Lyme disease is the most common vector-borne infectious disease in the United States. Post-treatment Lyme disease (PTLD) is a condition affecting 10–20% of patients in which symptoms persist despite antibiotic treatment. Cognitive complaints are common among those with PTLD, suggesting that brain changes are associated with the course of the illness. However, there has been a paucity of evidence to explain the cognitive difficulties expressed by patients with PTLD. This study administered a working memory task to a carefully screened group of 12 patients with well-characterized PTLD and 18 healthy controls while undergoing functional MRI (fMRI). A subset of 12 controls and all 12 PTLD participants also received diffusion tensor imaging (DTI) to measure white matter integrity. Clinical variables were also assessed and correlated with these multimodal MRI findings. On the working memory task, the patients with PTLD responded more slowly, but no less accurately, than did controls. FMRI activations were observed in expected regions by the controls, and to a lesser extent, by the PTLD participants. The PTLD group also hypoactivated several regions relevant to the task. Conversely, novel regions were activated by the PTLD group that were not observed in controls, suggesting a compensatory mechanism. Notably, three activations were located in white matter of the frontal lobe. DTI measures applied to these three regions of interest revealed that higher axial diffusivity correlated with fewer cognitive and neurological symptoms. Whole-brain DTI analyses revealed several frontal lobe regions in which higher axial diffusivity in the patients with PTLD correlated with longer duration of illness. Together, these results show that the brain is altered by PTLD, involving changes to white matter within the frontal lobe. Higher axial diffusivity may reflect white matter repair and healing over time, rather than pathology, and cognition appears to be dynamically affected throughout this repair process.
Lyme disease is the most common vector-borne infectious disease in the United States. Post-treatment Lyme disease (PTLD) is a condition affecting 10-20% of patients in which symptoms persist despite antibiotic treatment. Cognitive complaints are common among those with PTLD, suggesting that brain changes are associated with the course of the illness. However, there has been a paucity of evidence to explain the cognitive difficulties expressed by patients with PTLD. This study administered a working memory task to a carefully screened group of 12 patients with well-characterized PTLD and 18 healthy controls while undergoing functional MRI (fMRI). A subset of 12 controls and all 12 PTLD participants also received diffusion tensor imaging (DTI) to measure white matter integrity. Clinical variables were also assessed and correlated with these multimodal MRI findings. On the working memory task, the patients with PTLD responded more slowly, but no less accurately, than did controls. FMRI activations were observed in expected regions by the controls, and to a lesser extent, by the PTLD participants. The PTLD group also hypoactivated several regions relevant to the task. Conversely, novel regions were activated by the PTLD group that were not observed in controls, suggesting a compensatory mechanism. Notably, three activations were located in white matter of the frontal lobe. DTI measures applied to these three regions of interest revealed that higher axial diffusivity correlated with fewer cognitive and neurological symptoms. Whole-brain DTI analyses revealed several frontal lobe regions in which higher axial diffusivity in the patients with PTLD correlated with longer duration of illness. Together, these results show that the brain is altered by PTLD, involving changes to white matter within the frontal lobe. Higher axial diffusivity may reflect white matter repair and healing over time, rather than pathology, and cognition appears to be dynamically affected throughout this repair process.
IntroductionWorking memory describes the ability to maintain and manipulate information held in mind, and it is a fundamental aspect of executive function. Within drug addiction, impairments of executive control over behavior are thought to lead to poor decision making and risky behaviors. Previous research has demonstrated working memory (WM) and executive function difficulties in opioid-dependent individuals, but the neural underpinnings of such impairments in this population are not well understood.MethodsThis study used functional magnetic resonance imaging to examine the neural mechanisms involved in WM in 13 opioid-dependent, methadone-maintained participants (OP) and 13 matched, healthy controls (HC). A Sternberg item-recognition task was administered with three conditions: (1) a “verbal” condition in which participants determined whether any six visually presented target letters matched a probe item that was presented 4–6 s later, (2) a “non-verbal” condition in which participants were presented with a Chinese character and, following a 4–6 s delay, determined whether the character matched the probe item, and (3) a “control” condition in which participants were presented with three horizontal lines and following the same delay, determined whether the lines matched a probe item (always the same three lines). Functional magnetic resonance imaging (fMRI) contrasts focused on the delay (or “maintenance”) phase for verbal and non-verbal conditions relative to the control condition.ResultsAccuracy on the WM task did not differ between groups, but the OP group was significantly slower to respond. The fMRI imaging results indicated differences in brain activity between the OP and HC groups. fMRI-guided regions of interest correlated with age of first alcohol and THC use, suggesting that early substance use, in addition to years of opioid-abuse, may have played a role in the OP group’s WM performance.DiscussionA deeper understanding of these neural differences between opioid-dependent individuals and their healthy control counterparts helps shed light on fundamental ways in which substance use impacts the brain and cognition, potentially opening up novel avenues for therapeutic targets to treat substance use disorder.
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