Search

Background: Age reportedly affects headache prevalence differently in boys and girls. However, little empirical data exists regarding pediatric headache prevalence and headache-related burden in children and adolescents according to age and sex. In the present study, we considered age and sex while evaluating the distribution, characteristics, and impairment of primary headache disorders at a pediatric headache center in Germany. Methods: Medical records of children and adolescents attending the headache clinic of the Interdisciplinary Pain Center of the Carl Gustav Carus University Hospital in Dresden during the period 2015-2022 were retrospectively grouped and analyzed depending on age (< or ≥14 years) and sex. Results: The study population consisted of 652 children and adolescents, aged between 3 and 18 years. Almost two-thirds of the patients (≈60%) were females, and almost two-thirds of these females (58%) were ≥14 years of age. Generally, the most prevalent headache diagnoses as defined by the International Classification of Headache Disorders 3rd edition were episodic migraine without aura and the combination of tension-type headache and episodic migraine with or without aura i.e., mixed-type headache (each ≈27%). In the younger group (<14 years), the mixed-type headache was the most prevalent in girls (28.6%), whereas, for boys, episodic migraine without aura was the most prevalent headache diagnosis (47.4%). In the older group (≥14 years), the mixed-type headache continued to be the most prevalent for girls (30%), and it became the most prevalent for boys (26.3%). Before the age of 14, about 16% of children were severely affected by their headaches. After the age of 14, this proportion increased to roughly one-third (33%) of adolescents, driven mainly by teenage girls (26%) who were severely affected by their headaches. Furthermore, the prevalence of comorbidities was significantly higher among girls (67%), particularly in the adolescent group (74%). Conclusions: Our data shows that headache disorders in a specialized pediatric clinic impose a significant burden, especially among teenage girls indicating high therapy needs. Enhancing awareness of early diagnosis and preventive care is crucial to mitigate the development of chronic headaches, and mitigate their adverse effects on life quality and educational capability. [ABSTRACT FROM AUTHOR]

Much is known about the effect of odors on mood, cognition and behavior, but little is known about the relationship between odors and well-being. We investigated the neural processing of odors with different degrees of association with well-being (WB) through two large independent datasets. The study encompassed pre-testing and fMRI. During pre-testing, 100 and 80 (studies 1 and 2) young, healthy subjects participated, rating intensity, valence, and WB association for 14 (study 1) and 8 (study 2) different odors. Pre-testing resulted in the selection of two odors with high WB association (WB-associated) and two odors with lower WB association (neutral odors) for each study. Odors were delivered intranasally to the subjects who underwent fMRI scanning (44 and 41 subjects, respectively, for studies 1 and 2). We assessed brain activity for subjects when they experienced WB-associated versus neutral odors. In study 1, WB-associated odors showed increased activation in the right angular gyrus whereas in study 2, increased activity in the left angular gyrus existed, together with increased activity in the anterior cingulate cortex and posterior orbitofrontal cortex. The increased activity of higher-order cognitive and emotional regions during the processing of WB-associated odors in the two independent studies suggests a role of odors in influencing individual well-being. Moreover, the consistent activation of the angular gyrus might suggest its key role in shifting attention toward relevant emotional stimuli. [ABSTRACT FROM AUTHOR]

