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A Jacksonian and biopsychosocial hypothesis concerning borderline and related phenomena


  • Russell Meares,

  • Janine Stevenson,

  • Evian Gordon

  • Department of Psychiatry, Westmead Hospital, PO Box 533, Wentworthville, New South Wales 2145, Australia. Email:

RussellMeares Professor of Psychiatry (Correspondence); Janine Stevenson, Visiting Medical Officer; Evian Gordon, Head Neuroscience Unit


Objective: The aim of this paper is to develop an aetiological model for borderline personality disorder.

Method: The postulates of Hughlings Jackson are used to provide a preliminary explanatory framework for borderline phenomena. As a necessary background to this discussion, the findings concerning abuse in the early history of borderline personality disorder (BPD) and other conditions, notably somatisation disorder and dissociative states, are briefly reviewed. Other data, including family studies, which might have significance in the aetiology of BPD are also reviewed.

Results: The hypothesis is put forward that the symptoms of BPD are due to the failure of ‘experience-dependent’ maturation of a cascade of neural networks, with prefrontal connections, which become active relatively late in development and which coordinate disparate elements of central nervous system function. These networks subserve higher psychological functions, including attentional focus and affect regulation. They also underpin the reflective function necessary to the emergence of self as the stream of consciousness, which appears at about the age of 4 years.

Conclusion: Adverse developmental circumstances may produce an interrelated set of symptom clusters, with associated neural network disturbances that are amenable to investigation with psychometric and brain imaging techniques. Since these disturbances are seen as ‘experience-dependent’, they are considered reversible, at least in part.