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Guest Editor's conclusions
This article sets the scene for the current debate on the concept of complicated grief. Issues identified with diagnosis of individuals with complicated grief include concerns about misuse of the term, distinctions between normal and complicated grief and fears regarding stigmatisation associated with potential DSM-V classification of complicated grief. Use of the term as described by Prigerson and colleagues reflects current best evidence, addresses concerns related to definitional error and would assist in progressing research and clinical practice in a more consistent manner if this were used by clinicians, researchers, health policy makers and educators. Such progress will be further assisted when consensus on the diagnostic criteria for complicated grief is achieved.
A key theme in the bereavement literature is the recognition that every grief experience is unique and dependent on many variables, such as the circumstances of the death, characteristics of the bereaved individual, their relationship with the deceased, the provision and availability of support, and a myriad of sociocultural factors. Concurrently, there are corresponding efforts to define "normal" grief and delineate it from "complicated" grief experiences. The discord between these two potentially opposing statements remains a paradox evident within the three major tensions within the thanatological literature--the dominance of grief theories, the medicalization of grief, and the efficacy of grief interventions. Three recommendations for moving beyond the paradox are discussed--the provision of improved grief education for service providers, the bereaved, and the wider community; the conduct of research that emphasizes the context of grief and is relevant to service provision; and the examination of current grief interventions.
In this study the authors examined the functional neuroanatomy of grief, which to their knowledge has not been studied previously in functional neuroimaging research.
Grief was elicited in eight bereaved women through photographs of the deceased versus a stranger, combined with words specific to the death event versus neutral words. Use of both pictures and words resulted in a 2x2 factorial design.
Three brain regions were independently activated by the picture and word factors: posterior cingulate cortex, medial/superior frontal gyrus, and cerebellum. The two factors also activated distinct regions: for the picture factor, they were the cuneus, superior lingual gyrus, insula, dorsal anterior cingulate cortex, inferior temporal gyrus, and fusiform gyrus; and for the word factor, they were the precuneus, precentral gyrus, midbrain, and vermis. The interaction of the two factors showed significant activation in the cerebellar vermis.
Grief is mediated by a distributed neural network that subserves affect processing, mentalizing, episodic memory retrieval, processing of familiar faces, visual imagery, autonomic regulation, and modulation/coordination of these functions. This neural network may account for the unique, subjective quality of grief and provide new leads in understanding the health consequences of grief and the neurobiology of attachment.
Separation from loved ones commonly leads to grief reactions. In some individuals, grief can evolve into a major depressive episode. The brain regions involved in grief have not been specifically studied. The authors studied brain activity in women actively grieving a recent romantic relationship breakup. It was hypothesized that while remembering their ex-partner, subjects would have altered brain activity in regions identified in sadness imaging studies: the cerebellum, anterior temporal cortex, insula, anterior cingulate, and prefrontal cortex.
Nine right-handed women whose romantic relationship ended within the preceding 4 months were studied. Subjects were scanned using blood-oxygen-level-dependent functional magnetic resonance imaging while they alternated between recalling a sad, ruminative thought about their loved one (grief state) and a neutral thought about a different person they knew an equally long time.
Acute grief (grief minus neutral state) was associated with increased group activity in posterior brain regions, including the cerebellum, posterior brainstem, and posterior temporoparietal and occipital brain regions. Decreased activity was more prominent anteriorly and on the left and included the anterior brainstem, thalamus, striatum, temporal cortex, insula, and dorsal and ventral anterior cingulate/prefrontal cortex. When a more lenient statistical threshold for regions of interest was used, additional increases were found in the lateral temporal cortex, supragenual anterior cingulate/medial prefrontal cortex, and right inferomedial dorsolateral prefrontal cortex, all of which were adjacent to spatially more prominent decreases. In nearly all brain regions showing brain activity decreases with acute grief, activity decreases were greater in women reporting higher grief levels over the past 2 weeks.
During acute grief, subjects showed brain activity changes in the cerebellum, anterior temporal cortex, insula, anterior cingulate, and prefrontal cortex, consistent with the hypothesis. Subjects with greater baseline grief showed greater decreases in all these regions except for the cerebellum. Further imaging studies are needed to understand the relationship between normal sadness, grief, and depression.
In a 10-year follow-up of a survey from Oslo, 503 persons were reinterviewed using the same questionnaire.
The questionnaire includes information about social support, 'locus of control' and mental health as well as negative life events and long-lasting mental strain during the year prior to the follow-up.
The study confirms the "buffer hypothesis", that social support protects against the development of mental disorder only when the individual is exposed to stressors, like negative life events. This buffering effect was especially strong for depression.
The buffering effect only applies to the 'externals'--those who have personality-related feelings of powerlessness and lack of control over their own lives. The 'internals' do not have the same need for social support to cope with life stressors, and have low symptom scores even when negative life events are combined with relative weak social support.