Ischemic optic neuropathy

Ischemic optic neuropathy (ION), based on vascular anatomy of the optic nerve, pathogenesis and clinical picture, consists of two distinct entities: anterior (AION) and posterior (PION) ischemic optic neuropathies. AION is due to interference with posterior ciliary artery supply to the optic nerve head and retrolaminar part of the optic nerve; it initially presents with visual loss and optic disc edema which progresses to optic atrophy in a month or two. PION is due to occlusion of nutrient arteries to the posterior part of the optic nerve; in this condition during the initial stages the optic disc is normal in spite of marked visual loss, but the atrophy develops later on. Their pathogeneses, causes, clinical pictures, diagnosis and management are discussed briefly.Some of the figures have been reproduced by courtesy of the British Journal of Ophthalmology (Figs. 2, 5, 7), American Academy of Ophthalmology and Otolarngology (Fig. 1) and Springer-Verslag (Fig. 8). This investigation was supported by Public Health Service Grant EY-01151.     

Perioperative posterior ischemic optic neuropathy: review of the literature

Posterior ischemic optic neuropathy (PION) is an uncommon cause of perioperative visual loss. Perioperative PION has been most frequently reported after spinal surgery and radical neck dissection. The visual loss typically presents immediately after recovery from anesthesia, although it may be delayed by several days. Visual loss is often bilateral and profound with count fingers vision or worse. The examination findings are consistent with an optic neuropathy; however the funduscopic examination is initially normal. The cause is unknown, although patient-specific susceptibility to perioperative hemodynamic derangements is likely. No treatment has proven to be effective. The prognosis for visual recovery is generally poor.     

缺血性视神经病变的中医治疗进展

缺血性视神经病变（Ischemic Optic Neuropathy,ION）是50岁以上中老年人常见的急性视神经疾病,特别是伴有高血压、糖尿病或心脑血管等血流变异常及血管性疾病的患者。缺血性视神经病变可分为前段缺血性视神经病变（Anterior Ischemic Optic Neuropathy,AION）与后段缺血性视神经病变（Posterior Ischemic Optic Neuropathy,PION）,前段缺血性视神经病变发生在视神经筛板及其前后,缺血导致视盘水肿并常伴视盘周围出血,后段缺血病变发生在视盘后的眶内段视神经,病变早期视盘无异常,早期表现仅有视功能障碍。无论AION或PION均有动脉炎性和非动脉炎性的区别,并最终都会导致视神经萎缩。     

Uncommon ophthalmologic disorders in intensive care unit patients

Ophthalmologic complications are frequently encountered in intensive care unit (ICU) patients (Grixti et al. Ocul Surf 2012;10(1):26–42). However, eye care is often overlooked in the critical care setting or just limited to the ocular surface because treatment is focussed on the management of organ failures. Lack of awareness about other less common intraocular sight-threatening conditions may have a devastating effect on the patient's vision. To identify specific, frequently missed uncommon ocular disorders in ICU, a literature review using the keywords “Intensive Care,” “Eye care,” “ITU,” “ICU,” “Ophthalmological disorders,” “Eye disorders” was performed. The databases of CINAHL, PuBMed, EMBASE, and Cochrane library were searched. The higher quality studies are summarized in the table with statements of methodology to clarify the level of evidence. The most prevalent ophthalmologic disorders identified in critically ill subjects include exposure keratopathy, chemosis, and microbial keratitis. In addition, uncommon eye disorders reported in ICU include metastatic endogenous endophthalmitis, acute primary angle closure, ischemic optic neuropathy, pupil abnormalities, vascular occlusions, and rhino-orbital cerebral mucormycosis. Early diagnosis and effective treatment will help to prevent visual loss.     

Immunohistochemical characterization of γ-secretase activating protein expression in Alzheimer's disease brains

J. Satoh, H. Tabunoki, T. Ishida, Y. Saito and K. Arima (2012) Neuropathology and Applied Neurobiology 38, 132–141 Immunohistochemical characterization of γ‐secretase activating protein expression in Alzheimer's disease brains Aims: A recent study showed that γ‐secretase activating protein (GSAP), derived from a C‐terminal fragment of pigeon homolog (PION), increases amyloid‐β (Aβ) production by interacting with presenilin‐1 (PS1) and the β‐secretase‐cleaved C‐terminal fragment of amyloid precursor protein (APP‐CTF). In the study, knockdown of GSAP reduces production of Aβ and plaque formation in the brain of APPswe and PS1ΔE9 double transgenic mice without affecting the Notch‐dependent pathway. Therefore, GSAP is an ideal target for designing γ‐secretase modulators with least side effects in Alzheimer's disease (AD). However, at present, the precise distribution of GSAP in AD brains remains to be characterized. Methods: By immunohistochemistry, we studied GSAP expression in the frontal cortex and the hippocampus of 11 aged AD and 17 age‐matched control cases. Results: GSAP immunoreactivity exhibited distinct morphological features, such as fine granular cytoplasmic deposits, dense nodular and patchy deposits, beads and string‐like deposits, and diffuse dot‐like deposits. In both AD and control brains, a fairly small subset of cerebral cortical and hippocampal neurones expressed fine granular cytoplasmic deposits, while diffuse dot‐like deposits were more frequently found in the neuropil and neuronal processes, particularly enriched in the hippocampal CA2 and CA3 regions. Among GSAP‐immunoreactive deposits, dense nodular and patchy deposits, located in the neuropil and closely associated with PS1 expression and Aβ deposition, indicated the most distinguishing features of AD pathology. Conclusions: Aberrant regulation of GSAP expression plays a key role in acceleration of γ‐cleavage of APP‐CTF and accumulation of Aβ in AD brains.