神马文学网叩诊锤论坛[灌水]病例讨论 转发（八）（公布结果 Hallervorden–Spatz disease ）1
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[灌水]病例讨论 转发（八）（公布结果 Hallervorden–Spatz disease ） 
2007-9-29 22:15:00 
[灌水]病例讨论 转发（八）（公布结果 Hallervorden–Spatz disease ） A 8-year-old boy presented with a 2 year history of abnormal flexor posturing of the right hand and wrist with clenching of the fist. Over 6 months it became fixed and persistent and also involved the left hand. Subsequently, he developed extension of the neck and flexion of the trunk, with grimacing of the face, tight closure of the mouth and deterioration of speech and walking. He was the product of a non-consanguineous marriage and was born at full term. The labor was prolonged. His developmental milestones were delayed and speech was slurred with inability to speak difficult words. He was mentally retarded with poor scholastic performance and was sent to a school for mentally challenged children. No other family members had similar or other movement disorders. With levodopa with carbidopa he had a mild improvement. Later baclofen and trihexyphenadyl were added. He continued to worsen progressively.
On examination, he was bedridden with generalized dystonia, fixed contractures of the lower limbs and was incontinent. There was no evidence of Kayser-Fleischer ring More Details or retinitis pigmentosa. Serum ferritin, ceruloplasmin levels were normal and blood smear was negative for acanthocytes. Brain commuter tomography and MRI (low field strength) done 2 years back were normal. Repeat MRI showed hypointensity with an area of central hyperintensity in both globus pallidi on T2 weighted imaging [Figure - 1].
大致翻译 仅供参考
一个8岁的孩子有两年病史了 开始是右手和手腕握紧拳头时出现屈曲姿势 在6个月后这种现象变成持久性的了 左手也出现症状 随后出现脖子和躯干的弯曲 并出现扮鬼脸 口唇紧闭 语言和步态的变化 他不是近亲结婚 足月产 分娩时间延长 他发育延迟 说话含糊不清 不能说复杂的词语 他反应迟钝 学习成绩差 被送去特殊的学校 其他家庭成员没有相似或其他症状 用了美多巴 症状轻度改善 后来加用了巴氯酚 病情持续恶化
体格检查 他卧床不起 有肌张力障碍 下肢挛缩和尿失禁 没有k-f环和视网膜炎 血铁蛋白 铜蓝蛋白正常 血涂片没有见到棘红细胞 两年后脑ct及mri正常 复查mri是双侧苍白球t2上有中心高密度周围低密度区
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2007-9-29 22:32:00 Re:[灌水]病例讨论 转发（八） 看片子应该是典型的eye-of-the-tiger sign，我查查文献。
本贴已被 作者 于 2007-9-29 22:33:32 编辑过 查看此帖需要积分 0 分 2007-9-29 23:02:00 Re:[灌水]病例讨论 转发（八） The clinical symptoms showed progressive generlaized dystonia with childhood onset.
The most most common causes were idiopathic generalized dystonia (DYT1), Dopa-responsive dystonia (DYT5), myoclonic dystonia, metachromatic leukodystrophy, Niemann–Pick disease type C
and Lesch–Nyhan syndrome.
Mild response to levodopa and negative for acanthocytes or Kayser-Fleischer ring could exlcude DYT5, acanthicytosis or Wilson's disease.
The MRI of the brain showed typical "Eye-of-the-tiger" sign of bilateral globus pallidi.
The most famous disease is Hallervorden–Spatz disease, which is also compatible with the clinical picture of this poor boy.
Other rare differential diagnosis of "Eye-of-the-tiger" sign include
Early-onset levodopa-responsive parkinsonism, PSP, or CBD.
Judging from the clinical picture and neuroimaging, Hallervorden–Spatz disease is my first impression. Other rare differential diangosis include Dopa-responsive dystonia or idiopathic generalized dystonia.
