Lyme disease is a worldwide, tick-transmitted spirochetosis with endemic foci throughout North America, Europe, and Asia. Borrelia burgdorferi is the etiologic bacterium; the vector is a tick of the genus Ixodes.
Lyme disease is now the most common vector-borne illness in the United States. The seasonal pattern of tick activity determines the seasonal pattern of illness onset; symptoms typically begin in late spring or summer. Because ticks prefer forest underbrush, illness is more common in such areas.
Stages
Lyme disease begins locally and spreads systemically. Skin, heart, joints, and nervous system are the organ systems most often involved. Illness typically evolves in sequential stages:
| Stage | Clinical abnormality |
| Early localized |
|
| Early disseminated |
|
| Late disseminated |
|
Reviewed and revised March 2004 by Steven C. Schachter, MD, epilepsy.com Editorial Board.
Back to topIllness begins days to 1 month after tick bite. A red macule or papule arises at the tick bite site, which expands centrifugally to form an annular erythematous lesion. B. burgdorferi proliferation and the host’s immune reaction eventually produce the characteristic skin lesion, erythema migrans (EM) in about 80% of U.S. cases (40% in Europe). EM is the best clinical marker for Lyme disease. A photo of someone with Lyme disease can be found at http://www.cdc.gov/ncidod/dvbid/lyme/diagnosis.htm
Adapted from: Goldstein MA and Harden CL. Infectious states. In: Ettinger AB and Devinsky O, eds. Managing epilepsy and co-existing disorders. Boston: Butterworth-Heinemann; 2002;83-133.
With permission from Elsevier (www.elsevier.com).
Reviewed and revised March 2004 by Steven C. Schachter, MD, epilepsy.com Editorial Board.
Within days to weeks, B. burgdorferi spreads hematogenously. The organism also probably enters the CNS at this time (B. burgdorferi DNA, outer surface protein antigens, and the organism itself have been recovered from CSF as early as 18 days after inoculation). One to two months postinfection, B. burgdorferi localizes and becomes sequestered in certain tissues, including the CNS.
The CNS is involved in up to 20% of untreated North American patients (50% in European populations). Meningitis (typically lymphocytic) is the most common neuropathologic abnormality in early disseminated Lyme disease. Systemic symptoms can be present, but EM, fever, and lymphadenopathy are usually gone by the time neurologic complications develop. In fact, neurologic deficits, including seizure, can occur without antecedent EM and can be the initial disease manifestation. Neurologic abnormalities that have been reported to be associated with early CNS Lyme disease include:
- acute aseptic meningitis
- acute purulent meningitis
- chronic lymphocytic meningitis
- recurrent meningitis
- acute meningoencephalitis
- acute focal encephalitis
- encephalomyelitis
- leukoencephalitis
- acute cerebellar ataxia
- acute parkinsonian syndrome
- acute transverse myelitis
- subacute myelitis
- cognitive deficits
- affective disturbance
- seizures
Adapted from: Goldstein MA and Harden CL. Infectious states. In: Ettinger AB and Devinsky O, eds. Managing epilepsy and co-existing disorders. Boston: Butterworth-Heinemann; 2002;83-133.
With permission from Elsevier (www.elsevier.com).
Reviewed and revised March 2004 by Steven C. Schachter, MD, epilepsy.com Editorial Board.
Neurologic abnormalities of late Lyme disease usually develop a year or more after illness onset:
- progressive encephalomyelitis
- focal encephalitis
- cerebral vasculitis
- stroke
- multi-infarct dementia
- leukoencephalitis
- brain stem encephalitis
- late encephalopathy
- cerebellar ataxia
- transverse myelitis
- progressive spastic paraparesis or quadriparesis
- cognitive deficits
- affective disturbance
- seizures
The most common late CNS abnormalities are vague neuropsychiatric deficits such as somnolence, emotional lability, depression, impaired memory, and behavioral symptoms. The best-defined late CNS abnormality, however, is progressive Borrelia encephalomyelitis.27
Seizures can occur in 7% of these cases.25 Focal motor, partial complex, and generalized convulsions can all occur.
