- Email: [email protected]
Plasma catecholamines in post-traumatic stress disorder
BIOL PSYCHIATRY
34A
Stress: Basic and Clinical Studies
1989;25:33A-36A
to both the combat (p < .005) and the noncombat (p < .05) films, but showed greater heart rate (p < .Ol) response only to the combat film. PTSD subjects showed a greater increase in diastolic BP during both the combat (p < .005) and noncombat (p < .05) films. Plasma epinephrine (E) was increased in PTSD patients during the combat film (p < .05) only. Both diastolic BP (p < .05) and E (p < .05) remained elevated for thirty minutes following only the combat film. Plasma norepinephrine and systolic BP did not change for either group after either stressor. This data supports autonomic conditioning in PTSD .
70
PSYCHOTIC SYMPTOMS IN CHRONIC COMBAT-RELATED POST-TRAUMATIC STRESS DISORDER Robert Butler, David Braff San Diego, CA One of the critical diagnostic criteria for Post-Traumatic Stress Disorder (PTSD) involves intrusive re-experiencing of the trauma. Isolated reports have suggested that these intrusive experiences may form a continuum with frank auditory hallucinations occurring in the absence of other psychiatric symptoms in some PTSD patients. There has not been a systematic investigation on auditory hallucinations in PTSD using reliable and valid assessment measures, however. We administered the Schedule for Affective Disorders and Schizophrenia-Change Version (SADS-C), Scale for the Assessment of Positive Symptoms (SAPS) to a group of combat veterans who met DSMIII-R criteria for PTSD (N = 11) and a control group of combat veterans who did not have PTSD (N = 13). On the SADS, the PTSD group scored significantly higher levels of depression, anxiety, and agitation but were not significantly different from the control group on the Mania and Psychosis subscales. The PTSD group scored significantly higher on the SAPS when compared to the control group. SAPS subscales were investigated and it was determined that the PTSD group was characterized by greater hallucinations and delusions but not by significantly greater levels of bizarre behavior or thought disorder. The qualitative nature of the symptoms, diagnosis and treatment are discussed.
71
PLASMA CATECHOLAMINES DISORDER Mark Hamner, Bruce Diamond, Augusta,
IN POST-TRAUMATIC
STRESS
Ana Hitri
GA
Abnormalities of catecholamine (CA) function have been implicated in the pathophysiology of anxiety disorders. Hyperactivity of CA systems may contribute to posttraumatic stress disorder (PTSD) symptoms. To investigate the effects of exercise on plasma catecholamines in PTSD, seven male veterans with a DSM-III-R diagnosis of PTSD underwent a standard grade-incremented exercise treadmill test of maximal exercise intensity. They were compared with six age-matched male controls (CS). Plasma dopamine (DA), norepinephrine (NE), and 3-methoxy_Q-hydroxyphenyl-ethylene glycol (MHPG) at rest and post-exercise were assayed by HPLC with electrochemical detection. Plasma DA was higher at rest in PTSD versus CS (p < .05). Plasma NE values at rest tended to be higher in PTSD versus CS. MHPG levels were lower at rest in PTSD versus CS (p < .05). Exercise
increased
NE and DA levels
Stress: Basic and Clinical Studies
BIOL PSYCHIATRY 1989:25:33A-36A
35A
significantly in both groups. However, the magnitude of increase was greater in CS. MHPG increased in PTSD and decreased in CS with exercise. These data suggest an increased CA state in PTSD. Furthermore, the lower resting MHPG as well as the opposite MHPG response to exercise in PTSD suggests an altered CA metabolism.