本贴已被 作者 于 2007-9-29 23:2:45 编辑过 查看此帖需要积分 0 分 2007-9-30 1:33:00 Re:[灌水]病例讨论 转发（八） 儿童患者，锥体外系临床表现，MRI出现典型的“虎眼征”。考虑为：
Hallervorden-Spatz病（苍白球黑质色素变性） 查看此帖需要积分 0 分 2007-9-30 15:28:00 Re:[灌水]病例讨论 转发（八） 虎眼征常见于两个疾病，一个是低前β脂蛋白血症-棘红细胞增多症-视网膜色素变性-苍白球变性综合征,即HARP综合征，另一个是Hallervorden-Spatz综合征(HSS)又称苍白球黑质红核色素变性。HARP综合征与HSS临床表现类似,MRI也表现有“虎眼征”,对该病患者进行PANK2基因分析也发现有突变,表明这两种疾病属于“等位基因病”(allelic diseases)。
虎眼征产生的原因：HSS由于铁沉积在苍白球和黑质等部位,故MRIT2WI显示苍白球、黑质呈低信号。由于铁不断沉积在苍白球造成细胞死亡、胶质细胞增生、水含量增加以及空泡形成,因此T2WI显示苍白球周边低信号,而其前内侧出现高信号,即所谓的“虎眼征”。
引至另一篇文献：（The Eye-of-the-Tiger Sign，Radiology，December 2000）
The eye-of-the-tiger sign is most commonly referenced in association with Hallervorden-Spatz syndrome, but the sign has been reported in other extrapyramidal parkinsonian disorders,including cortical–basal ganglionic degeneration (19), earlyonset levodopa-responsive parkinsonism (20), and Steele-Richardson-Olszewski syndrome (progressive supranuclear palsy) (21).
大概是说，虎眼征可以见于以下疾病：Hallervorden-Spatz syndrome，皮质基底节变性（Molinuevo JL, Munoz E, Valldeoriola F, Tolosa E. The eye of the tiger sign in cortical-basal ganglionic degeneration. Mov Disord 1999; 14:169–171.），早发左旋多巴敏感帕金森病（Barbosa ER, Bitar MS, Bacheschi LA, Comerlati LR, Scaff M. Parkinsonismo precoce associado a leso˜es pallidais do tipo ’eye of the tiger.’ Arq Neuropsiquiatr 1995; 53:294–297.），核上性麻痹综合征（进行性核上性麻痹）（Davie CA, Barker GJ, Machado C, Miller DH, Lees AJ. Proton magnetic spectroscopy in Steele-Richardson-Olszewski syndrome.Mov Disord 1997; 12:767–771.）
下图：左侧为虎眼征，右侧为正常对照。
本贴已被 作者 于 2007-10-1 9:52:3 编辑过 查看此帖需要积分 0 分 2007-10-1 9:26:00 Re:[灌水]病例讨论 转发（八） Late adult onset chorea with typical pathology of Hallervorden-Spatz syndrome
J. Neurol. Neurosurg. Psychiatry 2000;69;392-395
Case report
A 76 year old woman was referred with a 1 year
history of unsteady gait and unusual movements
of her head and upper limbs that had
been noticed by her family. Her medical history
included myocardial infarction 20 years previously
with mild congestive heart failure,
peripheral vascular disease, and arthritis. Her
medications were digoxin, furosemide, and
ibuprofen. There was no known neuroleptic or
toxic exposure, no history of Sydenham’s chorea
or rheumatic fever, and no family history of
abnormal movements.
Her initial mental status examination
showed an alert, fully oriented woman with
only mild difficulty in tasks of attention. Her
motor examination was normal except for the
mild generalised choreic movements. The rest
of her neurological examination, including
extraocular movements, was normal except for
slight unsteadiness when walking and mild difficulty
with tandem gait.
Laboratory investigations including complete
blood count, blood smear, thyroid
studies, liver function tests, erythrocyte sedimentation
rate, ceruloplasmin, anticardiolipin
antibodies, antinuclear antibody, and rheumatoid
factor were normal. Huntington’s disease
molecular genetic testing for the CAG trinucleotide
repeat expansion was negative
(number of repeats=23 and 21). Neuropsychological
testing disclosed only mild decline in
cognitive functioning and was considered not
to be consistent with any significant degree of
dementia. Head MRI, done 2 years after the
onset of her chorea, demonstrated decreased
signal intensity in the putamen, caudate,
substantia nigra, and dentate nuclei bilaterally
(fig 1). There were also multiple small
non-specific focal white matter lesions seen in
the centrum semiovale and periventricular
regions bilaterally. She was diagnosed as having
“senile chorea” with the MRI findings thought
to represent iron deposition in the basal ganglia
of unknown cause.
