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The role of the parietal lobe in borderline personality disorder
Medical Hypotheses (2003) 60(2), 263–267 ª 2003 Elsevier Science Ltd. All rights reserved. doi:10.1016/S0306-9877(02)00384-5
The role of the parietal lobe in borderline personality disorder M. Swinton Ashworth Hospital, Maghull, Liverpool, UK
Summary Many patients with a diagnosis of borderline personality disorder describe multi-modal hallucinations. A likely cortical origin for multi-modal hallucinations is the inferior parietal lobule. Neuropsychological testing of borderline personality disorder reveals deficits of visuospatial capacity; a function which is also localised to the inferior parietal lobule. It is hypothesised that this brain area is likely to be dysfunctional in those patients with borderline personality disorder who have multi-modal hallucinations. A deficit in the inferior parietal lobe could plausibly explain a number of other clinical features; the gender dimorphism of this disorder, the lack of expressive gesture and the specific response to clozapine. More speculatively; the increased concern over this disorder over the past 40 years could result from the normal population showing an increase in functional ability in the parietal lobe, leaving patients with parietal deficits relatively more disabled. ª 2003 Elsevier Science Ltd. All rights reserved.
INTRODUCTION In a recent paper Corrigan et al. (1) suggested that borderline personality disorder could arise from a dysfunction of the amygdala. Taking emotional dysregulation as the core feature of BPD, the authors proposed that the disorder arises from impaired modulation of subcortical inputs to consciousness. There is some recent evidence that supports their hypothesis. Using MRI, Dreissen et al. (2) showed patients have reductions in size in the amygdala and hippocampal regions. Using functional MRI scanning; Herpetz et al. (3) reported enhanced activation in the amygdala in response to emotionally aversive slides in BPD patients. The basis of this approach is that BPD is seen primarily as a disorder of affect and impulse control. It is suggested here that this approach, although relevant,
Received 20 August 2002 Accepted 29 August 2002 Correspondence to: Mark Swinton MRCPsych, MD, Consultant Forensic Psychiatrist, Ashworth Hospital, Maghull, Liverpool L31 1HW, UK. Phone: +44-151-473-0303; E-mail: [email protected]
misses important clinical features of these patients and that other brain regions are likely to be implicated. SYMPTOMS IN BORDERLINE PERSONALITY DISORDER Hoch and Polatin (4) described a clinical syndrome they named pseudoneurotic schizophrenia. Their first paper was a case series describing patients with a range of both neurotic and psychotic symptoms. The psychotic symptoms were characteristically vague and fluctuating. The concept of pseudoneurotic schizophrenia later fell from favour; it was, however, one of the main intellectual precursors of the borderline personality disorder concept. While symptoms do not feature strongly in the DSM criteria; a number of authors have described psychotic symptoms in patients who meet diagnostic criteria for this disorder (5–7). Clinicians caring for BPD patients will be aware that patients have a wide range of mental symptoms beyond those of affect and impulse control. A disorder solely of a relatively primitive brain structure is inherently unlikely to be associated with complex pathological mental experiences The presence of such experiences implies some involvement of cortical structures.
