Brain (1990), 113, 1207-1221
LYME NEUROBORRELIOSIS PERIPHERAL NERVOUS SYSTEM MANIFESTATIONS by J. HALPERIN, 1 BENJAMIN J. LUFT, 2 DAVID J. VOLKMAN 3 and RAYMOND J. DATTWYLER 34 (From the ^Department of Neurology, 2Division of Infectious Diseases, Department of Medicine, Division of Allergy, Immunology and Rheumatology, Department of Medicine, and the Department of Pathology, State University of New York, Stony Brook NY, USA)
3
An ever increasing number of apparently unrelated peripheral nervous system (PNS) disorders has been associated with Lyme borreliosis. To ascertain their relative frequency and significance, we studied prospectively 74 consecutive patients with late Lyme disease, with and without PNS symptoms: 53% had intermittent limb paraesthesiae, 25% the carpal tunnel syndrome, 8% painful radiculopathy, and 3% Bell's palsy; 39% had disseminated neurophysiological abnormalities. To assess the interrelationships among these syndromes, we reviewed the neurophysiological findings in all 163 such patients that we have studied to date. Reversible abnormalities of distal conduction were the most common finding. Demyelinating neuropathy was extremely rare. The pattern of abnormality was similar in all patient groups, regardless of whether the symptoms suggested radiculopathy, Bell's palsy, or neuropathy. We conclude that (1) reversible PNS abnormalities occur in one-third of our patients with late Lyme borreliosis, and (2) the pattern of electrophysiological abnormalities is the same in all and is indicative of widespread axonal damage, suggesting that these different presentations reflect varying manifestations of the same pathological process. INTRODUCTION
Abnormalities of both the peripheral (PNS) and central (CNS) nervous systems are well recognized complications of infection with the tick-borne spirochaete, Borrelia burgdorferi (Garin and Bujadoux, 1922; Hellerstrom, 1930; Bannwarth, 1941; Dalsgaard-Nielsen and Kierkegaard, 1948; Schaltenbrandt, 1962; Bammer and Schenk, 1965; Hopf, 1975; Reiketal., 1979; Wulff etal., 1983; Pachner and Steere, 1985; Camponovoand Meier, 1986; Halperin tva/., 1987; Hirsch
LYME NEUROBORRELIOSIS PERIPHERAL NERVOUS SYSTEM MANIFESTATIONS by J. HALPERIN, 1 BENJAMIN J. LUFT, 2 DAVID J. VOLKMAN 3 and RAYMOND J. DATTWYLER 34 (From the ^Department of Neurology, 2Division of Infectious Diseases, Department of Medicine, Division of Allergy, Immunology and Rheumatology, Department of Medicine, and the Department of Pathology, State University of New York, Stony Brook NY, USA)
3
An ever increasing number of apparently unrelated peripheral nervous system (PNS) disorders has been associated with Lyme borreliosis. To ascertain their relative frequency and significance, we studied prospectively 74 consecutive patients with late Lyme disease, with and without PNS symptoms: 53% had intermittent limb paraesthesiae, 25% the carpal tunnel syndrome, 8% painful radiculopathy, and 3% Bell's palsy; 39% had disseminated neurophysiological abnormalities. To assess the interrelationships among these syndromes, we reviewed the neurophysiological findings in all 163 such patients that we have studied to date. Reversible abnormalities of distal conduction were the most common finding. Demyelinating neuropathy was extremely rare. The pattern of abnormality was similar in all patient groups, regardless of whether the symptoms suggested radiculopathy, Bell's palsy, or neuropathy. We conclude that (1) reversible PNS abnormalities occur in one-third of our patients with late Lyme borreliosis, and (2) the pattern of electrophysiological abnormalities is the same in all and is indicative of widespread axonal damage, suggesting that these different presentations reflect varying manifestations of the same pathological process. INTRODUCTION
Abnormalities of both the peripheral (PNS) and central (CNS) nervous systems are well recognized complications of infection with the tick-borne spirochaete, Borrelia burgdorferi (Garin and Bujadoux, 1922; Hellerstrom, 1930; Bannwarth, 1941; Dalsgaard-Nielsen and Kierkegaard, 1948; Schaltenbrandt, 1962; Bammer and Schenk, 1965; Hopf, 1975; Reiketal., 1979; Wulff etal., 1983; Pachner and Steere, 1985; Camponovoand Meier, 1986; Halperin tva/., 1987; Hirsch
