Peter Novak, MD, PhD
Division Chief, Autonomic Neurology
Director, Autonomic Laboratory
Department of Neurology, Brigham and Women’s Faulkner Hospital
Assistant Professor of Neurology, Harvard Medical School
Neurological correlates of Post Treatment Lyme Disease Syndrome
Peter Novak, MD, PhD is the Chief of the Division of Autonomic Neurology and Director of the Autonomic Laboratory at Brigham and Women’s Hospital. He is a board-certified neurologist and a board-certified autonomic specialist. He is a member of American Academy of Neurology, American Autonomic Society and a member of Autonomic Board of United Council for Neurologic Subspecialties (UCNS).
He graduated from medical school in Bratislava, Slovakia and completed his neurology residency at the Ohio State University. He also completed postdoctoral studies focusing on cardiovascular and autonomic research at Charles University (Prague), University of Montreal, McGill University (Montreal) and Mayo Clinic. He has special interests in autoimmune small fiber and autonomic neuropathies, orthostatic syndromes, multiple system atrophy and neurologic complications of Lyme disease. He has written over 70 papers and presented at numerous conferences.
Conference Lecture Summary
Lyme disease is a transmittable tick-borne infection caused by the spirochete Borrelia burgdorferi. Neurologic sequelae of Lyme disease, termed Lyme neuroborreliosis, occur in 10-15% of patients with untreated Lyme disease. Persistent symptoms despite standard antibiotic therapy of Lyme disease are reported in 10% to 36% of patients. These symptoms, when prolonged for a period of 6 months or longer, are referred to as post-treatment Lyme disease syndrome (PTLDS). Typical symptoms of PTLDS include widespread pain, fatigue, and cognitive disturbances. PTLDS results in considerable impairment of quality of life. The origin of PTLDS symptoms is unclear. Potential mechanisms include direct cytotoxicity by the spirochete, the presence of neurotoxic mediators occurring during host-pathogen interaction, autoimmune reactions or genetic predisposition. The main problem in PTLDS research is lack of the objective biomarker. In our study, we analyzed 10 PTLDS patients (all had history of Lyme disease satisfying CDC criteria) and patients all had evidence of small fiber neuropathy, dysautonomia and abnormal cerebral blood flow. The study suggest that SFN appears to be associated with PTLDS and may be responsible for certain sensory symptoms. Reduced orthostatic CBFv can be associated with cerebral hypoperfusion and may lead to cognitive dysfunction in PTLDS.