263
264 Swinton
MULTI-MODAL HALLUCINATIONS Characteristically patients with a BPD diagnosis will describe abnormal sensory experiences in multiple sensory modalities. Often these experiences are brief and indistinct and not given much emphasis by examining clinicians, perhaps sometimes disbelieved. Chesterman and Boast (8) described how multi-modal hallucinations have over time shifted from being seen by clinicians as a feature of mental illness to being seen as a feature of hysterical and factitious conditions. There has been no evidence that supports this shift in the beliefs and attitudes of clinicians. Most commonly patients with a BPD diagnosis will describe hearing voices. These voices have a differing quality to those reported by patients with unequivocal schizophrenia, consisting of short action-based words or phrases repeated over and over (e.g., cut, cut), often located by patients within their own head and often attributed by patients to someone known to them. In UK clinical practice the term ‘pseudo-hallucination’ is used to describe these experiences; however, this is unsatisfactory given the multiple meanings attached to this term (9,10). In practice these experiences are often regarded by clinicians as being either not real (i.e., fabricated) experiences or at least experiences which do not influence behaviour. Close examination of these patients will often reveal hallucinations in at least one additional sensory modality. Most often this is visual; patients will describe seeing disembodied faces often again this is of people they know. In addition some patients report hallucinations of smell and taste. Patients will report feeling they are being touched. There is often have a high rate of contact with physical health care professionals in the absence of major physical illness and as a result patients are often regarded as hypochondriacal. Close examination of symptoms will reveal descriptions of sensations in the abdomen such as burning or tickling, that cannot be linked to recognised physical disorders. In addition to hallucinatory experiences; some patients will report normal sensations becoming intense e.g., suddenly being irritated by noise around them. Nyman et al. (11) described ‘non-regressive schizophrenia’ a concept similar to pseudoneurotic schizophrenia. In their accounts, this latter feature (which they termed dishabituation) was given particular prominence. In his alternative classification of the major mental illnesses, Leonhard (12) documented a condition of ‘affective paraphrenia’ which was described in terms similar to that of Hoch and Nyman and included accounts of multi-modal hallucinations. Both Leonhard, Hoch and Nyman have in common an approach to these patients which stresses mental symptoms as opposed to
Medical Hypotheses (2003) 60(2), 263–267
behavioural features arising from presumed personality deficits. Conventional thinking on BPD patients regards these symptoms as accessory to the real disorder. Patients are, for example, described as having transient psychotic episodes implying that the ‘real’ disorder is something that carries on between these episodes; the ‘real’ disorder being seen as a disorder of emotional regulation. However, as the writings of Leonhard, Hoch and Nyman indicate, historically these psychotic symptoms have been seen as the key feature of the disorder. It is probably true that patients who now report multi-modal hallucinations are met with scepticism in psychiatric services. There is no clear way of validating self-report of such symptoms. However, if patients’ self-report were believed this would imply a disease process in cortical areas responsible for processing these sensations. COGNITIVE DEFICITS IN BORDERLINE PERSONALITY DISORDER The cortical receiving areas for the primary senses are widely dispersed involving frontal (taste), occipital (vision), medial temporal (sound), inferior temporal (smell), and anterior parietal (touch) areas. A disease process affecting two or more of those areas would be expected to cause a very major degree of overall cognitive impairment. Clinically this does not appear to be the case with typical patients. Neuropsychological testing of BPD patients identifies a persistent picture of relatively subtle deficits of cognitive functioning involving deficits in memory and visuospatial functioning (13). The latter finding, which has been recorded in three separate studies (14–16) is of particular relevance as this function is believed to be localised to the inferior parietal lobule (17). PRIMARY HYPOTHESIS: A DISORDER OF THE INFERIOR PARIETAL LOBULE? The inferior parietal lobule consists of the supramarginal and angular gyri (Broadman’s area 39 and 40). It is an established finding that, in addition to visuospatial functioning, one function of the inferior parietal lobule (IPL) is the integration of primary sensory inputs (18). Therefore on the basis of mainstream understanding of brain functioning it is proposed that patients with borderline personality disorder who have multi-modal hallucinations will have a disorder of their parietal lobe particularly the inferior parietal lobule. The scanning studies of BPD patients described above did not describe parietal dysfunction. However, this may be a result of patient selection. These studies above all
ª 2003 Elsevier Science Ltd. All rights reserved.
The role of the parietal lobe in borderline personality disorder
report on BPD patients on no medication and with no additional diagnoses. This approach causes the deselection of patients with any symptoms. In a similar study (of frontal lobe size in BPD patients) by Lyoo et al. (19) this system of selection led to a drop out of two-thirds of otherwise eligible BPD patients. These cited imaging studies thus describe a patient group with a disorder certainly milder than and possibly different to those found in hospital inpatient services. If BPD was a disorder localisable to the parietal lobe; four other features of these patients could be explicable (1) (2) (3) (4)
the the the the
apparent higher prevalence in women response to clozapine absence of expressive gesture possible increased prevalence over time.
