceptor antagonist activity. 5. Inotropic responses to isoprenaline were significantly prolonged by both 3-0-methyl isoprenaline and normetanephrine (10 muM). 6. These results indicate that blockade of extraneuronal accumulation of catecholamines causes potentiation of both metabolic and mechanical beta-adrenoceptor-mediated responses of the heart to isoprenaline. It is suggested that Uptake2 and the cardiac beta-adrenoceptor are separate entities, and that the beta-adrenoceptor is localized in the sarcolemma. The physiological function of Uptake2 may be to help clear the sympathetic synaptic gap of liberated neurotransmitter.