RESUMO
It is well known that cortical damage may affect cognitive functions, whereas subcortical damage, especially brainstem stroke, would be far less likely to cause cognitive decline, resulting in this condition being overlooked. Few studies have focused on cognitive dysfunction after a pontine stroke. Here, we begin with describing our nine new case reports of in-depth neuropsychological findings from patients with pontine stroke. The dominant domain of cognitive dysfunction was commonly characterized by executive dysfunction, almost in line with previous studies. The severity was relatively mild. We give an overview of the available literature on cognitive decline following a pontine stroke. This is followed by discussions regarding the prognosis of the cognitive disabilities. Based on previous neuroimaging findings, we would like to get to the core of the neuropathology underlying the cognitive declines in the context of "diaschisis", a phenomenon of a broad range of brain dysfunctions remote from the local lesions. Specifically, our unique paper, with two modalities of neuroimaging techniques, may help us better understand the pathology. SPECT scans yield evidence of frontal and thalamic hyper-perfusion and cerebellar hypo-perfusion in patients with pontine stroke. Functional near-infrared spectroscopy, when focusing on the supplementary motor area (SMA) as one of the hyper-perfusion areas, exhibits that SMA responses may be subject to the severity of cognitive decline due to a pontine stroke and would also be related to the recovery. Finally, we posit that cognitive decline due to pontine stroke could be explained by the failure of hierarchical cognitive processing in the fronto-ponto-cerebellar-thalamic loop.
RESUMO
Background: Cribriform plate dural arteriovenous fistulas (dAVFs) are rarely encountered. Here, we report a case of cribriform plate dAVF with a rare complication after endovascular therapy. Case Description: A 60-year-old man presented with severe sudden headache. Head computed tomography showed right subdural hematoma, and magnetic resonance angiography showed dilated bilateral frontal cortical vein. Digital subtraction angiography revealed cribriform plate dAVF fed by the anterior and posterior ethmoidal branches of the bilateral ophthalmic arteries. Transarterial embolization with liquid embolic material was performed and the fistula disappeared. Although magnetic resonance imaging showed the disappearance of the cribriform plate dAVF and subdural hematoma, the patient complained of anosmia after the procedure. Conclusion: Endovascular embolization is an effective treatment option for treating cribriform plate dAVFs. However, anosmia is a possible complication, and endovascular surgeons should take care of this complication, especially in cribriform plate dAVFs supplied with blood bilaterally.