Her chorea slowly increased in severity and 5
years after her first assessment reserpine (2
mg/day) was initiated with moderate improvement
in her chorea. Two years later tetrabenazine
(75 mg/day) was substituted with further
benefit because of concerns that the reserpine
may have been exacerbating her increasing
postural instability. She required placement in
a nursing home 8 years after the onset of her
chorea because of the worsening postural
stability and her increasing number of falls.
She was last examined at this time and had
moderate head rocking movements with mildgeneralised chorea that increased with movement.
She continued to have only minor
memory difficulties. She died suddenly at the
age of 85, 9 years after the onset of her chorea.
NEUROPATHOLOGICAL FINDINGS
Neuropathological examination was confined
to the right half of the brain. External
examination of the cerebral convexity showed
no significant cortical atrophy but there were
two small areas of subarachnoid haemorrhage
in the right occipital and superior parietal
areas. Coronal sections through the cerebral
hemisphere showed a slight flattening of the
head of the caudate nucleus. The medial
segment of the globus pallidum had a cribriform
appearance. The entorhinal cortex was
thinner than normal and there was mild
atrophy of the amygdala. A small area of cortical
infarction was seen underlying the area of
subarachnoid haemorrhage in the right superior
parietal area.A large haemorrhage measuring
3.5´4.0´8.0 cm was noted in the occipital
lobe extending into the posterior temporal
area. Horizontal sections through the brainstem
were unremarkable with the substantia
nigra and locus ceruleus well pigmented.
Sagittal sections through the cerebellum were
unremarkable, including the dentate nucleus.
Microscopic examination showed severe neuronal
loss in the globus pallidus, predominantly
in the medial segment, with abundant neuroaxonal
spheroids and a moderate degree of iron
deposition (fig 2 A and B). The iron deposition
was most abundant extracellularly and was
often perivascular (fig 2 C). It was also noted in
astrocytes and more rarely in neurons. The
striatum showed a moderate degree of neuronal
loss and gliosis affecting chiefly the large
neurons. Iron deposition was also noted,
although less abundant than in the globus pallidus
and in the same pattern of distribution.
Severe neuronal loss was noted in the pars
reticulata of the substantia nigra with a moderate
degree of iron deposition and neuroaxonal
spheroids (fig 2 D). The gracilis and cuneatus
nuclei showed large numbers of neuroaxonal
spheroids with no significant neuronal loss or
pigment deposition. Sections of neocortex
showed mild patchy neuronal loss and occasional
spheroids. The substantia nigra pars
compacta showed no significant neuronal loss
and gliosis but a rare spheroid. Mild Alzheimer
type changes were present (CERAD: neurofibrillary
tangles 0, neuritic plaques sparse, and
diffuse plaques moderate; BRAAK stage II/
VI). In addition to the degenerative changes,
there was an old haemorrhagic infarct in the
occipital lobe in close proximity to a recent
intracerebral haemorrhage. These vascular
changes were accompanied by severe amyloid
angiopathy.
NEUROPATHOLOGICAL DIAGNOSIS
The neuropathalogical diagnoses were:
Hallervorden-Spatz syndrome; old occipital
infarction; recent intracerebral haemorrhage
due to amyloid angiopathy; mild Alzheimer’s
changes.
