| |
| Investigating
the pathogenesis of posttraumatic stress disorder
with neuroimaging. |
Pitman RK, Shin LM, Rauch SL.
VA Research Service, Manchester, NH, USA.
Rapidly evolving brain neuroimaging techniques
such as magnetic resonance imaging (MRI) and positron
emission tomography (PET) are proving fruitful in
exploring the pathogenesis and pathophysiology of
posttraumatic stress disorder (PTSD). Structural
abnormalities in PTSD found with MRI include nonspecific
white matter lesions and decreased hippocampal volume.
These abnormalities may reflect pretrauma vulnerability
to develop PTSD, or they may be a consequence of
traumatic exposure, PTSD, and/or PTSD sequelae.
Functional neuroimaging symptom provocation and
cognitive activation paradigms using PET measurement
of regional cerebral blood flow have revealed greater
activation of the amygdala and anterior paralimbic
structures (which are known to be involved in processing
negative emotions such as fear), greater deactivation
of Broca's region (motor speech) and other nonlimbic
cortical regions, and failure of activation of the
cingulate cortex (which possibly plays an inhibitory
role) in response to trauma-related stimuli in individuals
with PTSD. Functional MRI research has shown the
amygdala to be hyperresponsive to fear-related stimuli
in this disorder. Research with PET suggests that
cortical, notably hippocampal, metabolism is suppressed
to a greater extent by pharmacologic stimulation
of the noradrenergic system in persons with PTSD.
The growth of knowledge concerning the anatomical
and neurochemical basis of this important mental
disorder will hopefully eventually lead to rational
psychological and pharmacologic treatments.
J Clin Psychiatry 2001;62 Suppl 17:41-6
Clin Psychol Rev 2001 Aug;21(6):931-48
Posttraumatic stress disorder and traumatic brain
injury: can they co-exist?
Bryant RA.
School of Psychology, University of New South Wales,
Sydney, Australia. r.bryant@unsw.edu.au
The possibility that posttraumatic stress disorder
(PTSD) can develop following traumatic brain injury
(TBI) has been the subject of considerable debate.
The traditional view has held that impaired consciousness
that occurs with TBI precludes encoding of the traumatic
experience, and this prevents subsequent reexperiencing
symptoms. This paper critically reviews available,
empirical studies on PTSD in TBI populations and
suggests that these two conditions can co-exist.
The various mechanisms that may mediate PTSD following
TBI are discussed, and special attention is given
to issues that recognize the distinctive features
of PTSD following TBI. These processes include implicit
processing, biologically mediated fear conditioning,
and reconstruction of trauma memories. Finally implications
for assessment, treatment, and forensic investigation
of PTSD in TBI populations are, addressed. This
review concludes that TBI populations provide a
useful means by which the role of traumatic memories
(and impaired memories) in posttraumatic adjustment
can be studied.
J Clin Psychiatry 2001;62 Suppl 17:41-6
Biology of posttraumatic stress disorder.
Yehuda R.
Mount Sinai School of Medicine and Bronx Veterans
Affairs, New York, NY, USA. rachel.yehuda@med.va.gov
Most biological findings in posttraumatic stress
disorder (PTSD) are compatible with those of the
chronic stress response, such as increased corticotropin-releasing
factor (CRF) concentrations, catecholamine depletion
within the central nervous system, and reduced hippocampal
volume. However, over the last 10 years, biological
observations have been made in PTSD that are different
from what has been typically associated with chronic
stress, notably certain hypothalamic-pituitary-adrenal
(HPA) axis findings. In particular, urinary and
plasma cortisol levels are considerably lower in
PTSD patients than in non-PTSD trauma survivors
and normal controls. Furthermore, the circadian
pattern of cortisol release from the adrenal glands
follows a greater dynamic range in PTSD than in
patients with major depression or in normal controls.
The reduction in cortisol levels results from an
enhanced negative feedback by cortisol, which is
secondary to an increased sensitivity of glucocorticoid
receptors in target tissues. This HPA axis alteration
contrasts with the well-known chronic stress cascade
in which CRF release results in erosion of negative
feedback and down-regulation of glucocorticoid receptors.
Sensitization of the HPA axis is consistent with
the clinical picture of hyperreactivity and hyperresponsiveness
in PTSD.
|