265
isting evidence that clozapine is specifically effective in these patients and that it has a direct and specific effect on one aspect of parietal lobe functioning. The absence of expressive gesture Many patients with BPD and psychotic symptoms have a marked reduction in expressive gesture. They can sit and discuss emotionally laden topics while their hands remain quite still. This occurs in the absence of a generalised reduction in motor activity. This observation was made by Leonard op cit and by Krystal in relation to similar patients with alexithymia (29) and will be familiar to experienced clinicians although it has not been studied systematically. Expressive gesture is thought to be a function of either the inferior or the posterior parietal lobe (30).
The apparent higher prevalence in women In clinical services most patients with this diagnosis are women. This could reflect a treatment bias (that there are an equal number of men with this disorder in the population but they do not get into services) or a true gender variation. The common explanation is that this is a true gender variation but that it is due to psychosocial factors (20). It is believed that women have a higher risk of experiencing childhood sexual trauma than men and this is understood as the cause of the female excess in this disorder which is often seen as a consequence of childhood trauma. An alternative explanation is, however, possible in relation to known gender differences in neuropsychological functioning. In healthy subjects the left inferior parietal lobule is smaller in women than in men (21). This area is involved in visuospatial processing in which men tend to outperform women (22). A pathological process operating in the inferior parietal lobule would be more likely to cause clinical manifestations in women than it would in men.
The response to clozapine There is some evidence that patients with these disorders show a specific response to clozapine (23–26) when they have not responded to other treatments. This evidence is relatively weak coming from case series rather than experimental studies. There have been studies that focus on the neuropsychological effects of clozapine (27). These studies show improvements in motor and mental speed, verbal learning and visuospatial functioning. The last of these is a function which is clearly localised to the parietal lobe. Similar studies of the effect of haloperidol and quetiapine (28) showed improvements in other aspects of cognitive functioning but not in visuospatial functioning. There is therefore some exª 2003 Elsevier Science Ltd. All rights reserved.
The possible increased prevalence over time There are no existing studies that describe the prevalence of borderline personality disorder over time. Nevertheless it could well be true that borderline personality disorder has become more common over the past 50 years as such a condition was not described by Kraepelin and only appeared in diagnostic classifications in the 1960s. Self injury is perhaps the most characteristic behavioural manifestation of this disorder. It could well be true that self injury has become more common over the past 50 years. It is hard to find clinical accounts of self injury prior to this time. As an example; a descriptive study of self injury in a large psychiatric hospital from 1960 contains no references to previous similar work (31). The detailed review of the history of self injury by Favazza (32) identified a 19th century medical book which described patients with self injury (33) but the title of the book (‘Anomalies and Curiosities of Medicine’) indicates that this was seen as a rare behaviour. The cause of borderline personality disorder is usually attributed to childhood physical, sexual or emotional abuse. Yet it would be hard to imagine that the prevalence of these traumas has increased over the past 100 years. If the disorder has really become more common while its putative causes have become less common; this would indicate that alternative causes should be considered. Overall IQ has risen persistently over the post war years. The evidence comes from the work of Flynn (34) and is based on IQ testing in those countries that use conscripts for their armed forces. The most substantial rises have taken place, not in tests of verbal and numeric skills, but on tests of visuospatial functioning. Howard (35) showed evidence that abilities in chess (a game based on visuospatial functioning) have improved Medical Hypotheses (2003) 60(2), 263–267
266 Swinton
