WordNet
- a pattern of symptoms indicative of some disease
- a complex of concurrent things; "every word has a syndrome of meanings"
PrepTutorEJDIC
- (疾患の徴候となる一群の)症徴候,症候群 / (事件・社会的状態などのパターンを示す)徴候形態
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出典(authority):フリー百科事典『ウィキペディア(Wikipedia)』「2017/07/02 18:52:37」(JST)
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Extrapyramidal system |
Medulla spinalis. (Extrapyramidal tracts are labeled as a group in red, at bottom left.)
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Details |
Identifiers |
Latin |
Systema extrapyramidale |
MeSH |
Extrapyramidal+tracts |
NeuroNames |
ancil-623 |
Dorlands
/Elsevier |
s_33/12787420 |
Anatomical terms of neuroanatomy
[edit on Wikidata]
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In anatomy, the extrapyramidal system is a biological neural network that is part of the motor system causing involuntary movements. The system is called "extrapyramidal" to distinguish it from the tracts of the motor cortex that reach their targets by traveling through the "pyramids" of the medulla. The pyramidal pathways (corticospinal and some corticobulbar tracts) may directly innervate motor neurons of the spinal cord or brainstem (anterior (ventral) horn cells or certain cranial nerve nuclei), whereas the extrapyramidal system centers on the modulation and regulation (indirect control) of anterior (ventral) horn cells.
Extrapyramidal tracts are chiefly found in the reticular formation of the pons and medulla, and target lower motor neurons in the spinal cord that are involved in reflexes, locomotion, complex movements, and postural control. These tracts are in turn modulated by various parts of the central nervous system, including the nigrostriatal pathway, the basal ganglia, the cerebellum, the vestibular nuclei, and different sensory areas of the cerebral cortex. All of these regulatory components can be considered part of the extrapyramidal system, in that they modulate motor activity without directly innervating motor neurons.
The extrapyramidal tracts include parts of the following:[1]
- rubrospinal tract
- pontine reticulospinal tract
- medullary reticulospinal tract
- lateral vestibulospinal tract
- tectospinal tract
See also
- List of regions in the human brain
- Extrapyramidal symptoms
- Rabbit syndrome, a rare extrapyramidal side effect
- tectospinal tract
- reticulospinal tract
- vestibulospinal tract
References
- ^ http://www.amazon.com/BRS-Physiology-Board-Review-Series/dp/0781798760/
The spinal cord
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General features |
- Cervical enlargement
- Lumbar enlargement
- Conus medullaris
- Filum terminale
- Cauda equina
- Meninges
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Grey matter |
Posterior grey column |
- Marginal nucleus
- Substantia gelatinosa of Rolando
- Nucleus proprius
- Spinal lamina V
- Spinal lamina VI
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Lateral grey column |
- Intermediolateral nucleus
- Posterior thoracic nucleus
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Anterior grey column |
- Interneuron
- Alpha motor neuron
- Gamma motor neuron
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Other |
- Rexed laminae
- Central gelatinous substance
- Gray commissure
- Central canal
- Terminal ventricle
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White matter |
Sensory |
Posterior |
- Posterior column-medial lemniscus pathway:
- Gracile
- Cuneate
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Lateral: |
- Spinocerebellar
- Spinothalamic
- Posterolateral
- Spinotectal
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- Spinoreticular tract
- Spino-olivary tract
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Motor |
Lateral |
- Corticospinal
- Extrapyramidal
- Rubrospinal
- Olivospinal
- Raphespinal
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Anterior |
- Corticospinal
- Extrapyramidal
- Vestibulospinal
- Reticulospinal
- Tectospinal
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Both |
- Anterior white commissure
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External features |
- Ventral
- Anterior median fissure
- Anterolateral sulcus
- Dorsal
- Posterior median sulcus
- Posterolateral sulcus
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Brain and spinal cord: neural tracts and fasciculi
