The corticobasal syndrome triggered by central pontine myelinolysis

Shamim, Ahmar; Siddiqui, B. K.; Josephs, Keith A.

doi:10.1111/j.1468-1331.2006.01221.x

Cited by 8 publications

(3 citation statements)

References 14 publications

(17 reference statements)

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“…This leads to loss of inhibitory striatonigral feedback regulation 16 . Shamim et al reported a case of corticobasal syndrome following CPM in an elderly lady who developed progressive asymmetric parkinsonism with ideomotor apraxia and cortical sensory deficits 17 . One of our patients (Patient‐8) had corticobasal syndrome like presentation but without cortical signs and FDG = PET was not consistent with corticobasal syndrome.…”

Section: Discussionmentioning

confidence: 74%

The Spectrum of Movement Disorders in Cases with Osmotic Demyelination Syndrome

Sindhu

Holla

Prasad

et al. 2021

Movement Disord Clin Pract

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Background Osmotic demyelination syndrome (ODS) can be a central pontine myelinolysis (CPM) and extrapontine myelinolysis (EPM) based on the regions involved even though they share the same disease process, aetiopathogenesis and time course. Objectives Present study aims to characterize the clinical, radiological features and the outcome of patients with ODS with movement disorders as the forthcoming manifestation. Methods Chart review of patients with ODS with movement disorders. Demographic, clinical and radiological details of the patients were reviewed. Results Eleven patients (six females; mean age: 48.3 ± 17.6 years) were included in the study. Parkinsonism alone and parkinsonism with dystonia was noted in four patients each (36.4%) while dystonia alone was noted in the other 3 (27.3%). Five patients (45.5%) had postural tremors. While 5 patients had dystonia early in the course of illness (3–7 days), it was delayed (6–9 months) in the other 2. A triphasic course was noted in two patients. The first phase of hyponatremia induced neurological impairment was followed by a second phase of worsening due to the immediate effect of ODS and a third delayed phase of worsening due to delayed effect of ODS. MRI showed both EPM and CPM in eight patients, EPM alone in two patients and CPM alone in 1 patient. Nine patients had a good outcome with mRS < 3. Conclusion Parkinsonism and dystonia are important manifestations of ODS. Triphasic course with a delayed phase of worsening of movement disorders is probably due to the maladaptive neuronal repair. The concept of triphasic ODS is first being described in our series.

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Section: Discussionmentioning

confidence: 74%

The Spectrum of Movement Disorders in Cases with Osmotic Demyelination Syndrome

Sindhu

Holla

Prasad

et al. 2021

Movement Disord Clin Pract

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“…In other patients, however, cerebral lesions compatible with myelinolysis were only evident in the pons, and they still had movement disorders, with parkinsonism as the most common manifestation. Symptoms usually manifest acutely, but also late presentations with a chronic and progressive course have been described, both for dystonia and parkinsonism [5,7]. We were not able to precisely date the myelinolysis of the pons in our patient, as the only symptom he manifested was an intense daily headache for many years before he underwent a first MRI, but we can affirm that the onset of parkinsonism was surely delayed with respect to the pontine lesion compatible with myelinolysis.…”

mentioning

confidence: 58%

“…Moreover, the lesions in deep nuclei remained stable over time (Figure 2). ODS and idiopathic Parkinson's disease (PD) could be independently present in our patient, but it has been postulated that pontine myelinolysis may act as a trigger of a neurodegenerative process [7]; this may be the case for our patient. Of note, the patient had no other non-motor symptoms typical of PD, i.e., sleep disturbances and sensory disturbances, such as reduced olfactory perception, a typical and early symptom of this disease [8,9].…”

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confidence: 71%

Development of Parkinsonism in a Patient with Central Pontine Myelinolysis

Antonioni

Rispoli

Fazio

et al. 2022

Neurology International

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Osmotic demyelination syndrome (ODS) is caused by damage to the pons myelin sheath and nerve cells. Although the pathophysiological mechanism responsible for the damage is not yet fully understood, it is currently believed that osmotic-type changes (especially if they are massive and too rapid) cause oedema that leads to compression and, subsequently, demyelination of white matter fibres. It generally manifests with acute paraparesis/tetraparesis, dysphagia, dysarthria, diplopia, and loss of consciousness, as well as hallucinations, spasms, and other neurological symptoms related to brainstem damage. In extreme cases, the locked-in syndrome may also appear. Of note, in some cases an association between osmotic demyelinating damage and the onset of movement disorders has been documented and, although the pathophysiology is still unknown, a correlation has been postulated between ODS and movement disorders. Here, we present a patient with ODS who developed parkinsonism, thus supporting the hypothesis of a correlation between these pathological events.

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Dose Dependency and Reversibility of Serotonin-Induced Valvular Heart Disease in Rats

et al. 2009

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Serotonergic drugs may lead to valvular heart disease in humans and more recently also in rats. Although clinical data suggest that dose dependency and reversibility after drug cessation might occur, proof of this is lacking. For that purpose, a total of 106 rats were prospectively enrolled: 22 control animals and 7 groups of 12 rats that received daily subcutaneous serotonin injections (5, 10, 20, 30, 40, 50 and 60 mg/kg respectively) for 12 weeks. At 12 weeks, half of the animals of each group were killed for histological analysis, whereas the remaining rats were further followed (without serotonin injections) for an additional 8 weeks. After 12 weeks of serotonin treatment, aortic and mitral regurgitation (AR, MR) were more frequently observed in the high dose groups (>30 mg/kg) compared to controls. Moreover, aortic and mitral valves were also thicker in the high dose groups compared to controls. After 8 weeks free of serotonin injections, AR and MR were no longer significantly higher than controls. Moreover, aortic and mitral valve thickness had normalized, returning to control levels. In conclusion, this study provides evidence for a dose-dependent valvular toxicity of serotonergic drugs, which appears to be reversible after drug withdrawal.

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The corticobasal syndrome triggered by central pontine myelinolysis

Cited by 8 publications

References 14 publications

The Spectrum of Movement Disorders in Cases with Osmotic Demyelination Syndrome

The Spectrum of Movement Disorders in Cases with Osmotic Demyelination Syndrome

Development of Parkinsonism in a Patient with Central Pontine Myelinolysis

Dose Dependency and Reversibility of Serotonin-Induced Valvular Heart Disease in Rats

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