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Query: UMLS:C0014070 (encephalomyelitis)
 13,017 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Lyme disease, like syphilis, a spirochetal infection, can appear with exacerbations and remissions in different stages. The clinical picture is marked by dermatological, neurological, rheumatic and cardiological complications. PNS complications appear in the second and third stage. Tick bite meningoradiculoneuritis neuritis (Garin-Bujadoux-Bannwarth-Syndrome), characterized by painful asymmetrical sensory and motor dysfunctions and inflamed CSF, is a typical manifestation of the second stage. Mononeuritis multiplex appearing in conjunction with acrodermatitis chronica atrophicans is a typical PNS manifestation of the third stage. CNS involvement may also occur in early and late stages of Lyme-Borreliosis, presenting as myelitis or progressive encephalomyelitis. Lyme-Borreliosis is a treatable condition, which should not be missed in the differential diagnosis of PNS and CNS disorders.
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PMID:Neurological complications of Lyme borreliosis. 134 45

The tick-borne Lyme Borreliosis may lead to a wide variety of sequels. Besides symptoms involving skin, joints and heart the infection provokes as a neurologic complication a meningopolyneuritis Garin-Bujadoux-Bannwarth in second state and a progressive encephalomyelitis in third state. Unexpected widespread--as modern laboratory investigations proved--the contamination only occasionally inflicts clinical manifestations. Involvement of the nervous system is substantiated by the demonstration of endogenous Borrelia antibodies in the cerebrospinal fluid. This prove is to claim especially for the assumption of a third state neuroborreliosis with progressive encephalomyelitis. Severe damage can be prevented by prompt diagnosis, specific treatment and follow-up.
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PMID:[Lyme borreliosis--epidemiology, etiology, diagnosis and therapy]. 176 Dec 73

After the isolation of Borrelia burgdorferi, the previously unknown causative agent of Lyme disease, two neurological disorders, Bannwarth's syndrome and acrodermatitis chronica atrophicans-associated neuropathy, which have been known in Europe for decades, gained new interest. With the availability of serodiagnostic tests, a chronic debilitating disorder--progressive borrelia encephalomyelitis--was found to be caused by chronic infection with B. burgdorferi. Beside these typical manifestations, a growing number of publications about various neurological phenomena appeared, which were thought to be caused by B. burgdorferi. This assumption was based in many cases on the results of serodiagnostic tests only. Considerations for causal connections were frequently lacking. While prior to the availability of serodiagnostic tests neurological manifestations of Lyme borreliosis frequently remained undiagnosed, we now face a tendency for overdiagnosis. The great variety of neurological manifestations in Lyme borreliosis--most of them can also be attributed to other conditions--and the high rate of seropositivity for B. burgdorferi amongst the population living in endemic areas require strict criteria for the correct diagnosis of new and typical neurological manifestations.
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PMID:Neurological manifestations of Lyme borreliosis. 180 27

The serological survey, analyzing sera which were obtained from Lyme disease suspected subjects was performed using immunoperoxidase (IP) test between July, 1987 and February, 1989. Fifteen seropositive subjects to Borrelia burgdorferi have been found in this survey, and these cases were considered to be true Lyme disease or highly suspected for this illness. Most of these seropositive cases geographically occurred in northern part of Japan, and both sexes and all age subjects were affected. In clinical manifestations, 5 cases developed a typical skin lesion of erythema chronicum migrans (ECM) followed by tick-bite. Neurologic manifestations were found in 6 cases, including one patient who also had ECM after a known tick bite. Of these neurologic manifestations, 4 cases had lymphocytic meningitis, 3 unilateral or bilateral facial palsy, and one encephalomyelitis. When 8 of these 15 sera were analyzed for antibodies to Lyme disease with ELISA, a poor agreement of serodiagnosis between IP test and ELISA has been found in the course of this study.
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PMID:[Studies on 15 seropositive cases to Lyme disease using immunoperoxidase test in Japan]. 188 Apr 40

