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finger-nose
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  指鼻
     Physical examination: the patient can not complete both hands alternating movement test, heel-knee-tibia test, and finger-nose test, and presented pyramidal sign.
     体格检查呈高腭弓,双手轮替动作试验、跟-膝-胫试验和指鼻试验均不能完成,并有锥体束征;
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  相似匹配句对
     Finger Drills
     儿童钢琴入门教程——“手指操”
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     finger performance training;
     手指弹奏能力训练;
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     Study on replantation of the finger-end severing.
     指末节断离再植探讨
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     On Ecology of Five-finger Mountain Fairyland
     五指山仙颜话生态
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     BEAUTY NOSE
     俏鼻保养秋令时
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  finger-nose
Eight signs were evaluated: anisocoria, jerky eye movements, facial palsy, difference in elbow extension force, abnormal finger-nose test, Barré sign, difference in knee jerk, and extensor plantar reflex.
      


Objective To review the clinical and autopsy neuropathological changes of one Menkes disease patient who was misdiagnosed as Wilson disease, and to reveal the clinical and neuropathological differences between these two diseases. Methods and Results A girl at 8 years old gradually presented lower limb weakness, multiple joint deformities, both hand as claw-like ulnar drift deformity, osteoporosis, extremities lead-pipe rigidity, tremor, dysphasia, and mental retardation. She had high palatal arch, gingival bleeding,...

Objective To review the clinical and autopsy neuropathological changes of one Menkes disease patient who was misdiagnosed as Wilson disease, and to reveal the clinical and neuropathological differences between these two diseases. Methods and Results A girl at 8 years old gradually presented lower limb weakness, multiple joint deformities, both hand as claw-like ulnar drift deformity, osteoporosis, extremities lead-pipe rigidity, tremor, dysphasia, and mental retardation. She had high palatal arch, gingival bleeding, nasal hemorrhage and retention of urine, etc. Physical examination: the patient can not complete both hands alternating movement test, heel-knee-tibia test, and finger-nose test, and presented pyramidal sign. Laboratory examination: serum ceruloplasmin was 0.02 μmol/L. Clinical diagnosis: hepatolenticular degeneration (also called Wilson disease) complicated with osteopathy. Treated with D-penicillamine (0.3 g) oral administration 3/d. Signs and symptoms progressively deteriorated. She died at 16 years old. Autopsy neuropathological results: cerebral parenchyma presented extensive atrophy, bilateral subcortical white matter of the frontoparietal lobe showed severe atrophy, degeneration and cavitation. Optical microscopic observation: Obvious changes in basal ganglion tissue were not seen. Irregular vascular lumen and endangium shrinkage may be occasionally found. In the cortex neurons of granular cell layer reduced obviously, and white matter showed extensive demyelinated degeneration with vesiculation. Massive astrocytes, phagocytes, ectopic neurons, and satellite cells proliferated, without perivascular inflammatory cells infiltration. Neuron loss and necrosis were not seen in the head of caudate nucleus, putamen, globus pallidus, and thalamus, but satellite cells around the neurons were markedly increased. There were many activated microgliocytes. Deposit could be found in the neurons at the tail of caudate nucleus. No Opaski cells and Alzheimer type Ⅱ cells were seen. The characteristic changes in cerebellum were as follow: residual Purkinje cells presented obvious abnormal dendritic arborization (so called ″weeping willow″), increased perisomatic processes, and focal axonal swelling (″torpedoes″) and Purkinje cells deposited in the granular cell layer. Conclusion 1) Menkes disease could be seen in females and could onset at childhood or early adult. 2) There are prominent massive white matter degeneration, necrosis, and cavitation. The construction of basal ganglia which remains quite well is inconsistent with the clinical signs and symptoms. Neurons markedly reduced in cortex granular cell layer. Purkinje cells of cerebellum emerge abnormal dendritic arborization. All of these are the characteristic presentations of Menkes disease.

目的对1例Menkes病患者的诊断与治疗过程进行回顾分析,以识别遗传性铜代谢异常引起的神经系统变性病Wilson病与Menkes病患者的临床及病理特点。方法与结果患者女性,8岁发病,逐渐出现下肢无力、关节变形、双手呈爪样偏向尺侧、骨质疏松、四肢肌张力铅管样增高、震颤、言语不利、精神障碍,以及牙龈出血、鼻出血及尿潴留等临床症状。体格检查呈高腭弓,双手轮替动作试验、跟-膝-胫试验和指鼻试验均不能完成,并有锥体束征;血清铜氧化酶0.02μmol/L。临床诊断为肝豆状核变性(亦称Wilson病)并骨质病。给予青霉胺0.25g口服,3次/d,治疗4年无效,改为0.25g口服,4次/d。治疗1年余,症状及体征渐进性加重,16岁死亡。尸检结果显示,脑实质呈广泛性萎缩,双侧额顶叶皮质下白质严重萎缩、变性形成空腔。光学显微镜下基底节组织结构无明显改变,血管管腔偶有不规则,内膜皱缩;皮质内颗粒细胞层神经元脱失明显,白质广泛脱髓鞘变性并有囊腔形成,可见大量增生的星形细胞、吞噬细胞、异位神经元及卫星细胞,血管周围无炎症细胞浸润;基底节区尾状核头、壳核、苍白球、丘脑均未见明显的神经元脱失和坏死,但是神经元中卫星细胞明显增多,有大量激活...

目的对1例Menkes病患者的诊断与治疗过程进行回顾分析,以识别遗传性铜代谢异常引起的神经系统变性病Wilson病与Menkes病患者的临床及病理特点。方法与结果患者女性,8岁发病,逐渐出现下肢无力、关节变形、双手呈爪样偏向尺侧、骨质疏松、四肢肌张力铅管样增高、震颤、言语不利、精神障碍,以及牙龈出血、鼻出血及尿潴留等临床症状。体格检查呈高腭弓,双手轮替动作试验、跟-膝-胫试验和指鼻试验均不能完成,并有锥体束征;血清铜氧化酶0.02μmol/L。临床诊断为肝豆状核变性(亦称Wilson病)并骨质病。给予青霉胺0.25g口服,3次/d,治疗4年无效,改为0.25g口服,4次/d。治疗1年余,症状及体征渐进性加重,16岁死亡。尸检结果显示,脑实质呈广泛性萎缩,双侧额顶叶皮质下白质严重萎缩、变性形成空腔。光学显微镜下基底节组织结构无明显改变,血管管腔偶有不规则,内膜皱缩;皮质内颗粒细胞层神经元脱失明显,白质广泛脱髓鞘变性并有囊腔形成,可见大量增生的星形细胞、吞噬细胞、异位神经元及卫星细胞,血管周围无炎症细胞浸润;基底节区尾状核头、壳核、苍白球、丘脑均未见明显的神经元脱失和坏死,但是神经元中卫星细胞明显增多,有大量激活的小胶质细胞,尾状核尾的神经元内有沉积物;未见AlzheimerⅡ型星形细胞和Opaski细胞;小脑的特征性变化为颗粒细胞层变薄,细胞减少,残留的Purkinje细胞有明显的树枝状突起(垂柳影样)及突起局限性肥大处树突增多,局灶性轴突肿胀(鱼雷样变);并可见Purkinje细胞沉入颗粒细胞层内。结论(1)Menkes病亦可发生于女性,可于儿童晚期或成年早期发病。(2)特征性表现为皮质下白质大片变性、坏死形成空腔,以及与临床症状、体征不平行的基底节结构保留完好,皮质内颗粒细胞层神经元脱失和小脑Purkinje细胞异常突起等。

 
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