Huang Brendan, Shafiian Neeva, Masi Paul Joseph, Gordon Marc L, Franceschi Ana M, Giliberto Luca
Department of Neurology, Northwell, New Hyde Park, NY, United States.
Zucker School of Medicine at Hofstra/Northwell, Hempstead, NY, United States.
Front Neurol. 2024 Aug 29;15:1428021. doi: 10.3389/fneur.2024.1428021. eCollection 2024.
Creutzfeldt-Jakob disease (CJD) is a spongiform encephalopathy caused by misfolded human prion proteins (PrP)s. Due to variability in presentation, the diagnosis may be missed in lieu of various psychiatric disorders. Our study reports on a prototypical case and psychiatric mimic for CJD, and the workup used to establish the correct diagnosis. A 54-year-old male with a past medical history of traumatic brain injury and major depressive disorder presented with chest pain. During the hospital stay, he was found to be increasingly aggressive, and behaved out of character. Further review of clinical history revealed that the patient was diagnosed with cognitive impairment and depression one year prior. The patient was agitated, poorly redirectable, and had unstable gait on neurological examination. Magnetic resonance imaging (MRI) of the brain demonstrated restricted diffusion (DWI) along the parietooccipital and temporal regions (L > R) and in the subcortical structures, including the basal ganglia and thalami, with accompanying subtle fluid attenuation inversion recovery (FLAIR) hyperintense signal abnormality in these regions, deemed as artifactual at the time. Repeat MRI brain two months later demonstrated progression of the DWI signal with ADC correlate and FLAIR findings. Cerebrospinal fluid 14-3-3 and RT-QuIC samples were positive. Upon passing a few months later, brain autopsy and Western Blot confirmed the CJD diagnosis. Literature review was conducted on PubMed to identify CJD cases initially diagnosed as psychiatric disorder. Search terms included "CJD" or "Creutzfeldt-Jakob disease" with three common psychiatric diagnoses, "Depression," "Psychosis," and "Mania." Positive EEG, MRI, PET, and CSF (including protein 14-3-3 and tau) findings for CJD were found in 66.7, 81.1, 50, and 72.7% of cases, respectively. Overall, CJD can present as a psychiatric mimic. In suspicious cases, EEG, imaging, and CSF studies should be promptly utilized to arrive at the correct diagnosis. Repeated MRI imaging is often required to help in the diagnostic process. Brain biopsy should be considered in selected cases.
克雅氏病(CJD)是一种由错误折叠的人类朊病毒蛋白(PrP)引起的海绵状脑病。由于临床表现具有变异性,在存在各种精神障碍的情况下,可能会漏诊。我们的研究报告了一例典型的克雅氏病病例及其精神症状模仿表现,以及用于确立正确诊断的检查过程。一名54岁男性,既往有创伤性脑损伤和重度抑郁症病史,因胸痛就诊。住院期间,发现他越来越有攻击性,行为异常。进一步回顾临床病史发现,该患者一年前被诊断为认知障碍和抑郁症。患者烦躁不安,难以转移注意力,神经系统检查时步态不稳。脑部磁共振成像(MRI)显示沿顶枕叶和颞叶区域(左侧>右侧)以及包括基底神经节和丘脑在内的皮质下结构存在扩散受限(DWI),同时这些区域伴有轻微的液体衰减反转恢复(FLAIR)高信号异常,当时认为是伪影。两个月后复查脑部MRI显示DWI信号进展,伴有表观扩散系数(ADC)相关性及FLAIR表现。脑脊液14-3-3和实时震颤诱导转化(RT-QuIC)样本呈阳性。几个月后患者去世,脑部尸检和免疫印迹证实了克雅氏病的诊断。在PubMed上进行了文献综述,以确定最初被诊断为精神障碍的克雅氏病病例。检索词包括“CJD”或“克雅氏病”以及三种常见的精神诊断“抑郁症”“精神病”和“躁狂症”。分别在66.7%、81.1%、50%和72.7%的病例中发现了克雅氏病的脑电图(EEG)、MRI、正电子发射断层扫描(PET)和脑脊液(包括蛋白14-3-3和tau)阳性结果。总体而言,克雅氏病可表现为精神症状模仿。在可疑病例中,应及时利用脑电图、影像学和脑脊液检查以得出正确诊断。通常需要重复进行MRI成像以辅助诊断过程。在某些选定病例中应考虑进行脑活检。