Auditory Brainstem Response and Fos Immunoreactivity in Central Auditory Pathway in an Acquired Audiogenic Seizure Model in Rats.

Background. Cortical hemispherectomy leads to degeneration of ipsilateral subcortical structures, which can be observed long term after the operation. Therefore, reorganization of the brainstem auditory pathway might occur. The aim of this study was to assess reorganization of brainstem auditory pathways by measuring the auditory brainstem response (ABR) in long-term hemispherectomized patients.Methods. We performed bilateral monaural stimulation and measured bilateral ABR in 8 patients~20 years after hemispherectomy and 10 control subjects. Magnetic resonance imaging (MRI) was performed in patients to assess structural degeneration.Results. All patients showed degenerated ipsilateral brainstem structures by MRI but no significant differences in bilateral recording ABR wave latencies. However, nonsurgical-side stimulation elicited significantly longer wave V latencies compared to surgical-side stimulation. Differences in bilateral ABR were observed between hemispherectomized patients and control subjects. Waves III and V latencies elicited by nonsurgical-side stimulation were significantly longer than those in control subjects; surgical-side stimulation showed no significant differences.Conclusions. (1) Differences in ABR latency elicited by unilateral stimulation are predominantly due to bilateral brainstem auditory pathway activity rather than to changes in brainstem volume; (2) ABR Waves III and V originate predominantly in the contralateral brainstem; and (3) subcortical auditory pathways appear to reorganize after long term hemispherectomy.

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Brainstem auditory pathway of children with acute lymphoid leukemia on chemotherapy with methotrexate

Arquivos de Neuro-Psiquiatria ◽

10.1590/0004-282x20190139 ◽

2020 ◽

Vol 78 (2) ◽

pp. 63-69 ◽

Cited By ~ 1

Author(s):

Renata Aparecida LEITE ◽

Jéssica Sales VOSGRAU ◽

Leticia CORTEZ NETO ◽

Nayara Pereira SANTOS ◽

Sandro Luiz de Andrade MATAS ◽

...

Keyword(s):

Acute Lymphoblastic Leukemia ◽

Auditory Brainstem Response ◽

Otoacoustic Emissions ◽

Lymphoblastic Leukemia ◽

Auditory Pathway ◽

Auditory Brainstem ◽

Intrathecal Methotrexate ◽

Lymphoid Leukemia ◽

Acute Lymphoid Leukemia ◽

Brainstem Response

Abstract Objective: Investigate the auditory pathway in the brainstem of children with acute lymphoblastic leukemia submitted to chemotherapy (by intravenous or intrathecal infusion). Methods: Fourteen children aged between 2 and 12 years with diagnosis of acute lymphoid leukemia were evaluated. The following procedures were used: meatoscopy, acoustic immitance measurements, tonal audiometry, vocal audiometry, transient otoacoustic emissions, and auditory brainstem response. Results: From the 14 children with normal auditory thresholds, 35.71% showed an alteration in auditory brainstem response, with a predominance of hearing impairment in the lower brainstem. It was found that 80% of the children with alteration had used intrathecal methotrexate less than 30 days and that 40% had the highest cumulative intravenous methotrexate doses. Conclusion: Children with acute lymphoblastic leukemia submitted to chemotherapy, present auditory pathway impairment in the brainstem, with a predominance of a low brainstem.

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Neuroprotective activation of astrocytes by methylmercury exposure in the inferior colliculus

Scientific Reports ◽

10.1038/s41598-019-50377-9 ◽

2019 ◽

Vol 9 (1) ◽

Cited By ~ 1

Author(s):

Yasuhiro Ishihara ◽

Kouichi Itoh ◽

Ami Oguro ◽

Yoichi Chiba ◽

Masaki Ueno ◽

...

Keyword(s):

Inferior Colliculus ◽

Neurotrophic Factor ◽

Auditory Brainstem Response ◽

Global Analysis ◽

Protein A ◽

Auditory Pathway ◽

Brain Derived Neurotrophic Factor ◽

Auditory Brainstem ◽

Protective Role ◽

Brainstem Response

Abstract Methylmercury (MeHg) is well known to induce auditory disorders such as dysarthria. When we performed a global analysis on the brains of mice exposed to MeHg by magnetic resonance imaging, an increase in the T1 signal in the inferior colliculus (IC), which is localized in the auditory pathway, was observed. Therefore, the purpose of this study is to examine the pathophysiology and auditory dysfunction induced by MeHg, focusing on the IC. Measurement of the auditory brainstem response revealed increases in latency and decreases in threshold in the IC of mice exposed to MeHg for 4 weeks compared with vehicle mice. Incoordination in MeHg-exposed mice was noted after 6 weeks of exposure, indicating that IC dysfunction occurs earlier than incoordination. There was no change in the number of neurons or microglial activity, while the expression of glial fibrillary acidic protein, a marker for astrocytic activity, was elevated in the IC of MeHg-exposed mice after 4 weeks of exposure, indicating that astrogliosis occurs in the IC. Suppression of astrogliosis by treatment with fluorocitrate exacerbated the latency and threshold in the IC evaluated by the auditory brainstem response. Therefore, astrocytes in the IC are considered to play a protective role in the auditory pathway. Astrocytes exposed to MeHg increased the expression of brain-derived neurotrophic factor in the IC, suggesting that astrocytic brain-derived neurotrophic factor is a potent protectant in the IC. This study showed that astrogliosis in the IC could be an adaptive response to MeHg toxicity. The overall toxicity of MeHg might be determined on the basis of the balance between MeHg-mediated injury to neurons and protective responses from astrocytes.

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