over a similar period. It has been argued that visuospatial functioning has improved as a result of improved education systems and in response to a greater need for abstract thought in more complex societies. Whatever the cause of the rise; if there was a disorder which affected visuospatial functioning then such a disorder would be likely to become more manifest as these abilities increased in the normal population. A small group of individuals would essentially become left behind. CONCLUSION The primary argument is that the symptoms and cognitive impairments of patients with a borderline personality disorder (multi-modal hallucinations and impaired visuospatial functioning) are suggestive of dysfunction of the inferior parietal lobe. This hypothesis here is not incompatible with that of Corrigan. The inferior parietal lobe has evolved from and provides a strong input into the amygdala (36). A disorder in the inferior parietal lobe is likely to effect amygdala functioning. The approach taken in this analysis does not negate the life history of abuse reported by so many patients with this disorder; it merely suggests an alternative way of thinking about their disorder. In clinical services, debates about whether these patients are really mentally ill or are personality disordered are common. Patients regarded as suffering from a personality disorder find it hard to access mental health care services. These arguments cannot be resolved by debate about phenomenology alone since it is not agreed that patients actually experience the symptoms that they claim or that the symptoms are the cause of observed behaviours. If the hypothesis that patients have a disorder of parietal lobe functioning is correct then such arguments would be resolved by higher order concepts; that of disordered brain functioning which can plausibly cause both symptoms and an abnormal pattern of interpersonal interactions. REFERENCES 1. Corrigan F. M., Davidson A., Heard H. The role of dysregulated amygdalic emotion in borderline personality disorder. Med Hypotheses 2000; 54: 574–579. 2. Driessen M., Herrmann J., Stahl K., Zwaan M., Meier S., Hill A., Osterheider M., Petersen D. Magnetic resonance imaging volumes of the hippocampus and the amygdala in women with borderline personality disorder and early traumatization. Arch Gen Psychiatry 2000; 57: 1115–1122. 3. Herpertz S. C., Dietrich T. M., Wenning B., Krings T., Erberich S. G., Willmes K., Thron A., Sass H. Evidence of abnormal amygdala functioning in borderline personality disorder: a functional MRI study. Biol Psychiatry 2001; 50: 292–298.
Medical Hypotheses (2003) 60(2), 263–267
4. Hoch P. H., Polatin P. Psuedoneurotic forms of schizophrenia. Psychiatr Q 1949; 23: 248–276. 5. Miller F. T., Abrams T., Dulit R., Fyer M. Psychotic symptoms in patients with borderline personality disorder and concurrent axis I disorder. Hosp Community Psych 1993; 44: 59–61. 6. Chopra H. D., Beatson J. A. Psychotic symptoms in borderline personality disorder. Am J Psychiatry 1986; 143: 1605–1607. 7. Dowson J. H., Sussams P., Grounds A. J., Taylor J. Associations of self-reported past ‘psychotic’ phenomena with features of personality disorders. Compr Psychiatry 2000; 41: 42–48. 8. Chesterman L. P., Boast N. Multi-modal hallucinations. Psychopathology 1994; 27: 273–280. 9. Berrios G. E., Dening T. R. Pseudohallucinations: a conceptual history. Psychol Med 1996; 26: 753–763. 10. Dening T. R., Berrios G. E. The enigma of pseudohallucinations: current meanings and usage. Psychopathology 1996; 29: 27–34. 11. Nyman G. E., Nyman A. K., Nylander B. I. Non-regressive schizophrenia: I. A comparative study of clinical picture, social prognosis, and heredity. Acta Psychiatr Scand 1978; 57: 165–192. 12. Leonhard K. Classification of Endogenous Psychoses and their Differentiated Etiology. New York: Irvington, 1979. 13. O’Leary K. M. Neuropsychological testing results. Psychiatr Clin North Am 2000; 23: 41–60. 14. O’Leary K. M., Brouwers P., Gardner D. L., Cowdry R. W. Neuropsychological testing of patients with borderline personality disorder. Am J Psychiatry 1991; 148: 106–111. 15. Judd P. H., Ruff R. M. Neuropsychological dysfunction in borderline personality disorder. J Personal Disord 1993; 7: 275–284. 16. Swirsky-Sacchetti T., Gorton G., Samuel S., Sobel R., Genetta-Wadley A., Burleigh B. Neuropsychological function in borderline personality disorder. J Clin Psychol 1993; 49: 385–396. 17. Frederikse M. E., Lu A., Aylward E., Barta P., Pearlson G. Sex differences in the inferior parietal lobule. Cereb Cortex 1999; 9: 896–901. 18. Luria A. R. The Working Brain. Penguin: Middlesex, 1973. 19. Lyoo I. K., Han M. H., Cho D. Y. A brain MRI study in subjects with borderline personality disorder. J Affect Disord 1998; 50: 235–243. 20. Widiger T. A., Weissman M. M. Epidemiology of borderline personality disorder. Hosp Community Psych 1991; 42: 1015–1021. 21. Frederikse M., Lu A., Aylward E. H., Barta P. E., Pearlson G. D. Sex differences in the inferior parietal lobule. Cereb Cortex 1999; 9: 901–986. 22. Halpern D. F. Sex Differences in Cognitive Abilities. New Jersey: Lawrence Erlbaum Associates, 1986. 23. Frankenburg F. R., Zanarini M. C. Clozapine treatment of borderline patients: a preliminary study. Compr Psychiatry 1993; 34: 402–405. 24. Benedetti F., Sforzini L., Colombo C., Maffei C., Smeraldi E. Low-dose clozapine in acute and continuation treatment of severe borderline personality disorder. J Clin Psychiatry 1998; 59: 103–107. 25. Chengappa K. N., Ebeling T., Kang J. S., Levine J., Parepally H. Clozapine reduces severe self-mutilation and aggression in psychotic patients with borderline personality disorder. J Clin Psychiatry 1999; 60: 477–484.
