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 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pulsatile tinnitus can be annoying for a patient and can also be the only clue to a potentially devastating and life-threatening disease. In order to understand its clinical spectrum and management better we analysed the files of 84 patients seen at our institution over a 10-year period. Noninvasive techniques (ultrasound, computed tomography, magnetic resonance imaging) and angiography were employed as investigations tailored to the individual patient. A vascular disorder [i.e. arteriovenous fistula, dissection of the internal carotid artery (ICA), fibromuscular dysplasia, aneurysm of the ICA and sinus thrombosis] was found in 36 patients (42%), most commonly a dural arteriovenous fistula or a carotid-cavernous sinus fistula. In 26 patients with a vascular abnormality, pulsatile tinnitus was the presenting symptom. In 12 patients (14%), nonvascular disorders such as glomus tumour or intracranial hypertension with a variety of causes explained the tinnitus. We conclude that patients with pulsatile tinnitus should be investigated with noninvasive techniques. If these are negative or to clarify abnormal findings of noninvasive techniques selective angiography is needed for diagnosis and to guide treatment.
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PMID:Pulsatile tinnitus--a review of 84 patients. 955 42

This paper offers a review of cranial nerve rhizopathies caused by vascular compression of cranial nerves in the posterior cranial fossa. We present our results of microvascular decompression for trigeminal neuralgia, hemifacial spasm, and glossopharyngeal neuralgia caused by compression of the 5th, 7th and 9th cranial nerves, respectively. After a median observation time of 38 months, 20 of 25 patients with trigeminal neuralgia were completely free of pain, and one patient reported more than 50% pain relief. Four out of five patients treated for hemifacial spasms were completely free of spasms. Of two patients treated for glossopharyngeal neuralgia, one reported complete pain relief, whereas the other reported less than 50% pain relief. No serious complications occurred. The results of microvascular decompression reported in the literature reviewed, including results of the treatment of tinnitus and positional vertigo due to compression of the 8th cranial nerve, hypertension due to compression of the 10th cranial nerve and spastic torticollis due to compression of the 11th cranial nerve. It is concluded that the rationale behind microvascular decompression is supported by an extensive amount of data.
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PMID:[Vascular compression and cranial nerve diseases]. 984 12

Chronic headaches due to intracranial hypo- or hypertension (IHS codes 7.2 and 7.1) may be difficult to diagnose. In this article, we review their principal clinical characteristics, etiologies and therapies. Intracranial hypotension may be caused by CSF linkage, e.g. after lumbar puncture. It may also be "idiopathic" in which case a CSF leak, usually at the spinal level, may be difficult to demonstrate. Postural headache is the clinical hallmark of intracranial hypotension. The diagnosis is confirmed by leptomeningeal enhancement on MRI scans. The headache of benign intracranial hypertension may be aggravated by the supine position and accompanied by transient visual obscurations and tinnitus. Papillary edema supports the diagnosis but may be absent in some cases. Increased opening pressure of the CSF will confirm the diagnosis. Etiologies such as cerebral venous thrombosis, have to be excluded by adequate imaging methods. In both hypo- and hypertension syndromes, various therapeutic strategies have been proposed.
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PMID:[Benign intracranial hypo- and hypertension]. 1054 94

We present two cases of Bell's palsy, and another with tinnitus, all in association with pre-eclampsia in the third trimester of pregnancy. We also systematically reviewed the published literature on both Bell's palsy and tinnitus in pregnancy and the puerperium using Medline from January 1966 to October 1998, and searched through the references from review articles and original research publications for further studies. Studies were limited to those published in the English language. We then pooled the rates of occurrence for Bell's palsy according to trimester of pregnancy, and postpartum, as well as the associated prevalence of pre-eclampsia or gestational hypertension. We found that the majority of cases of Bell's palsy arose during the third trimester (pooled event rate 71.1%, 95% confidence interval (CI) 64.1-77.2), while almost none arose in the first trimester. During the postpartum period, the distribution of Bell's palsy was 21.3% (95% CI 15.7-28.1) of all cases, with the majority arising within days of delivery. Gestational hypertension or pre-eclampsia was present in 22.2% of cases (95% CI 12.5-36.4), well above the 5% rate in the general population. Only one paper provided data on tinnitus in pregnancy, with the distribution equal across all three trimesters. When compared to non-pregnant controls, the odds ratio for the development of tinnitus during pregnancy was 2.8 (95% CI 1.0-8.1). In conclusion, Bell's palsy, and perhaps, tinnitus, occur more frequently during the third trimester of pregnancy. Both may be presenting prodromal signs of underlying early pre-eclampsia. The pathophysiologic mechanism relating these two entities to pre-eclampsia is also discussed.
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PMID:Bell's palsy and tinnitus during pregnancy: predictors of pre-eclampsia? Three cases and a detailed review of the literature. 1058 96

