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ObjectiveChildren and adolescents with functional neurological symptom disorder (FND) present with diverse neurological symptoms not explained by a disease process. Functional neurological symptoms have been conceptualized as somatoform dissociation, a disruption of the brain's intrinsic organization and reversion to a more primitive level of function. We used EEG to investigate neural function and functional brain organization in children/adolescents with FND.MethodEEG was recorded in the resting eyes-open condition in 57 patients (aged 8.5–18 years) and 57 age- and sex-matched healthy controls. Using a topographical map, EEG power data were quantified for regions of interest that define the default mode network (DMN), salience network, and somatomotor network. Source localization was examined using low-resolution brain electromagnetic tomography (LORETA). The contributions of chronic pain and arousal as moderators of differences in EEG power were also examined.ResultsChildren/adolescents with FND had excessive theta and delta power in electrode clusters corresponding to the DMN—both anteriorly (dorsomedial prefrontal cortex [dmFPC]) and posteriorly (posterior cingulate cortex [PCC], precuneus, and lateral parietal cortex)—and in the premotor/supplementary motor area (SMA) region. There was a trend toward increased theta and delta power in the salience network. LORETA showed activation across all three networks in all power bands and localized neural sources to the dorsal anterior cingulate cortex/dmPFC, mid cingulate cortex, PCC/precuneus, and SMA. Pain and arousal contributed to slow wave power increases in all three networks.ConclusionsThese findings suggest that children and adolescents with FND are characterized by overactivation of intrinsic resting brain networks involved in threat detection, energy regulation, and preparation for action.

ObjectiveStress, pain, injury, and psychological trauma all induce arousal-mediated changes in brain network organization. The associated, high level of arousal may disrupt motor-sensory processing and result in aberrant patterns of motor function, including functional neurological symptoms. We used the auditory oddball paradigm to assess cortical arousal in children and adolescents with functional neurological symptom disorder.MethodElectroencephalogram (EEG) data was collected in fifty-seven children and adolescents (41 girls; 16 boys, aged 8.5–18 years) with acute functional neurological symptoms and age- sex- matched controls during a conventional auditory oddball task. The high-resolution fragmentary decomposition technique was used to analyse the amplitude of event-related potentials (ERPs) to target tones at midline sites (Fz, Cz, and Pz).ResultsCompared to age- and sex-matched controls, and across all three midline sites, children and adolescents with functional neurological symptoms showed increased amplitude of all ERP components (P50, N100, P200, N200, and P300) (t-value range 2.28–8.20; p value-range 0.023 to < 0.001) to the emotionally-neutral auditory stimulus.ConclusionsOur findings add to a growing literature indicating that a baseline state of high arousal may be a precondition for generating functional neurological symptoms, a finding that helps explain why a range of psychological and physiological stressors can trigger functional neurological symptoms in some patients. Interventions that target cortical arousal may be central to the treatment of paediatric patients with functional neurological symptom disorder.

Functional somatic symptoms (FSS) emerge when the stress system is activated in response to physical or emotional stress that is either chronic or especially intense. In such cases, the heightened state of physiological arousal and motor activation can be measured through biological markers. Our team have integrated the use of biological markers of body state – respiratory rate, heart rate (HR) and heart rate variability (HRV) measurements – as a way of helping families to understand how physical symptoms can signal activation of the body’s stress systems. This study measured respiratory rates, HR and HRV in children and adolescents with FSS (and healthy controls) during baseline assessment to determine whether these biological markers were effective at differentiating patients with FSS. The study also implemented a biofeedback intervention during the assessment to determine whether patients with FSS were able to slow their respiratory rates and increase HRV. Patients with FSS had faster respiratory rates, faster HR, and lower HRV, suggesting activation of the autonomic nervous system coupled with activation of the respiratory motor system. Like controls, patients were able to slow their respiratory rates, but in contrast to controls, they were unable to increase their HRV. Our findings suggest that patients with FSS present in a state of physiological activation and struggle to regulate their body state. Patients with FSS are likely to need ongoing training and practice to regulate body state coupled with interventions that target regulatory capacity across multiple systems.

Background: Cannabinoid hyperemesis syndrome (CHS) is a diagnosis of exclusion with intractable nausea, cyclic vomiting, abdominal pain, and hot bathing behavior associated with ongoing tetrahydrocannabinol (THC) exposure. Increasing cannabis use may elevate CHS prevalence, exacerbating a public health issue with attendant costs and morbidity. Objective, Design, and Data Source: This study, the largest contemporaneous database, investigated genetic mutations underlying CHS. Patients with CHS diagnosis and ongoing symptoms were compared with current cannabis users lacking symptoms. Target Population: A screening questionnaire was posted online. Of 585 respondents, 205 qualified as the CHS pool and 54 as controls; a reduced pool of 28 patients and 12 controls ultimately completed genomic testing. Results: Patients and controls were high-frequency users of cannabis flower or concentrates (93%), using multiple grams/day of THC-predominant material. Among patients, 15.6% carried diagnoses of cannabis dependency or addiction, and 56.6% experienced withdrawal symptoms. About 87.7% of patients improved after cannabis cessation, most suffering recurrence rapidly after resumption. Findings in patients included mutations in genes COMT {odds ratio, 12 (95% confidence limit [CL], 1.3-88.1) p = 0.012}, transient receptor potential vanilloid receptor 1 (TRPV1) (odds ratio, 5.8 [95% CL, 1.2-28.4] p = 0.015), CYP2C9 (odds ratio, 7.8 [95% CL, 1.1-70.1] p = 0.043), gene coding dopamine-2 receptor (DRD2) (odds ratio, 6.2 [95% CL, 1.1-34.7] p = 0.031), and ATPbinding cassette transporter gene (ABCA1) (odds ratio, 8.4 [95% CL, 1.5-48.1] p = 0.012). Limitations: Some participants were reluctant to undergo genetic testing; only 28 of 99 CHS patients who agreed to testing ultimately returned a kit. Conclusion: This is the largest patient cohort of CHS examined to date, and first to note associated mutations in genes affecting neurotransmitters, the endocannabinoid system, and the cytochrome P450 complex associated with cannabinoid metabolism. Although the sample size was smaller than desired, these preliminary findings may contribute to the growing body of knowledge, stimulate additional investigation, help elucidate the pathophysiology of CHS, and, ultimately, direct future treatment.

Cannabis is the most commonly used illicit drug globally, and Canada has among the highest use rates.1 In 2014, 10% to 15% of general-population adults and 25% to 30% of adolescents or young adults report current (i.e., past-year) cannabis use.2 Arguably, the legalization of cannabis in Canada can be regarded as one of the most significant public health policy changes in the last 50 years. The stated aim of legalization of cannabis was to protect youth and eliminate the criminal element from the cannabis industry, and it has been challenging, as the government attempts to navigate the creation a new industry that can compete with the well-established illicit market.