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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

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

In 1987, follow-up studies were conducted on 72 patients who had had meningoradiculitis and encephalomyelitis (8 patients) due to Borrelia burgdorferi 5-27 years previously. These patients had not been treated with antibiotics, either during the acute disease or during the interval prior to follow-up studies. The patients had exhibited the typical symptoms of Bannwarth's syndrome during the acute phase. At the follow-up studies, 33 patients showed no, and 23 only mild, clinical residual symptoms including normal CSF findings and low-positive serum IgG borrelia antibody titres (IFT; ELISA). Three patients without sequelae exhibited persistent intrathecal secretion of oligoclonal B. burgdorferi-specific CSF IgG antibodies (Immunoblot; positive borrelia CSF IgG antibody titres). Thirteen patients exhibited mild-to-medium sequelae with persistent intrathecal formation of oligoclonal B. burgdorferi-specific CSF IgG antibodies, up to 21 years after the acute illness. This persistence can be interpreted as an "immunological scar syndrome". Our follow-up studies appear to indicate that neurological manifestations of B. burgdorferi infections are generally (with few exceptions) of a benign nature. Most patients can be classified as having been cured without antibiotic therapy. No late manifestations of chronic progressive CNS borreliosis comparable to that of neurosyphilis have been seen following acute untreated neuroborreliosis.
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PMID:Meningoradiculitis and encephalomyelitis due to Borrelia burgdorferi: a follow-up study of 72 patients over 27 years. 279 99

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

Neuroborreliosis, a manifestation of infection with the spirochete Borellia burgdorferi, has become the most frequently recognised arthropod-borne infection of the nervous system in Europe and the USA. The best criterion of an early infection with B. burgdorferi is erythema migrans (EM), but this is present in only about 40-60% of patients with validated borreliosis. Therefore use of the duration of the disease as a classification criterion for neuroborreliosis is increasing, the chronic form being distinguished from the acute when symptoms persist for more than 6 months. The diverse manifestations of neuroborreliosis require that it be included in the differential diagnosis of many neurological disorders. In Europe, meningopolyradiculoneuritis (Bannwarth's syndrome) represents the most common manifestation of acute neuroborreliosis, with the facial nerve being affected much more frequently than the other cranial nerves. Clinical symptoms affecting the central nervous system are rarely observed and then mostly in chronic courses. By far the most common manifestation of chronic neuroborreliosis is encephalomyelitis with spastic-ataxic disturbances and a disturbance of micturition. The current diagnosis of neuroborreliosis is a clinical one, which has to be confirmed by laboratory testing. In most patients, examination of the cerebrospinal fluid (CSF) reveals lymphocytic pleocytosis, damage to the blood-CSF-barrier and an intrathecal synthesis immunoglobulin (Ig) M, IgG, and sometimes IgA. Confirmation of a borrelial infection of the nervous system requires demonstration of an intrathecal synthesis of borrelial-specific antibodies in the CSF or detection of borrelial DNA in the CSF by polymerase chain reaction (PCR). There is no generally accepted therapeutic regime for the treatment of neuroborreliosis, but recent studies have shown ceftriaxone 2 g/day and cefotaxime 6 g/day to be effective in acute and chronic courses. Penicillin G 20 mega units/day and doxycycline 200 mg/day may be suitable for uncomplicated meningopolyneuritis, without involvement of the central nervous system. The durationof treatment--at least 2 weeks in the acute forms and 3 weeks in the chronic forms of neuroborreliosis--is very important for successful treatment. Corticosteroids are recommended only for patients with severe pain that does not respond to antibiotics an analgesics.
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PMID:Neuroborreliosis. 961 4

Any headache in the course of Lyme disease could be an early manifestation of invasion of the CNS by spirochaetes. The most characteristic symptoms of early neuroborreliosis are meningitis with cranial or peripheral neuropathies connected with radiculopathies, less common are encephalitis and myelitis, neuropathies, polyneuropathies, encephalopathies. Encephalomyelitis is the most serious form of neuroborreliosis. From the pathophysiologic point of view all cranial and peripheral neuropathies are forms of mononeuritis multiplex. Encephalopathy is due to neuroimmunomodulators, like lymphokins and or by toxico-metabolic effect could be connected with each form of systemic borreliosis. Certain diagnosis of neuroborreliosis is based on culturing of B. burgdorferi from CSF, detection of specific antispirochaetal antibodies produced in the subarachnoid space, detection of activated lymphocytes B producing specific antibodies, detection in CSF of other antigens of B. burgdorferi or DNA sequences.
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PMID:[Neurologic borreliosis]. 963 83

