Van Gerpen J A, Wider C, Broderick D F, Dickson D W, Brown L A, Wszolek Z K
Department of Neurology, Mayo Clinic, Jacksonville, FL 32224, USA.
Neurology. 2008 Sep 16;71(12):925-9. doi: 10.1212/01.wnl.0000325916.30701.21.
To report a new American family with hereditary diffuse leukoencephalopathy with spheroids (HDLS), including serial, presymptomatic and symptomatic, cranial MRIs from the proband.
We report clinical and genealogic investigations of an HDLS family, sequential brain MRIs of the proband, and autopsy slides of brain tissue from the proband's father.
We identified seven affected family members (five deceased). The mean age at symptomatic disease onset was 35 years (range: 20-57), and the mean disease duration was 16 years (range: 3-46). Five affected individuals initially manifested memory disturbance and behavioral changes, whereas two experienced a mood disorder as their presenting symptom. Our proband's father had been diagnosed clinically with vascular dementia, but his brain autopsy was consistent with HDLS. The proband had a cranial MRI prior to symptom onset, with two subsequent MRIs performed during follow-up. These serial images reveal a progressive, confluent, frontal-predominant leukoencephalopathy with symmetric cortical atrophy.
The proband of our newly identified hereditary diffuse leukoencephalopathy with spheroids (HDLS) kindred had subtle evidence of an incipient leukoencephalopathy on a presymptomatic cranial MRI. Conceivably, MRI may facilitate identifying affected presymptomatic individuals within known HDLS kindreds, increasing the likelihood of isolating the causative genes.
报告一个患有球形细胞遗传性弥漫性白质脑病(HDLS)的新美国家庭,包括先证者的系列、症状前和症状期头颅磁共振成像(MRI)。
我们报告了一个HDLS家系的临床和系谱调查、先证者的系列脑MRI以及先证者父亲脑组织的尸检切片。
我们确定了7名受影响的家庭成员(5名已故)。症状性疾病发作的平均年龄为35岁(范围:20 - 57岁),平均病程为16年(范围:3 - 46年)。5名受影响个体最初表现为记忆障碍和行为改变,而2名以情绪障碍作为首发症状。我们先证者的父亲临床诊断为血管性痴呆,但他的脑尸检结果与HDLS一致。先证者在症状发作前进行了头颅MRI检查,随访期间又进行了两次MRI检查。这些系列图像显示出一种进行性、融合性、以额叶为主的白质脑病,并伴有对称性皮质萎缩。
我们新确定的球形细胞遗传性弥漫性白质脑病(HDLS)家系的先证者在症状前头颅MRI上有早期白质脑病的细微证据。可以想象MRI可能有助于在已知HDLS家系中识别受影响的症状前个体,增加分离致病基因的可能性。