Abstract

There is increasing evidence and recognition that Lyme borreliosis (LB) causes mental symptoms. This article draws from databases, search engines and clinical experience to review current information on LB. LB causes immune and metabolic effects that result in a gradually developing spectrum of neuropsychiatric symptoms, usually presenting with significant comorbidity which may include developmental disorders, autism spectrum disorders, schizoaffective disorders, bipolar disorder, depression, anxiety disorders (panic disorder, social anxiety disorder, generalized anxiety disorder, posttraumatic stress disorder, intrusive symptoms), eating disorders, decreased libido, sleep disorders, addiction, opioid addiction, cognitive impairments, dementia, seizure disorders, suicide, violence, anhedonia, depersonalization, dissociative episodes, derealization and other impairments. Screening assessment followed by a thorough history, comprehensive psychiatric clinical exam, review of systems, mental status exam, neurological exam and physical exam relevant to the patient’s complaints and findings with clinical judgment, pattern recognition and knowledgeable interpretation of laboratory findings facilitates diagnosis. Psychotropics and antibiotics may help improve functioning and prevent further disease progression. Awareness of the association between LB and neuropsychiatric impairments and studies of their prevalence in neuropsychiatric conditions can improve understanding of the causes of mental illness and violence and result in more effective prevention, diagnosis and treatment.

Highlights

  • Lyme borreliosis (LB) is caused by Borrelia burgdorferi and other Borrelia species, such as Borrelia garinii and Borrelia afzelii

  • Many infections are associated with an early inflammatory reaction followed by adaptive immunity and a resolution of symptoms, but in some chronic infections that evade and suppress the immune system, such as B. burgdorferi and other Borreliae, inflammation can persist without adaptive immunity, autoimmune symptoms may occur, and relapses and reinfections are common. [2,17,18,19,20,21]

  • There are three basic types of B. burgdorferi infections causing neuropsychiatric symptoms—the meningovascular form associated with cerebrovascular infarcts; the second is infection within the central nervous system (CNS) which is the atrophic form of Lyme meningoencephalitis and is associated with cortical atrophy, gliosis and dementia and the third is infection outside the CNS

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Summary

Introduction

Lyme borreliosis (LB) is caused by Borrelia burgdorferi and other Borrelia species, such as Borrelia garinii and Borrelia afzelii. Other tick-borne and opportunistic infections may be present as well [1]. The most common co-infections seen with LB include Anaplasma phagocytophilum, Babesia species, Ehrlichia chaffeensis, Rickettsia species and Bartonella species; but there are other less common and yet unknown pathogens [1]. Secondary co-infections or opportunistic infections are commonly seen in patients with LB [1]. There is increasing evidence and recognition that LB causes mental symptoms, debate exists regarding the role of LB vs other tick-borne diseases (TBD) in the pathogenesis of neuropsychiatric symptoms [2]. There are over 400 peer-reviewed articles addressing different aspects of neuropsychiatric symptoms caused by LB [2]

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