Background: Although the amygdala is thought to be a crucial brain region for negative affect, neuroimaging studies do not always show enhanced amygdala response to aversive stimuli in patients with anxiety disorders. Serotonin (5-HT)-related genotypes may contribute to interindividual variability in amygdala responsiveness. The short (s) allele of the 5-HT transporter linked polymorphic region (5-HTTLPR) and the T variant of the G-703T polymorphism in the tryptophan hydroxylase-2 (TPH2) gene have previously been associated with amygdala hyperresponsivity to negative faces in healthy controls. We investigated the influence of these polymorphisms on amygdala responsiveness to angry faces in patients with social anxiety disorder (SAD) compared with healthy controls. Methods: We used positron emission tomography with oxygen 15-labelled water to assess regional cerebral blood flow in 34 patients with SAD and 18 controls who viewed photographs of angry and neutral faces presented in counterbalanced order. We genotyped all participants with respect to the 5-HTTLPR and TPH2 polymorphisms. Results: Patients with SAD and controls had increased left amygdala activation in response to angry compared with neutral faces. Genotype but not diagnosis explained a significant portion of the variance in amygdala responsiveness, the response being more pronounced in carriers of s and/or T alleles. Limitations: Our analyses were limited owing to the small sample and the fact that we were unable to match participants on genotype before enrolment. In addition, other imaging techniques not used in our study may have revealed additional effects of emotional stimuli. Conclusion: Amygdala responsiveness to angry faces was more strongly related to serotonergic polymorphisms than to diagnosis of SAD. Emotion activation studies comparing amygdala excitability in patient and control groups could benefit from taking variation in 5-HT-related genes into account. Contexte: Meme si l&apos;on considere l&apos;amygdale comme une region du cerveau cruciale pour l&apos;affect negatif, les epreuves de neuroimagerie ne revelent pas toujours un rehaussement de la reactivite amygdalienne aux stimuli aversifs chez les patients souffrant de troubles anxieux. Les genotypes lies a la serotonine (5-HT) pourraient contribuer a la variabilite interindividuelle de la reponse amygdalienne. L&apos;allele (s) court du gene polymorphe 5-HTTLPR (serotonin-transporter-linked polymorphic region), un transporteur de la 5-HT, et la variante T du polymorphisme G-703T du gene TPH2 (tryptophan hydroxylase-2) ont ete associes anterieurement a une hyperreactivite amygdalienne aux visages exprimant une emotion negative chez des temoins en bonne sante. Nous avons voulu mesurer l&apos;influence de ces polymorphismes sur la reactivite amygdalienne aux visages exprimant la colere chez des patients atteints de phobie sociale, comparativement a des temoins en bonne sante. Methodes : Nous avons utilise la tomographie par emission de positrons avec de l&apos;eau radioactive marquee a l&apos;oxygene 15 pour mesurer le debit sanguin cerebral regional chez 34 patients souffrant de phobie sociale et 18 temoins a qui l&apos;on presentait des photographies de visages en colere ou neutres en sequence contrebalancees. Nous avons etabli le genotype de tous les participants pour ce qui est des polymorphismes 5-HTTLPR et TPH2. Resultats : Les patients souffrant de phobie sociale et les temoins ont presente une activation amygdalienne gauche accrue en reponse aux visages en colere, par rapport aux visages neutres. Il a ete possible d&apos;expliquer une portion significative de la variance de la reactivite amygdalienne par le genotype, mais non par le diagnostic, la reponse ayant ete plus prononcee chez les porteurs des alleles s ou T. Limites : Nos analyses ont ete limitees en raison du petit echantillon et du fait que nous n&apos;ayons pas pu assortir les participants selon leurs genotypes avant leur inscription a l&apos;etude. De plus, d&apos;autres techniques d&apos;imagerie, non utilisees lors de notre etude, auraient pu reveler certains effets additionnels des stimuli emotionnels. Conclusion : La reactivite amygdalienne aux visages exprimant la colere a ete plus intimement liee aux polymorphismes serotoninergiques qu&apos;au diagnostic de phobie sociale. Les etudes d&apos;activation des emotions comparant l&apos;excitabilite de l&apos;amygdale chez des groupes de patients et de temoins pourraient utiliser avantageusement les variations des genes lies a la 5-HT., Introduction The amygdala has long been associated with fear reactions and detection of danger signals. (1) Studies in animals and humans have confirmed that the amygdala is a critical structure [...]

Introduction: Patients with chemosensory dysfunction frequently report symptoms of depression. The current study aims to clarify whether the type (smell dysfunction, taste dysfunction, and mixed smell and taste dysfunction), severity, duration, or cause of dysfunction have differential impacts on the symptoms of depression.Methods: 899 patients with chemosensory disorders and 62 controls were included. Following a structured interview and an otorhinolaryngological examination, subjects underwent olfactory tests (Sniffin' Sticks), gustatory tests (taste sprays) and an assessment of depressive symptoms (Beck Depression Inventory). Information on the cause and duration of disorders was also collected.Results: Patients with combined olfactory/gustatory dysfunction had higher depression scores than patients with smell dysfunction only and controls, and no significant difference was found between the smell dysfunction and controls. Anosmia patients, but not hyposmia patients, exhibited higher depression scores than controls. Among various causes of chemosensory disorders, patients from the posttraumatic group had higher depression scores than patients with other causes of chemosensory dysfunction (sinonasal, idiopathic, or postinfectious). Multiple linear regression analyses suggested that reduced olfactory function was associated with enhanced depression scores in the olfactory disorders group (B = -0.326, t = -2.294, and p = 0.02) and in all patients with chemosensory disorders (B = -0.374, t = -2.550, p = 0.017).Discussion/conclusion: Simultaneously decreased input of olfaction and gustation seems to have an additive effect on the exacerbation of emotional dysfunction. Early intervention should be considered for depression symptoms in patients with mixed olfactory/gustatory dysfunction in clinical practice. [ABSTRACT FROM AUTHOR]

