RESEARCH ROUNDUP: The Effects of Lyme Disease on the Central Nervous System

The Effects of Lyme Disease on the Central Nervous System

Lyme disease is caused by a bacterium, Borrelia burgdorferi, spread to humans by infected black-legged ticks.  Early symptoms may include headaches, fever, fatigue, and the hallmark skin rash of the disease called erythema migrans (Centers for Disease Control; CDC, 2015).  There are at least 4 disorders commonly referred to as “nervous system Lyme disease,” which are commonly confused and some remain controversial.  The first of these is actual central nervous system (CNS) infection by B. burgdorferi spirochetes that leads to increased white blood cell count in cerebrospinal fluid (CSF), as well as antibody production.  This can lead to neurologic damage and residual impairment, such as facial nerve palsy, despite successful antibiotic therapy.  This type of infection will rarely enter the brain or spinal parenchyma.  Also possible are 3 neurobehavioral syndromes without CNS infection that include Lyme encephalopathy, posttreatment Lyme disease syndrome (PTLDS), and chronic Lyme disease.  Lyme encephalopathy includes memory dysfunction and other cognitive problems that result from active systemic infection (not in the CNS) and typically responds to antibiotic therapy, while posttreatment Lyme syndrome and chronic Lyme disease do not.  PTLDS shares many of the same symptoms with Lyme encephalopathy, generally represents persistence of physical and cognitive symptoms for at least 6 months after appropriate treatment has been provided, and usually resolves over time.  Chronic Lyme lacks formal definition, but shares similar symptoms with PTLDS.  However, it’s diagnosis does not require objective evidence of Lyme disease or laboratory confirmation of B. burgdorferi infection (Halperin, 2014).  Lyme-related brain imaging findings, when present, often include white matter lesions in the periventricular white matter (Westervelt & McCaffrey, 2002).  In chronic Lyme disease, SPECT scanning has found abnormal perfusion, especially in frontal, temporal, and parietal lobes, in those with both seropositive and seronegative results (Donta, Noto, & Vento, 2012).  Neuropsychological impairments in chronic Lyme disease tend to be mild and include those in verbal memory (especially list-learning), verbal fluency, upper extremity fine motor speed and coordination, oral agility, and information processing speed, and are consistent with other autoimmune disorders that primarily show impairment in frontal systems.  Significant fatigue is a hallmark of the disease, and affective symptoms such as depression, are also common (Westervelt & McCaffrey, 2002).  


ABSTRACT:  Lyme Disease: Neurology, Neurobiology, and Behavior (2014)
The Lyme disease controversy can be largely linked to the misconception that neurobehavioral effects of illness constitute evidence of nervous system infection. Appropriate differentiation between neuroborreliosis (nervous system Borrelia burgdorferi infection) and Lyme encephalopathy (altered nervous system function in individuals with systemic but not nervous system infection)--or encephalopathies of other etiologies--would lessen the controversy considerably, as the attribution of nonspecific symptoms to supposed ongoing central nervous system infection is a major factor perpetuating the debate. Epidemiologic considerations suggest that the entities referred to as “posttreatment Lyme disease” and “chronic Lyme disease” may not actually exist but rather reflect anchoring bias, linking common, nonspecific symptoms to an antecedent medical event. On the other hand, there are data suggesting possible mechanisms by which posttreatment Lyme disease could occur.

Halperin, J. J.  (2014).  Lyme disease: Neurology, neurobiology, and behavior.  Clinical Infectious Diseases, 58, 1267-72.  http://cid.oxfordjournals.org/content/58/9/1267.full.pdf

 
WEBINAR:
CDC Grand Rounds- Lyme Disease: Challenges and Innovations
https://www.youtube.com/watch?v=k7L61d--GmI                           


FURTHER INFORMATION:

1. Donta, S. T., Noto, R. B., & Vento, J. A.  (2012).  SPECT brain imaging in chronic Lyme disease.  Clinical Nuclear Medicine, 37 (9), e219-e222.   http://journals.lww.com/nuclearmed/Abstract/2012/09000/SPECT_Brain_Imaging_in_Chronic_Lyme_Disease.33.aspx
   
2. Nadelman, R. B., Hanincova, K., Mukherjee, B. S., Liveris, D., Nowakowski, J., McKenna, D., Brisson, D., Cooper, D., Bittker, S., Madison, G., Holmgren, D., Schwartz, I., Wormser, G. P.  (2012).  Differentiation of reinfection from relapse in recurrent Lyme disease.  The New England Journal of Medicine, 367 (20), 1883-90. http://www.nejm.org/doi/pdf/10.1056/NEJMoa1114362
   
3. Fallon, B. A., Keilp, J., Prohovnik, I., Van Heertum, R. & Mann, J. J.  (2003). Regional cerebral blood flow and cognitive deficits in chronic Lyme disease.  The Journal of Neuropsychiatry and Clinical Neurosciences, 15 (3), 326-32. http://www.unboundmedicine.com/medline/citation/12928508/Regional_cerebral_blood_flow_and_cognitive_deficits_in_chronic_lyme_disease_
   
4.  Westervelt, H. J. & McCaffrey, R. J.  (2002).  Neuropsychological functioning in chronic Lyme disease.  Neuropsychology Review, 12 (3), 153-77. http://link.springer.com/article/10.1023/A%3A1020381913563
   

Contributor:

Abigail Lyon is a graduate student at Widener University Institute for Graduate Clinical Psychology