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Biomedical subjects

Neil S Longridge

Publications and source records attributed to Neil S Longridge.

7 recordsLinked to original sources
PubMed2005

Barotrauma presenting as temporal lobe injury secondary to temporal bone rupture.

We present the case of a scuba diver who experienced acute ear pain during ascent from a dive. CT imaging was performed because of severe unrelenting headache. Blood and gas was identified within the epidural space of the middle fossa and over the petrous bone, as well as hemorrhage within the adjacent temporal lobe. To the best of our knowledge, this is the first case of CT-documented barotrauma affecting the brain as a result of middle-ear gas rupturing through the tegmen tympani.

Adult↗
PubMed2003

Longitudinal analysis of hearing loss in a case of hemosiderosis of the central nervous system.

OBJECTIVE: To describe cochleovestibular aspects of superficial hemosiderosis of the central nervous system. BACKGROUND: Superficial hemosiderosis of the central nervous system is a rare disease in which cochleovestibular impairment, cerebellar ataxia, and myelopathy are the most frequent signs. Chronic recurrent subarachnoidal hemorrhage with bleeding into the cerebrospinal fluid is the cause of deposition of hemosiderin in leptomeningeal and subpial tissue, cranial nerves, and spinal cord. Removing the cause of bleeding can prevent irreversible damage to these structures. Because this is the only effective treatment, an early diagnosis is crucial. STUDY DESIGN: Retrospective case review. SETTING: Tertiary referral center. PATIENT: A 72-year-old woman with superficial hemosiderosis of the central nervous system that developed when she was age 39. METHODS: Neurologic and imaging diagnostic examinations and longitudinal evaluation of cochleovestibular features were performed. Neurosurgery was not performed. RESULTS: Progressive bilateral sensorineural hearing loss and severe vestibular hyporeflexia developed within 15 years, which can be attributed to lesions in the cochleovestibular system. Additional pathology of the central nervous system developed later. CONCLUSION: The patient demonstrated cochlear and vestibular findings that are typical of this pathologic condition. It is the first documented case with extensive serial audiometry used to precisely outline the degree of hearing deterioration during the course of the disease.

Aged↗
PubMed2002

Exostosis of the external auditory canal: a technical note.

OBJECTIVE: To describe the author's method of managing occlusive exostosis of the external auditory canal. STUDY DESIGN: Retrospective chart review. SETTING: Tertiary referral ambulatory otology clinic. PATIENTS: A case series of patients treated sequentially by the author over 15 years, all of whom had occlusive external auditory canal exostoses that could not be treated by medical management. INTERVENTION: Permeatal surgical removal of the anterior exostosis only. MAIN OUTCOME MEASURE: Surgical relief of occlusive external auditory canal disease by restoration of hearing and absence of infection with persistence of an external auditory canal and no symptoms of recurrence. RESULTS: A total of 8 men were treated by anterior exostosis removal. Follow-up continued on these patients for a period of 5 to 15 years after the operation, and none showed any evidence of recurrence or tendency to narrowing of the deep ear canal. One patient incurred a tympanic membrane perforation at escostosis surgery that was repaired during the operation. CONCLUSION: Anterior exostosis removal by a permeatal route is a safe, rapid, and effective method of relieving patients of occlusive external auditory canal exostosis. By leaving the posterior exostosis intact, patients are not put at risk for injury to the facial nerve, chorda tympani nerve, or ossicles. When the deep ear canal is drilled blind, there are no landmarks to indicate the true path of the external canal.

Adult↗
PubMed2002

Visual vestibular mismatch in patients treated with intratympanic gentamicin for Meniere's disease.

OBJECTIVE: To support the hypothesis that the symptom complex known as visual vestibular mismatch (VVM) can be induced by peripheral vestibular disease. DESIGN: Retrospective chart review; prospective questionnaire. SETTING: A tertiary/quaternary care hospital clinic. METHODS: The charts of 28 patients who were treated for Meniere's disease were studied. Their responses to a pretreatment VVM questionnaire were scored and compared with their answers in a telephone follow-up to the same questions posttreatment. These questionnaires were compared with those filled in by 100 control patients without ear disease. MAIN OUTCOME MEASURES: Patients' responses to a VVM-specific questionnaire. RESULTS: Seventeen of 28 patients had VVM. Gentamicin therapy increased the number of positive answers. There was no correlation between the development of VVM complaints, caloric scores, and posturography performance. No control patients had symptoms of VVM. CONCLUSION: We conclude that the development of VVM indicates the onset or worsening of vestibular disease as it can be induced or exacerbated by gentamicin therapy. As there is no correlation between VVM and caloric scores, we suggest that otolithic damage may be responsible for this symptom set developing.

Anti-Bacterial Agents↗
PubMed2002

Motion sickness and vestibular hypersensitivity.

OBJECTIVE: Motion sickness is poorly understood, although it has been recognized for years as debilitating. Vestibular function is required for motion sickness to occur, but motion sickness can also be brought on without body motion. The aim of this study was to see if there was a correlation between caloric response and motion sickness susceptibility. DESIGN: One experiment was a prospective study carried out on 200 patients. A second prospective study was carried out on 121 patients. SETTING: Patients referred to our tertiary/quaternary care dizziness clinic. METHODS: In experiment 1, caloric scores in patients were correlated with symptoms of motion sickness as established by responses to a simple question. In experiment 2, caloric scores were correlated with symptomatic responses to caloric testing itself. MAIN OUTCOME MEASURES: Caloric responses of the best ear were measured according to standardized caloric evaluation methods. RESULTS: There was no correlation between motion sickness and caloric scores. There was a significant difference in caloric scores between patients made symptomatic by calorics and those who were not. CONCLUSIONS: The autonomic response seen in some patients is not triggered by a specific level of semicircular canal response (as measured by caloric testing). We hypothesize that (similar to space motion sickness) the trigger is a signal differential that arises between semicircular canals and otoliths and that some patients are unable to suppress this response. These patients often suffer motion sickness on a long-term basis.

Adult↗