Adapted from: Goldstein MA and Harden CL. Infectious states. In: Ettinger AB and Devinsky O, eds. Managing epilepsy and co-existing disorders. Boston: Butterworth-Heinemann; 2002;83-133.
With permission from Elsevier (www.elsevier.com).
Reviewed and revised March 2004 by Steven C. Schachter, MD, epilepsy.com Editorial Board.
Lyme disease should be suspected in any patient with chronic lymphocytic meningitis or mild meningoencephalitis with associated cranial neuritis or radiculitis. Lab tests include serologic assays like immunofluorescent assay and enzyme-linked immunoassay tests for anti–B. burgdorferi antibodies. Specific anti–B. burgdorferi antibody also appears in CSF, where it can be detected even when serum antibody tests are negative. (To establish whether these antibodies are synthesized intrathecally, serum and CSF antibody levels should be measured simultaneously.28)
The CSF profile in Lyme disease encephalomeningitis includes these findings:
- Opening pressure: normal
- White blood cell count >100 (>90% lymphocytes)
- Glucose: normal
- Protein: mild to moderate increase
- Oligoclonal bands: present
- B. burgdorferi antibody: positive
Following are diagnostic criteria for Lyme neuroborreliosis:
| Possible neuroborreliosis | Compatible neurologic abnormality and history of tick bite or travel or residence in endemic area |
| Probable neuroborreliosis | Compatible neurologic abnormality and serum immunoreactivity to B. burgdorferi |
| Definite neuroborreliosis | Compatible neurologic abnormality
plus one of the following:
|
In most patients with late Lyme disease (especially those with cortical dysfunction, but also many without), the EEG demonstrates nonspecific generalized slowing, focal slowing, increases in sharp wave activity, or a combination of these.13
MRI may show multifocal white-matter abnormalities, infarct patterns, periventricular and subinsular encephalomalacia, and pontine and medullary atrophy.25,27
Lyme Neuroborreliosis Table adapted from L Reik. Lyme Disease. In WM Scheld, RJ Whitley, DT Durack (eds), Infections of the Central Nervous System. Philadelphia: Lippincott–Raven, 1997;685–718.
Adapted from: Goldstein MA and Harden CL. Infectious states. In: Ettinger AB and Devinsky O, eds. Managing epilepsy and co-existing disorders. Boston: Butterworth-Heinemann; 2002;83-133.
With permission from Elsevier (www.elsevier.com).
Reviewed and revised March 2004 by Steven C. Schachter, MD, epilepsy.com Editorial Board.
Seizures associated with Lyme disease are treated via routine antiepileptic management principles.
Antibiotic treatment regimens for Lyme disease vary according to stage and differ for adults and children:
| Lyme disease stage | Treatment options |
| Erythema migrans and systemic symptoms | |
| Adults |
|
| Children |
|
| Early neurologic involvement | |
| Facial palsy alone | Oral antibiotics, same treatment as above |
| All others | |
| Adults |
|
| Children |
|
| Late neurologic involvement | |
| Adults |
|
| Children |
|
Antibiotic treatment regimens Table adapted from L Reik. Lyme Disease. In WM Scheld, RJ Whitley, DT Durack (eds), Infections of the Central Nervous System. Philadelphia: Lippincott–Raven, 1997;685–718; DW Rahn, MW Felz. Lyme disease update. Postgraduate Medicine 1998;103:51–70; JR Miller. Spirochete Infections: Lyme Disease. In LP Rowland (ed), Merritt’s Textbook of Neurology. Baltimore: Williams & Wilkins, 1995;209–211.
Adapted from: Goldstein MA and Harden CL. Infectious states. In: Ettinger AB and Devinsky O, eds. Managing epilepsy and co-existing disorders. Boston: Butterworth-Heinemann; 2002;83-133.
With permission from Elsevier (www.elsevier.com).
Reviewed and revised March 2004 by Steven C. Schachter, MD, epilepsy.com Editorial Board.
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