Latimer Caitlin S, Flanagan Margaret E, Cimino Patrick J, Jayadev Suman, Davis Marie, Hoffer Zachary S, Montine Thomas J, Gonzalez-Cuyar Luis F, Bird Thomas D, Keene C Dirk
Department of Pathology, Division of Neuropathology, University of Washington School of Medicine, Seattle, WA, USA.
Department of Neurology, University of Washington School of Medicine, Seattle, WA, USA.
J Huntingtons Dis. 2017;6(4):337-348. doi: 10.3233/JHD-170261.
Huntington's disease (HD) is an autosomal dominant neurodegenerative disease caused by a trinucleotide (CAG) repeat expansion in huntingtin (HTT) on chromosome 4. Anticipation can cause longer repeat expansions in children of HD patients. Juvenile Huntington's disease (JHD), defined as HD arising before age 20, accounts for 5-10% of HD cases, with cases arising in the first decade accounting for approximately 1%. Clinically, JHD differs from the predominately choreiform adult onset Huntington's disease (AOHD) with variable presentations, including symptoms such as myoclonus, seizures, Parkinsonism, and cognitive decline.
The neuropathologic changes of AOHD are well characterized, but there are fewer reports that describe the neuropathology of JHD. Here we report a case of a six-year-old boy with paternally-inherited JHD caused by 169 CAG trinucleotide repeats who presented at age four with developmental delay, dysarthria, and seizures before dying at age 6. The boy's clinical presentation and neuropathological findings are directly compared to those of his father, who presented with AOHD and 54 repeats.
A full autopsy was performed for the JHD case and a brain-only autopsy was performed for the AOHD case. Histochemically- and immunohistochemically-stained slides were prepared from formalin-fixed, paraffin-embedded tissue sections.
Both cases had neuropathology corresponding to Vonsattel grade 3. The boy also had cerebellar atrophy with huntingtin-positive inclusions in the cerebellum, findings not present in the father.
Autopsies of father and son provide a unique opportunity to compare and contrast the neuropathologic findings of juvenile and adult onset HD while also providing the first immunohistochemical evidence of cerebellar involvement in JHD. Additionally this is the first known report to include findings from peripheral tissue in a case of JHD.
亨廷顿舞蹈症(HD)是一种常染色体显性神经退行性疾病,由4号染色体上亨廷顿蛋白(HTT)中的三核苷酸(CAG)重复扩增引起。遗传早现可导致HD患者子女的重复扩增更长。青少年型亨廷顿舞蹈症(JHD)定义为20岁之前发病的HD,占HD病例的5%-10%,其中在第一个十年发病的病例约占1%。临床上,JHD与以舞蹈样动作为主要表现的成人起病型亨廷顿舞蹈症(AOHD)不同,其表现多样,包括肌阵挛、癫痫、帕金森症和认知衰退等症状。
AOHD的神经病理学变化已得到充分描述,但描述JHD神经病理学的报告较少。在此,我们报告一例由169个CAG三核苷酸重复序列引起的父系遗传JHD病例,该男孩4岁时出现发育迟缓、构音障碍和癫痫,6岁时死亡。将该男孩的临床表现和神经病理学发现与他患有AOHD且有54个重复序列的父亲的情况进行直接比较。
对JHD病例进行了全面尸检,对AOHD病例进行了仅脑部的尸检。从福尔马林固定、石蜡包埋的组织切片制备组织化学和免疫组织化学染色玻片。
两例病例的神经病理学均符合冯·萨特尔3级。该男孩还存在小脑萎缩,小脑中有亨廷顿蛋白阳性包涵体,而其父亲没有这些发现。
父子尸检提供了一个独特的机会,可对青少年和成人起病型HD的神经病理学发现进行比较和对比,同时也提供了小脑受累于JHD的首个免疫组织化学证据。此外,这是已知的第一份包含JHD病例外周组织发现的报告。