ª 2003 Elsevier Science Ltd. All rights reserved.
The role of the parietal lobe in borderline personality disorder
26. Swinton M. Clozapine in severe borderline personality disorder. J Forensic Psychiatr 2001; 12: 580–591. 27. Purdon S. E., Labelle A., Boulay L. Neuropsychological change in schizophrenia after 6 weeks of clozapine. Schizophr Res 2001; 48: 57–67. 28. Purdon S. E., Malla A., Labelle A., Lit W. Neuropsychological change in patients with schizophrenia after treatment with quetiapine or haloperidol. J Psychiatr Neurosci 2001; 26: 137–149. 29. Krystal H. Alexithymia and psychotherapy. Am J Psychother 1979; 33: 17–31. 30. Choi S. H., Na D. L., Kang E., Lee K. M., Lee S. W., Na D. G. Functional magnetic resonance imaging during pantomiming tool-use gestures. Exp Brain Res 2001; 139: 311–317.
ª 2003 Elsevier Science Ltd. All rights reserved.
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31. Offer D., Barglow P. Adolescent and young adult selfmutilation incidents in a general psychiatric hospital. Arch Gen Psychiatry 1960; 3: 102–112. 32. Favazza A. R. Bodies Under Siege. Baltimore: John Hopkins University Press, 1987. 33. Gould G. M., Pyle L. W. Anomalies and Curiosities of Medicine. New York: Sydenham, 1882. 34. Flynn J. R. Massive IQ gains in 14 nations: what IQ tests really measure. Psychol Bull 1987; 101: 171–191. 35. Howard R. W. Preliminary real-world evidence that average human intelligence really is rising. Intelligence 1999; 27: 235–250. 36. Joseph R. Neuropsychology, Neuropsychiatry and Clinical Neuroscience. Baltimore, MD: Williams and Wilkins, 1990.
Medical Hypotheses (2003) 60(2), 263–267
The role of the parietal lobe in borderline personality disorder M. Swinton Ashworth Hospital, Maghull, Liverpool, UK
Summary Many patients with a diagnosis of borderline personality disorder describe multi-modal hallucinations. A likely cortical origin for multi-modal hallucinations is the inferior parietal lobule. Neuropsychological testing of borderline personality disorder reveals deficits of visuospatial capacity; a function which is also localised to the inferior parietal lobule. It is hypothesised that this brain area is likely to be dysfunctional in those patients with borderline personality disorder who have multi-modal hallucinations. A deficit in the inferior parietal lobe could plausibly explain a number of other clinical features; the gender dimorphism of this disorder, the lack of expressive gesture and the specific response to clozapine. More speculatively; the increased concern over this disorder over the past 40 years could result from the normal population showing an increase in functional ability in the parietal lobe, leaving patients with parietal deficits relatively more disabled. ª 2003 Elsevier Science Ltd. All rights reserved.
