The autonomic nervous system (ANS) controls the body’s internal environment by sending impulses from the central nervous system to the peripheral organs. The ANS is subdivided into the sympathetic nervous system (red) and parasympathetic nervous systems (grey). The sympathetic nervous system, which starts in the hypothalamus, is most active in times of stress, and stimulation of the peripheral organs (blue) produces a panic response (yellow).
There is consistent evidence from MRI volumetric studies that hippocampal volume is reduced in posttraumatic stress disorder (PTSD). This atrophy of the hippocampus is thought to represent decreased neuronal density. However, other studies suggest that hippocampal changes are explained by whole brain atophy and generalised white matter atrophy is exhibited by people with PTSD.
During passive activity, patients with generalized anxiety disorder (GAD) exhibit increased metabolic rates in the occipital, temporal and frontal lobes and in the cerebellum and thalamus compared with healthy controls. Increased metabolic activity in the basal ganglia has also been reported in patients with GAD during vigilance tasks. These finding suggest that there may be hyperactive brain circuits in GAD.
Patients with generalised anxiety disorder (GAD) exhibit increased metabolic rates in several brain regions compared with healthy controls. Hyperactive neurotransmitter circuits between the cortex, thalamus, amygdala and hypothalamus have been implicated in the disorder. Hypofunction of serotonergic neurones arising from the dorsal raphe nucleus and GABAergic neurones that are widely distributed in the brain may result in a lack of inhibitory effect on the putative GAD pathway. Furthermore, overactivity of noradrenergic neurones arising from the locus coeruleus may produce excessive excitation in the brain areas implicated in GAD.
In obsessive compulsive disorder (OCD) there is abnormal metabolic activity in the orbitofrontal cortex, the anterior cingulate/caudal medial prefrontal cortex, and the caudate nucleus. Activity within this cortico-basal ganglia network is increased at rest compared with controls. During provocation of symptoms this activity is accentuated: it is reduced following successful treatment.
Patients with obsessive compulsive disorder (OCD) exhibit increased metabolic activity in the cortico-basal ganglia network compared with healthy controls. Hyperactive neurotransmitter circuits between the cortex, basal ganglia and thalamus have been implicated in the disorder. Hypofunction of serotonergic neurones arising from the rostral raphe nucleus may result in a lack of inhibitory effect on the putative OCD pathway. Furthermore, overactivity of dopaminergic neurones arising from the substantia nigra may produce excessive excitation in the brain areas implicated in OCD.
There are a number of areas of the brain affected in panic disorder. Increased serotonin activity in the amygdala and frontal cortex induces symptoms of anxiety, whereas increased activity in the periaquaductal grey results in defensive behaviours and postural freezing. The locus coeruleus increases noradrenaline release mediating physiological and behavioural arousal, while the hypothalamus mediates the sympathetic nervous system.
Hyperactive neurotransmitter circuits between the cortex, thalamus, hippocampus, amygdala, hypothalamus and peri-adqueductal grey matter have been implicated in panic disorder. Hypofunction of serotonergic neurones arising from the rostral raphe nucleus may result in a lack of inhibitory effect on the putative panic pathways in the brain. While, overactivity of noradrenergic neurones arising from the locus coeruleus may produce excessive excitation in the regions implicated in panic disorder. Physiological symptoms of the panic response are medicated by the autonomic nervous system through connections with the locus coeruleus and hypothalamus.
There are a number of areas of the brain affected in phobia. Activation of the amygdala causes anticipatory anxiety or avoidance (conditioned fear) while activation of the hypothalamus activates the sympathetic nervous system. Other regions of the brain involved in phobia include the thalamus and the cortical structures, which may form a key neural network along with the amygdala. Stimulation of the locus coeruleus increases noradrenaline release mediating physiological and behavioural arousal.
Sensory input, memory formation and stress response mechanisms are affected in patients with post-traumatic stress disorder (PTSD). The regions of the brain involved in memory processing that are implicated in PTSD include the hippocampus, amygdala and frontal cortex. While the heightened stress response is likely to involve the thalamus, hypothalamus and locus coeruleus.
Based on early neuroanatomical observations and studies with psychoactive drugs, the septohippocampal circuit has been proposed as a model for anxiety disorders. The circuit that links the septum, amygdala, hippocampus and fornix is thought to process external stimuli and regulate the behavioural response through wider projections in the brain. Hyperstimulation of this putative ‘behavioural inhibition’ circuit, through dysfunctional noradrenergic and serotonergic neurotransmission, has been implicated in producing anxiety, and increased arousal and attention.