Objective: Functional magnetic resonance imaging (fMRI) is a non-invasive neuroimaging technique widely used in olfactory research. During a typical fMRI olfactory block-design, one functional "run" refers to a combination of multiple blocks with continuous brain image acquisition. The current study investigated the length of functional runs on odor-induced brain response signals (blood oxygen level dependent [BLOD]) within the primary and key secondary olfactory areas.Methods: Twenty-five female adults (age range 19 to 30 years, mean age 25 years) underwent a block-design fMRI measurement with odor stimulation. Twelve participants received the odor stimuli within a short run paradigm (six blocks in each 4-minute run, eight runs in total), and 13 participants received the odor stimulation with a long-run paradigm (12 blocks in each 8-minute run, four runs in total). For each paradigm, two odors (peach and rose) were alternatingly presented between runs. Participants rated odor intensity and pleasantness at the end of each run. Ratings and fMRI data were analyzed for different subsections and compared between groups.Results: There was a higher level of brain activation in the insula and orbitofrontal cortex during the short-run paradigm as compared to the long-run paradigm. However, there was no difference for odor intensity or pleasantness ratings.Conclusion: The current study suggested the employment of short runs with multiple repetitions for odor stimulation during fMRI research.Level Of Evidence: 3 Laryngoscope, 130:1110-1115, 2020. [ABSTRACT FROM AUTHOR]

Social anxiety disorder (SAD) can come in different forms, presenting problems for diagnostic classification. Here, we examined personality traits in a large sample of patients (N = 265) diagnosed with SAD in comparison to healthy controls (N = 164) by use of the Revised NEO Personality Inventory (NEO-PI-R) and Karolinska Scales of Personality (KSP). In addition, we identified subtypes of SAD based on cluster analysis of the NEO-PI-R Big Five personality dimensions. Significant group differences in personality traits between patients and controls were noted on all Big Five dimensions except agreeableness. Group differences were further noted on most lower-order facets of NEO-PI-R, and nearly all KSP variables. A logistic regression analysis showed, however, that only neuroticism and extraversion remained significant independent predictors of patient/control group when controlling for the effects of the other Big Five dimensions. Also, only neuroticism and extraversion yielded large effect sizes when SAD patients were compared to Swedish normative data for the NEO-PI-R. A two-step cluster analysis resulted in three separate clusters labelled Prototypical (33%), Introvert-Conscientious (29%), and Instable-Open (38%) SAD. Individuals in the Prototypical cluster deviated most on the Big Five dimensions and they were at the most severe end in profile analyses of social anxiety, self-rated fear during public speaking, trait anxiety, and anxiety-related KSP variables. While additional studies are needed to determine if personality subtypes in SAD differ in etiological and treatment-related factors, the present results demonstrate considerable personality heterogeneity in socially anxious individuals, further underscoring that SAD is a multidimensional disorder. [ABSTRACT FROM AUTHOR]

Background: Selective serotonin reuptake inhibitors (SSRIs) and cognitive-behavioural therapy (CBT) are often used concomitantly to treat social anxiety disorder (SAD), but few studies have examined the effect of this combination.Aims: To evaluate whether adding escitalopram to internet-delivered CBT (ICBT) improves clinical outcome and alters brain reactivity and connectivity in SAD.Method: Double-blind, randomised, placebo-controlled neuroimaging trial of ICBT combined either with escitalopram (n = 24) or placebo (n = 24), including a 15-month clinical follow-up (trial registration: ISRCTN24929928).Results: Escitalopram+ICBT, relative to placebo+ICBT, resulted in significantly more clinical responders, larger reductions in anticipatory speech state anxiety at post-treatment and larger reductions in social anxiety symptom severity at 15-month follow-up and at a trend-level (P = 0.09) at post-treatment. Right amygdala reactivity to emotional faces also decreased more in the escitalopram+ICBT combination relative to placebo+ICBT, and in treatment responders relative to non-responders.Conclusions: Adding escitalopram improves the outcome of ICBT for SAD and decreased amygdala reactivity is important for anxiolytic treatment response. [ABSTRACT FROM AUTHOR]

