Ischemic strokes and other brain problems due to LD

Topics with information and discussion about published studies related to Lyme disease and other tick-borne diseases.
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Yvonne
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Re: Ischemic strokes and other brain problems due to LD

Post by Yvonne » Sat 7 Feb 2009 15:58

http://www.springerlink.com/content/lm04k5h5t347h467/

Chronic progressive neurological involvement in Borrelia burgdorferi infection
Summary Five patients with chronic meningitis were hospitalized several times for progressive neurological symptoms. The clinical manifestations included cranial neuritis, radiculoneuritis, myelitis and encephalitis. In two cases cerebral infarction occurred. The course was commonly characterized by a tendency to deteriorate. From the clinical point of view, it was repeatedly difficult to exclude multiple sclerosis or tuberculous meningitis. Finally, specific antibodies against Borrelia burgdorferi were detected by indirect immunofluorescence assay. The diagnosis of a borreliosis was not considered initially because there was no history of tick-bite or erythema chronicum migrans, and the neurological involvement of the central nervous system seemed unusual. The latency between the first symptoms and diagnosis varied from 3 months to 5 years. After a parenteral, high-dose therapy with penicillin, there was a significant improvement in all patients. In two cases, there was evidence of intrathecally produced antibodies to myelin basic protein.
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Re: Ischemic strokes and other brain problems due to LD

Post by Yvonne » Tue 25 Aug 2009 11:07

http://www.neurology.org/cgi/content/abstract/48/2/520

Subarachnoid hemorrhage in a patient with lyme disease

subarachnoid hemorrhage = http://en.wikipedia.org/wiki/Subarachnoid_hemorrhage

Article abstract-
Neuroborreliosis can cause a wide variety of seemingly unrelated neurologic abnormalities. Although the epidemiology, etiology, and pathology of this infection have been well documented, the pathogenesis and diagnosis continue to be problematic. In the current study we report a case of Lyme disease in which subarachnoid hemorrhage was the presenting feature of a patient with polyradiculoneuropathy and encephalopathy. Magnetic resonance imaging of the spine demonstrated diffuse pial and meningeal enhancement with more focal nodular areas of involvement.
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Re: Ischemic strokes and other brain problems due to LD

Post by Yvonne » Mon 8 Mar 2010 15:57

http://www.actaneurologica.be/acta/down ... t%20al.pdf

Acute ischaemic pontine stroke revealing Lyme Neuroborreliosis in a young adult
Abstract
We report the case of a 23 year old malepatient who
suddenly developed right hemiparesis ,cerebellar ataxia,
dysarthria and bilateral dysmetria
Brain magnetig resonance (MR) examination demonstrated hyperacute
ischaemic lesions within the pons.
CSF analysis revealed a high proteing content, lymphocytic pleocytosis and
oligoclonal IgG bands not present in the serum .
Elevated IgMg and IgG anti Borreliag burgdorferi antibodies were
shown in both serum and CSF samples, associated with
an intrathecal synthesis of these antibodies ,
Ischaemic CNS lesions have been rarely observed as the first
manifestation of Lyme neuroborreliosis .
The putative mechanism for parenchymal ischaemia is the glocal extension
of inflammatory changes from meninges to the wall of penetrating arterioles
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Yvonne
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Re: Ischemic strokes and other brain problems due to LD

Post by Yvonne » Sun 21 Mar 2010 10:22

Nervenarzt. 1997 Apr;68(4):339-41.

Vasculitis course of neuroborreliosis with thalamic infarct

[Article in German]

Keil R, Baron R, Kaiser R, Deuschl G.

Klinik für Neurologie, Christian-Albrechts-Universität, Kiel.

A-20-year-old man without vascular risk factors presented with paraesthesia of the left side of the body with acute onset. Cerebral magnetic resonance imaging showed an infarction in the right thalamus. Intra-arterial digital subtraction angiography revealed stenosis of the right thalamic vessels. Recent infection by Borrelia burgdorferi was demonstrated by typical findings in the cerebrospinal fluid: lymphocytic pleocytosis and intrathecal synthesis of borrelial-specific antibodies. The diagnosis of a borrelial-induced vasculitis with secondary thalamic infarction was made from these findings. After antibiotic treatment with cefrtriaxone, the patient was discharged without residual complaints.

PMID: 9273464
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Re: Ischemic strokes and other brain problems due to LD

Post by Yvonne » Sun 21 Mar 2010 10:23

Nervenarzt. 1999 Feb;70(2):167-71.

