by Roberto Acampora
Symposium 6 shed light on the autonomic disorders across a broad range of conditions through both pre-clinical and clinical studies as well as novel treatment approaches. The first speaker, Prof. Gregor K. Wenning, spoke about disease modifying therapies in multiple systems atrophy (MSA), focusing first on the pathogenesis of the disease: α-synuclein and neuroinflammation. Concerning clinical trials that have been conducted in this field so far, one applied the use of mesenchymal stem cells to small numbers of MSA-C patients and showed an encouraging positive effect on disease progression. Several other ongoing agents in development are looking promising, such as the M-STAR trial of verdiperstat, which suppresses microglial activation and oxidative stress, or the novel quinazolinone that has demonstrated a reduction in α-synuclein aggregation and neuronal death in mice. Last but not least, encouraging results came from a phase I trial using vaccines in both MSA and PD patients.
The next speaker was Prof. Roland D. Thijs, who gave a lecture on how seizures can dramatically impact on autonomic function, especially frequent nocturnal tonic-clonic seizures (TCs) and temporal lobe seizures with impaired awareness. Drug-resistant epilepsy may indirectly be responsible for SUDEP (sudden unexpected death in epilepsy) if the central autonomic network is involved. However, autonomic alterations including tachycardia, increased blood pressure and sweating may also provide a tool for early seizure detection and facilitate timely interventions. Post-ictal arrhythmias triggered by TCs and due to cardiac comorbidity or ion channel mutations may indeed lead to SUDEP, which usually occurs several minutes after a convulsive seizure. Raising an alarm at seizure onset through a night-watch device as well as nocturnal supervision and optimisation of antiepileptic medication may help facilitate prevention and timely intervention.
Prof. Mario Habek talked about the clinical implications of autonomic nervous system (ANS) dysfunction in multiple sclerosis (MS). He showed that ANS dysfunction consisting of gastrointestinal (constipation, diarrhoea, irritable bowel syndrome) and urinary symptoms may be evident up to ten years prior to diagnosis of MS. In addition, disease activity in clinically isolated syndrome and early relapsing-remitting MS is associated with sympathetic nervous system dysfunction,whereas parasympathetic nervous system dysfunction becomes more evident with progression of disease. On a molecular level, changes in expression of different receptors responsible for communication between the ANS and the immune system may modulate inflammatory responses and thus exert an influence on MS disease activity. Damage to the brainstem and spinal cord in MS may contribute to more severe ANS dysfunction whilst, conversely, ANS dysfunction can predict development of disease activity in MS. Furthermore, ANS dysfunction in early MS, mainly driven by sympathetic nervous system abnormalities, may explain the increased risk of cardiovascular disease after MS onset. Small fibre neuropathy may also be evident in a significant proportion of MS patients. This may be a consequence of spinal cord involvement or represent additional peripheral nervous system involvement. Further investigations are needed to clarify this aspect.
The last talk was given by Prof. Jens Jordan, who talked about the influence of space conditions on cardiovascular, haemodynamic autonomic control. He showed that space travel alters human haemodynamics, including blood volume changes in different anatomical compartments and autonomic function at rest, during routine activities and following various interventions. Studies investigating changes in the ANS in astronauts are giving us a unique new perspective on long‐term human autonomic neuroplasticity.