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Sensory/
ascending |
PCML |
1°: |
- Pacinian corpuscle/Meissner's corpuscle → Posterior column (Gracile fasciculus/Cuneate fasciculus) → Gracile nucleus/Cuneate nucleus
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2°: |
- → sensory decussation/arcuate fibers (Posterior external arcuate fibers, Internal arcuate fibers) → Medial lemniscus/Trigeminal lemniscus → Thalamus (VPL, VPM)
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3°: |
- → Posterior limb of internal capsule → Postcentral gyrus
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Anterolateral/
pain |
Fast/lateral |
- 1° (Free nerve ending → A delta fiber) → 2° (Anterior white commissure → Lateral and Anterior Spinothalamic tract → Spinal lemniscus → VPL of Thalamus) → 3° (Postcentral gyrus) → 4° (Posterior parietal cortex)
2° (Spinomesencephalic tract → Superior colliculus of Midbrain tectum)
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Slow/medial |
- 1° (Group C nerve fiber → Spinoreticular tract → Reticular formation) → 2° (MD of Thalamus) → 3° (Cingulate cortex)
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Motor/
descending |
Pyramidal |
- flexion: Primary motor cortex → Posterior limb of internal capsule → Decussation of pyramids → Corticospinal tract (Lateral, Anterior) → Neuromuscular junction
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Extrapyramidal |
flexion: |
- Primary motor cortex → Genu of internal capsule → Corticobulbar tract → Facial motor nucleus → Facial muscles
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flexion: |
- Red nucleus → Rubrospinal tract
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extension: |
- Vestibulocerebellum → Vestibular nuclei → Vestibulospinal tract
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extension: |
- Vestibulocerebellum → Reticular formation → Reticulospinal tract
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- Midbrain tectum → Tectospinal tract → muscles of neck
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Basal ganglia |
direct: |
1° (Motor cortex → Striatum) → 2° (GPi) → 3° (Lenticular fasciculus/Ansa lenticularis → Thalamic fasciculus → VL of Thalamus) → 4° (Thalamocortical radiations → Supplementary motor area) → 5° (Motor cortex)
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indirect: |
1° (Motor cortex → Striatum) → 2° (GPe) → 3° (Subthalamic fasciculus → Subthalamic nucleus) → 4° (Subthalamic fasciculus → GPi) → 5° (Lenticular fasciculus/Ansa lenticularis → Thalamic fasciculus → VL of Thalamus) → 6° (Thalamocortical radiations → Supplementary motor area) → 7° (Motor cortex)
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nigrostriatal pathway: |
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Cerebellar |
Afferent |
- Vestibular nuclei → Vestibulocerebellar tract → ICP → Cerebellum → Granule cell
- Pontine nuclei → Pontocerebellar fibers → MCP → Deep cerebellar nuclei → Granule cell
- Inferior olivary nucleus → Olivocerebellar tract → ICP → Hemisphere → Purkinje cell → Deep cerebellar nuclei
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Efferent |
- Dentate nucleus in Lateral hemisphere/pontocerebellum → SCP → Dentatothalamic tract → Thalamus (VL) → Motor cortex
- Interposed nucleus in Intermediate hemisphere/spinocerebellum → SCP → Reticular formation, or → Cerebellothalamic tract → Red nucleus → Thalamus (VL) → Motor cortex
- Fastigial nucleus in Flocculonodular lobe/vestibulocerebellum → Vestibulocerebellar tract → Vestibular nuclei
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Bidirectional:
Spinocerebellar |
Unconscious
proprioception |
- lower limb → 1° (muscle spindles → DRG) → 2° (Posterior thoracic nucleus → Dorsal/posterior spinocerebellar tract → ICP → Cerebellar vermis)
- upper limb → 1° (muscle spindles → DRG) → 2° (Accessory cuneate nucleus → Cuneocerebellar tract → ICP → Anterior lobe of cerebellum)
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Reflex arc |
- lower limb → 1° (Golgi tendon organ) → 2° (Ventral/anterior spinocerebellar tract→ SCP → Cerebellar vermis)
- upper limb → 1° (Golgi tendon organ) → 2° (Rostral spinocerebellar tract → ICP → Cerebellum)
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UpToDate Contents
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English Journal
- C9orf72 repeat expansions are restricted to the ALS-FTD spectrum.