Neuroborreliosis with extensive cerebral vasculitis and multiple cerebral infarcts

[Article in German]

Schmitt AB, Küker W, Nacimiento W.

Neurologische Klinik, Medizinische Einrichtungen der RWTH, Aachen.

We report on a patient who suffered from borreliosis-induced severe cerebral vasculitis accompanied by multiple cerebral infarctions leading to hemiparesis, hemianopsia and reduced consciousness. Despite antibiotic and immunosuppressive therapy with ceftriaxon and prednisolone the patients condition deteriorated. Cerebral angiography showed multiple stenoses of large arteries of the posterior circulation and ubiquitous irregularities of small vessel wails. General reduced perfusion reflected an increased peripheral resistance. After 4 weeks of additional immunosuppressive treatment with cyclophosphamide the neurological status and angiographic findings improved dramatically.

PMID: 10098153
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Re: Ischemic strokes and other brain problems due to LD

Post by Yvonne » Sun 21 Mar 2010 10:28

http://www.neurologyindia.com/article.a ... t=Buchwald

Fatal course of cerebral vasculitis induced by neuroborreliosis
Borreliosis is a tick-borne illness caused by the spirochete Borrelia and the different causative strains identified include B. burgdorferi sensu strictu in America and B. garinii and B. afzelii in Europe. Clinical manifestations are wide and vary in severity. The disease is divided into three stages: 1) early localized disease characterized by skin lesions (erythema migrans); 2) early disseminated disease characterized by neurologic and/or cardiac involvement; and 3) late disease characterized by arthritis and/or rare neurologic complications. [1],[2] Cerebral vasculitis is a very rare, usually a nonfatal complication. [3],[4],[5] A fatal case of neuroborreliosis complicated by cerebral vasculitis in a young male patient prompted us to present this case.

In May 2008 a 25-year-old male smoker presented with a sudden onset of right-sided hemiparesis and at admission he had partially recovered. Computerized tomography (CT) scan and magnetic resonance imaging (MRI) revealed a small left subcortical infarction. Angiographic sequences, both CT-angiography and MR-angiography, were essentially normal [Figure 1] a-c. Diagnostic work-up for vascular risk factors was normal. During springtime he had been bitten by a tick but as he had no erythema, headache, fever or other alarming symtoms the possibility of neuroborreliosis was excluded. He was put on aspirin 160 mg once a day and dipyridamole 200 mg twice a day. His state continued to improve and one week later he was discharged.

About five weeks after discharge, his condition slowly worsened. His original symptoms progressed in severity and, in addition, he developed dysphasia and paresis of his left leg. He returned to our emergency room about 3 weeks later and a repeat neuroradiological investigation with MRI and CT, including angiographic sequences, showed an infarction in the territory of the left anterior cerebral artery (ACA) and extensive changes in the calibre of basilar artery, both middle cerebral arteries (MCA) and left ACA, the latter being occluded. These features were consistent with cerebral vasculitis [Figure 1] d-f. Cerebrospinal fluid (CSF) examination revealed elevated protein (1.88 g/l) and increased white blood cells (monocytes 6.3 x 106/l). CSF was positive for specific borrelia IgM-antibodies (1.35 ELISA index pos) and serum borrelia IgG-antibodies titers were elevated. These findings were strongly suggestive of neuroborreliosis, even though the CSF polymerase chain reaction (PCR) showed no borrelia-DNA. Extensive radiological and laboratory work-up for systemic vasculitis and connective tissue diseases was negative. Work-up for other infectious diseases was also negative.

He was treated with oral doxycycline 200 mg twice daily for 12 days. His vasculitis was initially treated with IV methylprednisolone 1 g for three consecutive days followed by oral prednisone 60 mg per day. In spite of this treatment, his state continued to deteriorate. Repeat MRI including angiographic sequences showed progression of cerebral vasculitic changes and more ischemic areas [Figure 1]g. Repeat CSF examination after antibiotic treatment revealed normal levels of specific borrelia IgM-antibodies. He was further treated with IV cyclophosphamid, 15 mg/kg every second week. Three weeks later he developed brain edema due to extensive bihemispheric infarctions [Figure 1]h-i and died of transtentorial and subfalcine herniation. With respect to his family's wish, an autopsy was not performed

