Dystonia in central pontine myelinolysis without evidence of extrapontine myelinolysis.

Salerno, Sergio; Kurlan, Roger; Joy, Stephen E.; Shoulson, Ira

doi:10.1136/jnnp.56.11.1221

Cited by 15 publications

(6 citation statements)

References 9 publications

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“…However, given the probable occurrence of CPM-EPM in the early post-operative period, we hypothesize a delayed movement disorder related to extrapontine myelin damage. Similar cases have been previously reported (14)(15)(16)(17)(18), with a latency as long as two years (15). We considered also a possible side-effect of CyA, but the low plasma levels, the tardive onset and the permanence of the symptoms do not favor this hypothesis.…”

Section: Discussionsupporting

confidence: 53%

No neurological improvement after liver transplantation for Wilson's disease

Guarino

Stracciari

D’Alessandro

et al. 2009

Acta Neurologica Scandinavica

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Orthotopic liver transplantation (OLT) represents the sole etiological treatment for Wilson's disease (WD), but its efficacy in resolving the neurological symptoms is still a matter of debate. We present the case of a young male affected by WD with hepatic and neurological involvement, who underwent OLT for subacute liver failure. Clinical, neuropsychological and neuroradiological assessment were performed before and after OLT. OLT had no effect on neurological symptoms, suggesting that the basal ganglia damage may be irreversible. Nineteen months after OLT, the patient went on to develop new permanent extrapyramidal symptoms. We postulate a sequela of an early post‐operative central pontine and extrapontine myelinolysis.

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Section: Discussionsupporting

confidence: 53%

No neurological improvement after liver transplantation for Wilson's disease

Guarino

Stracciari

D’Alessandro

et al. 2009

Acta Neurologica Scandinavica

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“…In central pontine myolinolysis, dystonic movement disorders have been repeatedly described. There is evidence that dystonia may occur in cases of central pontine myolinolysis without evidence of extrapontine lesions 24. Moreover, McNaught and colleagues found perinuclear inclusion bodies in the midbrain reticular formation of four patients with DYT1 primary torsion dystonia while the basal ganglia appeared to be unaffected 5…”

Section: Discussionmentioning

confidence: 99%

Dystonia Associated with pontomesencephalic lesions

Loher

Krauss

2008

Movement Disorders

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Secondary dystonia is well known subsequent to lesions of the basal ganglia or the thalamus. There is evidence that brainstem lesions may also be associated with dystonia, but little is known about pathoanatomical correlations. Here, we report on a series of four patients with acquired dystonia following brainstem lesions. There were no basal ganglia or thalamic lesions. Three patients suffered tegmental pontomesencephalic hemorrhage and one patient diffuse axonal injury secondary to severe craniocerebral trauma. Dystonia developed with a delay of 1 to 14 months, at a mean delay of 6 months. The patients' mean age at onset was 33 years (range 4-56 years). All patients presented with hemidystonia combined with cervical dystonia, and two patients had craniofacial dystonia in addition. Three patients had postural or kinetic tremors. Dystonia was persistent in three patients, and improved gradually in one. There was little response to medical treatment. One patient with hemidystonia combined with cervical dystonia improved after thalamotomy. Overall, the phenomenology of secondary dystonia due to pontomesencephalic lesions is similar to that caused by basal ganglia or thalamic lesions. Structures involved include the pontomesencephalic tegmentum and the superior cerebellar peduncles. Such lesions are often associated with fatal outcome. While delayed occurrence of severe brainstem dystonia appears to be rare, it is possible that mild manifestations of dystonia might be ignored or not be emphasized in the presence of other disabling deficits.

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“…19 If the published report did not use the specific terms to describe symptoms, categorization was performed based on definitions within the aforementioned consensus statements. 1,19 For example, if the authors did not explicitly use the term “generalized dystonia,” but described the body parts affected (e.g., Ref. 20), this could be classified based on the definition by Albanese et al 1 (“The trunk and at least 2 other sites are involved”).…”

Section: Methodsmentioning

confidence: 99%

Clinical and Structural Findings in Patients With Lesion-Induced Dystonia

et al. 2022

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Background and Objectives:Brain lesions are a well-recognized etiology of dystonia. These cases are especially valuable as they offer causal insight into the neuroanatomical substrates of dystonia. To date, knowledge of lesion-induced dystonia comes mainly from isolated case reports or small case series, restricting broader description and analysis.Methods:Cases of lesions-induced dystonia were first identified from a systematic review of published literature. Latent class analysis then investigated whether patients could be classified into subgroups based on lesion location and body regions affected by dystonia. Regression analyses subsequently investigated whether subgroup membership predicted clinical characteristics of dystonia.Results:359 published cases were included. Lesions causing dystonia occurred in heterogeneous locations, most commonly in the basal ganglia (46.2%), followed by the thalamus (28.6%), brainstem (22.6%), and white matter (21.2%). The most common form of lesion-induced dystonia was focal dystonia (53.2%), with the hand (49.9%) and arm (44.3%) most commonly affected. Of all cases, 86.6% reported co-occurring neurological manifestations, and 26.1% reported other movement disorders. Latent class analysis identified three distinct subgroups of patients: those with predominantly limb dystonias, which were associated with basal ganglia lesions; those with predominantly cervical dystonia, associated with brainstem and cerebellar lesions; and those with predominantly hand dystonia, associated with thalamic lesions. Regression demonstrated significant differences between these subgroups on a range of dystonia symptoms, including dystonic tremor, symptom latency, other movement disorders, and dystonia variability.Discussion:While dystonia can be induced by lesions to numerous brain regions, there are distinct relationships between lesion locations and dystonic body parts. This suggests that the affected brain networks are different between types of dystonia.

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Dystonia in central pontine myelinolysis without evidence of extrapontine myelinolysis.

Cited by 15 publications

References 9 publications

No neurological improvement after liver transplantation for Wilson's disease

No neurological improvement after liver transplantation for Wilson's disease

Dystonia Associated with pontomesencephalic lesions

Clinical and Structural Findings in Patients With Lesion-Induced Dystonia

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