Lyme disease presenting as recurrent acute meningitis.

Pal, Garima; Baker, Joanne; Humphrey, P R

doi:10.1136/bmj.295.6594.367

Cited by 13 publications

(1 citation statement)

References 5 publications

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“…Clinical and complementary data in this series CSF oligoclonal bands in this syndrome. Most of our patients showed normal levels of IgG in successive CSF samples and rule out conditions such as Lyme disease (Pal et al, 1987;Steere, 1989), neurosyphilis (López de Munain et al, 1990), no patient, not even those with some IgG elevation, had positive CSF oligoclonal bands, thus suggesting that local neurobrucellosis (Pascual et al, 1988;Roldán-Montaud, 1991), mycoplasma infections (Dalton and Newton, 1991), synthesis of immunoglobulins does not occur in the CSF in PMP (MacLean et al, 1990;Bhigjee and Bill;1996). The HIV meningitis (Hollander and Stringari, 1987) and granulomatous (Tozman, 1991;Roch-Le Foch et al, 1992) finding of normal or, at most, only slightly elevated ADA values in our PMP cases also helps in the differential diagnosis and neoplastic (Grossman and Moynihan, 1991) arachnoiditis which could theoretically account for clinical symptoms such of this condition from chronic infectious, granulomatous and neoplastic arachnoiditis, where ADA levels are usually as those observed in this syndrome before the availability of serological testing.…”

Section: Discussionmentioning

confidence: 57%

Pseudomigraine with temporary neurological symptoms and lymphocytic pleocytosis. A report of 50 cases

Gómez-Aranda

Cañadillas²,

Martí-Massó³

et al. 1997

Brain

175

239

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This is the first large series, comprising 50 patients who suffered a total of 164 episodes, of pseudomigraine with temporary neurological symptoms and lymphocytic pleocytosis (PMP syndrome). Onset of PMP was between the ages of 14 and 39 years and was most frequent in males (68%). Eight males (24%) and five females (31%) had a personal history of migraine. One-quarter had had a viral-like illness up to 3 weeks prior to the onset of the syndrome. The clinical picture consisted of one to 12 episodes of changing variable neurological deficits accompanied by moderate-to-severe headache and occasionally fever. The headaches were described as predominantly throbbing and bilateral with variable duration (mean, 19 h). The mean duration of the transient neurological deficits was 5 h. Sensory symptoms were most common (78% of episodes), followed by aphasic (66%) and motor (56%) symptoms. Visual symptoms appeared in only 12% of episodes. The most frequent combinations were motor aphasia plus sensory and motor right hemibody symptoms (19% of episodes), motor aphasia plus right sensory symptoms (10%) and isolated right (9%) or left (9%) sensory symptoms. All patients were asymptomatic between episodes and following the symptomatic period (maximum duration 49 days). Lymphocytic pleocytosis ranged from 10 to 760 lymphocytic cells/mm3 CSF (mean, 199). In CSF, protein was increased in 96% of patients, IgG was normal in 80% of cases and oligoclonal bands were not found. Adensoine deaminase values were slightly above normal in two out of 16 patients tested. Extensive microbiological determinations, including viral HIV and borrelia serologies, were negative. Brain CT and MRI were always within normal limits, while EEG frequently showed focal slowing. Conventional cranial angiography was performed on 12 patients. In only one were there abnormalities suggestive of localized vascular inflammation, coincident with the focal neurological symptoms. Two patients developed PMP symptoms immediately after angiography. SPECT, performed on only three patients in the symptomatic period, revealed focal areas of decreased uptake consistent with the clinical symptoms. PMP aetiology remains a mystery; chronic arachnoiditis, viral meningoencephalitis or migraine are not plausible aetiological explanations. Because a number of patients had had a prodromic viral-like illness, we hypothesize here that such a viral infection could activate the immune system, thereby producing antibodies that would induce an aseptic inflammation of the leptomeningeal vasculature, possibly accounting for this clinical picture.

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Section: Discussionmentioning

confidence: 57%

Pseudomigraine with temporary neurological symptoms and lymphocytic pleocytosis. A report of 50 cases

Gómez-Aranda

Cañadillas²,

Martí-Massó³

et al. 1997

Brain

175

239

View full text Add to dashboard Cite

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Neurologische Manifestationen der Lyme-Borreliose

Kristoferitsch

1991

Infection

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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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Lyme disease

Bourke

1989

Biomedicine & Pharmacotherapy

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Neurological problems form an important part of the clinical spectrum of Lyme disease. A triad of aseptic meningoencephalitis, cranial neuritis and peripheral neuritis is unique to the disease. However, the list of neurological manifestations described includes pseudotumour cerebri, hemiparesis, demyelinating disorders, optic atrophy, recurrent laryngeal nerve palsy and purulent meningitis so that Lyme disease must now be considered in the differential diagnosis of a wide range of neurological disorders.

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Lyme disease presenting as recurrent acute meningitis.

Abstract: immune haemolytic anaemia in a patient treated with chlorpropamide; in vitro testing showed cross reactivity with glibenclamide and related compounds. Immune haemolysis in vivo caused by glibenclamide, however, does not seem to have been reported before.

Cited by 13 publications

References 5 publications

Pseudomigraine with temporary neurological symptoms and lymphocytic pleocytosis. A report of 50 cases

Pseudomigraine with temporary neurological symptoms and lymphocytic pleocytosis. A report of 50 cases

Neurologische Manifestationen der Lyme-Borreliose

Lyme disease

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