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louse-borne relapsing fevers were medical curiosities that did not involve neurologists However, in the late 1970s, a multisystem disease with prominent neurologic features cropped up in the eastern United States It was named after the town of Lyme, Connecticut, where a cluster of cases was rst recognized in 1975 In 1982, Burgdorfer and colleagues identi ed the causative spirochetal agent, Borrelia burgdorferi An early skin manifestation of the disease had previously been described in western Europe and referred to as erythema chronicum migrans Later manifestations of the disease taking the form of acute radicular pain followed by chronic lymphocytic meningitis and frequently accompanied by peripheral and cranial neuropathies had long been known in Europe as the Bannwarth or Garin-Bujadoux syndrome The identity of these diseases has been established, as well as their close relationship to relapsing fever a disease that is also caused by spirochetes of the genus Borrelia and transmitted by ticks The entire group is now classed as the borrelioses In humans, all these spirochetoses induce a subacute or chronic illness that evolves in ill-de ned stages, with early spirochetemia, vascular damage in many organs, and a high level of neurotropism As in syphilis, the nervous system is invaded early in the form of an asymptomatic meningitis Later, neurologic abnormalities appear, but only in a proportion of such cases The early neurologic complications are mainly derivations of meningitis In this disease, unlike syphilis, peripheral and cranial nerves may be implicated (see further on and Chap 46) Immune factors may be important in the later phases of the latent periods and in the development of the neurologic syndromes Lyme disease is less acute than leptospirosis (Weil disease) and less chronic than syphilis It successively involves the skin, nervous system, heart, and articular structures over a period of a year and then burns out The infective organism, as stated above, is the spirochete B burgdorferi, and the vector in the United States is the common ixodid tick The precise roles of the infecting spirochete, the antibodies it induces, and other features of the human host response in the production of clinical symptoms and signs are not fully understood, but the development of an animal model by Pachner and colleagues suggests that there is a chronic form of Borrelia infection in the CNS Lyme borreliosis has a worldwide distribution, but the typical neurologic manifestations differ slightly in Europe and America, as emphasized in the review by Garcia-Monico and Benach In the United States, where approximately 13,000 cases are reported annually, the disease is found mainly in the Northeast and the North Central states Most infections are acquired from May to July In 60 to 80 percent of cases, a skin lesion (erythema chronicum migrans) at the site of a tick bite is the initial manifestation, occurring within 30 days of exposure It is a solitary, enlarging, ring-like erythematous lesion that may be surrounded by annular satellite lesions Usually fatigue and in uenza-like symptoms (myalgia, arthralgia, and headache) are associated, and these seem to be more prominent in the North American than the European form of the illness possibly attributable to a more virulent species of spirochete (Nadelman and Wormser) Weeks to months later, neurologic or cardiac symptoms appear in 15 and 8 percent of the cases, respectively Still later, if the patient remains untreated, arthritis or, more precisely, synovitis develops in about 60 percent of the cases Death from this disease does not occur; therefore little is known of the pathology A long period of disability is to be expected if the disease is not recognized and treated Diagnosis is not dif cult during the summer season in regions where the disease is endemic.

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and when all the clinical manifestations are present But in some cases, a skin lesion is not observed or may have been forgotten, or there may have been only a few or no secondary lesions and the patient is rst seen in the neurologic phase of the illness Then clinical diagnosis may be dif cult Neurologic Manifestations The usual pattern of neurologic involvement is one of an aseptic meningitis or a uctuating meningoencephalitis with cranial or peripheral neuritis, lasting for months (Reik) By the time the neurologic disturbances appear, the systemic symptoms and skin lesions may have long since receded An infrequent cardiac disorder, which may accompany or occur independently of the neurologic changes, takes the form of myocarditis, a pericarditis, or an atrioventricular block The initial nervous system symptoms are rather nonspeci c They consist of headache, mild stiff neck, nausea and vomiting, malaise, and chronic fatigue, uctuating over a period of weeks to months These symptoms relate to the meningitis There is a CSF lymphocytosis with cell counts from 50 to 3000/mL and protein levels from 75 to 400 mg/dL, but both values are typically in the lower part of the range Polymorphonuclear cells may be prominent in the early part of the illness Usually the glucose content is normal Somnolence, irritability, faulty memory, depressed mood, and behavioral changes have been interpreted as marks of encephalitis but are dif cult to separate from the effects of meningitis Seizures, choreic movements, cerebellar ataxia, and dementia have been reported but are infrequent A myelitic syndrome, causing quadriparesis, is also documented In about half the cases, cranial neuropathies become manifest within weeks of onset of the illness The most frequent is a unilateral or bilateral facial palsy, but involvement of other cranial nerves, including the optic nerve, has been observed, usually in association with meningitis One-third to one-half of the patients with meningitis have multiple radicular or peripheral nerve lesions in various combinations These are described in Chap 46 In addition to facial palsies, a severe and painful meningoradiculitis of the cauda equina (Bannwarth syndrome) is particularly characteristic and seems to be more common in Europe than in the United States (there are other causes of this syndrome, including herpesvirus and cytomegalovirus) There is also an infrequent occurrence of Guillain-Barre syndrome following Lyme infection, but there is no reason to believe that the illness then differs from other cases of the acute in ammatory demyelinating polyneuropathy that follows numerous other infections Because of the paucity of autopsy material, knowledge of the nature of Lyme encephalitis is still imprecise Such pathologic material as is available has shown a perivascular lymphocytic in ammatory process of the leptomeninges and the presence of subcortical and periventricular demyelinative lesions, like those of multiple sclerosis (Fig 32-6) Oski and colleagues have recovered B burgdorferi DNA from the involved areas, suggesting that the encephalitis is due to direct invasion by the spirochete A problematic aspect of Lyme disease relates to the development in some patients of a mild chronic encephalopathy, coupled with extreme fatigue That such a disorder may occur after a welldocumented attack of Lyme disease is undoubted However, in the absence of a history of the characteristic rash, arthritis, or welldocumented aseptic meningitis, the attribution to Lyme disease of fatigue alone or various other vague mental symptoms, such as dif culty in concentration, is almost always erroneous, even if there is serologic evidence of prior exposure to the spirochete It would.

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intravenous drugs For late abnormalities, no treatment has proved to be effective However, most of the symptoms tend to regress regardless of the type of treatment given