INTRODUCTION In a recent paper Corrigan et al. (1) suggested that borderline personality disorder could arise from a dysfunction of the amygdala. Taking emotional dysregulation as the core feature of BPD, the authors proposed that the disorder arises from impaired modulation of subcortical inputs to consciousness. There is some recent evidence that supports their hypothesis. Using MRI, Dreissen et al. (2) showed patients have reductions in size in the amygdala and hippocampal regions. Using functional MRI scanning; Herpetz et al. (3) reported enhanced activation in the amygdala in response to emotionally aversive slides in BPD patients. The basis of this approach is that BPD is seen primarily as a disorder of affect and impulse control. It is suggested here that this approach, although relevant,
Received 20 August 2002 Accepted 29 August 2002 Correspondence to: Mark Swinton MRCPsych, MD, Consultant Forensic Psychiatrist, Ashworth Hospital, Maghull, Liverpool L31 1HW, UK. Phone: +44-151-473-0303; E-mail: [email protected]
misses important clinical features of these patients and that other brain regions are likely to be implicated. SYMPTOMS IN BORDERLINE PERSONALITY DISORDER Hoch and Polatin (4) described a clinical syndrome they named pseudoneurotic schizophrenia. Their first paper was a case series describing patients with a range of both neurotic and psychotic symptoms. The psychotic symptoms were characteristically vague and fluctuating. The concept of pseudoneurotic schizophrenia later fell from favour; it was, however, one of the main intellectual precursors of the borderline personality disorder concept. While symptoms do not feature strongly in the DSM criteria; a number of authors have described psychotic symptoms in patients who meet diagnostic criteria for this disorder (5–7). Clinicians caring for BPD patients will be aware that patients have a wide range of mental symptoms beyond those of affect and impulse control. A disorder solely of a relatively primitive brain structure is inherently unlikely to be associated with complex pathological mental experiences The presence of such experiences implies some involvement of cortical structures.
263
264 Swinton
MULTI-MODAL HALLUCINATIONS Characteristically patients with a BPD diagnosis will describe abnormal sensory experiences in multiple sensory modalities. Often these experiences are brief and indistinct and not given much emphasis by examining clinicians, perhaps sometimes disbelieved. Chesterman and Boast (8) described how multi-modal hallucinations have over time shifted from being seen by clinicians as a feature of mental illness to being seen as a feature of hysterical and factitious conditions. There has been no evidence that supports this shift in the beliefs and attitudes of clinicians. Most commonly patients with a BPD diagnosis will describe hearing voices. These voices have a differing quality to those reported by patients with unequivocal schizophrenia, consisting of short action-based words or phrases repeated over and over (e.g., cut, cut), often located by patients within their own head and often attributed by patients to someone known to them. In UK clinical practice the term ‘pseudo-hallucination’ is used to describe these experiences; however, this is unsatisfactory given the multiple meanings attached to this term (9,10). In practice these experiences are often regarded by clinicians as being either not real (i.e., fabricated) experiences or at least experiences which do not influence behaviour. Close examination of these patients will often reveal hallucinations in at least one additional sensory modality. Most often this is visual; patients will describe seeing disembodied faces often again this is of people they know. In addition some patients report hallucinations of smell and taste. Patients will report feeling they are being touched. There is often have a high rate of contact with physical health care professionals in the absence of major physical illness and as a result patients are often regarded as hypochondriacal. Close examination of symptoms will reveal descriptions of sensations in the abdomen such as burning or tickling, that cannot be linked to recognised physical disorders. In addition to hallucinatory experiences; some patients will report normal sensations becoming intense e.g., suddenly being irritated by noise around them. Nyman et al. (11) described ‘non-regressive schizophrenia’ a concept similar to pseudoneurotic schizophrenia. In their accounts, this latter feature (which they termed dishabituation) was given particular prominence. In his alternative classification of the major mental illnesses, Leonhard (12) documented a condition of ‘affective paraphrenia’ which was described in terms similar to that of Hoch and Nyman and included accounts of multi-modal hallucinations. Both Leonhard, Hoch and Nyman have in common an approach to these patients which stresses mental symptoms as opposed to
Medical Hypotheses (2003) 60(2), 263–267