72
CHRONIC STRESS PRODUCES DELAYED AND PROLONGED SUBSENSITIZATION OF A NICOTINIC MECHANISM Jason Peck, Max McGee, Richard S. Jaeckle, Steven C. Dilsaver Columbus, OH
Nicotinic receptors in the hypothalamus mediate certain neurobiologic effects of stress. We studied the effects of chronic inescapable swim stress on a nicotinic mechanism which regulates core body temperature. Twelve male rats were given twice daily swim stress (8 minutes/session at 12C) for 14 days. We challenged the animals with nicotine (1.0 mg/kg, ip) at baseline, after seven and 14 days of stress, and weekly thereafter for five weeks following the cessation of stress. The mean hypothermic response to nicotine was subsensitized after 14 days of stress. We observed a continued progressive subsensitization of the response during the first two weeks after cessation of stress. The response gradually returned to baseline over the following three weeks. Our results suggests: (1) chronic inescapable stress subsensitizes what is thought to be a hypothalamic nicotinic mechanism; (2) this nicotinic mechanism continues to become progressively subsensitized after the stressor is terminated; (3) the nicotinic mechanism is more resistant to the effects of stress than are muscarinic and alpha* adrenergic mechanisms regulating core body temperature. Our results suggest that alterations in central nicotinic mechanisms may play a role in stress-related diseases such as major depression.
73
CHRONIC STRESS SUBSENSITIZES AN ALPHA* ADRENERGIC MECHANISM WHICH REGULATES CORE BODY TEMPERATURE Max McGee, Jason Peck, Richard S. Jaeckle, Steven C. Dilsaver Columbus, OH
Chronic inescapable stress is hypothesized to produce alterations in brain noradrenergic systems. We studied the effects of chronic swim stress on an alpha* adrenergic mechanism which regulates core body temperature. Twelve male rats were given twice daily swim stress (8 minutes/session at 12C) for seven days. We challenged the animals with clonidine (0.1 mg/kg, ip) on the days before and after chronic swim stress. The pre-stress clonidine challenge produced a mean thermic response of - 0.50 ? 0.13C (mean + SEM). After one week of chronic stress, the mean thermic response was subsensitized (-0.05 + 0.06C). The mean thermic response returned to baseline seven days after the cessation of chronic stress. Thus, one week of chronic stress was sufficient to subsensitize what is thought to be a hypothalamic alpha2 adrenergic mechanism, and alpha* sensitivity normalized during one week of recovery from stress. The neurobiologic responses to stress may be relevant to the pathophysiology of stressrelated diseases such as major depression. Chronic uncontrollable stressors and some subtypes of major depression may be accompanied by hyperactivity of central nor-
34A
Stress: Basic and Clinical Studies
1989;25:33A-36A
to both the combat (p < .005) and the noncombat (p < .05) films, but showed greater heart rate (p < .Ol) response only to the combat film. PTSD subjects showed a greater increase in diastolic BP during both the combat (p < .005) and noncombat (p < .05) films. Plasma epinephrine (E) was increased in PTSD patients during the combat film (p < .05) only. Both diastolic BP (p < .05) and E (p < .05) remained elevated for thirty minutes following only the combat film. Plasma norepinephrine and systolic BP did not change for either group after either stressor. This data supports autonomic conditioning in PTSD .
70
PSYCHOTIC SYMPTOMS IN CHRONIC COMBAT-RELATED POST-TRAUMATIC STRESS DISORDER Robert Butler, David Braff San Diego, CA One of the critical diagnostic criteria for Post-Traumatic Stress Disorder (PTSD) involves intrusive re-experiencing of the trauma. Isolated reports have suggested that these intrusive experiences may form a continuum with frank auditory hallucinations occurring in the absence of other psychiatric symptoms in some PTSD patients. There has not been a systematic investigation on auditory hallucinations in PTSD using reliable and valid assessment measures, however. We administered the Schedule for Affective Disorders and Schizophrenia-Change Version (SADS-C), Scale for the Assessment of Positive Symptoms (SAPS) to a group of combat veterans who met DSMIII-R criteria for PTSD (N = 11) and a control group of combat veterans who did not have PTSD (N = 13). On the SADS, the PTSD group scored significantly higher levels of depression, anxiety, and agitation but were not significantly different from the control group on the Mania and Psychosis subscales. The PTSD group scored significantly higher on the SAPS when compared to the control group. SAPS subscales were investigated and it was determined that the PTSD group was characterized by greater hallucinations and delusions but not by significantly greater levels of bizarre behavior or thought disorder. The qualitative nature of the symptoms, diagnosis and treatment are discussed.
