Hostname: page-component-78c5997874-fbnjt Total loading time: 0 Render date: 2024-11-06T07:48:45.616Z Has data issue: false hasContentIssue false

Loss of consciousness and post-traumatic stress disorder

A clue to aetiology and treatment

Published online by Cambridge University Press:  03 January 2018

Maureen O'Brien*
Affiliation:
St David's Hospital, Carmarthen, Dyfed
David Nutt
Affiliation:
Psychopharmacology Unit, University of Bristol, Bristol
*
Professor David Nutt. University of Bristol. Psychopharmacology Unit. School of Medical Sciences. University Walk. Bristol BS8 ITD. Fax: 0117 927 70S7 Voice-mail: 0117 925 3066
Rights & Permissions [Opens in a new window]

Extract

Core share and HTML view are not available for this content. However, as you have access to this content, a full PDF is available via the ‘Save PDF’ action button.

Post-traumatic stress disorder (PTSD) is a condition that appears to be becoming increasingly prevalent in psychiatric and general practice. Davidson (1992) reports a lifetime prevalence of 1–9% in the community, with high levels of chroniciry and comorbidity. It routinely features in the general as well as medical literature following major traumas such as the Herald of free enterprise disaster. PTSD is also growing more important in medicolegal terms, as the recent police attempt to obtain compensation for their experiences in the Hillsborough tragedy demonstrates. Despite the high profile of the condition and the repeated descriptions of its development and (partial) resolution after every major disaster, there is very little research into the most effective means of preventing or treating PTSD. The usual approach of debriefing has been shown to be without effect (Deahl et al, 1994) and a recent review of drug treatments revealed only a few small-scale studies, none of which would be suitable tor [he licensing of a drug for this disorder (Davidson, 1992). This may be because most drug treatments are initiated well after the trauma, which may be too late to prevent the laying down of immutable brain traces for the memories, behaviours and affect that trauma causes and which develop into PTSD.

Type
Editorials
Copyright
Copyright © 1998 The Royal College of Psychiatrists 

References

Adamec, R. E. (1998) Evidence that NMDA dependent limbic neuronal plasticity in the right hemispheric mediates stressor induced lasting increases in anxiety-like behavior – a model of limbic plasticity in post-traumatic stress disorder? Journal of Psychopharmacology (in press).CrossRefGoogle Scholar
Adler, A. (1943) Neuropsychiatrie complications in victims of Bostons Coconut Grove Disaster. Journal of the American Medical Association. 123, 10981101.CrossRefGoogle Scholar
Adler, A. (1945a) Two different types of post-traumatic neuroses. American Journal of Psychiatry. 102, 237240.Google Scholar
Adler, A. (1945b) Mental symptoms following head injury. Archives of Neurology and Psychiatry. 53, 3443.Google Scholar
Braun, P., Greenberg, D., Dasberg, H., et al (1990) Core symptoms of post-traumatic stress disorder unimproved by alprazolam treatment. Journal of Clinical Psychiatry. 51, 236238.Google Scholar
Coupland, N. J., Lillywhite, A., Bell, C. E., et al (1997) A pilot controlled study of the effects of flumazenil in post-traumatic stress disorder. Biological Psychiatry. 41, 988990.CrossRefGoogle Scholar
Collingridge, G. L. & Bliss, T. V. (1995) Memories of NMDA receptors and LTP. Trends in Neurosciences. 18, 5456.Google Scholar
Davidson, J. (1992) Drug therapy of post-traumatic stress disorder. British Journal of Psychiatry. 160, 309314.CrossRefGoogle ScholarPubMed
Davidson, J., Glover, V., Clow, A., et al (1988) Tribulin in post-traumatic stress disorder. Psychological Medicine. 4, 833836.CrossRefGoogle Scholar
Deahl, M. P., Gillham, A. B., Thomas, J., et al (1994) Psychological sequelae following the Gulf War. Factors associated with subsequent morbidity and the effectiveness of psychological debriefing, British Journal of Psychiatry, 165, 6065.Google Scholar
Glue, P., Nutt, D. J. & Coupland, N. J. (1993) Stress and psychiatric disorder: reconciling social and biological approaches. In Stress: An Integrated Approach (eds Stanford, S. C. & Salmon, P.), pp. 5373. London: Academic Press.Google Scholar
Harley, C. W., Lalies, M. D. & Nutt, D. J. (1996) Estimating the synaptic concentration of norepinephrine in dentate gyrus which produces beta-receptor mediated long-lasting potentiation in vivo using microdialysis and intracerebroventricular norepinephrine. Brain Research. 710, 293298.Google Scholar
Izquierdo, I. & Medina, J. H. (1991) GABA-A receptor modulation of memory: the role of endogenous benzodiazepines. Trends in Pharmacological Sciences. 121, 260265.CrossRefGoogle Scholar
Mayou, R., Bryant, B. & Duthie, R. (1993) Psychiatric consequences of road traffic accidents. British Medical Journal, 307, 647651.Google Scholar
McMillan, T. M. (1991) Post-traumatic stress disorder and severe head injury, British Journal of Psychiatry. 159, 431433.Google Scholar
Mongan, L. & Calloway, E. (1990) Buprenorphine responders. Biological Psychiatry, 28, 10781080.Google Scholar
Nutt, D. J. & Peters, T. J. (1994) Alcohol: the drug. British Medical Bulletin, 50, 517.Google Scholar
Randall, P. K., Bremner, J. D., Krystal, J. H., et al (1995) Effects of the benzodiazepine antagonist flumazenil in PTSD. Biological Psychiatry, 38, 319324.Google Scholar
Southwick, S. M., Krystal, J. H., Morgan, C. A., et al (1993) Abnormal noradrenergic function in posttraumatic stress disorder. Archives of General Psychiatry. 50, 266274.Google Scholar
Submit a response

eLetters

No eLetters have been published for this article.