Welcome to the WCN 2021 Interactive Program
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Please note that all sessions will run at their scheduled time and be followed by a LIVE Q&A/Discussion at the end
The viewing of sessions, cannot be accessed from this conference calendar. All sessions are accessible via the Virtual Platform
- Mario Habek (Croatia)
AUTONOMIC FAILURE IN MULTIPLE SCLEROSIS, COMPLICATION OR PRECURSOR?
- Mario Habek (Croatia)
Autonomic nervous system abnormalities are being increasingly recognized as an important aspect of multiple sclerosis (MS) on a clinical, neurophysiological and molecular level. Autonomic dysfunction in MS shows a distinctive pattern: the disease activity (manifested with relapses and MRI activity) is associated with sympathetic nervous system dysfunction, while the disease progression (manifested by increasing neurological disability) is associated with parasympathetic nervous system dysfunction, with highest percentages of involvement seen in advanced progressive MS. Furthermore, in MS, not only that autonomic symptoms are present, but may influence the disease course. A recent study has shown that presence of autonomic symptoms increase the risk of the second relapse after the diagnosis of clinically isolated syndrome by 2.7 folds.
On the other hand, there is evidence suggesting that multiple sclerosis (MS) starts years before the first clinical presentation, and this period has become known as the MS prodrome. This period can span for more than a decade and the most well characterized symptom of it lies in the spectrum of autonomic nervous system abnormalities. Autonomic symptoms before the diagnosis increase the risk for the first clinical manifestation of MS, and if they are present at the diagnosis of MS, they increase the likelihood of the second relapse. All this data, emphasize the importance of studying ANS involvement in MS.
LOWER URINARY TRACT DYSFUNCTION IN NEUROINFLAMMATORY DISEASES
- Jalesh N. Panicker (United Kingdom)
Lower urinary tract (LUT) dysfunction is a commonly reported sequelae of neuroinflammatory disorders such as Multiple sclerosis, NMO spectrum disorders and MOG associated transverse myelitis, and have a significant impact on quality of life. The pattern of LUT dysfunction is influenced by the site of neurological lesion and patients may present with storage and/or voiding dysfunction . The risk for developing upper urinary tract damage is considerably lower, compared to other disorders such as spinal cord injury or spina bifida. History taking forms the cornerstone of assessment, and urinalysis, ultrasonography and urodynamics provide information about the cause and nature of LUT dysfunction. Antimuscarinic agents are the first line management of urinary incontinence, however the side effect profile and anticholinergic burden should be considered when prescribing these medications. Beta-3 receptor agonists are a promising alternative oral medication. Tibial and sacral neuromodulation have been shown to be effective for managing neurogenic incontinence. Intradetrusor injections of onabotulinumtoxinA have revolutionised the management of neurogenic detrusor overactivity. Patients with neuroinflammatory disorders reporting LUT symptoms require a comprehensive evaluation for planning a patient-tailored approach to management.
GASTROINTESTINAL DYSFUNCTION IN NEUROINFLAMMATORY DISEASES
- Ryuji Sakakibara (Japan)
Nervous system has ‘guts’ to produce a variety of gastrointestinal (GI) dysfunction. Among these, focal brain disease causes appetite loss (hypothalamus), decreased peristalsis (presumably the basal ganglia, pontine defecation center/ Barrington’s nucleus), decreased abdominal strain (presumably parabrachial nucleus/ Kolliker-Fuse nucleus), hiccup and vomiting (area postrema/ dorsal vagal complex); spinal cord disease causes decreased peristalsis and anismus (tracts, the intermediolateral nucleus) (CNS); and disease affecting the peripheral nerve including the myenteric plexus causes decreased peristalsis with/without loss of bowel sensation (PNS).
Recently inflammatory causes of the nervous diseases, particularly those affecting the PNS, are being recognized to contribute to GI dysfunction of previously-unknown etiology. We briefly review neuroinflammatory diseases that potentially cause GI dysfunction, e.g., multiple sclerosis, neuromyelitis optica spectrum disorder (anti-aquaporin 4 or MOG antibody), autoimmune acute myelitis, subacute disseminated encephalomyelitis, and autoimmune encephalitis (anti-NMDA glutamate receptor antibody etc.) (CNS); Guillain-Barre syndrome (anti-ganglioside antibody etc.), acute sensory-autonomic neuropathy/ acute pandysautonomia (anti-nicotinic ganglionic acetylcholine receptor [gAChR] antibody), pure autonomic failure (anti-gAChR antibody in some), paraneoplastic sensory-autonomic neuropathy (anti-Hu, CRPMP5, gAChR, VGKC antibody etc.), (selective organs) paraneoplastic/idiopathic intestinal pseudo-obstruction and achalasia (anti-gAChR antibody in some), and collagen diseases affecting both CNS and PNS (Sjogren syndrome, scleroderma, etc.).
These GI dysfunctions may occur solely, predate, or occur concurrent with other nervous system symptoms. Such patients may visit gastroenterologists or physicians first before the correct diagnosis was made. Therefore, collaboration of gastroenterologists and neurologists are highly recommended in order for the early diagnosis and optimal management.