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The ongoing developments of psychiatric classification systems have largely improved reliability of diagnosis, including that of schizophrenia. However, with an unknown pathophysiology and lacking biomarkers, its validity still remains low, requiring further advancements. Research has helped establish multiple sclerosis (MS) as the central nervous system (CNS) disorder with an established pathophysiology, defined biomarkers and therefore good validity and significantly improved treatment options. Before proposing next steps in research that aim to improve the diagnostic process of schizophrenia, it is imperative to recognize its clinical heterogeneity. Indeed, individuals with schizophrenia show high interindividual variability in terms of symptomatic manifestation, response to treatment, course of illness and functional outcomes. There is also a multiplicity of risk factors that contribute to the development of schizophrenia. Moreover, accumulating evidence indicates that several dimensions of psychopathology and risk factors cross current diagnostic categorizations. Schizophrenia shares a number of similarities with MS, which is a demyelinating disease of the CNS. These similarities appear in the context of age of onset, geographical distribution, involvement of immune-inflammatory processes, neurocognitive impairment and various trajectories of illness course. This article provides a critical appraisal of diagnostic process in schizophrenia, taking into consideration advancements that have been made in the diagnosis and management of MS. Based on the comparison between the two disorders, key directions for studies that aim to improve diagnostic process in schizophrenia are formulated. All of them converge on the necessity to deconstruct the psychosis spectrum and adopt dimensional approaches with deep phenotyping to refine current diagnostic boundaries.
We aimed to determine the role of the European Psychiatric Association (EPA) and the European Academy of Neurology (EAN) in the management of post-COVID conditions. This is a joint statement from the EAN and the EPA on post-COVID. It is published in the official journals of the two associations, the European Journal of Neurology and European Psychiatry.
This chapter discusses the main types of eye movement paralysis resulting from brainstem lesions, and the related pathophysiology. The abnormalities are easily detected at the bedside by studying three main types of eye movements: saccades; smooth pursuit; and the vestibular ocular reflex (VOR). The chapter reviews eye movement disturbances due to cerebellar and cerebral hemispheric lesions, resulting in relatively more subtle syndromes. The stroke-related lesions that most often involve horizontal gaze are located in the cerebral hemispheres and the pons. The hemispheral lesions are most often relatively large hemorrhages or infarcts that include the lateral aspect of the frontal lobe and/or the deep basal ganglia-capsular regions. Outside the brainstem, a number of suprareticular structures, located in the cerebellum and the cerebral hemispheres, control eye movements. Damage to these structures results in saccade and/or smooth pursuit disturbances usually much more subtle than those due to brainstem lesions.
Sleep disorders are commonly found in the general population. In stroke patients, their frequency is even higher, because brain damage can affect sleep–wake mechanisms and because cerebrovascular and sleep disorders can arise from similar predisposing factors. Sleep disorders often influence negatively general well-being, physical and mental performance, and, as a consequence, rehabilitation and final outcome. In addition, sleep-disordered breathing (SDB) – one of the most common forms of post-stroke sleep disorders – may increase the risk of stroke recurrence. For these reasons, sleep disturbances should be adequately diagnosed and treated after stroke.
Changes in sleep and breathing were reported in stroke patients as early as in the beginning of the nineteenth century. Cheyne (1818) first described periodic breathing in a patient with cardiac disease and “apoplexy.” Jackson later recognized that this breathing pattern frequently accompanies bilateral hemispheric stroke (quoted by Brown and Plum, 1961). Symptoms of obstructive sleep apnea (OSA) were first reported in a patient with intracerebral hemorrhage by Broadbent (1877). In the nineteenth century, it was also already known that stroke may cause profound changes of sleep patterns. Post-stroke hypersomnia was recognized by MacNish as early as 1830 (see Lavie, 1991), but it was only in the beginning of the twentieth century that its preferential association with thalamic and mesencephalic strokes was recognized (Freund, 1913). Neurogenic insomnia (agrypnia) related to thalamomesecephalic stroke was first described by Lhermitte (1922) and van Bogaert (1926). Lhermitte (1922) coined the term peduncular hallucinosis to describe vivid, colorful, and dream-like hallucinations following midbrain stroke. Asymmetries of the electroencephalogram (EEG) during sleep, with a reduction of spindle activity over the affected hemisphere, were first reported by Cress and Gibbs (1948). During subsequent decades, other authors described abnormalities in rapid eye movement (REM) and non-REM sleep in patients with supra- and infratentorial strokes. More recently, the link between SDB and vascular disease has been suggested.
Circadian rhythms and stroke
Cerebrovascular events, such as myocardial infarction and sudden death, appear most frequently in the morning hours – between 6 a.m. and noon – and particularly within the first hour after awakening. A meta-analysis of 31 publications with 11 816 patients found a 49% increase in all types of stroke (ischemic, hemorrhagic, transient ischemic attack) during that time of the day compared with other times (Elliott, 1998).
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