I Hate You, Don't Leave Me

Inside the mind of a borderline.

Is Good Psychiatric Management Good Enough to Treat BPD?

DBT vs MBT vs SFT vs TFP...all are well-documented treatment approaches for Borderline Personality. But how do you help the borderline who can't commit to these intensive and expensive programs. Gunderson's description of "Good Psychiatric Management" may open up an approach more practical for more people. Read More

A better approach includes biology

Borderline personality disorder is a heritable brain disease
Current Psychiatry 2014 April;13(4):19-20, 32.
Henry A. Nasrallah, MD
Editor-in-Chief
The prevailing view among many psy­chiatrists and mental health profession­als is that borderline personality disorder (BPD) is a “psychological” condition. BPD often is conceptualized as a behav­ioral consequence of childhood trauma; treatment approaches have emphasized intensive psychotherapeutic modali­ties, less so biologic interventions. You might not be aware that a large body of research over the past decade provides strong evidence that BPD is a neuro­biological illness—a finding that would drastically alter how the disorder should be conceptualized and managed.
Neuropathology underpins the personality disorder
Foremost, BPD must be regarded as a serious, disabling brain disorder, not simply an aberration of personality. In DSM-5, symptoms of BPD are listed as: feelings of abandonment; unstable and intense interpersonal relationships; un­stable sense of self; impulsivity; suicidal or self-mutilating behavior; affective in­stability (dysphoria, irritability, anxiety); chronic feelings of emptiness; intense anger episodes; and transient paranoid or dissociative symptoms. Clearly, these clusters of psychopathological and be­havioral symptoms reflect a pervasive brain disorder associated with abnormal neurobiology and neural circuitry that might, at times, stubbornly defy thera­peutic intervention.
No wonder that 42 published stud­ies report that, compared with healthy controls, people who have BPD display extensive cortical and subcortical abnor­malities in brain structure and function.1 These anomalous patterns have been detected across all 4 available neuroim­aging techniques.

Magnetic resonance imaging. MRI studies have revealed the following abnormalities in BPD:
• hypoplasia of the hippocampus, caudate, and dorsolateral prefrontal cortex
• variations in the CA1 region of the hippocampus and subiculum
• smaller-than-normal orbitofrontal cortex (by 24%, compared with healthy controls) and the mid-temporal and left cingulate gyrii (by 26%)
• larger-than-normal volume of the right inferior parietal cortex and the right parahippocampal gyrus
• loss of gray matter in the frontal, temporal, and parietal cortices
• an enlarged third cerebral ventricle
• in women, reduced size of the me­dial temporal lobe and amygdala
• in men, a decreased concentra­tion of gray matter in the anterior cingulate
• reversal of normal right-greater-than-left asymmetry of the orbitofron­tal cortex gray matter, reflecting loss of gray matter on the right side
• a lower concentration of gray mat­ter in the rostral/subgenual anterior cin­gulate cortex
• a smaller frontal lobe.
In an analysis of MRI studies,2 cor­relation was found between structural brain abnormalities and specific symp­toms of BPD, such as impulsivity, sui­cidality, and aggression. These findings might someday guide personalized in­terventions—for example, using neuro­stimulation techniques such as repetitive transcranial magnetic stimulation and deep brain stimulation—to modulate the activity of a given region of the brain (depending on which symptom is most prominent or disabling).

Magnetic resonance spectroscopy. In BPD, MRS studies reveal:
• compared with controls, a higher glutamate level in the anterior cingulate cortex
• reduced levels of N-acetyl aspar­tate (NAA; found in neurons) and cre­atinine in the left amygdala
• a reduction (on average, 19%) in the NAA concentration in the dorsolat­eral prefrontal cortex.
Functional magnetic resonance im­aging. From fMRI studies, there is evi­dence in BPD of:
• greater activation of the amygdala and prolonged return to baseline
• increased functional connectiv­ity in the left frontopolar cortex and left insula
• decreased connectivity in the left cuneus and left inferior parietal and the right middle temporal lobes
• marked frontal hypometabolism
• hypermetabolism in the motor cor­tex, medial and anterior cingulate, and occipital and temporal poles
• lower connectivity between the amygdala during a neutral stimulus
• higher connectivity between the amygdala during fear stimulus
• higher connectivity between the amygdala during fear stimulus
• deactivation of the opioid system in the left nucleus accumbens, hypothal­amus, and hippocampus
• hyperactivation of the left medial prefrontal cortex during social exclusion
• more mistakes made in differenti­ating an emotional and a neutral facial expression.

