Slowly Progressive Dystonia Following Central Pontine and Extrapontine Myelinolysis.

Yoshida, Yukie; Akanuma, Jun; Tochikubo, Sanae; Hoshi, Akihiko; Matsuura, Yutaka; Homma, Mari; Yamamoto, Toshiyuki

doi:10.2169/internalmedicine.39.956

Cited by 11 publications

(5 citation statements)

References 8 publications

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“…The relative role of residual corticospinal function in modulating this manifestation is not clear. It is interesting to note that dystonia has been associated with pontine and extrapontine myelinolysis [11][12][13][14][15][16]. However, the pathophysiology of progressive and delayed dystonia from an osmotic demyelinating process with ineffective reorganization of neuronal structures is not entirely comparable to those associated with a structural lesion.…”

Section: Discussionmentioning

confidence: 99%

Hemidystonia precipitated by acute pontine infarct

Tan

Chan

Auchus

2005

Journal of the Neurological Sciences

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Section: Discussionmentioning

confidence: 99%

Hemidystonia precipitated by acute pontine infarct

Tan

Chan

Auchus

2005

Journal of the Neurological Sciences

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“…1 However, dystonia has also been associated with structural changes or lesions in the brainstem, spinal cord, and peripheral nerves. [2][3][4] Most cases of dystonia, however, occur in the absence of an identified cause or structural lesion in the nervous system. When dystonia occurs without a known cause or recognized pathological condition, it is classified as primary or idiopathic dystonia.…”

mentioning

confidence: 99%

Pathophysiology of dystonia: A neuronal model

2002

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Dystonia has commonly been thought to represent a disorder of basal ganglia function. Although long considered a hyperkinetic movement disorder, the evidence to support such a classification was based on the presence of excessive involuntary movement, not on physiological data. Only recently, with the return of surgical procedures using microelectrode guidance for the treatment of dystonia, has electrophysiological data demonstrated an alteration in mean discharge rate, somatosensory responsiveness and the pattern of neuronal activity in the basal ganglia thalamocortical motor circuit. Previous models of dystonia suggested that reduced mean discharge rates in the globus pallidus internus (GPi) led to unopposed increases in activity in the thalamocortical circuit that precipitated the development of involuntary movement associated with dystonia. This model has subsequently been modified given the clear improvement in dystonic symptoms following lesions in the GPi, a procedure that is associated with a further reduction in pallidal output. The improvement in dystonia following pallidal lesions is difficult to reconcile with the "rate" hypothesis for hypokinetic and hyperkinetic movement disorders and has led to the development of alternative models that, in addition to rate, incorporate changes in pattern, somatosensory responsiveness and degree of synchronization of neuronal activity. Present models of dystonia, however, must not only take these changes into account but must reconcile these changes with the reported changes in cortical excitability reported with transcranial magnetic stimulation, the changes in metabolic activity in cortical and subcortical structures documented by positron emission tomography (PET), and the alterations in spinal and brainstem reflexes. A model incorporating these changes together with the reported changes in neuronal activity in the basal ganglia and thalamus is presented.

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“…Although a cause and effect relationship has not been established, the sites of the brain that are disproportionately involved compared with others include the basal ganglia (particularly the putamen), the thalamus, and cortex 1. However, dystonia has also been associated with structural changes or lesions in the brainstem, spinal cord, and peripheral nerves 2–4. Most cases of dystonia, however, occur in the absence of an identified cause or structural lesion in the nervous system.…”

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confidence: 99%

Vesicular glutamate transporter DNPI/VGLUT2 is expressed by both C1 adrenergic and nonaminergic presympathetic vasomotor neurons of the rat medulla

Stornetta

Sevigny

Schreihofer

et al. 2002

J of Comparative Neurology

182

153

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The main source of excitatory drive to the sympathetic preganglionic neurons that control blood pressure is from neurons located in the rostral ventrolateral medulla (RVLM). This monosynaptic input includes adrenergic (C1), peptidergic, and noncatecholaminergic neurons. Some of the cells in this pathway are suspected to be glutamatergic, but conclusive evidence is lacking. In the present study we sought to determine whether these presympathetic neurons express the vesicular glutamate transporter BNPI/VGLUT1 or the closely related gene DNPI, the rat homolog of the mouse vesicular glutamate transporter VGLUT2. Both BNPI/VGLUT1 and DNPI/VGLUT2 mRNAs were detected in the medulla oblongata by in situ hybridization, but only DNPI/VGLUT2 mRNA was present in the RVLM. Moreover, BNPI immunoreactivity was absent from the thoracic spinal cord lateral horn. DNPI/VGLUT2 mRNA was present in many medullary cells retrogradely labeled with Fluoro-Gold from the spinal cord (T2; four rats). Within the RVLM, 79% of the bulbospinal C1 cells contained DNPI/VGLUT2 mRNA. Bulbospinal noradrenergic A5 neurons did not contain DNPI/VGLUT2 mRNA. The RVLM of six unanesthetized rats subjected to 2 hours of hydralazine-induced hypotension contained tenfold more c-Fos-ir DNPI/VGLUT2 neurons than that of six saline-treated controls. c-Fos-ir DNPI/VGLUT2 neurons included C1 and non-C1 neurons (3:2 ratio). In seven barbiturate-anesthetized rats, 16 vasomotor presympathetic neurons were filled with biotinamide and analyzed for the presence of tyrosine hydroxylase immunoreactivity and/or DNPI/VGLUT2 mRNA. Biotinamide-labeled neurons included C1 and non-C1 cells. Most non-C1 (9/10) and C1 presympathetic cells (5/6) contained DNPI/VGLUT2 mRNA. In conclusion, DNPI/VGLUT2 is expressed by most blood pressure-regulating presympathetic cells of the RVLM. The data suggest that these neurons may be glutamatergic and that the C1 adrenergic phenotype is one of several secondary phenotypes that are differentially expressed by subgroups of these cells.

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Slowly Progressive Dystonia Following Central Pontine and Extrapontine Myelinolysis.

Cited by 11 publications

References 8 publications

Hemidystonia precipitated by acute pontine infarct

Hemidystonia precipitated by acute pontine infarct

Pathophysiology of dystonia: A neuronal model

Vesicular glutamate transporter DNPI/VGLUT2 is expressed by both C1 adrenergic and nonaminergic presympathetic vasomotor neurons of the rat medulla

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