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Neurology AND Movement disorders [keywords]
- Botulinum toxin therapy of cervical dystonia: duration of therapeutic effects. [JOURNAL ARTICLE]
- J Neural Transm 2014 Jul 23.
We sought to explore the therapeutic effect of botulinum toxin (BT) therapy by analysing the time between the BT application and the onset of its decrease (treatment duration, TD), the inter-injection interval (II), and the excess time (ET, ET = II-TD). For this we studied 59 patients (37 females, 22 males, age 52.6 ± 10.9 years) with cervical dystonia (CD, Tsui score 9.0 ± 4.1) and BT therapy with Botox(®) and/or Xeomin(®) sequentially. Altogether 1,289 treatment cycles were evaluated. On average 21.8 ± 14.0 (4-66) treatment cycles were recorded for each patient. TD was 11.8 ± 2.7 weeks (7.8 ± 1.4 to 21.0 ± 3.9 weeks), II 15.4 ± 3.4 weeks (11.3 ± 1.3 to 27.8 ± 11.6 weeks) and ET 3.5 ± 2.4 weeks (23 % of II). TD and II were stable throughout the treatment course. In 36 % of the patients we found TD ≤10 weeks, in 83 % TD ≤12 weeks. In 17 % of the patients we saw treatment delays due to appointment difficulties, due to the patient's attempts to explore TD or his actual CD severity, from fear of adverse effects or due to psychiatric comorbidity. 19 % of the patients showed prolonged treatment effects probably due to CD fluctuations. 0.38 % of the injection series produced singular unexplained therapy failure (SUTF). Antibody-induced therapy failure did not occur. TD and II are stable on long-term monitoring. SUTF, treatment delays, and CD fluctuations can occur. 23 % of the time patients are treated suboptimally. Our data suggest to reduce II. If II is to be reduced to ≤12 weeks, use of low antigenicity BT drugs might be useful.
- Teaching Video NeuroImages: Semiology and localization of ballistic movements. [Journal Article]
- Neurology 2014 Jul 22; 83(4):e56-7.
- Natural history of falls in a population-based cohort of patients with Parkinson's disease: An 8-year prospective study. [JOURNAL ARTICLE]
- Parkinsonism Relat Disord 2014 Jul 9.
Prospective long-term studies of falls in Parkinson's disease (PD) are scarce.To examine the development of falls over 8 years in a population-based cohort of ambulatory patients with PD, and to investigate predictors of future falls in non-fallers at baseline.All patients were examined at baseline and after 4 and 8 years, including the UPDRS, MMSE, Montgomery and Aaberg Depression Rating Scale, Functional Comorbidity Index, and a clinical dementia interview. Logistic regression models were applied to investigate baseline risk factors for future falls. A total of 211 patients were included at baseline, whereas 121 and 64 were re-examined at 4 and 8 years, respectively.The prevalence of falls increased from 41% (87 of 211) at baseline to 72% (46 of 64) after 8 years of prospective follow-up (disease duration 16.2 ± 4.8 years). Forty-seven non-falling patients at baseline completed all study visits, of these 68% (n = 32) changed fall status during follow-up. Predictive variables for current falling after 4 years were rare or occasional freezing of gait (OR 6.6, 95% CI 1.2-36.9), higher levodopa equivalent doses and more severe speech and axial impairment (both OR 1.3, 95% CI 1.0-1.7) in non-fallers at baseline. Higher baseline age was the only risk factor for current falling after 8 years.Nearly ¾ of the PD cohort reported falling after 8 years of follow-up. Disease-specific gait and axial impairments were the major risk factors for future falls in non-fallers at baseline. This has implications for patient education and management.
- Reply: The FM/AM world is shaping the future of deep brain stimulation. [LETTER]
- Mov Disord 2014 Jul 17.
- All in the blink of an eye: new insight into cerebellar and brainstem function in DYT1 and DYT6 dystonia. [JOURNAL ARTICLE]
- Eur J Neurol 2014 Jul 18.