Diffusion tensor imaging. DTI white-matter integrity studies of BPD show:
• a bilateral decrease in fractional an­isotropy (FA) in frontal, uncinated, and occipitalfrontal fasciculi
• a decrease in FA in the genu and rostrum of the corpus callosum
• a decrease in inter-hemispheric connectivity between right and left ante­rior cigulate cortices.
Genetic Studies
There is substantial scientific evidence that BPD is highly heritable—a finding that suggests that brain abnormalities of this disorder are a consequence of genes involved in brain development (similar to what is known about schizophrenia, bipolar disorder, and autism).
A systematic review of the heritabil­ity of BPD examined 59 published stud­ies that were categorized into 12 family studies, 18 twin studies, 24 association studies, and 5 gene-environment inter­action studies.3 The authors concluded that BPD has a strong genetic compo­nent, although there also is evidence of gene-environment (G.E) interactions (ie, how nature and nurture influence each other).
The G.E interaction model appears to be consistent with the theory that ex­pression of plasticity genes is modified by childhood experiences and environ­ment, such as physical or sexual abuse. Some studies have found evidence of hypermethylation in BPD, which can ex­ert epigenetic effects. Childhood abuse might, therefore, disrupt certain neuro­plasticity genes, culminating in morpho­logical, neurochemical, metabolic, and white-matter aberrations—leading to pathological behavioral patterns identi­fied as BPD.

The neuropsychiatric basis of BPD must guide treatment
There is no such thing as a purely psycho­logical disorder: Invariably, it is an abnor­mality of brain circuits that disrupts normal development of emotions, thought, behavior, and social cognition. BPD is an exemplar of such neuropsychiatric illness, and treat­ment should support psychotherapeutic ap­proaches to mend the mind at the same time it moves aggressively to repair the brain.

A better approach includes biology

Borderline personality disorder is a heritable brain disease
Current Psychiatry 2014 April;13(4):19-20, 32.
Henry A. Nasrallah, MD
Editor-in-Chief
The prevailing view among many psy­chiatrists and mental health profession­als is that borderline personality disorder (BPD) is a “psychological” condition. BPD often is conceptualized as a behav­ioral consequence of childhood trauma; treatment approaches have emphasized intensive psychotherapeutic modali­ties, less so biologic interventions. You might not be aware that a large body of research over the past decade provides strong evidence that BPD is a neuro­biological illness—a finding that would drastically alter how the disorder should be conceptualized and managed.
Neuropathology underpins the personality disorder
Foremost, BPD must be regarded as a serious, disabling brain disorder, not simply an aberration of personality. In DSM-5, symptoms of BPD are listed as: feelings of abandonment; unstable and intense interpersonal relationships; un­stable sense of self; impulsivity; suicidal or self-mutilating behavior; affective in­stability (dysphoria, irritability, anxiety); chronic feelings of emptiness; intense anger episodes; and transient paranoid or dissociative symptoms. Clearly, these clusters of psychopathological and be­havioral symptoms reflect a pervasive brain disorder associated with abnormal neurobiology and neural circuitry that might, at times, stubbornly defy thera­peutic intervention.
No wonder that 42 published stud­ies report that, compared with healthy controls, people who have BPD display extensive cortical and subcortical abnor­malities in brain structure and function.1 These anomalous patterns have been detected across all 4 available neuroim­aging techniques.

