Charcot's early descriptions of patients with multiple sclerosis noted “enfeeblement of memory” and “concepts formed slowly,” along with the classic triad of nystagmus, intention tremor, and ataxic dysarthria.1 Charcot was trained in psychiatry and neurology, but for decades neither discipline took note of his psychological observations. Psychiatrists in the 1920s used interviews to probe mental status in people with multiple sclerosis, but estimates of the frequency of cognitive impairment were unreliable, ranging from two to 72%.
We take our vision for granted, rarely stopping to consider that the human visual system is a marvel of evolution capable of correctly—and almost instantaneously—identifying a multitude of objects from a variety of angles, and often while impeded by motion or poor lighting. Our understanding of human vision is still far from complete, but what we have learned so far has helped us to understand other aspects of the human brain, and this is the central theme in We know it when we see it, by the great neurobiologist Richard Masland (1942-2019).
Parkinson's disease is one of the most common neurological disorders and its prevalence more than doubled between 1990 and 2016 to over 6 million patients worldwide. This increase cannot be solely attributed to population ageing. The relatively high contribution of Parkinson's disease to the global burden of neurological diseases reflects its progressive, debilitating nature. In recognition of the importance of and need for large-scale data collection efforts to enable meaningful progress in the development of new therapies to treat this disease, the Accelerating Medicines Partnership for Parkinson's Disease (AMP-PD) initiative was established in 2018.
The word pandemic is now everywhere we look, courtesy of COVID-19. In their book Ending Parkinson's disease, Ray Dorsey, Todd Sherer, Michael Okun, and Bastiaan Bloem talk about a figurative pandemic though. The number of individuals to be diagnosed with Parkinson's disease could increase dramatically in the coming years due to population ageing and because of environmental factors; this book is a call to action, with a prescriptive list on how to prevent these factors.
The introduction of monoclonal antibodies targeting the calcitonin gene-related peptide (CGRP) or its receptor for migraine prevention has been a great success. In The Lancet Neurology, Wim M Mulleners and colleagues report data that complete findings from a series of randomised, controlled trials targeting CGRP in patients with migraine in whom previous prophylactic treatment attempts had been unsuccessful.1 These trials have shown that erenumab,2 fremanezumab,3 and, as reported now in this Article, galcanezumab1 can provide beneficial effects for these patients.
Galcanezumab was superior to placebo in the preventive treatment of migraine and was safe and well tolerated in patients for whom multiple previous standard-of-care preventive treatments had failed. Galcanezumab might represent an important treatment option for patients who have not benefited from or tolerated previous standard-of-care treatments.
In the past decade, many tropical regions have had arboviruses epidemics, including of Zika, dengue, and chikungunya viruses. Factors related to arboviral infection epidemics include population growth, unplanned urbanisation, increased travel, climate change, and decline of vector control programmes. The geographical distribution of Zika, dengue, and chikungunya viruses overlap and co-circulation became a serious concern in regions where Aedes spp mosquito vectors are endemic. Particularly, the Americas suffered from simultaneous outbreaks and co-circulation of these arthropod-borne viruses.
There is a wide and overlapping spectrum of neurological manifestations caused by Zika or chikungunya mono-infection and by dual infections. The possible increased risk of acute cerebrovascular disease in patients with dual infection merits further investigation.
In his study of Beckett's Waiting for Godot, Martin Esslin argued that although inherent meaning might exist in the universe, we are incapable of understanding it because of our intrinsic limitations.1 Like Beckett's play, dreams invite boundless speculation about their origin and meaning. Psychiatrist Allan Hobson long ago called the oneiric protoconsciousness of rapid eye movement (REM) sleep a primordial state of brain organisation,2 to which we revert every night, as to our own theatre of the absurd.
We present, to our knowledge, the first evidence of statistically robust genetic associations in sporadic human prion disease that implicate intracellular trafficking and sphingolipid metabolism as molecular causal mechanisms. Risk SNPs in STX6 are shared with progressive supranuclear palsy, a neurodegenerative disease associated with misfolding of protein tau, indicating that sCJD might share the same causal mechanisms as prion-like disorders.