The Role of Neuron Creation in Anxiety Disorders

 

THE NEUROPHYSIOLOGY OF PTSD

According to Mike Membrino, anxiety and stress disorders are among the major prevalent of PTSD.

Separately, the clinical manifestations of these disorders provide a spectrum of alterations. To some extent, the present original trauma effects and when untreated, the disease can develop a significant impairment in functioning, reduced quality of life, and enormous economic burden. Recent studies have examined the underlying literature review on the neural mechanism when regulating impaired pattern present in anxiety.

According to the note submitted by Rene Hen, Ph.D., of Columbia’s Department of Psychiatry and the NY Psychiatric Institute, suggest that the production of the neuron or the in the brain have assisted in the treatment of anxiety that is associated with PTSD (Duval et al., 2015).
They further note that the thalamus is an implicated sensory integration. In effect, through activation, the thalamus is associated with high degree of anxiety and disgust in blood-injury-injection phobia, as well as automatic arousal in snake phobia. In the treatment with paroxetine reduces the activation of the thalamus, therefore, tend to reduce anxiety. Additionally, in the hippocampus, the dentate gyrus that is that separate is among the two areas of the brain where neurogenesis takes place. Among the possible improving patterns separation is the addition in the number of adult-generated neurons, so they are better able to process information. Besides, there is enough evidence that shows that reduced hippocampal can be achieved through functional neuroimaging.
THE NEUROPHYSIOLOGY OF PTSD
Moreover, recent studies provide that in the current models of PTSD, hypoactivity in frontal regions suggests a reduced potential for top-down regulation of fear and fear extinction (Holzschneider & Mulert, 2011). The hippocampus provides information about the context of a situation, and the attenuated hippocampal response might be attributable to difficulties in identifying safe circumstances (Holzschneider & Mulert, 2011). Besides, the above mentioned functional modalities in the brain, including the hippocampus, amygdala, and medial prefrontal cortex, have shown possibilities in the patients with PTSD (Holzschneider & Mulert, 2011).
Therefore, the studies as mentioned earlier researchers emphasize on the using better use of technological advancement in imaging. Finally, research should be conducted on patient with impairments in pattern-separation tasks and decreased neurogenesis in the dentate gyrus.

References:

Holzschneider, K., & Mulert, C. (2011). Neuroimaging in anxiety disorders. Dialogues in Clinical Neuroscience, 13(4), 453–461.

Duval, E. R., Javanbakht, A., & Liberzon, I. (2015). Neural circuits in anxiety and stress disorders: a focused review. Therapeutics and Clinical Risk Management, 11, 115–126. http://doi.org/10.2147/TCRM.S48528

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