The prevalence of migraine has an exponential trajectory that is most obvious in young females between puberty and early adulthood. Adult females are affected twice as much as males. During development, hormonal changes may act on predetermined brain circuits, increasing the probability of migraine. However, little is known about the pediatric migraine brain and migraine evolution. Using magnetic resonance imaging, we evaluated 28 children with migraine (14 females and 14 males) and 28 sex-matched healthy controls to determine differences in brain structure and function between (1) females and males with migraine and (2) females and males with migraine during earlier (10-11 years) vs later (14-16 years) developmental stages compared with matched healthy controls. Compared with males, females had more gray matter in the primary somatosensory cortex (S1), supplementary motor area, precuneus, basal ganglia, and amygdala, as well as greater precuneus resting state functional connectivity to the thalamus, amygdala, and basal ganglia and greater amygdala resting state functional connectivity to the thalamus, anterior midcingulate cortex, and supplementary motor area. Moreover, older females with migraine had more gray matter in the S1, amygdala, and caudate compared to older males with migraine and matched healthy controls. This is the first study showing sex and developmental differences in pediatric migraineurs in brain regions associated with sensory, motor, and affective functions, providing insight into the neural mechanisms underlying distinct migraine sex phenotypes and their evolution that could result in important clinical implications increasing treatment effectiveness. [ABSTRACT FROM AUTHOR]

In patients with social anxiety disorder (SAD) it has been reported that selective serotonin reuptake inhibitors (SSRIs) and placebo induce anxiolytic effects by attenuating neural activity in overlapping amygdala subregions, i.e. left basolateral and right ventrolateral amygdala. However, it is not known whether these treatments inhibit amygdala subregions via similar or distinct brain pathways. As anxiolytic treatments may alter amygdala-frontal couplings we investigated differences and similarities in amygdala-frontal functional co-activation patterns between responders and nonresponders to SSRIs and placebo in patients with SAD. Positron emission tomography (PET) with oxygen-15-labeled water was used to measure anxiety-related regional cerebral blood flow in 72 patients with SAD before and after 6–8 wk of treatment under double-blind conditions. Functional couplings were evaluated with a seed region approach using voxel values from the left basolateral and right ventrolateral amygdala. Responders and nonresponders to SSRIs and placebo showed different treatment-induced co-activations between the left amygdala and the dorsolateral prefrontal cortex (dlPFC) as well as the rostral anterior cingulate cortex (ACC). Conjunction analysis suggested shared anxiolysis-dependent inverse co-activations in SSRI and placebo responders between the left amygdala-dlPFC and left amygdala-rostral ACC, and a shared positive co-activation between left amygdala-dorsal ACC. We demonstrate that amygdala-frontal co-activation patterns differentiate effective from ineffective anxiolytic treatments and that SSRI and placebo responders share overlapping neuromodulatory paths that may underlie improved emotion regulation and reduced expression of anxiety.TRIAL REGISTRATION: clinicaltrials.gov Identifier: NCT00343707. [ABSTRACT FROM AUTHOR]

The amygdala is a key structure in the pathophysiology of anxiety disorders, and a putative target for anxiolytic treatments. Selective serotonin reuptake inhibitors (SSRIs) and placebo seem to induce anxiolytic effects by attenuating amygdala responsiveness. However, conflicting amygdala findings have also been reported. Moreover, the neural profile of responders and nonresponders is insufficiently characterized and it remains unknown whether SSRIs and placebo engage common or distinct amygdala subregions or different modulatory cortical areas. We examined similarities and differences in the neural response to SSRIs and placebo in patients with social anxiety disorder (SAD). Positron emission tomography (PET) with oxygen-15-labeled water was used to assess regional cerebral blood flow (rCBF) in 72 patients with SAD during an anxiogenic public speaking task, before and after 6-8 weeks of treatment under double-blind conditions. Response rate was determined by the Clinical Global Impression-Improvement scale. Conjunction analysis revealed a common rCBF-attenuation from pre- to post-treatment in responders to SSRIs and placebo in the left basomedial/basolateral and right ventrolateral amygdala. This rCBF pattern correlated with behavioral measures of reduced anxiety and differentiated responders from nonresponders. However, nonanxiolytic treatment effects were also observed in the amygdala. All subgroups, including nonresponders, showed deactivation of the left lateral part of the amygdala. No rCBF differences were found between SSRI responders and placebo responders. This study provides new insights into the brain dynamics underlying anxiety relief by demonstrating common amygdala targets for pharmacologically and psychologically induced anxiety reduction, and by showing that the amygdala is functionally heterogeneous in anxiolysis. [ABSTRACT FROM AUTHOR]