- Ticozzi N1, Tiloca C2, Calini D3, Gagliardi S4, Altieri A3, Colombrita C5, Cereda C4, Ratti A5, Pezzoli G6, Borroni B7, Goldwurm S6, Padovani A7, Silani V5.Author information 1Department of Neurology and Laboratory of Neuroscience, Istituto di Ricovero e Cura a Carattere Scientifico Istituto Auxologico Italiano, Milan, Italy; Department of Pathophysiology and Transplantation, Dino Ferrari Center, Università degli Studi di Milano, Milan, Italy. Electronic address: n.ticozzi@auxologico.it.2Department of Neurology and Laboratory of Neuroscience, Istituto di Ricovero e Cura a Carattere Scientifico Istituto Auxologico Italiano, Milan, Italy; Doctoral School in Molecular Medicine, Department of Sciences and Biomedical Technologies, University of Milan, Milan, Italy.3Department of Neurology and Laboratory of Neuroscience, Istituto di Ricovero e Cura a Carattere Scientifico Istituto Auxologico Italiano, Milan, Italy.4Laboratory of Experimental Neurology, Istituto di Ricovero e Cura a Carattere Scientifico C. Mondino National Neurological Institute, Pavia, Italy.5Department of Neurology and Laboratory of Neuroscience, Istituto di Ricovero e Cura a Carattere Scientifico Istituto Auxologico Italiano, Milan, Italy; Department of Pathophysiology and Transplantation, Dino Ferrari Center, Università degli Studi di Milano, Milan, Italy.6Parkinson Institute, Istituti Clinici di Perfezionamento, Milan, Italy.7Centre for Neurodegenerative Disorders, University of Brescia, Brescia, Italy.AbstractExpansion of a GGGGCC repeat (RE) in the C9orf72 gene has been recently reported as the main genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). Given the growing evidence of genetic and clinicopathologic overlap among ALS, FTD, and other neurodegenerative diseases, we investigated the occurrence of RE in a subset of 9 patients with ALS-plus syndromes, including Parkinson's disease (PD), progressive supranuclear palsy (PSP), corticobasal syndrome (CBS), and multiple system atrophy. We identified RE in 2 ALS-plus individuals (22.2%) displaying PSP and CBS features. On the basis of this finding, we extended our analysis to a cohort composed of 190 PD, 103 CBS, 107 PSP, and 177 Alzheimer's disease cases. We did not identify any RE in these patients, indicating that C9orf72 is in all probability not involved in the pathogenesis of these disorders. However, the high frequency of C9orf72 RE in patients with ALS-plus syndromes suggests that, similar to ALS-FTD patients, individuals with combined motor neuron and extrapyramidal features should be screened for RE, independent of their family history.
- Neurobiology of aging.Neurobiol Aging.2014 Apr;35(4):936.e13-7. doi: 10.1016/j.neurobiolaging.2013.09.037. Epub 2013 Oct 2.
- Expansion of a GGGGCC repeat (RE) in the C9orf72 gene has been recently reported as the main genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). Given the growing evidence of genetic and clinicopathologic overlap among ALS, FTD, and other neurodegenerative disease
- PMID 24169076
- CLIPPERS: chronic lymphocytic inflammation with pontine perivascular enhancement responsive to steroids. Review of an increasingly recognized entity within the spectrum of inflammatory central nervous system disorders.
- Dudesek A1, Rimmele F, Tesar S, Kolbaske S, Rommer PS, Benecke R, Zettl UK.Author information 1Department of Neurology, University of Rostock, Rostock, Germany.AbstractChronic lymphocytic inflammation with pontine perivascular enhancement responsive to steroids (CLIPPERS) is a recently defined inflammatory central nervous system (CNS) disorder, prominently involving the brainstem and in particular the pons. The condition features a combination of clinical symptoms essentially referable to brainstem pathology and a characteristic magnetic resonance imaging (MRI) appearance with punctate and curvilinear gadolinium enhancement 'peppering' the pons. The radiological distribution is focused in the pons and adjacent rhombencephalic structures such as the cerebellar peduncles, cerebellum, medulla and the midbrain. While the lesion burden with a perivascular pattern is typically most dense in these pontine and peripontine regions, enhancing lesions may additionally extend into the spinal cord and supratentorial structures such as the thalamus, basal ganglia, capsula interna, corpus callosum and the cerebral white matter. Another core feature is clinical and radiological responsiveness to glucocorticosteroid (GCS)-based immunosuppression. As withdrawal of GCS treatment results commonly in disease exacerbation, long-term immunosuppressive therapy appears to be mandatory for sustained improvement. Diagnosis of CLIPPERS is challenging, and requires careful exclusion of alternative diagnoses. A specific serum or cerebrospinal fluid (CSF) biomarker for the disorder is currently not known. Pathogenesis of CLIPPERS remains poorly understood, and the nosological position of CLIPPERS has still to be established. Whether CLIPPERS represents an independent, actual new disorder or a syndrome that includes aetiologically heterogeneous diseases and/or their prestages remains a debated and not finally clarified issue. Clinicians and radiologists should be aware of this condition and its differential diagnoses, given that CLIPPERS constitutes a treatable condition and that patients may benefit from an early introduction of GCS ensued by long-term immunosuppression. Based on previous reports in literature - currently encompassing more than 50 reported cases of CLIPPERS - this review addresses clinical features, diagnostic criteria, differential diagnoses and therapeutic management of this peculiar disorder.
