Thursday, July 31, 2014

Inability to Ignore Irrelevant Stimuli Impairs Working Memory and Cognition in Schizophrenia


This new research article helps explain one of the symptoms I have notice in clients suffering from the symptoms identified as schizophrenia - an apparent inability to filter external (and internal) stimuli. One of the intrusive elements seems to be memory, and because so many people with schizophrenia have histories of severe neglect and/or trauma, random details from those memories seem to frequently invade consciousness.

One of the ways I have seen this manifest is in what appears to be random verbal associative thinking. One name, place, or idea will lead to an internal association that seems random from the outside but for the client it flows naturally, from one thing to the next.

Anyway, this is important new material for those of us who serve clients with these symptoms.

'Noisy' memory in schizophrenia (7/25/2014)


Philadelphia, PA, July 14, 2014 - The inability to ignore irrelevant stimuli underlies the impaired working memory and cognition often experienced by individuals diagnosed with schizophrenia, reports a new study in the current issue of Biological Psychiatry.

Our brains are usually good at focusing on the information that we are trying to learn and filtering out the "noise" or thoughts that aren't relevant. However, memory impairment in schizophrenia may be related in part to a problem with this filtering process, which Dr. Teal Eich at Columbia University and her colleagues studied.

"Our assumption was that understanding the impairments in the component processes of working memory - the ability to hold and manipulate information in the mind - among patients with schizophrenia could be fundamental to understanding not only cognitive function in the disorder, which is widespread and has debilitating consequences, but also the disorder itself," Eich explained.

The researchers recruited patients with schizophrenia and a control group of healthy volunteers to complete an item recognition task in the laboratory while undergoing a functional magnetic resonance imaging scan. In particular, they focused on analyzing potential activation differences in the ventro-lateral prefrontal cortex (VLPFC), a region of the brain implicated in working memory.

The design of the task allowed for the assessment of the various components of working memory: 1) maintaining the memory itself, 2) inhibiting or ignoring irrelevant information, and 3) during memory retrieval, controlling the interference of irrelevant information.

While simply maintaining the memory, both groups showed a similar degree of activation in the VLPFC. During the inhibition phase, VLPFC activity is expected to decrease, which was indeed observed in the healthy group, but not in the patients. Finally, during interference control, patients performed worse and showed increased VLPFC activation compared to the healthy volunteers. Overall, the patients showed altered VLPFC functioning and significant impairments in their ability to control working memory.

"Our findings show that these patients have a specific deficit in inhibiting information in working memory, leading to impaired distinctions between relevant and irrelevant thoughts," said Eich. "This result may provide valuable insights into the potential brain mechanisms underlying the reasons why these affected individuals are unable to control or put out of mind certain thoughts or ideas."

This study adds to a growing literature suggesting that cognitive functions require both the activation of one set of regions and the inhibition of others. The failure to suppress activation may be just as disruptive to cortical functions as deficits in cortical activation.

Many years ago, the pioneering scientist Patricia Goldman-Rakic and her colleagues showed that the inhibition of regional prefrontal cortical activity was dependent upon the integrity of the GABA (gamma-aminobutyric acid) system in the brain, a chemical system with abnormalities associated with schizophrenia.

"We need to determine whether the cortical inhibitory deficits described in this study can be attributed to particular brain chemical signaling abnormalities," said Dr. John Krystal, Editor of Biological Psychiatry. "If so, this type of study could be used to guide therapeutic strategies to enhance working memory function."

Note: This story has been adapted from a news release issued by the Elsevier

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Here is the abstract from the original article at Biological Psychiatry.

Full Citation:
Eich, TS, Nee, DE, Insel, C, Malapani, C, Smith, EE. (2014, Jul 15). Neural Correlates of Impaired Cognitive Control over Working Memory in Schizophrenia. Biological Psychiatry; 76(2): 146–153. DOI: http://dx.doi.org/10.1016/j.biopsych.2013.09.032 [Epub ahead of print, Nov. 18, 2013]

Neural Correlates of Impaired Cognitive Control over Working Memory in Schizophrenia

Teal S. Eich, Derek Evan Nee, Catherine Insel, Chara Malapani, Edward E. Smith [†]
†Deceased (EES).

ABSTRACT

Background

One of the most common deficits in patients with schizophrenia (SZ) is in working memory (WM), which has wide-reaching impacts across cognition. However, previous approaches to studying WM in SZ have used tasks that require multiple cognitive-control processes, making it difficult to determine which specific cognitive and neural processes underlie the WM impairment.

Methods

We used functional magnetic resonance imaging to investigate component processes of WM in SZ. Eighteen healthy controls (HCs) and 18 patients with SZ performed an item-recognition task that permitted separate neural assessments of 1) WM maintenance, 2) inhibition, and 3) interference control in response to recognition probes.

Results

Before inhibitory demands, posterior ventrolateral prefrontal cortex (VLPFC), an area involved in WM maintenance, was activated to a similar degree in both HCs and patients, indicating preserved maintenance operations in SZ. When cued to inhibit items from WM, HCs showed reduced activation in posterior VLPFC, commensurate with appropriately inhibiting items from WM. However, these inhibition-related reductions were absent in patients. When later probed with items that should have been inhibited, patients showed reduced behavioral performance and increased activation in mid-VLPFC, an area implicated in interference control. A mediation analysis indicated that impaired inhibition led to increased reliance on interference control and reduced behavioral performance.

Conclusions

In SZ, impaired control over memory, manifested through proactive inhibitory deficits, leads to increased reliance on reactive interference-control processes. The strain on interference-control processes results in reduced behavioral performance. Thus, inhibitory deficits in SZ may underlie widespread impairments in WM and cognition.

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