Frontal Cortex

In recent years, neuropsychological investigations of PTSD have begun to shed light on cognitive control deficits in PTSD, and cognitive neuroscience studies have suggested the neural bases of these deficits. For example, using an array of attention and memory tests, Vasterling (1998) found a pattern of generalized disinhibition in cognitive and behavioral domains among combat veterans with PTSD compared to combat veterans without PTSD. Work in rats and monkeys in a variety of neuroscience laboratories indicates that stress exposure impairs cognitive functions dependent on prefrontal structures. Arnsten et al. (1991) used repetitive transcranial magnetic stimulation (rTMS)

of the dorsolateral prefrontal cortex (DLPFC) to produce temporary functional lesions that resulted in worsened performance on a working memory task; these researchers simultaneously used PET to demonstrate that performance decrements caused by rTMS were associated with decreased regional cerebral blood flow in the DLPFC.

The prefrontal structures implicated in PTSD include the left inferior prefrontal cortex, or Broca's area, and the dorsolateral prefrontal cortex. Decreased activation in Broca's area in response to script-driven imagery or remembering was found in the first neuroimaging study of PTSD (Rauch et al., 1996) and has been replicated in two subsequent PET studies by Shin and colleagues (1997, 1999). Decreased activation in the dorsolateral prefrontal cortex (DLPFC; Brodmann's areas 9/46) has been found in a functional MRI study of subjects with PTSD (Lanius et al., 2002).

Recently Shaw et al. (2002) investigated distributed brain systems in PTSD patients and matched controls during performance of a working memory task. They found that the patient group was characterized by relatively more activation in the bilateral inferior parietal lobes and the left precentral gyrus than the control group, and less activation in the inferior medial frontal lobe, bilateral middle frontal gyri, and right inferior temporal gyrus. Their procedure provided direct evidence that working memory updating was abnormal in PTSD patients relative to matched controls.

Lanius et al. (2001) found that PTSD subjects showed significantly less activation of the thalamus, and the medial frontal gyrus (Brodmann's area 10/11), than did the comparison subjects upon trauma exposure. In women with child abuse histories Bremner et al. (1999a) found increases in blood flow in portions of anterior prefrontal cortex (superior and middle frontal gyri—areas 6 and 9).

Decreased dorsolateral frontal cortex activation in response to trauma scripts provides yet another level of understanding why people with PTSD plunge into reex-periencing their trauma with limited consciousness that they are simply remembering elements of experiences belonging to the past. In our treatment outcome study, subjects showed increased activation of the dorsolateral prefrontal cortex following effective treatment (Levin et al., 1999).

A study by Carter et al. (1999) demonstrated that, consistent with a role in cognitive control, the DLPFC is more active on trials requiring inhibition of an automatic (word-reading) response. Breakdowns of cognitive control in PTSD often occur in the context of "competition"—between processing external information and responses appropriate to the situation, on the one hand, and processing internally generated posttraumatic information and automatic but maladaptive posttraumatic responses. More generally, the DLPFC has been implicated in capacities for deliberate reflection, problem-solving, planning, and response selection. Thus impaired DLPFC function in the presence of posttraumatic "triggers" may cause traumatized people to experience situations and respond to them as if they were "back there" in the trauma.

Davidson and his colleagues have proposed that one of the key components of affective style is the capacity to regulate negative emotion and, specifically to decrease the duration of negative affect once it arises (Davidson, 1998; Davidson and Irwin, 1999). Their studies suggest that the connections between the PFC and amygdala play an important role in this regulatory process. They found that subjects with greater baseline levels of left prefrontal activation are better able to voluntarily suppress negative affect (Jackson et al., 2000). When subjects voluntarily regulate negative emotions this is reflected in changes in amygdala recorded signal intensity.

Anxiety and Depression 101

Anxiety and Depression 101

Everything you ever wanted to know about. We have been discussing depression and anxiety and how different information that is out on the market only seems to target one particular cure for these two common conditions that seem to walk hand in hand.

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