- Clinical and experimental immunology.Clin Exp Immunol.2014 Mar;175(3):385-96. doi: 10.1111/cei.12204.
- Chronic lymphocytic inflammation with pontine perivascular enhancement responsive to steroids (CLIPPERS) is a recently defined inflammatory central nervous system (CNS) disorder, prominently involving the brainstem and in particular the pons. The condition features a combination of clinical symptoms
- PMID 24028073
- Drosophila Myc, a novel modifier suppresses the poly(Q) toxicity by modulating the level of CREB binding protein and histone acetylation.
- Singh MD1, Raj K1, Sarkar S2.Author information 1Department of Genetics, University of Delhi, South Campus, Benito Juarez Road, New Delhi 110 021, India.2Department of Genetics, University of Delhi, South Campus, Benito Juarez Road, New Delhi 110 021, India. Electronic address: sarkar@south.du.ac.in.AbstractPolyglutamine or poly(Q) disorders are dominantly inherited neurodegenerative diseases characterised by progressive loss of neurons in cerebellum, basal ganglia and cortex in adult human brain. Overexpression of human form of mutant SCA3 protein with 78 poly(Q) repeats leads to the formation of inclusion bodies and increases the cellular toxicity in Drosophila eye. The present study was directed to identify a genetic modifier of poly(Q) diseases that could be utilised as a potential drug target. The initial screening process was influenced by the fact of lower prevalence of cancer among patients suffering with poly(Q) disorders which appears to be related to the intrinsic biological factors. We investigated if Drosophila Myc (a homologue of human cMyc proto-oncogene) harbours intrinsic property of suppressing cellular toxicity induced by an abnormally long stretch of poly(Q). We show for the first time that targeted overexpression of Drosophila Myc (dMyc) mitigates the poly(Q) toxicity in eye and nervous systems. Upregulation of dMyc results in a significant reduction in accumulation of inclusion bodies with residual poly(Q) aggregates localising into cytoplasm. We demonstrate that dMyc mediated suppression of poly(Q) toxicity is achieved by alleviating the cellular level of CBP and improved histone acetylation, resulting restoration of transcriptional machinery which are otherwise abbreviated due to poly(Q) disease conditions. Moreover, our study also provides a rational justification of the enigma of poly(Q) patients showing resistance to the predisposition of cancer.
- Neurobiology of disease.Neurobiol Dis.2014 Mar;63:48-61. doi: 10.1016/j.nbd.2013.11.015. Epub 2013 Nov 27.
- Polyglutamine or poly(Q) disorders are dominantly inherited neurodegenerative diseases characterised by progressive loss of neurons in cerebellum, basal ganglia and cortex in adult human brain. Overexpression of human form of mutant SCA3 protein with 78 poly(Q) repeats leads to the formation of incl
- PMID 24291519
Japanese Journal
- A Case of Idiopathic Basal Ganglia Calcification Associated with Membranoproliferative Glomerulonephritis
- Tsuchiya Yoshiki,Ubara Yoshifumi,Anzai Makoto,Hiramatsu Rikako,Suwabe Tatsuya,Hoshino Junichi,Sumida Keiichi,Hasegawa Eiko,Yamanouchi Masayuki,Hayami Noriko,Marui Yuji,Sawa Naoki,Hara Shigeko,Takaichi Kenmei,Oohashi Kenichi
- Internal Medicine 50(20), 2351-2356, 2011
- … Idiopathic basal ganglia calcification (IBGC) is a syndrome in which bilateral cerebral calcification occurs despite the absence of abnormal calcium metabolism. … Pyramidal and extrapyramidal signs started to develop at the age of 27 years and progressed, resulting in death from aspiration pneumonia at the age of 32 years. …
- NAID 130001087746
- 山内 健,井崎 ゆみ子,大森 哲郎
- 精神神經學雜誌 = Psychiatria et neurologia Japonica 108(5), 459-465, 2006-05-25
- NAID 10018585037
Related Pictures
★リンクテーブル★
[★]
- 英
- extrapyramidal syndrome, extrapyramidal tract syndrome (SP)
- 関
- 大脳基底核疾患
- 大脳基底核の障害(=大脳基底核疾患)によって生じる症状群
- 筋緊張の異常
- 不随意運動
- 麻痺を伴わない運動減少
- 注意:錐体外路症候群だからと言って、錐体路とか錐体外路のどちらかが関係しなくなることはない。両方とも関わっている。
[★]
[★]
- 関
- extrapyramidal tract
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