The increases in parasympathetic and overall cardiac autonomic modulation and in BRS seen with fingolimod initiation are theoretically beneficial for the MS patient's cardiovascular system. However, long-term studies must show whether these effects persist or are attenuated (e.g. due to S1P1 receptor down-regulation upon continued fingolimod therapy).

Background: In women with multiple sclerosis (MS), depression and sexual dysfunction (SD) are common. Whether SD promotes depression or vice versa remains unclear despite therapeutic relevance. Therefore, we aimed to assess whether SD more likely triggers depression or vice versa. Methods: In 83 female MS patients and 21 age-matched healthy women, we assessed depression, using the Beck Depression Inventory-V (BDI-V), and SD using the Female Sexual Function Index (FSFI). We diagnosed depression with BDI-V-scores >35 and SD with FSFI scores < 26.55. We divided patients into groups with and without SD, with and without depression. Between groups, we compared prevalence of SD and depression (Fisher’s-exact-test), age, MS-duration, MS-severity, BDI-V-, and FSFI scores (Mann-Whitney U-test; significance: p < 0.05). Results: A total of 37/83 MS patients and 1/21 controls had SD; 28/83 patients and 3/21 controls had depression; 51.4% patients with SD but only 19.6% without SD had depression (p = 0.003). SD was present in 67.9% depressed and 32.7% non-depressed patients. BDI-V-scores were higher in patients with SD than in patients without SD. FSFI scores were lower in depressed than non-depressed patients. Conclusion: In conclusion, SD was more common than depression. SD afflicted 67.9% depressed MS patients and was also more common in non-depressed MS patients than controls. SD may occur independently from depression while increased depressiveness seems linked to coexistent SD.

Serial chest computed tomography scans of four patients since symptom onset. (1) Patient A: (A and D) diffuse bilateral groundglass opacities (GGOs) predominantly involving perihilar and midzones with relative subpleural sparing at 3 weeks after symptom onset. (B and E) A mixed pattern of GGOs, reticulation and air space consolidation, cystic airspaces, decreased lung volume, and compensatory increased anteriorposterior chest diameter at 9 weeks. (C and F) Partial resolution of various lesions at 12 weeks. (2) Patient B: (A and D) diffuse irregular GGOs mainly with subpleural and peripheral involvement 10 days after symptom onset. (B and E) Confluence of peripheral lesions in the left upper lung and a mixed pattern of ground-glass and reticular opacities in the lower lung bilaterally at six weeks. (C and F) Lesion resolution with some remnant GGOs at 8 weeks. (3) Patient C: (A) irregular GGOs at the periphery of the lower lung bilaterally 4 weeks after symptom onset. (B) Enlarged areas of GGOs bilaterally and an irregular nodule in the right lower lung at 6 weeks. (C) minimal residual opaque lesions at eight weeks. (4) Patient D: (A) wedge-shaped GGOs at the periphery of the right upper lung and the left upper lung medially 2 days after symptom onset. (B) Enlarging area of GGOs bilaterally with reticulation and consolidation in the left lung at three weeks. (C) Partial resolution of GGOs at 5 weeks

Autonomic dysfunction is common in neuro-critical care patients and may compromise the function of various organs. Among the many diseases causing or being associated with autonomic dysfunction are traumatic brain injury, cerebrovascular diseases, epilepsy, Guillain-Barré syndrome (GBS), alcohol withdrawal syndrome, botulism and tetanus, among many others. Autonomic dysfunction may afflict various organs and may involve hyper- or hypo-activity of the sympathetic or parasympathetic system. In this short overview, we address only a small number of neuro-intensive care diseases with autonomic dysfunction. In GBS, autonomic dysfunction is frequent and may account for increased mortality rates; rapid changes between sympathetic and parasympathetic hypo- or hyper-activity may cause life-threatening cardiovascular complications. Paroxysmal sympathetic hyperactivity occurs after brain injury, hypoxia and cerebrovascular and other events, causes paroxysmal tachycardia, hypertension, tachypnoea and hyperthermia and is associated with a poorer prognosis and prolonged intensive care treatment. Other, at times life-threatening autonomic complications with exaggerated sympathetic activity and compromised baroreflex sensitivity arise during the alcohol withdrawal syndrome triggered by abrupt cessation of alcohol consumption. Botulism and tetanus are examples of life-threatening autonomic dysfunction caused by bacterial neurotoxins. Common neurological diseases, such as epilepsy, stroke or subarachnoid haemorrhage, are also associated with autonomic dysfunction that can on occasion cause critical deterioration of disease severity and prognosis.

Background and PurposeParkinson's disease (PD) and multiple-system atrophy of the parkinsonian type (MSA-P) are progressive neurodegenerative disorders that in addition to dysfunction of the motor system also present with features of dysautonomia, frequently manifesting as orthostatic hypotension (OH). The pathophysiology of OH has been proposed to differ between these two disorders. This study investigated the spontaneous and cardiovagal baroreflex sensitivity (BRS) in Parkinson's disease patients with orthostatic hypotension (PDOH) and multiple system atrophy of Parkinsonian type with orthostatic hypotension in an attempt to differentiate the two disorders.MethodsTwo methods were used for determining the BRS: a spontaneous method (spontaneous BRS) and the reflexive baroreflex gain (cardiovagal BRS) from phases II and IV of the Valsalva maneuver (VM) in PDOH and MSA-POH.ResultsThe spontaneous BRS (5.04±0.66 ms/mm Hg vs. 4.78±0.64 ms/mm Hg, p=0.54) and the cardiovagal BRS from phase II of the VM (0.96±0.75 ms/mm Hg vs. 1.34±1.51 ms/mm Hg, p=0.76) did not differ between PDOH and MSA-POH, but the cardiovagal BRS from phase IV of the VM (0.03±0.07 ms/mm Hg vs. 2.86±2.39 ms/mm Hg, p=0.004) was significantly lower in PDOH.ConclusionsThe cardiovagal BRS from phase IV of the VM has potential for differentiating PDOH and MSA-POH, indicating a difference in the pathophysiological mechanisms underlying the autonomic dysfunction in the two disorders.