71
PLASMA CATECHOLAMINES DISORDER Mark Hamner, Bruce Diamond, Augusta,
IN POST-TRAUMATIC
STRESS
Ana Hitri
GA
Abnormalities of catecholamine (CA) function have been implicated in the pathophysiology of anxiety disorders. Hyperactivity of CA systems may contribute to posttraumatic stress disorder (PTSD) symptoms. To investigate the effects of exercise on plasma catecholamines in PTSD, seven male veterans with a DSM-III-R diagnosis of PTSD underwent a standard grade-incremented exercise treadmill test of maximal exercise intensity. They were compared with six age-matched male controls (CS). Plasma dopamine (DA), norepinephrine (NE), and 3-methoxy_Q-hydroxyphenyl-ethylene glycol (MHPG) at rest and post-exercise were assayed by HPLC with electrochemical detection. Plasma DA was higher at rest in PTSD versus CS (p < .05). Plasma NE values at rest tended to be higher in PTSD versus CS. MHPG levels were lower at rest in PTSD versus CS (p < .05). Exercise
increased
NE and DA levels
Stress: Basic and Clinical Studies
BIOL PSYCHIATRY 1989:25:33A-36A
35A
significantly in both groups. However, the magnitude of increase was greater in CS. MHPG increased in PTSD and decreased in CS with exercise. These data suggest an increased CA state in PTSD. Furthermore, the lower resting MHPG as well as the opposite MHPG response to exercise in PTSD suggests an altered CA metabolism.
72
CHRONIC STRESS PRODUCES DELAYED AND PROLONGED SUBSENSITIZATION OF A NICOTINIC MECHANISM Jason Peck, Max McGee, Richard S. Jaeckle, Steven C. Dilsaver Columbus, OH
Nicotinic receptors in the hypothalamus mediate certain neurobiologic effects of stress. We studied the effects of chronic inescapable swim stress on a nicotinic mechanism which regulates core body temperature. Twelve male rats were given twice daily swim stress (8 minutes/session at 12C) for 14 days. We challenged the animals with nicotine (1.0 mg/kg, ip) at baseline, after seven and 14 days of stress, and weekly thereafter for five weeks following the cessation of stress. The mean hypothermic response to nicotine was subsensitized after 14 days of stress. We observed a continued progressive subsensitization of the response during the first two weeks after cessation of stress. The response gradually returned to baseline over the following three weeks. Our results suggests: (1) chronic inescapable stress subsensitizes what is thought to be a hypothalamic nicotinic mechanism; (2) this nicotinic mechanism continues to become progressively subsensitized after the stressor is terminated; (3) the nicotinic mechanism is more resistant to the effects of stress than are muscarinic and alpha* adrenergic mechanisms regulating core body temperature. Our results suggest that alterations in central nicotinic mechanisms may play a role in stress-related diseases such as major depression.
73
CHRONIC STRESS SUBSENSITIZES AN ALPHA* ADRENERGIC MECHANISM WHICH REGULATES CORE BODY TEMPERATURE Max McGee, Jason Peck, Richard S. Jaeckle, Steven C. Dilsaver Columbus, OH
Chronic inescapable stress is hypothesized to produce alterations in brain noradrenergic systems. We studied the effects of chronic swim stress on an alpha* adrenergic mechanism which regulates core body temperature. Twelve male rats were given twice daily swim stress (8 minutes/session at 12C) for seven days. We challenged the animals with clonidine (0.1 mg/kg, ip) on the days before and after chronic swim stress. The pre-stress clonidine challenge produced a mean thermic response of - 0.50 ? 0.13C (mean + SEM). After one week of chronic stress, the mean thermic response was subsensitized (-0.05 + 0.06C). The mean thermic response returned to baseline seven days after the cessation of chronic stress. Thus, one week of chronic stress was sufficient to subsensitize what is thought to be a hypothalamic alpha2 adrenergic mechanism, and alpha* sensitivity normalized during one week of recovery from stress. The neurobiologic responses to stress may be relevant to the pathophysiology of stressrelated diseases such as major depression. Chronic uncontrollable stressors and some subtypes of major depression may be accompanied by hyperactivity of central nor-