UNLABELLED: Pharmacological treatments do have a role to play in the treatment of PTSD. Several agents have been shown to be superior to a placebo and many PTSD sufferers do appear to benefit from medication. The overall effect sizes are relatively small. It is to be hoped that in the future better pharmacological agents will be developed. INTRODUCTION: In recent years there has been a large increase in the amount of research looking at the neurobiology of post-traumatic stress disorder (PTSD). We now know that certain areas of the brain become active at the time of trauma, resulting in emotional and behavioural responses, and changes in neurochemicals and hormones. The amygdala, for example, is involved in the normal fear response, determines the significance of external stimuli and triggers responses such as fight, flight and freezing. These responses lead to alterations in stress hormones, neurochemicals and activity in other parts of the brain, such as the hippocampus and medial prefrontal cortex. One hypothesis is that in PTSD there is a failure of other networks to regulate amygdala reactivity, resulting in hyper reactivity to threat commonly seen in PTSD sufferers.1 Some, but not all studies have suggested that cortisol levels are lower in PTSD sufferers than in individuals without PTSD,2 and that there is adrenergic overactivity shortly after traumatic events. Our current knowledge of the neurobiology of PTSD, although not complete, suggests that certain drugs should be able to prevent its development and reduce its symptoms.
UNLABELLED: Pharmacological treatments do have a role to play in the treatment of PTSD. Several agents have been shown to be superior to a placebo and many PTSD sufferers do appear to benefit from medication. The overall effect sizes are relatively small. It is to be hoped that in the future better pharmacological agents will be developed. INTRODUCTION: In recent years there has been a large increase in the amount of research looking at the neurobiology of post-traumatic stress disorder (PTSD). We now know that certain areas of the brain become active at the time of trauma, resulting in emotional and behavioural responses, and changes in neurochemicals and hormones. The amygdala, for example, is involved in the normal fear response, determines the significance of external stimuli and triggers responses such as fight, flight and freezing. These responses lead to alterations in stress hormones, neurochemicals and activity in other parts of the brain, such as the hippocampus and medial prefrontal cortex. One hypothesis is that in PTSD there is a failure of other networks to regulate amygdala reactivity, resulting in hyper reactivity to threat commonly seen in PTSD sufferers.1 Some, but not all studies have suggested that cortisol levels are lower in PTSD sufferers than in individuals without PTSD,2 and that there is adrenergic overactivity shortly after traumatic events. Our current knowledge of the neurobiology of PTSD, although not complete, suggests that certain drugs should be able to prevent its development and reduce its symptoms.
Authors: Laurence Astill Wright; Marit Sijbrandij; Rob Sinnerton; Catrin Lewis; Neil P Roberts; Jonathan I Bisson Journal: Transl Psychiatry Date: 2019-12-09 Impact factor: 6.222