Letter to the editors: comment on “Dissociation of caloric and head impulse tests: a marker of Meniere’s disease”

Eighty years of Medication-Overuse Headache: what about Medication-Overuse Backpain? Abstract Introduction Although chronic low back pain (CLBP) is one of the most common pain syndromes, up to now, clear pathophysiological causes or specific treatment options are missing. Medication-overuse has been associated with chronic headache, but never with CLBP. Hypothesis Based on several similarities between CLBP and Medication-Overuse Headache (MOH), we hypothesized that medication-overuse might contribute to CLBP as well, maybe even as an own entity. Might there be something like Medication-Overuse Backpain (MOB)? Methods We substantiate our hypothesis with a preliminary case-series analyzing five patients suffering from CLBP with a marked medication-overuse. In these patients, a stepwise analgesic withdrawal was recommended. Results Within 6 months of recruitment, five patients fulfilled the inclusion criteria and successfully completed discontinuation of their medication. All patients reported noticeable pain relief, despite the discontinuation of their analgesics. Withdrawal was well tolerated in all cases. Conclusions Considering our results, the described withdrawal method seems to be a simple and safe method to achieve pain reduction while simultaneously preventing organ damage. Despite the preliminary character of our results, our hypothesis might stimulate a new understanding of CLBP’s pathophysiology.

Gaetano Rummo (1853–1917)

High-dose steroid therapy for CNS inflammatory diseases increases INR in patients taking oral vitamin K antagonist

Multiple sclerosis associated with pembrolizumab in a patient with non-small cell lung cancer

Early MRI predictors of prognosis in multiple sclerosis

Correction to: How satisfied are cervical dystonia patients after 3 years of botulinum toxin type A treatment? Results from a prospective, long-term observational study The article How satisfied are cervical dystonia patients after 3 years of botulinum toxin type A treatment?

Clinical features, outcomes and prognostic factors of tuberculous meningitis in adults worldwide: systematic review and meta-analysis Abstract Background Tuberculous meningitis (TBM) is one of the most life-threatening infectious diseases. We performed a systematic review and meta-analysis of the clinical features, outcomes, and prognostic factors for TBM in adults. Methods PubMed, EMBASE, Cochrane CENTRAL, and Web of Science were searched for studies that reported the clinical outcomes and/or risk factors for death in adults with TBM between January 1990 and July 2018. A random-effects meta-analysis model was used to pool data on clinical features, outcomes, and risk factors for death. Results Thirty-two studies that examined 5023 adults who had TBM met the inclusion criteria. Overall, the mortality was 22.8% [95% confidence interval (CI) 18.9–26.8] and the risk of neurological sequelae was 28.7% (95% CI 22.8–35.1). The major risk factors for death (OR > 2 and P < 0.05) were advanced stage of disease (OR = 6.06, 95% CI 4.31–8.53), hydrocephalus (OR = 5.27, 95% CI 2.25–12.37), altered consciousness (OR 3.33, 95% CI 1.51–7.36), altered sensorium (OR 3.31, 95% CI 2.20–4.98), advanced age (> 60 years; OR = 2.64, 95% CI 1.27–5.51), and cerebral infarction (OR = 2.35, 95% CI 1.63–3.38). The clinical features and diagnostic findings present in more than four-fifths of the patients were fever (86.3%, 95% CI 82.4–89.8) and low CSF/serum glucose ratio (80.6%, 95% CI 64.8–92.6). Conclusions Adults with TBM have high rates of mortality. Clinicians should maintain a high clinical suspicion for patients who present with certain clinical features, and should pay more attention to prognostic factors.

Unexpected emergence from the vegetative state: delayed discovery rather than late recovery of consciousness Abstract Background The vegetative state, also known as the unresponsive wakefulness syndrome, is one of the worst possible outcomes of acquired brain injury and confronts rehabilitation specialists with various challenges. Emergence to (minimal) consciousness is classically considered unlikely beyond 3–6 months after non-traumatic or 12 months after traumatic etiologies. A growing body of evidence suggests that these timeframes are too narrow, but evidence regarding chances of recovery is still limited. Objective To identify the moment of recovery of consciousness in documented cases of late emergence from a vegetative state. Methods Four cases of apparent late recovery of consciousness, identified within a prospective cohort study, were studied in-depth by analyzing medical, paramedical and nursing files and interviewing the patients’ families about their account of the process of recovery. Results All patients were found to have shown signs of consciousness well within the expected time frame (5 weeks–2 months post-ictus). These behaviors, however, went unnoticed or were misinterpreted, leading to a diagnostic delay of several months to over 5 years. Absence of appropriate diagnostics, the use of erroneous terminology, sedative medication but also patient-related factors such as hydrocephalus, language barriers and performance fluctuations are hypothesized to have contributed to the delay. Conclusions Delayed recognition of signs of consciousness in patients in a vegetative state may not only lead to suboptimal clinical care, but also to distorted prognostic figures. Discriminating late recovery from the delayed discovery of consciousness, therefore, is vital to both clinical practice and science.

Genetic and clinical analyses of spinocerebellar ataxia type 8 in mainland China Abstract Background Spinocerebellar ataxia type 8 (SCA8) is a rare autosomal dominant neurodegenerative disease caused by CTA/CTG repeat expansion in the ATXN8/ATXN8OS gene. Methods To analyze the frequency and clinical characteristics of SCA8 patients in mainland China, we combined polymerase chain reaction (PCR) and triplet repeat-primed PCR (TRP-PCR) to detect the CTA/CTG expansion. We studied a cohort of 362 ataxia patients in which the other known causative genes had been previously excluded, from among 1294 index patients. Positive samples were validated by southern blotting. Results The CTA/CTG expansion was observed in six probands, accounting for approximately 0.46% (6/1294) in all patients, and 1.66% (6/362) in patients without definite molecular diagnosis. Clinically, aside from the typical SCA8 phenotype, some patients carrying the CTA/CTG expansion exhibited the cerebellar form of multisystem atrophy (MSA-C) and ataxia with paroxysmal kinesigenic dyskinesia (PKD). Conclusion For the first time, we described the PKD phenotype in association with CTA/CTG expansion, suggesting that CTA/CTG expansion might play a role in the pathogenesis of paroxysmal dyskinesia symptoms.