European Journal of Neurology 2014, 21: 1425–1434
Recent advances in neurology 2013–2014
The advent of modern neuro-imaging modalities transformed the practice of neurology and neurosurgery. Advances in this area continue with increased resolution and three-dimensional reconstructions, but perhaps the most exciting area of neuroradiology is the application of radiotracers or receptor ligands to the diagnosis of neurological diseases. The areas of stroke and the neurodegenerative diseases have perhaps been those that have beneﬁted most from the new imaging modalities, but inﬂammatory disorders and common clinical problems such as headache have also seen novel applications. Probably the next most important area for advance and clinical application has been in the ﬁeld of molecular neuroscience and genetics in particular. The ability to identify the genetic basis of disease has transformed the way we recognize the spectrum of the clinical phenotype of a particular mutation; indeed this has led us to reconsider the criteria for diagnosis in certain diseases such as Parkinson’s disease. These advances have also provided invaluable insight into the pathogenesis of neurological diseases and potential targets for novel therapeutic interventions. The past year has seen these advances reﬂected in the number and range of articles published in the European Journal of Neurology. Again, stroke is the most active area for publication followed by Parkinson’s disease and other movement disorders. The pathophysiology of stroke [1–22] has seen advances in the genetics of stroke that include identiﬁcation of a single gene but more frequently multiple gene associations that confer increased risk. The observation that vitamin D levels can be associated with stroke risk is interesting, bearing in mind that levels have also been associated with the risk for Parkinson’s disease and multiple sclerosis. The management of acute stroke [23–38] is focused on intravascular thrombolysis, now with a longer time window for intervention but with diminishing returns in terms of improved outcome. The management of blood glucose and blood pressure remain of importance in the acute stage as well as in prevention and post-stroke management. The treatment and prevention of stroke [39–47] to improve outcomes [48–72] has as much to do with therapeutic intervention as it has to do with education of the general public as well as physicians. The swift recognition of transient ischaemic attacks and stroke is essential to improve outcome. The identiﬁcation and correct stratiﬁcation
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for treatment of patients with atrial ﬁbrillation is a major feature of stroke prevention. Multiple sclerosis [73–101] is considered the prototypic neuro-inﬂammatory disease. It is now recognized to have a signiﬁcant genetic component, although no single gene mutations have been identiﬁed, so again this is likely to be a complex genetic inﬂuence on risk. Other insights into pathogenesis include the role of axonal degeneration and the possible contribution of mitochondrial dysfunction. Disease-modifying therapies have had a signiﬁcant impact upon relapse rate and outcome but are not without adverse events. Attempts to stratify patients manifesting with a single episode of demyelination into prognostic groups may enable the identiﬁcation of those patients who might beneﬁt more from earlier as opposed to later intervention with these drugs. Our understanding of the cause and pathophysiology of Parkinson’s disease (PD) [102–123] has beneﬁted considerably from the molecular and imaging advances referred to above. Several monogenetic forms of PD are recognized, and recent genome-wide association studies have conﬁrmed alpha-synuclein, tau, immune pathway and glucocerebrosidase (GBA) genes as playing important roles in determining risk. GBA gene mutations are now recognized as numerically the most important risk factor for PD. Studies have conﬁrmed this in several ethnic groups, although the prevalence of GBA mutations varies between groups, being most common in the Ashkenazi population. Attention is focused on the prodromal period of PD where subtle clinical abnormalities, e.g. hyposmia, rapid eye movement sleep behaviour, can precede the onset of motor problems by several years. It is hoped that a combination of genetic, clinical and biochemical biomarkers may oﬀer clinicians the opportunity to identify those most at risk for PD and therefore those most suitable for early intervention with a diseasemodifying drug, should one become available. Novel imaging modalities to detect microglial activation and alpha-synuclein oﬀer beneﬁts for early detection, but in particular a means potentially to follow the course of the disease and the success or not of therapies to slow progression. Advances in the clinical prodrome and pathogenesis of PD have called into question the traditional clinically based diagnosis of PD. Guidelines on the diagnosis of PD provide a rational basis for diagnosis , and for practical clinical practice the clinically