A 40-year-old normotensive man suddenly developed diplopia, tinnitus and a burning sensation on the left side of his body while driving a motorcycle. He did not complain of headache, nausea or vomiting. Neurologic examination revealed left trochlear nerve palsy and impaired pinprick, temperature and joint position sensation of the left limbs. There was no ptosis or motor deficit. He had a mild bleeding diathesis due to alcoholic liver cirrhosis. Computerized tomography and magnetic resonance image of the brain disclosed hemorrhages in the right midbrain tectum and the left temporal lobe. After nine months of observation, there was nearly complete recovery of symptoms, except for mild residual diplopia. From a literature review, only nine case of midbrain tectal hemorrhage involving the inferior colliculus have been reported. These patients had a unique clinical presentation. Diplopia due to trochlear nerve palsy, either unilateral or bilateral, was present in all of the cases. Tinnitus and sensory disturbance contralateral to the lesion side were very common. Only three patients had risk factors for hemorrhage, including bleeding diathesis, hypertension and vascular anomalies. In the majority of patients, no underlying causes were detected. The outcome was favorable with conservative treatment.
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PMID:Midbrain hemorrhage presenting with trochlear nerve palsy. 1067 25

Tinnitus is a frequent symptom but a tinnitus that is rhythmic and synchronous with the patient's heartbeat is rare. The symptom "pulsating noise in the ear" may be due to various cause but most frequently, by glomus tumors, intracranial hypertension and atherosclerosis of the carotid arteries. Pulsatile tinnitus can often present a serious diagnostic problem. The diagnostic evaluation includes physical examination, audiologic assessment and imaging techniques (ultrasonic examination of cervical vessels, high-resolution computed tomography of the temporal bones, nuclear magnetic resonance, angiography of the carotid arteries and magnetic resonance angiography). Evaluation should be individualized but must include a thorough ENT work up. The evaluation of the patient includes otomicroscopy, palpation and auscultation of ears and cervical region and the head positioning test. The cause of pulsatile tinnitus may be even identified on otoscopic examination. Further investigations by other specialities (neurology, internal medicine, ophthalmology) may become necessary. Life-threatening causes such as arteriovenous shunts or carotid artery stenosis must be ruled out. Nevertheless, in several cases it will not be possible to determine the etiology of tinnitus. Finally, therapeutic options which occasionally can include surgical techniques or interventional radiology are discussed.
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PMID:[Pulsating tinnitus]. 1070 57

The subject of tinnitus in the population extremes-children and the elderly-is ignored by the literature, probably because children do not complain of tinnitus spontaneously, whereas it is only one challenge among other major health problems in the elderly. A short review of the literature on this subject is presented. Presbytinnitus, defined as tinnitus that accompanies the progressive hearing loss of presbycusis is classified as: type 1 (normal aging affecting the cochlea), and type II (preexistent sensorineural hearing loss accompanied by multiple systemic complaints, especially of sensory ones). The incidence of tinnitus in presbycusis is 11%. Like in other age groups, there is no significant gender predilection in the prevalence of tinnitus, but a correlation was demonstrated between the severity of tinnitus and exposure to noise. Hypertension was associated with a lower incidence of tinnitus, as compared to normotension and hypotension. Several treatment modalities of geriatric tinnitus are reviewed: the superiority of the band-noise masker in patients with presbycusis, as compared to electrical promontory stimulation; amino-oxyacetic in presbycusis and Meniere's disease; zinc supplementation in marginally zinc-deficient elderly patients in improving sensorineural hearing loss and tinnitus; aeration of the middle ear in presbycusis caused by secretory otitis media. Pediatric tinnitus has an incidence of 13% in children who passed an audiometric screening test, and 23-60% in those with hearing loss, 44% in secretory otitis media, but only 3% complain spontaneously because that the child considers tinnitus to be a normal event. There is no significant difference between children with tinnitus and those without in terms of hearing level, age, gender, or etiology of the deafness. Despite the fact that often children do not mention it, tinnitus may incite behavioral problems.
Int Tinnitus J 1997
PMID:Pediatric and Geriatric Tinnitus. 1075 70