Figure 2 (A) Neuronal loss, (B) spheroids (arrows), and (C) iron pigment deposition (arrow) in the medial segment of the globus pallidus. (D) Spheroids in the substantia nigra, pars reticulata (arrows). Haematoxylin and eosin luxol fast blue (A, B, and D). Perl’s Prussian blue reaction for iron (C
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2007-9-29 22:15:00 [灌水]病例讨论 转发（八）（公布结果 Hallervorden–Spatz disease ） A 8-year-old boy presented with a 2 year history of abnormal flexor posturing of the right hand and wrist with clenching of the fist. Over 6 months it became fixed and persistent and also involved the left hand. Subsequently, he developed extension of the neck and flexion of the trunk, with grimacing of the face, tight closure of the mouth and deterioration of speech and walking. He was the product of a non-consanguineous marriage and was born at full term. The labor was prolonged. His developmental milestones were delayed and speech was slurred with inability to speak difficult words. He was mentally retarded with poor scholastic performance and was sent to a school for mentally challenged children. No other family members had similar or other movement disorders. With levodopa with carbidopa he had a mild improvement. Later baclofen and trihexyphenadyl were added. He continued to worsen progressively. On examination, he was bedridden with generalized dystonia, fixed contractures of the lower limbs and was incontinent. There was no evidence of Kayser-Fleischer ring More Details or retinitis pigmentosa. Serum ferritin, ceruloplasmin levels were normal and blood smear was negative for acanthocytes. Brain commuter tomography and MRI (low field strength) done 2 years back were normal. Repeat MRI showed hypointensity with an area of central hyperintensity in both globus pallidi on T2 weighted imaging [Figure - 1].
大致翻译 仅供参考
一个8岁的孩子有两年病史了 开始是右手和手腕握紧拳头时出现屈曲姿势 在6个月后这种现象变成持久性的了 左手也出现症状 随后出现脖子和躯干的弯曲 并出现扮鬼脸 口唇紧闭 语言和步态的变化 他不是近亲结婚 足月产 分娩时间延长 他发育延迟 说话含糊不清 不能说复杂的词语 他反应迟钝 学习成绩差 被送去特殊的学校 其他家庭成员没有相似或其他症状 用了美多巴 症状轻度改善 后来加用了巴氯酚 病情持续恶化
体格检查 他卧床不起 有肌张力障碍 下肢挛缩和尿失禁 没有k-f环和视网膜炎 血铁蛋白 铜蓝蛋白正常 血涂片没有见到棘红细胞 两年后脑ct及mri正常 复查mri是双侧苍白球t2上有中心高密度周围低密度区
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2007-9-29 22:32:00 Re:[灌水]病例讨论 转发（八） 看片子应该是典型的eye-of-the-tiger sign，我查查文献。本贴已被 作者 于 2007-9-29 22:33:32 编辑过 查看此帖需要积分 0 分
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2007-9-29 23:02:00 Re:[灌水]病例讨论 转发（八） The clinical symptoms showed progressive generlaized dystonia with childhood onset.The most most common causes were idiopathic generalized dystonia (DYT1), Dopa-responsive dystonia (DYT5), myoclonic dystonia, metachromatic leukodystrophy, Niemann–Pick disease type C
and Lesch–Nyhan syndrome.
Mild response to levodopa and negative for acanthocytes or Kayser-Fleischer ring could exlcude DYT5, acanthicytosis or Wilson's disease.
The MRI of the brain showed typical "Eye-of-the-tiger" sign of bilateral globus pallidi.
The most famous disease is Hallervorden–Spatz disease, which is also compatible with the clinical picture of this poor boy.
Other rare differential diagnosis of "Eye-of-the-tiger" sign include
Early-onset levodopa-responsive parkinsonism, PSP, or CBD.
Judging from the clinical picture and neuroimaging, Hallervorden–Spatz disease is my first impression. Other rare differential diangosis include Dopa-responsive dystonia or idiopathic generalized dystonia.