Lyme-Borreliosis which in Europe is transmitted by Ixodes ricinus presents in three stages with 1st a localised infection (erythema chronicum migrans), 2nd a disseminated infection (e.g., meningoradiculitis), and 3rd a persistent chronic infection (e.g., encephalomyelitis, cerebral vasculitis), whereby not all stages invariably become clinically apparent. The diagnosis is based on the typical clinical presentation, the lumbar puncture (lymphocytic pleocytosis), and serological test from the blood as well as from the CSF (intrathecal antibody production!). The frequency of positive serological results depends on the duration and the type of the disease. In stage 1 20-50% of the patients show increased IgM-antibodies, in stage 2 70-90% show increased IgM- and or IgG-antibodies, and in stage 3 almost 100% of the patients have positive IgG-antibodies. The Lyme-Neuroborreliosis usually is treated with Ceftriaxon 2 g/d intravenously over 14 (Stage 2) or 21 (Stage 3) days.
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PMID:[Diagnosis and therapy of Lyme neuroborreliosis]. 1059 80

Lyme borreliosis, multisystem disease, when involve neurologic system is named neuroborrelosis. Symptomatology of neuroborreliosis is rich and various. Difficulties in recognition are connected usually with long period from tick bite to late neurological signs. Any headache and psychiatric disorder in the course of Lyme disease could be an early manifestation of invasion of the CNS by the spirochaetes. Each part of neurologic system could be involved. The most common clinical picture of neuroborreliosis is meningitis with cranial or peripheral neuropathies connected with radiculalgia, less common are encephalitis and myelitis, neuropathies and polyneuropathies, encephalopathies. Encephalomyelitis is the most serious form of neuroborreliosis. From the pathophysiologic point of view all cranial and peripheral neuropathies are forms of mononeuritis multiplex. Vasculitis and autoimmunology processes are present. Encephalopathy is due to neuroimmunomodulators, like lymphokines and by toxico-metabolic effect could be connected with each form of systemic borreliosis. Spheroplast L-form of borrelia could be responsible for difficulties with their eradication. Diagnosis of neuroborreliosis is based on culturing of B. burgdorferi from CSF, detection of specific antispirochaetal antibodies produced in subarachnoid space, detection of activated lymphocytes, other antigens detection in CSF (also after dissociation of complexes) or borrelial DNA sequences.
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PMID:[Neurologic syndromes in Lyme disease]. 1108 32

Neurological manifestations are characteristic of stage 2 and stage 3 borreliosis. In stage 2, some 15% of the patients have neurological symptoms expressed as a triad of aseptic meningitis, cranial neuritis and radiculitis. Stage 3--chronic neuroborreliosis affects some 5% of untreated patients. The condition has its onset at the earliest 6 months after the infection, and is characterized by encephalopathic symptoms, such as fatigue, sleep and memory disturbances, and depressive states. Further manifestations of this stage may be Lyme polyneuropathy, in rare cases also progressive borrelia encephalomyelitis and cerebrovascular neuroborreliosis. The treatment of choice is intravenous administration of cephalosporins over 2-4 weeks. The success of treatment should be assessed on the basis of the clinical course rather than on laboratory results. Patience is required in the treatment of the post-Lyme syndrome, characterized by residual symptoms, recurrences or a relapsing course.
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PMID:[Diagnosis and therapy of neuroborreliosis. On the hunt for the "great imitator"]. 1211 69

Chronic manifestations (knee arthritis, encephalomyelitis, axonal polyneuropathy) may occur in the late phase of Lyme disease. Contrasting with such well-defined manifestations, the "post-Lyme syndrome" includes symptoms such as fatigue, algia, malaise, cognitive disorders, after treatment of a documented Lyme disease. The analysis of clinical, neuropsychological, bacteriological, immunological, epidemiological, quality of life, and treatment data does not support the reality of such a syndrome. Moreover, no physiopathological data can relate Borrelia infection to such symptoms in patients without previously documented Lyme disease symptoms but who are seropositive (or even sometimes without serodiagnosis as for instance in the Munchausen by proxy, or Gulf war syndromes).
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PMID:[Could aspecific symptoms be related to Borrelia infection?]. 1736 Jan 37


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