Traditionally dystonia has been considered a disorder of basal ganglia dysfunction. However, recent research has advocated a more complex neuroanatomical network. In particular, there is increasing interest in the pathophysiological role of the cerebellum. Patients with cervical and focal hand dystonia have impaired cerebellar associative learning using the paradigm eyeblink conditioning. This is perhaps the most direct evidence to date that the cerebellum is implicated in patients.Eleven patients with DYT1 dystonia and five patients with DYT6 dystonia were examined and rates of eyeblink conditioning were compared with age-matched controls. A marker of brainstem excitability, the blink reflex recovery, was also studied in the same groups.Patients with DYT1 and DYT6 dystonia have a normal ability to acquire conditioned responses. Blink reflex recovery was enhanced in DYT1 but this effect was not seen in DYT6.If the cerebellum is an important driver in DYT1 and DYT6 dystonia our data suggest that there is specific cerebellar dysfunction such that the circuits essential for conditioning function normally. Our data are contrary to observations in focal dystonia and suggest that the cerebellum may have a distinct role in different subsets of dystonia. Evidence of enhanced blink reflex recovery in all patients with dystonia was not found and recent studies calling for the blink recovery reflex to be used as a diagnostic test for dystonic tremor may require further corroboration.
- Discrimination of cortical laminae using MEG. [JOURNAL ARTICLE]
- Neuroimage 2014 Jul 16.
Typically MEG source reconstruction is used to estimate the distribution of current flow on a single anatomically derived cortical surface model. In this study we use two such models representing superficial and deep cortical laminae. We establish how well we can discriminate between these two different cortical layer models based on the same MEG data in the presence of different levels of co-registration noise, Signal-to-Noise Ratio (SNR) and cortical patch size. We demonstrate that it is possible to make a distinction between superficial and deep cortical laminae for levels of co-registration noise of less than 2mm translation and 2 degree rotation at SNR>11dB. We also show that an incorrect estimate of cortical patch size will tend to bias layer estimates. We then use a 3D printed head-cast (Troebinger et al., 2013) to achieve comparable levels of co-registration noise, in an auditory evoked response paradigm and show that it is possible to discriminate between these cortical layer models in real data.
- Neuroprotection by Orexin-A via HIF-1α Induction in a Cellular Model of Parkinson's Disease. [JOURNAL ARTICLE]
- Neurosci Lett 2014 Jul 16.
Orexin-A, a neuropeptide secreted by hypothalamic neurons, may be neuroprotective in many neurological conditions such as cerebral ischemia. One mechanism postulated to be involved in the neuroprotection by Orexin-A is the induction of hypoxia inducible factor 1 alpha (HIF-1α). Parkinson's disease (PD) is a progressive neurodegenerative disorder and mitochondrial dysfunction has been demonstrated to play a role in its pathogenesis. Mitochondrial dysfunction may cause reduction of O2 consumption and subsequently activate prolyl hydroxylase, which leads to decreased levels of HIF-1α. In this study, we used MPP(+)-treated SH-SY5Y cells as an in vitro cellular model of PD to test the role of Orexin-A as an inducer of HIF-1α. Our results showed that Orexin-A not only induced HIF-1α but also activated downstream targets of HIF-1α, such as vascular endothelial growth factor and erythropoietin. Thus, Orexin-A treatment attenuated MPP(+)-induced cell injury and this effect was blocked when HIF-1α was suppressed. Hence, we conclude that induction of HIF-1α is one of the mechanisms involved in the neuroprotection by Orexin-A.
- Persistent frequent subclinical seizures and memory impairment after clinical remission in smoldering limbic encephalitis. [JOURNAL ARTICLE]
- Epileptic Disord 2014 Jul 18.
Aim. To delineate a possible correlation between clinical course and EEG abnormalities in non-infectious "smoldering" limbic encephalitis. Methods. Long-term clinical data, including video-EEG monitoring records, were analysed in two patients. Results. The two patients were positive for anti-voltage-gated potassium channel complex antibody and unspecified antineuronal antibody, respectively. The latter patient had small cell lung carcinoma. Both patients had memory impairment and clinical seizures. EEG showed frequent subclinical seizure patterns in the bilateral temporal regions. Subclinical seizure patterns and memory impairment persisted over one to two years after clinical seizure remission. Therapy (prednisolone and chemoradiation in the two patients, respectively) resulted in decreased occurrence of subclinical seizure patterns and memory improvement. Conclusions. EEG seizure patterns may persist years after clinical seizure remission in "smoldering" limbic encephalitis and lead to memory impairment.