Placebo may yield beneficial effects that are indistinguishable from those of active medication, but the factors underlying proneness to respond to placebo are widely unknown. Here, we used functional neuroimaging to examine neural correlates of anxiety reduction resulting from sustained placebo treatment under randomized double-blind conditions, in patients with social anxiety disorder. Brain activity was assessed during a stressful public speaking task by means of positron emission tomography before and after an 8 week treatment period. Patients were genotyped with respect to the serotonin transporter-linked polymorphic region (5-HTTLPR) and the G-703T polymorphism in the tryptophan hydroxylase-2 (TPH2) gene promoter. Results showed that placebo response was accompanied by reduced stress-related activity in the amygdala, a brain region crucial for emotional processing. However, attenuated amygdala activity was demonstrable only in subjects who were homozygous for the long allele of the 5-HTTLPR or the G variant of the TPH2 G-703T polymorphism, and not in carriers of short or T alleles. Moreover, the TPH2 polymorphism was a significant predictor of clinical placebo response, homozygosity for theGallele being associated with greater improvement in anxiety symptoms. Path analysis supported that the genetic effect on symptomatic improvement with placebo is mediated by its effect on amygdala activity. Hence, our study shows, for the first time, evidence of a link between genetically controlled serotonergic modulation of amygdala activity and placebo-induced anxiety relief. [ABSTRACT FROM AUTHOR]

Social anxiety disorder (SAD) is associated with aberrant emotional information processing while little is known about non-emotional cognitive processing biases. The dorsal anterior cingulate cortex (dACC) has been implicated in SAD neuropathology and is activated both by emotional and non-affective cognitive challenges like the Multisource Interference Task (MSIT). Here, we used fMRI to compare dACC activity and test performance during MSIT in 69 SAD patients and 38 healthy controls. In addition to patient-control comparisons, we examined whether neural activity in the dACC correlated with social anxiety, trait anxiety or depression levels. The MSIT activated the dACC as expected but with no differences in task performance or neural reactivity between SAD patients and controls. There were no significant correlations between dACC activity and social or trait anxiety symptom severity. In patients, there was a significant negative correlation between dACC activity and depressive symptoms. In absence of affective challenge, we found no disorder-related cognitive profile in SAD patients since neither MSIT task performance nor dACC neural activity deviated in patients relative to controls. • Cognitive task performance and neural activity is unaffected in social anxiety disorder. • Anxiety severity does not correlate with dorsal anterior cingulate cortex activity. • Depressive symptoms correlate with neural activity in social anxiety disorder. [ABSTRACT FROM AUTHOR]

Social anxiety disorder (SAD) is associated with altered brain function and structure, but most structural studies include small samples and findings are mixed. This study compared regional gray matter volume between 48 SAD patients and 29 healthy controls (HC) as well as the relationship between volume and symptom severity. Structural magnetic resonance images from SAD patients and HC were evaluated using standard voxel-based morphometry (VBM) processing in the SPM8 software package. Social anxiety symptom severity was rated in SAD patients by a clinician using the Liebowitz Social Anxiety Scale (LSAS). SAD patients had greater regional gray matter volume in the lingual gyrus and lateral occipital cortex than the controls, and within the SAD group a positive correlation was found between symptom severity and regional gray matter volume in the lingual gyrus and the retrosplenial cortex. These findings replicate and extend earlier reports of enlarged visual processing areas in SAD. Increased gray matter volume in regions involved in visual processing and self-consciousness could underlie, or be the result of, abnormal emotional information processing and self-focused attention previously demonstrated in patients with SAD. [ABSTRACT FROM AUTHOR]