Bilateral fornix infarction presented with acute amnesia: case report.

Acute episodes of amnestic syndrome can be a challenging diagnostic problem. Except for nonvascular etiology, thalamic strokes or infarction involving several temporal lobe structures has been reported in earlier cases. The authors report a patient who suddenly developed memory loss without any other focal neurologic deficits. Brain magnetic resonance imaging (MRI) with diffusion-weighted imaging (DWI) performed 1 day after onset revealed acute infarction involving the bilateral fornix column and the genu of corpus callosum. Because simple fornix infarcts often have no obvious positive neurological signs, most of the related manifestations were provided by family members, are easy to be diagnosed falsely, and missed in clinical areas, we suggest that bilateral fornix infarction should be considered in the diagnosis of an acute onset amnestic syndrome.

Memory Impairment Due to a Small Acute Infarction of the Columns of the Fornix.

BACKGROUND: Clinically infarction of the columns of the fornix is very rare. It is also easy to be overlooked during imaging examination due to the special anatomical localization and features of columns of the fornix. In the meantime, with memory disorder to be its most prominent manifestation, it is very easily false diagnosed as other diseases when the lesion focus is overlooked, causing unnecessary invasive examinations like cerebrospinal fluid tests. METHODS: Case report and Literature review. RESULTS: We presented a 66-year-old woman with memory impairment due to a small acute infarction of the columns of the fornix. Through her diagnosis and treatment, we believed that early diagnosis and treatment were important to these patients who were enduring the disease. In addition, literature review informed us that for those unwilling to undergo cerebral angiography or for small cerebrovascular lesions that cannot be detected by angiography, 7T magnetic resonance imaging (MRI) might be an ideal diagnostic method. CONCLUSION: This case illustrated the significance of MRI in diagnosis for patients with acute memory impairment. When reading MRI results, one needs to pay attention to identify small lesions at special locations. In addition, cerebral apoplexy is still the first consideration of diagnosis when acute memory impairment occurs in patients with cerebrovascular disease risk factors.

Vertebral Artery Dissection Leading to Fornix Infarction: A Case Report.

BACKGROUND: The subcallosal artery is a proximal branch of the anterior communicating artery and has been recognized as the vessel responsible for fornix infarction. Fornix infarction caused by vascular damage to the posterior circulation has not been reported previously. RESULTS: A 26-year-old woman suffered from fornix infarction due to artery-to-artery embolism after vertebral artery dissection. Cerebral infarctions were also found in the left thalamus, body of the left caudate nucleus, and the left occipital lobe other than the fornix. CONCLUSIONS: Occlusion of the subcallosal artery results in cerebral infarction of fornix, anterior cingulate cortex, and genu of the corpus callosum. However, in our case, lesions were restricted to the territory of posterior circulation. In addition to subcallosal artery, lateral posterior choroidal artery, a perforating branch of the posterior cerebral artery, has been described to send branches to the fornix, so we speculated that the left lateral posterior choroidal artery was actually responsible for fornix infarction.

Subcallosal artery stroke: infarction of the fornix and the genu of the corpus callosum. The importance of the anterior communicating artery complex. Case series and review of the literature.

INTRODUCTION: Despite the variable anatomy of the anterior communicating artery (AcoA) complex, three main perforating branches can be typically identified the largest of which being the subcallosal artery (ScA). We present a case series of infarction in the vascular territory of the ScA to highlight the anatomy, the clinical symptomatology, and the presumed pathophysiology as it pertains to endovascular and surgical management of vascular pathology in this region. METHODS: In this retrospective multicenter case series study of patients who were diagnosed with symptomatic ScA stroke, we analyzed all available clinical records, MRI, and angiographic details. Additionally, a review of the literature is provided. RESULTS: We identified five different cases of ScA stroke, leading to a subsequent infarction of the fornix and the genu of the corpus callosum. The presumed pathophysiology in non-iatrogenic cases is microangiopathy, rather than embolic events; iatrogenic SCA occlusion can present after both surgical and endovascular treatment of AcoA aneurysms that may occur with or without occlusion of the AcoA. CONCLUSION: Stroke in the vascular territory of the ScA leads to a characteristic imaging and clinical pattern. Ischemia involves the anterior columns of the fornix and the genu of the corpus callosum, and patients present with a Korsakoff's syndrome including disturbances of short-term memory and cognitive changes. We conclude that despite its small size, the ScA is an important artery to watch out for during surgical or endovascular treatment of AcoA aneurysms.

Amnesia due to fornix infarction.

Background and Purpose-The fornix connects various structures involved in memory. We report a patient with anterograde amnesia after an acute ischemic infarct in the anterior fornix. Case Description-A 71-year-old female with acute-onset amnesia had neuroimaging studies showing ischemic infarction of both columns and the body of the fornix and the genu of the corpus callosum. Neuropsychological evaluation revealed anterograde amnesia without evidence of callosal disconnection. The patient showed marked improvement in her memory function on the follow-up visit. Conclusions-Amnesia in this case is likely due to infarction of the anterior fornix structures.

An analysis of atrophy in the medial mammillary nucleus following hippocampal and fornix lesions in humans and nonhuman primates.

Lesions of the hippocampal formation or transections of the fornix are followed by shrinkage of the medial mammillary nucleus (MMN). We determined whether the shrinkage of this nucleus was due to loss and/or shrinkage of neurons in addition to the loss of neuropil. We examined the MMN in a patient (KB) with an infarct that led to marked atrophy of the left hippocampus and subiculum, leaving the right MMN intact. Unbiased, stereological measurement techniques were used to compare the total cell number and individual neuronal cross-sectional areas in both left and right MMN in this patient and in two control human brains. We also analyzed the MMN in four macaque monkeys that underwent experimental unilateral transections of the fornix. The volume of the MMN on the lesioned side in KB was 55% of the unlesioned side (2.8 mm(3) vs 5.1 mm(3)); the MMN in the monkey cases were reduced to 47-58% of the volume of the nonlesioned side. Neurons in the deafferented MMN of KB and of the monkey subjects were decreased in cross-sectional area (16-20%, P < 0.0001). There was a trend toward decreased cell numbers (11-15%) on the lesioned side in all cases. We have estimated that the loss in cell number and shrinkage of remaining cells contribute negligibly to the 45% reduction in MMN volume. Therefore, the loss of neuropil (dendrites and afferent and efferent axons) appears to be the major contributor to the change in MMN volume.