An area of recent interest in psychiatric research is the application of neuroimaging techniques to investigate neural events associated with the development and the treatment of symptoms in a number of psychiatric disorders.

To examine whether psychological therapies modulate brain activity and, if so, to examine whether these changes similar to those found with relevant pharmacotherapy in various mental disorders.

Relevant data were identified from Pubmed and PsycInfo searches up to July 2005 using combinations of keywords including ‘psychological therapy’, ‘behaviour therapy’, ‘depression’, ‘panic disorder’, ‘phobia’, ‘obsessive compulsive disorder’, ‘schizophrenia’, ‘psychosis’, ‘brain activity’, ‘brain metabolism’, ‘PET’, ‘SPECT’ and ‘fMRI’.

There was ample evidence to demonstrate that psychological therapies produce changes at the neural level. The data, for example in depression, panic disorder, phobia and obsessive compulsive disorder (OCD), clearly suggested that a change in patients' symptoms and maladaptive behaviour at the mind level with psychological techniques is accompanied with functional brain changes in relevant brain circuits. In many studies, cognitive therapies and drug therapies achieved therapeutic gains through the same neural pathways although the two forms of treatment may still have different mechanisms of action.

Empirical research indicates a close association between the ‘mind’ and the ‘brain’ in showing that changes made at the mind level in a psychotherapeutic context produce changes at the brain level. The investigation of changes in neural activity with psychological therapies is a novel area which is likely to enhance our understanding of the mechanisms for therapeutic changes across a range of disorders.

Depression and pain are both burdensome ailments that affect a major proportion of the population. It is evident that depression and pain frequently coexist, with treatment and outcome implications.

To review the literature on the nature, prevalence and co-morbidity of depression and pain, the biological and psychological mechanisms involved and treatment options, thus presenting a broad overview of the current information available.

Relevant sources were identified from PubMed and Medline databases using a combination of keywords including depression, pain, prevalence, co-morbidity, biological and psychological mechanisms, serotonin (5-HT), norepinephrine (NE), hypothalamic-pituitary-adrenal (HPA) axis, amygdala, functional magnetic resonance imaging (fMRI), antidepressant and psychological therapy.

It is evident from the research that depression and pain are common co-morbidities. Pain as a physical symptom of depression affects approximately 65% of patients, leading to less favourable outcomes and greater health care utilization. Moreover, depression is a common feature in chronic pain patients and can affect pain threshold and tolerance. Evidence from biological and psychological studies has revealed mechanisms that link chronic pain to depression. Several classes of anti-depressants and psychological interventions have been used successfully in the treatment of somatic symptoms of depression and for a variety of pain syndromes.

Pain and depression are linked by overlapping phenomenology, neurobiology and therapy. They are mutually interacting, and the interaction has significant treatment and outcome implications.

Our understanding of the neural circuitry involved in mood disorders is rapidly expanding through the ever-increasing application of functional brain imaging techniques.

A selective review of functional neuroimaging studies in patients with primary mood disorders was undertaken in order to identify points of commonality and controversy in the existing literature.

Articles published between 1980 and July 2005 were identified using a range of keywords from relevant on-line databases and key journals.

Increased activity within limbic regions has been consistently associated with depressive states and may also be present in manic states too. Dorsal and ventral prefrontal regions appear compromised as suggested by emerging evidence of cortical inefficiency within prefrontal regions or reductions in their connectivity with limbic areas. Most of the functional changes observed are at least partly reversible following clinical remission although deficits in prefrontal regions may be state-related.

Despite the use of disparate functional imaging modalities, there is a convergence of findings, and the results described do not appear to differ between unipolar and bipolar depression. However, further data are required in order to fully determine the functional changes occurring during manic states. Future work will also need to elucidate the effects of medication, the utility of specific cognitive tasks, and blood oxygenation level-dependent interactions within these affective states.

The orienting reflex (OR) is a fundamental biological mechanism thought to reflect automatic adaptive processing of environmental stimuli necessary for successful interaction with the environment. It has been hypothesized that the OR is generated in response to novelty such as in the case where a mismatch results between an internal neuronal template stored in working memory and incoming stimuli. Recent blood oxygenated level dependant (BOLD) activation studies that have investigated networks involved in the processing of novelty have suggested the recruitment of a distributed limbic-neocortical network. In the present study, event-related functional resonance imaging with simultaneous autonomic electrodermal activity was used to detect single trials of an auditory oddball task associated with the OR.

The pattern of activations indicated two distinct, but partially overlapping, networks. Predominantly, frontal activations were seen for the target stimuli that did elicit an OR, including the orbitofrontal gyrus and anterior cingulate gyrus, as well as activations in the anterior thalamus and cerebellum. On contrary, parietal activations including the supramarginal gyrus and precuneus were seen for the target stimuli that that did not elicit an OR.

To develop and test a novel fMRI compatible comprehensive and expressive language task that reliably and predictably activates both Wernicke's and Broca's cortical brain regions, respectively, and has utility for the determination of hemispheric language dominance.

Ten healthy men (seven) and women (three) were administered a task based on the television game Jeopardy that was adapted for fMRI presentation. The task was programmed using E-PRIME software and designed to run as an event-related experiment. The study was conducted on 3 T MRI Phillips Intera scanner, and data was anlysed using Brain Voyager QX. All subjects provided written informed consent.

The Jeopardy task produced robust left hemisphere activation in regions corresponding to Wernicke's and Broca's areas.

This novel fMRI compatible task (Jeopardy) reliably maps both Broca's and Wernicke's areas with robust hemispheric lateralization. It is potentially useful in language localization studies as it offers advantages over conventional procedures and other fMRI tasks by virtue of being non-invasive and mapping both language areas in one experiment.

Animal models of depression and psychopharmacological mechanisms of action suggest the importance of the gamma-amino butyric acid (GABA) system in the pathophysiology of mood disorders. Mood stabilizers have overlapping effects on GABAergic neurotransmission, and antidepressant use has been associated with alterations in GABAB receptor function. Magnetic resonance spectroscopy (MRS) provides an opportunity to noninvasively assess cerebral GABA concentrations in anterior paralimbic circuits that have been implicated in mood disorders.

In bipolar disorder patients and healthy control subjects, we used MRS with a modified GABA-edited point resolved spectroscopy sequence (TE 68 ms, TR 1500 ms, 512 averages, total scan time 26 min) to assess GABA in an 18-cm3 occipital voxel. In addition, in another cohort of bipolar disorder patients and healthy control subjects, we similarly assessed GABA in a 12.5-cm3 medial prefrontal/anterior cingulate (MPF/AC) voxel. The concentration of GABA was referenced to creatine (Cr) from unedited spectra.

In bipolar patients and controls, we consistently detected 3.0 p.p.m. GABA peaks in occipital lobe and MPF/AC. In 16 bipolar (nine bipolar I and seven bipolar II) disorder patients, compared with six healthy control subjects, mean occipital GABA/Cr concentration was 61% higher. In addition, in 15 bipolar (five bipolar I, nine bipolar II, and one bipolar not otherwise specified) disorder patients, compared with six healthy control subjects, mean MPF/AC GABA/Cr concentration tended to be 41% higher.

Patients with bipolar disorders may have increased cerebral GABA concentrations. Although this was more evident in the occipital lobe, MPC/AC GABA disturbance may be of greater potential interest in view the more established role of MPF/AC in affective processing. Additional studies are warranted to assess changes in GABAergic neurotransmission and the influences of diagnosis, mood state, and medication status in bipolar disorder patients.