Genesis and dissemination of a controversial disease: Chronic Lyme.

OBJECTIVES: To describe the role of the internet and cognitive biases in the controversy surrounding chronic Lyme disease. The attribution of chronic but aspecific symptoms to Lyme borreliosis is a source of worldwide controversy. PATIENTS AND METHODS: Some patients attribute their aspecific symptoms to Lyme borreliosis even though, in fact, they have a functional somatic syndrome. RESULTS: These patients' diagnostic and therapeutic wandering contributes to the above attribution and to their suffering. The Internet has deregulated the information market. Cognitive confirmation bias contributes to confinement in belief. Negativity bias explains the tendency of the human brain to select the most alarming information available. The narrative force of alarmist videos or personal testimonies acts like a nocebo effect. The social exclusion generated by adherence to this belief is a factor of reinforcement and aggravation. CONCLUSIONS: Deconstructing chronic Lyme disease with empathy and conviction is in patients' best interests.

Somatic symptom disorder should be suspected in children with alleged chronic Lyme disease.

We report a case series of seven children admitted to a tertiary level pediatric ward for long-lasting physical symptoms with a previous diagnosis of chronic Lyme disease. In these children, medical history and clinical features were strongly suggestive of a psychopathological disorder, mainly a somatic symptom disorder. What is Known: • There is an increasing number of diagnoses of chronic Lyme disease both in North America and in Europe. Adults receive this diagnosis to explain chronic physical complaints often with negative history and serology. What is New: • Somatic symptom disorder should be suspected in children and adolescents with non-specific symptoms diagnosed with chronic Lyme disease.

Functional neuroimaging in patients presenting with somatoform disorders: A model for investigating persisting symptoms after tick bites and post-treatment Lyme disease syndrome?

Approximately 10% of patients presenting with Lyme disease experience fatigue, musculoskeletal pain, concentration disorders, or short-term memory deficits in the six months following treatment. This entity has been defined as post-Lyme disease syndrome or post-treatment Lyme disease syndrome. The pathophysiology of this syndrome is unknown, but neither persistence of the bacterium nor effectiveness of antibiotics are currently reported in the literature. The French High Council for Public Health (French acronym HCSP) has recently defined a new entity called "persistent polymorphic symptoms after a tick bite" allowing for designing studies to better understand these subjective presentations, for which objective biomarkers are currently lacking. This entity encompasses patients experiencing fatigue and generalized pain in the months following a tick bite and can be associated with several subjective symptoms with major impact on the quality of life. In the field of somatoform disorders, this article reviews functional neuroimaging studies in patients presenting with subjective complaints and discusses potential clinical implications for persisting symptoms after tick bites and post-treatment Lyme disease syndrome.

Neurocognition in Post-Treatment Lyme Disease and Major Depressive Disorder.

OBJECTIVE: Neurocognitive dysfunction in patients with residual or emergent symptoms after treatment for Lyme Disease is often attributed to comorbid depression. In this study, patients with Post-Treatment Lyme Disease Syndrome (PTLDS) were compared to patients with Major Depressive Disorder (MDD), as well as healthy comparison subjects (HC), on neurocognitive measures administered through the same laboratory, to determine if patterns of performance were similar. METHODS: Two analyses were conducted. First, performance on the Wechsler Adult Intelligence Scale (WAIS-III) and on subtests from the Wechsler Memory Scale (WMS-III) was compared among the groups. Second, comparable subgroups of PTLDS and MDD patients with at least one low WMS-III score were compared on an additional set of measures assessing motor function, psychomotor performance, attention, memory, working memory, and language fluency, to determine if the overall profile of performance was similar in the two subgroups. RESULTS: In the first analysis, PTLDS patients performed more poorly than both MDD and HC on tasks assessing verbal abilities, working memory, and paragraph learning. Processing speed in the two patient groups, however, was equally reduced. In the second analysis, MDD patients with low WMS-III exhibited concomitantly greater difficulties in psychomotor speed and attention, while low-WMS-III PTLDS patients exhibited greater difficulties in language fluency. CONCLUSIONS: MDD and PTLDS can be confused neuropsychologically because both exhibit similar levels of psychomotor slowing. However, problems on memory-related tasks, though mild, are more pronounced in PTLDS. PTLDS patients with poorer memory also exhibit poorer language fluency, and less deficit in processing speed and attention compared to MDD.

Cognitive Decline in Post-treatment Lyme Disease Syndrome.

OBJECTIVE: Patient-reported cognitive complaints are common in those with post-treatment Lyme disease syndrome (PTLDS). Objective evidence of cognitive impairment in this population is variable in part due to methodological variability in existing studies. In this study, we sought to use a systematic approach to characterizing PTLDS based on the most current consensus diagnosis. We further examined PTLDS-related cognitive decline, operationalized as a significant decline in cognitive test performance relative to premorbid cognitive ability. METHOD: We enrolled a case series of 124 patients with confirmed PTLDS defined by Infectious Diseases Society of America-proposed case definition. Cognitive functioning was evaluated using standardized neuropsychological measures. RESULTS: The majority (92%) of participants endorsed some level of cognitive difficulty, yet 50% of the sample showed no statistically or clinically significant cognitive decline, 26% of the sample evidenced significant cognitive decline on measures of memory and variably on measures of processing speed, and 24% of the sample were excluded from analyses due to suboptimal test engagement. CONCLUSIONS: The current findings are consistent with the literature showing that the most robust neurocognitive deficit associated with PTLDS is in verbal memory and with variable decline in processing speed. Compared to population normative comparison standards, PTLDS-related cognitive decline remains mild. Thus, further research is needed to better understand factors related to the magnitude of subjective cognitive complaints as well as objective evidence of mild cognitive decline.