Glufosinate ammonium (GLA) is a broad-spectrum herbicide used worldwide. As the use of GLA-containing herbicides has increased, poisoning from incidental and deliberate ingestion has also increased, and has been mostly reported from Japan. Most of glufosinate poisoning events were associated with suicide attempts using BASTA® (Bayer, Leverkusen, Germany). BASTA®, a herbicide containing glufosinate ammonium (18.5%) and the anionic surfactant, polyoxyethylene alkylether sulfate (30%), has been widely used in many countries since 1984 (1). Glufosinate poisoning has been reported to induce central nervous system (CNS) symptoms, such as drowsiness, memory impairment, and seizures. Also, the included anionic surfactant, which increases blood vessel permeability, may cause symptoms such as reduced circulatory blood volume, altered cardiac function, and systemic peripheral vessel resistance (1). Periventricular white matter ischemias, hippocampal lesions, and both hippocampal and striatal lesions have been reported following GLA intoxication, together with radiological findings (2, 3). We describe a patient who developed a reversible callosal lesion by ingesting a GLA-containing herbicide in an attempted suicide.
Objectives: To evaluate the magnetic resonance imaging (MRI) findings of labyrinthine hemorrhage as a cause of sudden sensorineural hearing loss (SSNHL).Methods: MRI scans of 59 patients with SSNHL were retrospectively analyzed and compared to clinical features and audiometry data. MR images included pre-enhanced T1-weighted, 3D FLAIR volume isometric turbo spin-echo acquisition (VISTA), post-enhanced T1-weighted and 4-h-delayed enhanced FLAIR VISTA, and 3D thin-section proton density-weighted images.Results: High labyrinth signals were seen on pre-enhanced T1-weighted and 3D FLAIR VISTA images with no enhancement for 6 of 59 (10.2%) patients with SSNHL. In these six patients with presumed inner-ear hemorrhage, high signal intensity was seen in the endolymphatic and perilymphatic portions of the labyrinth on T1-weighted and 3D FLAIR VISTA images. In patients with SSNHL with nonhemorrhagic causes such as vestibular schwannoma or labyrinthitis, high signal or labyrinthine enhancement was seen only in the perilymphatic portion of the labyrinth on pre- or post-enhanced 3D FLAIR VISTA images.Conclusions: MRI using pre-enhanced T1-weighted, 3D FLAIR VISTA, and post-enhanced T1-weighted, 4-h delayed enhanced FLAIR VISTA images is able to identify labyrinthine hemorrhage as the cause of SSNHL. High signals in both the endolymphatic and perilymphatic portions of the labyrinth on pre- or post-enhanced 3D FLAIR VISTA images without enhancement indicate labyrinthine hemorrhage.
This study was performed to evaluate the relationship between callosal microbleeds and anoxic brain injury.Twenty-seven patients with anoxic brain injuries were analyzed and retrospectively compared to the control group of patients without a history of anoxic brain injury using Fisher's exact test regarding comorbidities and cerebral microbleeds. The patient group was subdivided according to the presence of callosal microbleeds. Fisher's exact test was used to compare the presence of typical MRI findings of anoxic brain injury, use of cardiopulmonary resuscitation, and prognosis. The Mann-Whitney U test was used to compare the interval between the occurrence of anoxic brain injury to MRI acquisition.The prevalence of cerebral microbleeds in the patient group was 29.6%, which was significantly higher than that in the control group at 3.7% (p = 0.012). All cerebral microbleeds in the patient group were in the corpus callosum. Compared with the callosal microbleed-absent group, the callosal microbleed-present group showed a tendency of good prognosis (6/8 vs. 11/19), fewer typical MRI findings of anoxic brain injury (2/8 vs. 10/19), and more cardiopulmonary resuscitation (6/8 vs. 12/19), although these differences did not reach statistical significance (p = 0.35, p = 0.19, and p = 0.45, respectively).Callosal microbleeds may be an adjunctive MRI marker for anoxic brain injury.뇌량 미세출혈이 저산소 뇌 손상과 상관관계가 있는지 알아보고자 하였다.임상적으로 진단된 27명의 저산소 뇌 손상 환자군을 대상으로 후향적으로 연구를 진행하였다. 나이와 성별을 매칭한 대조군과 Fisher's exact test로 동반 질환, 뇌 미세출혈 유무를 비교하였다. 환자군은 뇌량 미세출혈의 유무로 나누어 비교하였다. Fisher's exact test로 두 그룹 간의 저산소 뇌 손상의 전형적인 자기공명영상 특징 유무, 심폐소생술 유무, 예후정도를 비교하였고, Mann-Whitney U test로 저산소 뇌 손상 사건 발생 후 자기공명영상 획득까지의 시간 간격을 비교하였다.환자군에서 뇌 미세출혈은 29.6%에서 보였으며, 이는 대조군의 3.7%보다 통계적으로 유의하게 높았다(p = 0.012). 환자군에서의 모든 뇌 미세출혈은 뇌량에 국한됐다. 비뇌량 미세출혈군과 비교하여, 뇌량 미세출혈군은 좋은 예후를 보이는 경우가 많았고(6/8 vs. 11/19), 저산소 뇌 손상의 전형적인 자기공명영상 특징을 작은 비율에서 보이며(2/8 vs. 10/19), 심폐소생술이 많은 비율에서 시행됐으나(6/8 vs. 12/19) 통계적 유의성을 보이진 못하였다(p = 0.35, p = 0.19, p = 0.45, respectively).뇌량 미세출혈은 저산소 뇌 손상을 시사하는 부수적인 자기공명영상 특징이 될 수 있겠다.
Parkinson disease (PD) is a heterogeneous neurodegenerative disorder. Dopamine transporter imaging using 123I-2β-carbomethoxy-3β-(4-iodophenyl)-N-(3-fluoropropyl)-nortropane (FP-CIT) and noradrenergic cardiac imaging using 123I-meta-iodobenzylguanidine (MIBG) have been used in combination or separately to study PD patients. Published results regarding uptake of the 2 tracers in each motor subtype are fairly abundant and mostly in agreement. However, data on the intrasubject association between dopaminergic and noradrenergic systems in PD patients are relatively scant and vary. We aimed to assess the intrasubject relationship between striatal dopamine transporter density using a PET tracer and cardiac sympathetic innervation in tremor-dominant subtype (TD) and akinetic-rigid subtype (AR) of PD.This study has a cross-sectional design. Thirty-one patients with early PD (17 TD/14 AR) who underwent both 123I-MIBG cardiac scintigraphy and 18F-FP-CIT PET/CT were retrospectively selected. We assessed the relationship between heart-to-mediastinum ratio (H/M) of 123I-MIBG and specific (striatal)-to-nonspecific (cerebellar) dopamine transporter binding ratio (S/N) measured from 4 separate regions-of-interest (bilateral caudate nuclei and lentiform nuclei) of 18F-FP-CIT in each motor subtype.S/N of all 4 striatal regions were significantly lower in the AR subgroup than in the TD subgroup. H/M was not significantly different. There was a significant intrasubject correlation between H/M and S/N of the lentiform nucleus in AR-PD but no correlation between H/M and any of 4 S/N in TD-PD.Our data suggest a coupled degeneration of nigrostriatal dopaminergic and myocardial sympathetic denervation in AR subtype, but not in TD subtype, of early PD patients. These different results between the 2 motor subtypes likely reflects the heterogeneous pathophysiology of PD.
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