The most common neurological manifestation of Lyme disease is lymphocytic meningoradiculitis (Banwarth's syndrome, stage II). In rare cases, chronic progressive encephalomyelitis (stage III) with symptoms similar to multiple sclerosis is observed. Antibodies against Borrelia burgdorferi are detectable in 70-90% of stage II cases, with IgM-antibodies predominating in the first two weeks, and IgG-antibodies thereafter. Detection of specific intrathecal antibodies is the best serodiagnostic parameter for diagnosing neuroborreliosis. With the aid of a CSF/serum index determination (on the basis of a comparison of IgG-antibody ELISA titers in CSF and serum with identical IgG concentrations) involvement of the nervous system was shown in 64% and 77%, respectively, of 76 stage II cases (diagnostic significance 98% and 100%, respectively). In particular when tertiary forms of the disease are suspected immunoblot techniques (Western blot, IEF-affinity blot) are recommended confirmatory tests.
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PMID:[Diagnosis of Lyme neuroborreliosis. Detection of intrathecal antibody formation]. 193 23

Lyme borreliosis is a multisystem disorder common in childhood. It is an acute and persistent anthropozoonotic infection caused by the spirochete Borrelia burgdorferi (Bb) which is transmitted by Ixodes ticks. After the tick bite in summer, erythema migrans, meningoradiculoneuritis, or carditis may develop within the same season. Later manifestations may be oligo-arthritis, progressive encephalomyelitis, or acrodermatitis chronica atrophicans. The most common course is probably asymptomatic. Connatal infection is possible. Diagnosis is established mainly by history and clinical manifestations. The antibody response to Bb can be measured in serum and cerebrospinal fluid. Tests may be false-negative early in the course of the disease or after early treatment. False-positive results may be caused by cross-reactions. Interpretation of test results must also consider unrelated anamnestic titres or asymptomatic infection. Treatment with appropriate antibiotics cures the disease in most patients, however some patients may not respond. The optimal drug has not yet been found. Best prophylaxis is by early removal of the tick from the skin.
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PMID:Childhood Lyme borreliosis in Europe. 222 64

Lyme disease is a multisystem disorder caused by a tick-transmitted spirochete, Borrelia burgdorferi. Clinical manifestations typically begin with characteristic skin lesions, erythema (chronicum) migrans. Weeks to months later, some patients develop the second stage of the illness characterized by neurologic abnormalities, migratory joint pain, cardiac involvement. Months to years later, in many patients the disease progresses to the third stage of manifestation such as chronic arthritis, chronic encephalomyelitis, acrodermatitis chronica atrophicans and keratitis. Zoonotic infection with B. burgdorferi is also widespread within endemic regions among domestic as well as wild animals. The diagnosis is based on clinical and epidemiological findings in most patients, particularly those with erythema migrans or tick bites. Detection of specific antibodies to B. burgdorferi is a useful confirmatory test in many patients. In atypical cases, a positive test result can be valuable for determining the diagnosis. However, serologic testing in Lyme disease is not yet standardized and the results obtained from different assay systems or commercial kits may vary. Moreover, because of poor agreement in sensitivity and/or specificity, data obtained from different laboratories are not comparable. We emphasize that serologic findings must be interpreted with caution; the physician must beware of its strengths and limitations.
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PMID:[Lyme disease]. 227 65

In Switzerland 5-35% of Ixodes ricinus ticks are infested with Borrelia burgdorferi (B.b.). There is a high risk of transmission of this infectious agent from any tick bite and 4-5% of affected subjects subsequently contract evident Lyme borreliosis. However, both tick bite and erythema chronicum migrans are unreliable diagnostic pointers as they are not usually found in the history of Lyme borreliosis patients. Similarly, an increased titer of antibodies against B.b. is not evidence of Lyme borreliosis, since this increased titer is found in some 10% of the healthy population. Finally, even a negative antibody titer does not rule out the diagnosis. The special problems of diagnosis are investigated in 7 patients with articular Lyme borreliosis and 9 patients with CNS symptoms. Articular Lyme borreliosis must be diagnosed by elimination even where there is an increased titer of antibodies against B.b., since neither the clinical picture, nor laboratory analysis of the synovial fluid, nor histologic and radiologic investigations show specific findings. There is a wide spectrum of neurologic symptoms. Diagnosis is easiest in cases with typical clinical findings (meningopolyneuritis), but in all other cases it is still by elimination. Among laboratory tests, calculation of an antibody index has proven helpful. Nevertheless, it is not always possible to differentiate Lyme borreliosis from encephalomyelitis disseminata. Antibiotic treatment has been tried in doubtful cases.
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PMID:[Diagnostic possibilities and limitations in Lyme borreliosis]. 269 51