behavioural features arising from presumed personality deficits. Conventional thinking on BPD patients regards these symptoms as accessory to the real disorder. Patients are, for example, described as having transient psychotic episodes implying that the ‘real’ disorder is something that carries on between these episodes; the ‘real’ disorder being seen as a disorder of emotional regulation. However, as the writings of Leonhard, Hoch and Nyman indicate, historically these psychotic symptoms have been seen as the key feature of the disorder. It is probably true that patients who now report multi-modal hallucinations are met with scepticism in psychiatric services. There is no clear way of validating self-report of such symptoms. However, if patients’ self-report were believed this would imply a disease process in cortical areas responsible for processing these sensations. COGNITIVE DEFICITS IN BORDERLINE PERSONALITY DISORDER The cortical receiving areas for the primary senses are widely dispersed involving frontal (taste), occipital (vision), medial temporal (sound), inferior temporal (smell), and anterior parietal (touch) areas. A disease process affecting two or more of those areas would be expected to cause a very major degree of overall cognitive impairment. Clinically this does not appear to be the case with typical patients. Neuropsychological testing of BPD patients identifies a persistent picture of relatively subtle deficits of cognitive functioning involving deficits in memory and visuospatial functioning (13). The latter finding, which has been recorded in three separate studies (14–16) is of particular relevance as this function is believed to be localised to the inferior parietal lobule (17). PRIMARY HYPOTHESIS: A DISORDER OF THE INFERIOR PARIETAL LOBULE? The inferior parietal lobule consists of the supramarginal and angular gyri (Broadman’s area 39 and 40). It is an established finding that, in addition to visuospatial functioning, one function of the inferior parietal lobule (IPL) is the integration of primary sensory inputs (18). Therefore on the basis of mainstream understanding of brain functioning it is proposed that patients with borderline personality disorder who have multi-modal hallucinations will have a disorder of their parietal lobe particularly the inferior parietal lobule. The scanning studies of BPD patients described above did not describe parietal dysfunction. However, this may be a result of patient selection. These studies above all
ª 2003 Elsevier Science Ltd. All rights reserved.
The role of the parietal lobe in borderline personality disorder
report on BPD patients on no medication and with no additional diagnoses. This approach causes the deselection of patients with any symptoms. In a similar study (of frontal lobe size in BPD patients) by Lyoo et al. (19) this system of selection led to a drop out of two-thirds of otherwise eligible BPD patients. These cited imaging studies thus describe a patient group with a disorder certainly milder than and possibly different to those found in hospital inpatient services. If BPD was a disorder localisable to the parietal lobe; four other features of these patients could be explicable (1) (2) (3) (4)
the the the the
apparent higher prevalence in women response to clozapine absence of expressive gesture possible increased prevalence over time.
265
isting evidence that clozapine is specifically effective in these patients and that it has a direct and specific effect on one aspect of parietal lobe functioning. The absence of expressive gesture Many patients with BPD and psychotic symptoms have a marked reduction in expressive gesture. They can sit and discuss emotionally laden topics while their hands remain quite still. This occurs in the absence of a generalised reduction in motor activity. This observation was made by Leonard op cit and by Krystal in relation to similar patients with alexithymia (29) and will be familiar to experienced clinicians although it has not been studied systematically. Expressive gesture is thought to be a function of either the inferior or the posterior parietal lobe (30).
The apparent higher prevalence in women In clinical services most patients with this diagnosis are women. This could reflect a treatment bias (that there are an equal number of men with this disorder in the population but they do not get into services) or a true gender variation. The common explanation is that this is a true gender variation but that it is due to psychosocial factors (20). It is believed that women have a higher risk of experiencing childhood sexual trauma than men and this is understood as the cause of the female excess in this disorder which is often seen as a consequence of childhood trauma. An alternative explanation is, however, possible in relation to known gender differences in neuropsychological functioning. In healthy subjects the left inferior parietal lobule is smaller in women than in men (21). This area is involved in visuospatial processing in which men tend to outperform women (22). A pathological process operating in the inferior parietal lobule would be more likely to cause clinical manifestations in women than it would in men.