based diagnosis of PD remains intact. The symptomatic treatment of PD over the past year has been reﬁned rather than revolutionized. Dopamine agonists are now available as once-a-day treatments and have a similar eﬃcacy and adverse event proﬁle to the traditional shorter acting preparations. However, it is clear that patients prefer the convenience of once-aday medication. The European Federation of Neurological Societies guidelines on the treatment of PD provide an excellent evidence-based review . However, the recognition and treatment of non-motor symptoms remain a major unmet need for PD patients [124–132]. Although traditionally associated with features such as cognitive abnormalities, autonomic dysfunction etc., sleep disorders and pain are commonly recognized problems; the latter may be exacerbated by dopaminergic medication. Unfortunately, eﬀective treatments for non-motor symptoms are very limited. Movement disorders other than PD have also beneﬁted from the major developments in genetics and imaging [133–147]. Huntington’s disease is a good example where the use of longitudinal magnetic resonance imaging can follow progression in pre-symptomatic mutation carriers and potentially be used as a marker for eﬃcacy of disease-modifying interventions. Imaging can also be helpful to distinguish some forms of parkinsonism although not necessarily with great sensitivity. Genetics has enabled the identiﬁcation of several novel parkinsonism dystonia syndromes and has also opened up the essential tremor and dystonia ﬁelds [148–153]. The main focus of attention for Alzheimer’s disease and other dementias [154–163] remains the discovery of an intervention that will slow or prevent progression. However, once again, novel imaging techniques have enabled the identiﬁcation of dementia variants more accurately and the correlation of these with genetics. The burden of vascular disease to cognitive decline can now be more accurately assessed in a longitudinal fashion. Amyotrophic lateral sclerosis (motor neuron disease) genetics have had a prominent advance with the identiﬁcation of fus gene mutations and these may lead to important insights into pathogenesis and therefore potential targets for intervention. In the interim, the practising neurologist still faces the diﬃculties of management, particularly of respiratory complications [164–168]. Genetic associations in headache [169–173] and epilepsy [174–183] continue to appear and help deﬁne diﬀerent phenotype correlations. New treatment strategies are becoming available for both, also incorporating lifestyle changes for headache management and new drugs for epilepsy.
The neuromuscular ﬁeld [184–203] was perhaps the ﬁrst area of neurology to be transformed by genetics when Duchenne gene mutations were identiﬁed. Mutations of primary myopathies including the limb girdle dystrophies and congenital and metabolic myopathies have been identiﬁed and have transformed the diagnostic approach to muscle disease. The role of muscle biopsy has changed with this and the European Federation of Neurological Societies guidelines on the use of this investigation in myalgia are welcomed . The genetic discoveries have yet to lead to treatments, but some progress is being made in this ﬁeld. Neuromuscular disorders and myasthenia gravis are important cases of morbidity and treatment protocols are now reﬁned by autoimmune proﬁles. Similarly, the diagnosis of immune-based neuropathies and their management has improved outcome in these disorders. Trauma-related neurological dysfunction remains an important cause of long-term disability that encompasses cognitive and physical deﬁcits, epilepsy and spinal cord injury sequelae that are not only of clinical but also of legal relevance [49,56,204–207]. The role of rehabilitation and research into its best delivery and eﬃcacy is an area that deserves greater attention. Inﬂammatory non-multiple-sclerosis neurological disease [208–216] has traditionally been associated with sarcoid or the vasculopathies, but the discovery of anti-aquaporin antibodies in neuromyelitis optica provided valuable insight into a rather heterogeneous and poorly deﬁned clinical entity. New treatment strategies are now being deﬁned. The same holds for the autoimmune limbic encephalitides. Guidelines [102,105,193,217] remain a vitally important area for education and the development of best medical practice. An enormous amount of work goes into the writing of these and the European Academy of Neurology will be continuing this role through the Scientiﬁc Committee. Neurology is a huge area of clinical activity and we have seen publications that cannot easily be incorporated into the major categories above [218–232]. The overlaps with psychiatry, oncology and cardiology in particular are a source of valuable clinical insight. Neurotoxicology is also an important ﬁeld of development and has the ability to provide valuable insights into potential mechanisms of disease that may in turn have relevance to metabolic pathways involved in genetic neurological disorders.
A. H. V. Schapira Department of Clinical Neurosciences, UCL Institute of Neurology, London, UK
(e-mail: [email protected]
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