Lyme disease is a tick-borne multisystemic Borrelia infection to which the following diseases belong: erythema migrans, lymphadenosis benigna cutis, lymphocytic meningoradiculitis (Bannwarth's syndrome), Lyme-arthritis and acrodermitis chronica atrophicans. The infection rate of ticks with Borrelia Burgdorferi in Germany amounts to 13.6% compared to the infection with the European spring summer meningoencephalitis virus with 1.1%. Recent investigations show that lipopolysaccharides and interleukin-1 play an important role in the pathogenesis of Lyme disease. Lipopolysaccharides (LPS) are a constitutive part of the outer wall of gram negative bacteria. Its biological activities include pyrogenicity, mitogenicity for lymphocytes and the induction of interleukin-1 (IL-1). IL-1 is the major macrophage-derived immunoregulatory protein. Lyme disease is characterized by a variety of symptoms which could be explained by the effects of IL-1 on host systems. These symptoms include: fever, malaise, erythema migrans and arthritis. The clinical course can be divided into three stages. Erythema migrans, lymphadenosis benigna cutis and general symptoms characterize the first stage. In the second stage disorders of the heart and the neurological system may follow including Bannwarth's syndrome. 60% of the patients develop facial palsy and 30% of these patients bilateral palsy. In 40% of all cases the facial palsy is the only motor disorder. Other cranial nerves can also be affected. The third stage consists of the Lyme-arthritis, acrodermitis chronica atrophicans and encephalomyelitis. The determination of specific spirochetal antibodies in serum and cerebrospinal fluid (CSF) is the most valuable diagnostic aid for this borreliosis. The CSF examination may also be helpful.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Lyme borreliosis and its significance for the ENT physician]. 278 72

The neurological spectrum of Borrelia burgdorferi infections is still enlarging. We review epidemiological, pathological and serological data of Lyme disease. The course of the disease is divided in three stages: stage 1 during the first month is characterised by erythema chronicum migrans and associated manifestations; stage 2 includes not only the classical European meningoradiculitis but also less specific neurological symptoms: isolated lymphocytic meningitis with an acute or even relapsing course, apparently idiopathic facial palsy, neuritis of other cranial nerves, polyneuritis cranialis, Argyll-Robertson sign, peripheral nerve involvement, acute transverse myelitis, severe encephalitis, myositis. During stage 3, three to five months or longer after the onset of the disease, chronic arthritis, acrodermatitis chronica atrophicans and various neurological symptoms can be observed: chronic neuropathy with mainly sensory or motor signs, recurrent strokes due to cerebral angiopathy and progressive encephalomyelitis; this third stage the central nervous system involvement is characterised by slowly progressive or fluctuating course during months or years, ataxic or spastic gait disorder, bladder disturbances, cranial nerve dysfunction including optic atrophy and hypoacusia, dysarthria, focal and diffuse encephalopathy. This chronic central nervous system disease can mimic multiple sclerosis, anorexia nervosa, psychic disorders or subacute presenile dementia. It is often associated with pleiocytosis, abnormal EEG and evoked potentials, sometimes multifocal and mainly periventricular white matter lesions visualised by CT or MRI, and as a rule high antibody titers against Borrelia burgdorferi. High doses of penicillin can halt the disease, sometimes induce spectacular regression of symptoms or sometimes be inefficient; ceftriaxone could be a more powerful therapy. Similarities between syphilis and Borreliosis are multiple: both of these spirochetes contain plasmids, can be transmitted through the placenta and progress for many years through successive stages, with multiorgan symptoms, including parenchymatous and vascular lesions of the central nervous system. Borrelia burgdorferi is the new great imitator.
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PMID:[Multiple neurologic manifestations of Borrelia burgdorferi infection]. 307 Jun 90


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