Magnetic resonance imaging. MRI studies have revealed the following abnormalities in BPD:
• hypoplasia of the hippocampus, caudate, and dorsolateral prefrontal cortex
• variations in the CA1 region of the hippocampus and subiculum
• smaller-than-normal orbitofrontal cortex (by 24%, compared with healthy controls) and the mid-temporal and left cingulate gyrii (by 26%)
• larger-than-normal volume of the right inferior parietal cortex and the right parahippocampal gyrus
• loss of gray matter in the frontal, temporal, and parietal cortices
• an enlarged third cerebral ventricle
• in women, reduced size of the me­dial temporal lobe and amygdala
• in men, a decreased concentra­tion of gray matter in the anterior cingulate
• reversal of normal right-greater-than-left asymmetry of the orbitofron­tal cortex gray matter, reflecting loss of gray matter on the right side
• a lower concentration of gray mat­ter in the rostral/subgenual anterior cin­gulate cortex
• a smaller frontal lobe.
In an analysis of MRI studies,2 cor­relation was found between structural brain abnormalities and specific symp­toms of BPD, such as impulsivity, sui­cidality, and aggression. These findings might someday guide personalized in­terventions—for example, using neuro­stimulation techniques such as repetitive transcranial magnetic stimulation and deep brain stimulation—to modulate the activity of a given region of the brain (depending on which symptom is most prominent or disabling).

Magnetic resonance spectroscopy. In BPD, MRS studies reveal:
• compared with controls, a higher glutamate level in the anterior cingulate cortex
• reduced levels of N-acetyl aspar­tate (NAA; found in neurons) and cre­atinine in the left amygdala
• a reduction (on average, 19%) in the NAA concentration in the dorsolat­eral prefrontal cortex.
Functional magnetic resonance im­aging. From fMRI studies, there is evi­dence in BPD of:
• greater activation of the amygdala and prolonged return to baseline
• increased functional connectiv­ity in the left frontopolar cortex and left insula
• decreased connectivity in the left cuneus and left inferior parietal and the right middle temporal lobes
• marked frontal hypometabolism
• hypermetabolism in the motor cor­tex, medial and anterior cingulate, and occipital and temporal poles
• lower connectivity between the amygdala during a neutral stimulus
• higher connectivity between the amygdala during fear stimulus
• higher connectivity between the amygdala during fear stimulus
• deactivation of the opioid system in the left nucleus accumbens, hypothal­amus, and hippocampus
• hyperactivation of the left medial prefrontal cortex during social exclusion
• more mistakes made in differenti­ating an emotional and a neutral facial expression.

Diffusion tensor imaging. DTI white-matter integrity studies of BPD show:
• a bilateral decrease in fractional an­isotropy (FA) in frontal, uncinated, and occipitalfrontal fasciculi
• a decrease in FA in the genu and rostrum of the corpus callosum
• a decrease in inter-hemispheric connectivity between right and left ante­rior cigulate cortices.
Genetic Studies
There is substantial scientific evidence that BPD is highly heritable—a finding that suggests that brain abnormalities of this disorder are a consequence of genes involved in brain development (similar to what is known about schizophrenia, bipolar disorder, and autism).
A systematic review of the heritabil­ity of BPD examined 59 published stud­ies that were categorized into 12 family studies, 18 twin studies, 24 association studies, and 5 gene-environment inter­action studies.3 The authors concluded that BPD has a strong genetic compo­nent, although there also is evidence of gene-environment (G.E) interactions (ie, how nature and nurture influence each other).
The G.E interaction model appears to be consistent with the theory that ex­pression of plasticity genes is modified by childhood experiences and environ­ment, such as physical or sexual abuse. Some studies have found evidence of hypermethylation in BPD, which can ex­ert epigenetic effects. Childhood abuse might, therefore, disrupt certain neuro­plasticity genes, culminating in morpho­logical, neurochemical, metabolic, and white-matter aberrations—leading to pathological behavioral patterns identi­fied as BPD.

The neuropsychiatric basis of BPD must guide treatment
There is no such thing as a purely psycho­logical disorder: Invariably, it is an abnor­mality of brain circuits that disrupts normal development of emotions, thought, behavior, and social cognition. BPD is an exemplar of such neuropsychiatric illness, and treat­ment should support psychotherapeutic ap­proaches to mend the mind at the same time it moves aggressively to repair the brain.

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Jerold Kreisman, M.D., is a psychiatrist and best-selling author of numerous books.

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