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2007-9-30 1:33:00 Re:[灌水]病例讨论 转发（八） 儿童患者，锥体外系临床表现，MRI出现典型的“虎眼征”。考虑为：Hallervorden-Spatz病（苍白球黑质色素变性） 查看此帖需要积分 0 分
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2007-9-30 15:28:00 Re:[灌水]病例讨论 转发（八） 虎眼征常见于两个疾病，一个是低前β脂蛋白血症-棘红细胞增多症-视网膜色素变性-苍白球变性综合征,即HARP综合征，另一个是Hallervorden-Spatz综合征(HSS)又称苍白球黑质红核色素变性。HARP综合征与HSS临床表现类似,MRI也表现有“虎眼征”,对该病患者进行PANK2基因分析也发现有突变,表明这两种疾病属于“等位基因病”(allelic diseases)。虎眼征产生的原因：HSS由于铁沉积在苍白球和黑质等部位,故MRIT2WI显示苍白球、黑质呈低信号。由于铁不断沉积在苍白球造成细胞死亡、胶质细胞增生、水含量增加以及空泡形成,因此T2WI显示苍白球周边低信号,而其前内侧出现高信号,即所谓的“虎眼征”。
引至另一篇文献：（The Eye-of-the-Tiger Sign，Radiology，December 2000）
The eye-of-the-tiger sign is most commonly referenced in association with Hallervorden-Spatz syndrome, but the sign has been reported in other extrapyramidal parkinsonian disorders,including cortical–basal ganglionic degeneration (19), earlyonset levodopa-responsive parkinsonism (20), and Steele-Richardson-Olszewski syndrome (progressive supranuclear palsy) (21).
大概是说，虎眼征可以见于以下疾病：Hallervorden-Spatz syndrome，皮质基底节变性（Molinuevo JL, Munoz E, Valldeoriola F, Tolosa E. The eye of the tiger sign in cortical-basal ganglionic degeneration. Mov Disord 1999; 14:169–171.），早发左旋多巴敏感帕金森病（Barbosa ER, Bitar MS, Bacheschi LA, Comerlati LR, Scaff M. Parkinsonismo precoce associado a leso˜es pallidais do tipo ’eye of the tiger.’ Arq Neuropsiquiatr 1995; 53:294–297.），核上性麻痹综合征（进行性核上性麻痹）（Davie CA, Barker GJ, Machado C, Miller DH, Lees AJ. Proton magnetic spectroscopy in Steele-Richardson-Olszewski syndrome.Mov Disord 1997; 12:767–771.）
下图：左侧为虎眼征，右侧为正常对照。
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2007-10-1 9:26:00 Re:[灌水]病例讨论 转发（八） Late adult onset chorea with typical pathology of Hallervorden-Spatz syndromeJ. Neurol. Neurosurg. Psychiatry 2000;69;392-395
Case report
A 76 year old woman was referred with a 1 year
history of unsteady gait and unusual movements
of her head and upper limbs that had
been noticed by her family. Her medical history
included myocardial infarction 20 years previously
with mild congestive heart failure,
peripheral vascular disease, and arthritis. Her
medications were digoxin, furosemide, and
ibuprofen. There was no known neuroleptic or
toxic exposure, no history of Sydenham’s chorea
or rheumatic fever, and no family history of
abnormal movements.
Her initial mental status examination
showed an alert, fully oriented woman with
only mild difficulty in tasks of attention. Her
motor examination was normal except for the
mild generalised choreic movements. The rest
of her neurological examination, including
extraocular movements, was normal except for
slight unsteadiness when walking and mild difficulty
with tandem gait.
Laboratory investigations including complete
blood count, blood smear, thyroid
studies, liver function tests, erythrocyte sedimentation
rate, ceruloplasmin, anticardiolipin
antibodies, antinuclear antibody, and rheumatoid
factor were normal. Huntington’s disease
molecular genetic testing for the CAG trinucleotide
repeat expansion was negative
(number of repeats=23 and 21). Neuropsychological
testing disclosed only mild decline in
cognitive functioning and was considered not
to be consistent with any significant degree of
dementia. Head MRI, done 2 years after the
onset of her chorea, demonstrated decreased
signal intensity in the putamen, caudate,
substantia nigra, and dentate nuclei bilaterally
(fig 1). There were also multiple small
non-specific focal white matter lesions seen in
the centrum semiovale and periventricular
regions bilaterally. She was diagnosed as having
“senile chorea” with the MRI findings thought
to represent iron deposition in the basal ganglia
of unknown cause.
Her chorea slowly increased in severity and 5
years after her first assessment reserpine (2
mg/day) was initiated with moderate improvement
in her chorea. Two years later tetrabenazine
(75 mg/day) was substituted with further
benefit because of concerns that the reserpine
may have been exacerbating her increasing
postural instability. She required placement in
a nursing home 8 years after the onset of her
chorea because of the worsening postural
stability and her increasing number of falls.