Pulsatile tinnitus (PT) is a perception of a rhythmical sound that is synchronous with the heartbeats. Despite being seen rarely in daily practice, frequently it is associated with identifiable causes, thus warranting special attention in regard to the etiological diagnosis. PT results from blood flow turbulence, which in turn results from changes in flow velocity or in the vessel lumen. One of the most important causes of PT is the paraganglioma, a vascular tumor that appears as a reddish retrotympanic mass. However, a normal tympanic membrane mandates differentiating among other diagnoses, such as arteriovenous malformations or fistulas, intracranial or extracranial aneurysms, a high or dehiscent jugular bulb, and persistent stapedial artery. Owing to the progress of radiological evaluation, magnetic resonance angiography (MRA) has proven to be excellent for evaluating vascular diseases. From January 1995 to June 1997, the authors prospectively studied 16 patients with PT and normal otoscopic examination. The study comprised 1 male and 15 female patients (ages 25-71 years; mean age, 42.5 years). All were subjected to MRA evaluation, which revealed the etiological diagnosis in 13 cases (81.25%), including 2 aneurysms and 1 case of intracranial hypertension. Of the 13 patients 9(69.23%) presented with at least one variation of vascular anatomy of the skull, showing a close correlation, in most cases, with the side on which PT occurred. Our results confirm that MRA is an excellent primary screening modality for patients with PT and normal otoscopic findings. The authors point out the importance of making etiological diagnoses in such cases, suggesting that variations of the vascular anatomy of the skull are a possible etiology.
Int Tinnitus J 1998
PMID:Magnetic Resonance Angiography in Pulsatile Tinnitus: The Role of Anatomical Variations. 1075 99

The authors report a case of high flow CCF with intracerebral hemorrhage during treatment with endovascular coil embolization. A 52-year-old woman had been in good health until a sudden onset of orbital bruit and left orbital tinnitus occurred. Conjunctival chemosis and diplopia caused by left abducens palsy gradually progressed. Left internal carotid arteriography revealed a carotid-cavernous sinus fistula with direct high-flow shunt. The fistula drained into the superior orbital vein, inferior petrosal sinus, intercavernous sinus and sphenoparietal sinus with significant cortical reflux. The attempt at transarterial balloon occlusion failed. Then transvenous coil embolization was performed. During the course of endovascular treatment, follow up CT depicted intracerebral hemorrhage. Intracerebral hemorrhage was asymptomatic and thought to be caused by venous hypertension from cortical reflux. The patient underwent direct occlusion of the left sphenoparietal sinus for prevention of further hemorrhage via craniotomy. Lastly, the cavernous sinus was completely occluded by transvenous coil embolization. The signs and symptoms resolved 3 months after the procedures.
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PMID:[A case of high flow CCF with congestive hemorrhage]. 1092 Aug 27

Hearing loss, vertigo, and tinnitus have been related to arterial hypertension. The aim of the present work was to study the permeability of the blood-perilymph and of the labyrinthine barrier, between endolymph and perilymph, to small molecules during chronic and acute hypertension. Experiments were performed in normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR). Acute hypertension was induced by phenylephrine. Perilymph was sampled from the first turn of the scala vestibuli and the Na, K, urea, and radioactive concentrations ((14)C-urea and (3)H-mannitol) were measured. In another experimental set, the endocochlear potential was recorded from the basal turn of scala media, before and after phenylephrine injection. The composition of the perilymph and the kinetic constants for (14)C-urea and (3)H-mannitol were similar in WKY and SHR, and not modified after acute hypertension. In endolymph, the endocochlear potential in SHR (+80+/-2.7 mV, n=24) was lower (P<0.001) than in WKY (+98+/-1.5 mV, n=29). The endocochlear potential was decreased by 40 mV during acute hypertensive peak in seven out of 19 WKY but not in SHR rats (n=13). In conclusion, chronic or acute hypertension did not severely alter the permeability to small molecules of the blood-perilymph barrier. The relationship between the low endocochlear potential and hypertension in SHR remains to be evaluated. After acute hypertensive peak, the presence of vascular protective mechanisms in the cochlea could account for the stable endocochlear potential recorded in SHR and 60% of normotensive rats.
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PMID:Effects of acute and chronic hypertension on the labyrinthine barriers in rat. 1112 68


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