Kretz Alexandra, Preul Christoph, Fricke Hans-Joerg, Witte Otto W, Terborg Christoph
Department of Neurology, University of Jena Medical School, Erlanger Allee 101, Jena D-07747, Germany.
J Med Case Rep. 2010 Jan 22;4:19. doi: 10.1186/1752-1947-4-19.
Unilateral optic neuropathy is commonly due to a prechiasmatic affliction of the anterior visual pathway, while losses in visual hemifields result from the damage to brain hemispheres. Here we report the unusual case of a patient who suffered from acute optic neuropathy following hemispherical subdural hematoma. Although confirmed up to now only through necropsy studies, our case strongly suggests a local, microcirculatory deficit identified through magnetic resonance imaging in vivo.
A 70-year-old Caucasian German who developed a massive left hemispheric subdural hematoma under oral anticoagulation presented with acute, severe visual impairment on his left eye, which was noticed after surgical decompression. Neurologic and ophthalmologic examinations indicated sinistral optic neuropathy with visual acuity reduced nearly to amaurosis. Ocular pathology such as vitreous body hemorrhage, papilledema, and central retinal artery occlusion were excluded. An orbital lesion was ruled out by means of orbital magnetic resonance imaging. However, cerebral diffusion-weighted imaging and T2 maps of magnetic resonance imaging revealed a circumscribed ischemic lesion within the edematous, slightly herniated temporomesial lobe within the immediate vicinity of the affected optic nerve. Thus, the clinical course and morphologic magnetic resonance imaging findings suggest the occurrence of pressure-induced posterior ischemic optic neuropathy due to microcirculatory compromise.
Although lesions of the second cranial nerve following subdural hematoma have been reported individually, their pathogenesis was preferentially proposed from autopsy studies. Here we discuss a dual, pressure-induced and secondarily ischemic pathomechanism on the base of in vivo magnetic resonance imaging diagnostics which may remain unconsidered by computed tomography.
单侧视神经病变通常是由于视交叉前视觉通路的病变引起的，而视野缺损则是由于脑半球受损所致。在此，我们报告一例罕见病例，患者在半球硬膜下血肿后出现急性视神经病变。尽管目前仅通过尸检研究得到证实，但我们的病例强烈提示通过磁共振成像在活体中发现的局部微循环缺陷。
一名70岁的德国白人男性，在口服抗凝剂治疗期间发生巨大的左侧半球硬膜下血肿，在手术减压后出现左眼急性、严重视力损害。神经科和眼科检查提示左侧视神经病变，视力几乎降至黑矇。排除了玻璃体出血、视乳头水肿和视网膜中央动脉阻塞等眼部病变。通过眼眶磁共振成像排除了眼眶病变。然而，磁共振成像的脑弥散加权成像和T2加权像显示，在受累视神经附近的水肿、轻度颞叶疝出的颞叶内侧有一个局限性缺血性病变。因此，临床病程和磁共振成像形态学表现提示，由于微循环受损导致压力性后部缺血性视神经病变。
尽管硬膜下血肿后第二脑神经病变已有个别报道，但其发病机制主要是通过尸检研究提出的。在此，我们基于活体磁共振成像诊断讨论一种双重的、压力性诱导和继发性缺血性发病机制，而计算机断层扫描可能未考虑到这一点。