The response to clozapine There is some evidence that patients with these disorders show a specific response to clozapine (23–26) when they have not responded to other treatments. This evidence is relatively weak coming from case series rather than experimental studies. There have been studies that focus on the neuropsychological effects of clozapine (27). These studies show improvements in motor and mental speed, verbal learning and visuospatial functioning. The last of these is a function which is clearly localised to the parietal lobe. Similar studies of the effect of haloperidol and quetiapine (28) showed improvements in other aspects of cognitive functioning but not in visuospatial functioning. There is therefore some exª 2003 Elsevier Science Ltd. All rights reserved.
The possible increased prevalence over time There are no existing studies that describe the prevalence of borderline personality disorder over time. Nevertheless it could well be true that borderline personality disorder has become more common over the past 50 years as such a condition was not described by Kraepelin and only appeared in diagnostic classifications in the 1960s. Self injury is perhaps the most characteristic behavioural manifestation of this disorder. It could well be true that self injury has become more common over the past 50 years. It is hard to find clinical accounts of self injury prior to this time. As an example; a descriptive study of self injury in a large psychiatric hospital from 1960 contains no references to previous similar work (31). The detailed review of the history of self injury by Favazza (32) identified a 19th century medical book which described patients with self injury (33) but the title of the book (‘Anomalies and Curiosities of Medicine’) indicates that this was seen as a rare behaviour. The cause of borderline personality disorder is usually attributed to childhood physical, sexual or emotional abuse. Yet it would be hard to imagine that the prevalence of these traumas has increased over the past 100 years. If the disorder has really become more common while its putative causes have become less common; this would indicate that alternative causes should be considered. Overall IQ has risen persistently over the post war years. The evidence comes from the work of Flynn (34) and is based on IQ testing in those countries that use conscripts for their armed forces. The most substantial rises have taken place, not in tests of verbal and numeric skills, but on tests of visuospatial functioning. Howard (35) showed evidence that abilities in chess (a game based on visuospatial functioning) have improved Medical Hypotheses (2003) 60(2), 263–267
266 Swinton
over a similar period. It has been argued that visuospatial functioning has improved as a result of improved education systems and in response to a greater need for abstract thought in more complex societies. Whatever the cause of the rise; if there was a disorder which affected visuospatial functioning then such a disorder would be likely to become more manifest as these abilities increased in the normal population. A small group of individuals would essentially become left behind. CONCLUSION The primary argument is that the symptoms and cognitive impairments of patients with a borderline personality disorder (multi-modal hallucinations and impaired visuospatial functioning) are suggestive of dysfunction of the inferior parietal lobe. This hypothesis here is not incompatible with that of Corrigan. The inferior parietal lobe has evolved from and provides a strong input into the amygdala (36). A disorder in the inferior parietal lobe is likely to effect amygdala functioning. The approach taken in this analysis does not negate the life history of abuse reported by so many patients with this disorder; it merely suggests an alternative way of thinking about their disorder. In clinical services, debates about whether these patients are really mentally ill or are personality disordered are common. Patients regarded as suffering from a personality disorder find it hard to access mental health care services. These arguments cannot be resolved by debate about phenomenology alone since it is not agreed that patients actually experience the symptoms that they claim or that the symptoms are the cause of observed behaviours. If the hypothesis that patients have a disorder of parietal lobe functioning is correct then such arguments would be resolved by higher order concepts; that of disordered brain functioning which can plausibly cause both symptoms and an abnormal pattern of interpersonal interactions. REFERENCES 1. Corrigan F. M., Davidson A., Heard H. The role of dysregulated amygdalic emotion in borderline personality disorder. Med Hypotheses 2000; 54: 574–579. 2. Driessen M., Herrmann J., Stahl K., Zwaan M., Meier S., Hill A., Osterheider M., Petersen D. Magnetic resonance imaging volumes of the hippocampus and the amygdala in women with borderline personality disorder and early traumatization. Arch Gen Psychiatry 2000; 57: 1115–1122. 3. Herpertz S. C., Dietrich T. M., Wenning B., Krings T., Erberich S. G., Willmes K., Thron A., Sass H. Evidence of abnormal amygdala functioning in borderline personality disorder: a functional MRI study. Biol Psychiatry 2001; 50: 292–298.
Medical Hypotheses (2003) 60(2), 263–267
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