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• W2025680773 abstract "To the Editor: Tinnitus is the perception of a noise, described by the patient as a murmur, in the ear or in the head, and is a symptom of various nervous or systemic diseases.1 The most frequent cause of this symptom is a vascular condition of the head and neck, followed by those situations creating a high heart output syndrome, but its cause is often difficult to find; hence, its treatment is sometimes less than satisfactory. Tinnitus has many causes. The most common cause is otological in.2 Other causes include neurological injuries, metabolic and drug-induced disorders, and collagenosis.2,3 Hypertensive intracraneal syndrome (HTIC), regardless of its etiology, can cause both objective and subjective tinnitus.4–6 The patient was a 74-year-old male, who had no neurological or otorhinolaryngological antecedents but did have a history of insulin-dependent diabetes mellitus and ischemic heart disease. He arrived at the emergency department with acute continuous frontal-occipital headache, vomiting, and a feeling of unsteadiness that had been developing over 3 days. General physical examination was normal. The patient was conscious and well orientated, although bradyphrenia was present. He had central left facial paralysis, an ataxic gait, right limb-ataxia, and impaired osteotendinous reflexes in the lower limbs with suppression of both Achilles tendons'reflexes and with a bilateral Babinski reflex. Hyperglycemia (191 mg/dL) was the only abnormal evidence seen in the laboratory tests. The ECG was normal. An emergency brain CT scan was obtained and showed a laminar subdural hematoma and cerebellar intraparenchymal hematoma on the right hemisphere, without signs of hydrocephalus or perilesional edema. Two weeks after admission, the patient developed a pulsating tinnitus, which was located in front of the left external auditory canal and which decreased on moving the head to this side, when the Valsalva maneuver was performed, and on compression of the jugular vein, whereas it increased on inspiration and when the right jugular vein was compressed. Two days later, the patient began experiencing decreased level of consciousness, continuous holocraneal headache, and vomiting. The otoscopic, audiometric and X-ray findings were seen to be normal for his age. The acouphenometry showed a 50-Db non-masking tinnitus between 1000 and 2000 Hz. The new brain CT scan showed a triventricular hydrocephalus, secondary to the perilesional edema. Because of the age of the patient and the underlying condition, the HTIC syndrome and the edema were treated conservatively with dexamethasone (4 mg/h), and the hydrocephalia subsided in several days, as did the tinnitus. The patient was discharged with several mild neurological sequelae secondary to his cerebral lesions. According to Meador,6 the physiopathogenic mechanism inducing tinnitus in the HTIC is a venous noise resulting from the turbulence created when the blood flows from the hypertensive intracraneal portion to the low-pressure zone of the jugular bulb. This noise is unilateral owing to the assymmetry of the right and left jugular flow (anatomical variant of normality). Tinnitus is located on the side with the greater venous flow. This theory is supported by its direct relationship with intracraneal pressure (when the intracraneal pressure decreases, so does the tinnitus), its occurrence in front of the external auditory canal, its pulsating character, and its attenuation by maneuvers that decrease jugular flow (ipsilateral jugular compression, Valsalva maneuver and ipsilateral head movement). The finding of a pulsating tinnitus responding to jugular compression or to the Valsalva maneuver, may suggest HTIC. Both subjective and objective tinnitus have been associated with increased intracraneal pressure.4–6 Tinnitus has been seen in cases of idiopathic communicating hydrocephalus, pseudotumor cerebri, and primary brain tumor.6 In the case reported, the tinnitus was caused by increased intracraneal pressure attributable to hydrocephalus secondary to right laminal and cerebellar intraparenchymal hematomas. The tinnitus disappeared spontaneously when the hydrocephalus remitted after treatment of the cerebral edema. The tinnitus caused by an idiopathic communicating hydrocephalus remits temporarily with repeated lumbar punctions and completely when peritoneal ventricular shunts or shunts from the lateral ventricle to the cisterna magna are made, whereas cases of tinnitus attributable to pseudotumor cerebri are also alleviated by repeated lumbar punctures.6–8 The interest of our case report is the presence of tinnitus as an advisory symptom of a HTIC syndrome. In conclusion, the presence of tinnitus in a patient with a recent history of cerebrovascular disease can point to the existence of an HTIC or hydrocephalus, this diagnosis being most likely when the tinnitus responds to jugular compression or to the Valsalva maneuver." @default.
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• W2025680773 title "TINNITUS AS THE FIRST CLINICAL MANIFESTATION OF HYDROCEPHALUS" @default.
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• W2025680773 doi "https://doi.org/10.1111/j.1532-5415.1996.tb05656.x" @default.
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