She was last examined at this time and had
moderate head rocking movements with mildgeneralised chorea that increased with movement.
She continued to have only minor
memory difficulties. She died suddenly at the
age of 85, 9 years after the onset of her chorea.
NEUROPATHOLOGICAL FINDINGS
Neuropathological examination was confined
to the right half of the brain. External
examination of the cerebral convexity showed
no significant cortical atrophy but there were
two small areas of subarachnoid haemorrhage
in the right occipital and superior parietal
areas. Coronal sections through the cerebral
hemisphere showed a slight flattening of the
head of the caudate nucleus. The medial
segment of the globus pallidum had a cribriform
appearance. The entorhinal cortex was
thinner than normal and there was mild
atrophy of the amygdala. A small area of cortical
infarction was seen underlying the area of
subarachnoid haemorrhage in the right superior
parietal area.A large haemorrhage measuring
3.5´4.0´8.0 cm was noted in the occipital
lobe extending into the posterior temporal
area. Horizontal sections through the brainstem
were unremarkable with the substantia
nigra and locus ceruleus well pigmented.
Sagittal sections through the cerebellum were
unremarkable, including the dentate nucleus.
Microscopic examination showed severe neuronal
loss in the globus pallidus, predominantly
in the medial segment, with abundant neuroaxonal
spheroids and a moderate degree of iron
deposition (fig 2 A and B). The iron deposition
was most abundant extracellularly and was
often perivascular (fig 2 C). It was also noted in
astrocytes and more rarely in neurons. The
striatum showed a moderate degree of neuronal
loss and gliosis affecting chiefly the large
neurons. Iron deposition was also noted,
although less abundant than in the globus pallidus
and in the same pattern of distribution.
Severe neuronal loss was noted in the pars
reticulata of the substantia nigra with a moderate
degree of iron deposition and neuroaxonal
spheroids (fig 2 D). The gracilis and cuneatus
nuclei showed large numbers of neuroaxonal
spheroids with no significant neuronal loss or
pigment deposition. Sections of neocortex
showed mild patchy neuronal loss and occasional
spheroids. The substantia nigra pars
compacta showed no significant neuronal loss
and gliosis but a rare spheroid. Mild Alzheimer
type changes were present (CERAD: neurofibrillary
tangles 0, neuritic plaques sparse, and
diffuse plaques moderate; BRAAK stage II/
VI). In addition to the degenerative changes,
there was an old haemorrhagic infarct in the
occipital lobe in close proximity to a recent
intracerebral haemorrhage. These vascular
changes were accompanied by severe amyloid
angiopathy.
NEUROPATHOLOGICAL DIAGNOSIS
The neuropathalogical diagnoses were:
Hallervorden-Spatz syndrome; old occipital
infarction; recent intracerebral haemorrhage
due to amyloid angiopathy; mild Alzheimer’s
changes.
Figure 2 (A) Neuronal loss, (B) spheroids (arrows), and (C) iron pigment deposition (arrow) in the medial segment of the globus pallidus. (D) Spheroids in the substantia nigra, pars reticulata (arrows). Haematoxylin and eosin luxol fast blue (A, B, and D). Perl’s Prussian blue reaction for iron (C
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2007-10-1 16:48:00 Re:[灌水]病例讨论 转发（八）
叩诊锤论坛[灌水]病例讨论 转发（八）（公布结果 Hallervorden–Spatz disease ）1
叩诊锤论坛[灌水]病例讨论 转发（八）（公布结果 Hallervorden–Spatz disease ）2
叩诊锤论坛-脑室出血，病因？(有明确结论！) 1
叩诊锤论坛典型影像常春藤征(ivy sign)1
军团病（Legionnaires disease）
叩诊锤论坛--脑室出血，病因？(有明确结论！)2
叩诊锤论坛---脑室出血，病因？(有明确结论！)3
叩诊锤论坛--脑室出血，病因？(有明确结论！)4
叩诊锤论坛---脑室出血，病因？(有明确结论！)5
叩诊锤论坛典型影像，大家看看2
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