Tone burst electrocochleography disproves a diagnosis of Meniere's disease treated aggressively.

Reliable confirmation of the presence or absence of endolymphatic hydrops is essential to avoid confusing vestibular migraine with Meniere's disease. MRI inner ear imaging is a promising new method to confirm hydrops, avoiding both unnecessary invasive or destructive inner ear treatments, but it is not universally available. Tone burst electrocochleography is an older simple, quick, safe, and sensitive test that is potentially available, with existing (or minorly upgraded) equipment at most tertiary medical centers. In Meniere's disease hydrops remains after intratympanic treatments. A case is presented of a 45 year-old man with a long history of recurrent vertigo attacks who, due to an erroneous diagnosis of Meniere's disease, was given five intratympanic treatments with no effect. He was subsequently found by tone burst electrocochleography to have no hydrops and was differentially diagnosed with probable vestibular migraine. Response to treatment confirms this diagnosis. This patient's electrocochleographic findings are compared with two other patients with definite Meniere's disease, one of whom had demonstrable hydrops despite intratympanic gentamycin treatments.

Magnetic resonance imaging for Ménière's disease: correlation with tone burst electrocochleography.

The newly developed use of magnetic resonance imaging of the human inner ear, on a 3 Tesla scanner with intratympanically administered gadolinium, can now reliably distinguish perilymph from endolymph and visually confirm the presence or absence of endolymphatic hydrops. Transtympanic tone burst electrocochleography is an established, and under-utilised evoked response electrophysiological test for hydrops, but it relies on a symptom score to indicate the likelihood of hydrops being present. The current diagnostic criteria for Ménière's disease make no allowance for any in vivo test, making diagnostic errors likely. In this small pilot study of three patients undergoing tone burst electrocochleography, subsequent magnetic resonance imaging confirmed or excluded the hydrops that the electrocochleography predicted. Magnetic resonance imaging of the inner ear is a safe technique that can be performed in conjunction with imaging of the VIIIth cranial nerves. As this report comprised only three patients in a pilot study, rigorous clinical studies are required to define the possible role of magnetic resonance imaging in the diagnosis of Ménière's disease.

Audiological screening of neonatal intensive care unit graduates at high risk of sensorineural hearing loss.

AIM: To audit the identification and screening of graduates from a neonatal intensive care unit with risk factors for sensorineural hearing loss. METHODS: Hospital medical records of newborn infants discharged from the neonatal intensive care unit, Christchurch Womens Hospital, between 1 July 1994 and 30 June 1995 (n=564), were examined to identify those at risk for sensorineural hearing loss according to the American Speech-Language Hearing Association risk criteria 1991. Auditory brainstem response test results were obtained from the Christchurch Hospital Audiology Department. Outcome measures were: presence of hearing loss risk factors, numbers tested with auditory brainstem response, age at test and presence and degree of hearing impairment. RESULTS: Of 5,215 live births in Christchurch, 564 infants were discharged through the neonatal intensive care unit. Of these, 86 had risk factors for sensorineural hearing loss. There were 72 (84%) infants tested at audiology, with fifteen (17%) having abnormal test results. There were fourteen with risk factors who did not get audiology screening. CONCLUSION: A high proportion (84%) of high risk newborn infants had auditory brainstem response testing. Further improvement would require strict implementation of standard procedures. Auditory brainstem response screening is part of a wider population surveillance approach to identify hearing loss as early as possible.

Characteristics of reactive hyperemia in the cerebral circulation.

Reactive hyperemia has been characterized in many vascular beds, but little is known about quantitative characteristics of reactive hyperemia in the cerebral circulation. We measured velocity of blood flow and pial artery diameter to characterize the time course of reactive hyperemia and used microspheres to study regional blood flow in the brain. Cerebral ischemia was produced by raising intracranial pressure or by arterial occlusion with a cuff around the neck. Five seconds of ischemia produced virtually maximal peak reactive hyperemia, and 30 s of ischemia produced maximal peak reactive hyperemia. During reactive hyperemia after 30 s of cerebral ischemia, there was a three- to fourfold increase in cerebral blood flow. The magnitude of reactive hyperemia was greater in gray matter than in white matter. Minimal resistance during reactive hyperemia, after ischemia produced by arterial occlusion, is similar to minimal resistance during seizures or hypercapnia, which suggests that reactive hyperemia produces maximal vasodilatation. Oxygen saturation of cerebral venous blood increased almost twofold during reactive hyperemia, which indicates that factors in addition to venous (and presumably tissue) oxygen are important determinants of reactive hyperemia. In summary, 1) we have characterized the time course of reactive hyperemia in the cerebral circulation; 2) reactive hyperemia after arterial occlusion produces maximal cerebral vasodilatation; and 3) there is marked heterogeneity of the response, with much larger increases in flow in cortical gray matter than white matter.

Effects of nimodipine on cerebral blood flow.

The purposes of this study were to compare the effects of the calcium entry blocker nimodipine (Bay e 9736) on blood flow with brain and other organs and to examine effects on regional cerebral blood flow. Cerebral blood flow was measured by the microsphere method. Determinations were made during intracarotid and i.v. nimodipine infusions in anesthetized and unanesthetized rabbits. In unanesthetized rabbits, i.v. infusion of 0.1 micrograms/kg x min nimodipine produced a 2-fold increase in cerebral blood flow and a 1.5-fold increase in myocardial flow without an increase in blood flow to other organs and with a small decrease in arterial pressure. A dose of 1.0 micrograms/kg x min produced further increases in flow to brain, myocardium and muscle despite reducing arterial pressure. Blood flow increased significantly in both cerebral gray and white matter and increased similarly in cerebrum, cerebellum and brainstem. In anesthetized rabbits, intracarotid infusion of nimodipine produced dose-dependent increases in cerebral blood flow; i.v. nimodipine produced an increase in cerebral blood flow with no change in cerebral O2 consumption. Thus, at low doses that have little effect on aortic pressure, nimodipine causes a selective increase in cerebral and myocardial blood flow. Nimodipine increases blood flow in all regions of the brain. The increase in blood flow is the result of a direct vasodilator effect and is not secondary to increased cerebral metabolism.