Social anxiety disorder it’s linked to imbalance between serotonin and dopamine

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The balance between the neurotransmitters serotonin and dopamine may affect whether a person develops social anxiety disorder.

Previous research has mainly focused on either the serotonin or the dopamine system individually.

Now researchers at Uppsala University have demonstrated the existence of a previously unknown link between the two. The results are published in Molecular Psychiatry.

“We see that there is a different balance between serotonin and dopamine transport in people with social anxiety disorder compared with control subjects.

The interaction between serotonin and dopamine transport explained more of the difference between the groups than each carrier individually.

This suggests one should not focus exclusively on one signal substance at a time, the balance between different systems may be more important,” says Olof Hjorth, Ph.D. student at the Department of Psychology at Uppsala University, Sweden.

Social anxiety can be a highly debilitating psychiatric disorder with negative impacts on the individual’s relationships and working life.

This study shows that affected people may have an imbalance between the serotonin and dopamine transporters in the amygdala and other brain areas that are important for fear, motivation and social behavior.

The functioning of the brain’s signal substances is affected by the amount of reuptake by the transmitter cell, which is controlled by specific transporter proteins.

“Previously, we have found an increased production and altered reuptake of serotonin in sufferers of social anxiety disorder, a finding we now, in part, replicate,” says Hjorth. He adds, “We can now show that dopamine reuptake is also directly related to the severity of the social anxiety symptoms that the individual is experiencing.”

The method used in the study is called positron emission tomography (PET), in which radioactive agents, injected into the blood stream, decay and release a signal that allows the scientists to determine the density of available transporter proteins in different areas of the brain.

Social anxiety can be a highly debilitating psychiatric disorder with negative impacts on the individual’s relationships and working life.

The researchers hope that the current findings can lead to a better understanding of the causes of social anxiety and ultimately to new, more effective treatments.

“Many of the patients we meet have symptoms that affect all parts of their everyday life, and many of them have suffered for most of their lives, so understanding the cause and finding effective treatments are our highest priority,” says Hjorth.


Individuals may experience anxiety as a warning sign in unknown situations, especially in response to fear and anticipation of danger.1However, it is considered pathological when it directly affects the individual’s quality of life, affecting social relations, cognitive function, and the wake–sleep cycle.24 Anxiety disorders represent one of the major psychiatric disorders today that can impair the quality of life of adults.24

The Diagnostic and Statistical Manual of Mental Disorders – Fifth Edition (DSM-5) defines the presence of an anxiety disorder when some criteria are met, for example: symptoms occurring more than six months, excessive anxiety and worry, panic attacks, restlessness or feeling nervous, fatigue, irritability, sleep and eating disorder.

Based on the symptomatology, anxiety disorders can be classified in: Generalized Anxiety Disorder (GAD), Social Anxiety Disorder, Panic Disorder (PD), Agoraphobia, Separation Anxiety Disorder, Selective Mutism and Specific Phobias. In addition to anxiety disorders, anxiety can be a symptom or comorbidity in several other pathologies, such as Major Depression,5 Obsessive Compulsive Disorder,6 TBI,7 among others.

Neuromodulation minimizes the impact of mood changes811 and repetitive transcranial magnetic stimulation (rTMS) is receiving attention in the last decade.12,17 TMS is a non-invasive method of stimulating the motor cortex neurons through the scalp and skull based on the principle of electromagnetic induction.18,19 

TMS was approved by the Food and Drug Administration (FDA) in 2008 as an alternative treatment for Major Depression Disorder,20 and has been shown to decrease the symptoms of Post Traumatic Stress Disorder (PTSD),21 Obsessive Compulsive Disorder (OCD),22 and Anxiety Disorders.14

Non-invasive brain stimulation techniques allow researchers to study in real-time the human brain activity, characterize the balance of excitation and cortical inhibition, and help guide plastic changes.8 

With TMS, you can apply repetitive induced current pulses that can increase or decrease cortical excitability and stimulate the process of neuronal plasticity.9,23,24 A coil of wire is placed on the scalp generating an electric current that flows through the target area, inducing neuronal depolarization.

Possible effects are depended on subject’s age, pharmacological treatment, number of technical parameters, including the intensity and number of stimulations (ie, frequency), coil orientation, focus, and depth of stimulation.9,25,26

Although TMS pulses (simple and repetitive) are considered safe, it is contraindicated for people who use a pacemaker or other implantable electronic devices.21,27 Patients with bone defects and craniotomy pose another concern, because the conductance of the structures would be modified.21,24 Some adverse effects might occur, such as headache and minor muscle spasms at the stimulation site.21,25,28,29

Recent literature reviews discussed the use of TMS as an intervention strategy for anxiety. Vicario et al’s30 study addressed the use of TMS and transcranial direct current stimulation (tDCS) and other studies portray its efficacy for other psychiatric disorders, without major insights.14,3032 

However, there is a gap in the literature regarding rTMS efficacy in anxiety symptoms (primary and secondary outcomes) in clinical trials. Our study focused on the effectiveness of TMS for Anxiety Disorders and as an intervention for Anxiety Symptoms arising from other pathologies. We make the division between anxiety arising from Neurological Disorders and Psychiatric Disorders.

Our hypothesis was that high-frequency rTMS on the dorsolateral prefrontal cortex (DLPFC) will decrease anxiety symptoms in patients with anxiety disorders, considering anxiety as the primary outcome.


Source:
Uppsala University

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