Probably this is the only reported case of fatal cerebral vasculitis due to neuroborreliosis. The diagnosis of cerebral vasculitis was based on clinical course, CSF findings, MRI and CT/MR-angiographic findings even though conventional cerebral angiography and histopathological confirmation were not performed in this patient. [6],[7] Elevated titers of specific borrelia IgM-antibodies in the CSF suggest that the cerebral vasculitis in this patient probably was a complication of neuroborreliosis. [3],[4],[5] The absence of a preceding erythema migrans is not unusual, [1],[2],[8] however, total absence of other symptoms and signs of borreliosis as seen in this patient is rare. The histopathological substrate for neuroborreliosis is assumed to be an angiopathy of small vessels with mononuclear perivascular infiltration. Cerebral vasculitis in neuroborreliosis is rare and the pathogenesis of the angiopathy is uncertain. [9] Cerebral vasculitis in neuroborreliosis improves in som patients with specific antibiotic treatment [3],[4],[5],[9] thus suggesting that cerebral vasculitis in neuroborreliosis may be due to direct angio-invasion by the spirochetes. In patients who fail to respond to specific antibiotics, immunosuppressive treatment may be necessary [6] thus suggesting immune-mediated mechanisms. In our patient CSF specific borrelia-IgM-antibodies returned to normal levels after adequate antibiotic treatment [10] while vasculitic changes progressed, thus supporting the latter theory.

In our patient delayed institution of appropriate specific treatment might have resulted in the fatal outcome. A contributing factor was failure on the part of the patient by not calling on us in spite of three weeks of deterioration. This case illustrates the importance of having an index of suspicion of borrelia infection, especially in high-endemic areas such as southern Sweden, [2] both when dealing with "cryptogenic" stroke and cerebral vasculitits.

http://en.wikipedia.org/wiki/Cerebral_vasculitis
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Yvonne
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Re: Ischemic strokes and other brain problems due to LD

Post by Yvonne » Sat 8 May 2010 10:50

Rev Neurol (Paris). 2010 Apr 29. [Epub ahead of print]

Multiple ischemic strokes due to Borrelia garinii meningovasculitis.

[Article in French]

Rey V, Du Pasquier R, Muehl A, Péter O, Michel P.

Service de neurologie, département des neurosciences cliniques, centre hospitalier universitaire Vaudois, BH 13, 1011 Lausanne, Suisse.

Abstract
The most frequent clinical manifestation of borreliosis in Switzerland is erythema migrans, with about 2500 patients each year. Neurological manifestations are rare, mostly hyperalgesic radiculitis (Bannwarth syndrome), aseptic meningitis or cranial nerve involvement. We report the first Swiss patient with meningovasculitis due to neuroborreliosis, with recurrent multiple ischemic strokes in multiple vascular territories. The treatment with ceftriaxone stopped the progression, but the patient is still suffering from severe invalidating cognitive disorders. We also comment on the pathophysiology and review the literature of other clinical cases.
Copyright © 2010 Elsevier Masson SAS. All rights reserved.

PMID: 20434741
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Yvonne
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Re: Ischemic strokes and other brain problems due to LD

Post by Yvonne » Mon 2 Aug 2010 9:58

Cerebral sinuvenous thrombosis associated with Lyme neuroborreliosis :


http://www.springerlink.com/content/mx4769u6550t8505/




Cerebral venous sinus thrombosis =

http://en.wikipedia.org/wiki/Cerebral_v ... thrombosis
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Yvonne
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Re: Ischemic strokes and other brain problems due to LD

Post by Yvonne » Fri 13 Aug 2010 11:59

Arkh Patol. 2010 Mar-Apr;72(2):36-7.

Early recurrence of neuroborreliosis with a fatal outcome

[Article in Russian]

[No authors listed]

Abstract
The authors describe a case of Lyme disease--neuroborreliosis. In neuroborreliosis, there are morphohistological changes: pronounced dystrophic processes in the brain nerve cells, spongiosis, perivascular hemorrhagic infiltrations, glial proliferation with the formation of perivascular glial granulomas.

PMID: 20698315
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Re: Ischemic strokes and other brain problems due to LD

Post by Yvonne » Sat 14 Aug 2010 20:38

Dement Geriatr Cogn Disord. 1997 Nov-Dec;8(6):384-90.

Borrelia burgdorferi-seropositive chronic encephalomyelopathy: Lyme neuroborreliosis? An autopsied report.

Kobayashi K, Mizukoshi C, Aoki T, Muramori F, Hayashi M, Miyazu K, Koshino Y, Ohta M, Nakanishi I, Yamaguchi N.

Department of Neuropsychiatry, Kanazawa University School of Medicine, Japan.

Abstract
A 36-year-old Japanese woman presented with progressive cerebellar signs and mental deterioration of subacute course after her return from the USA. Her serum antibody to spirochete Borrelia burgdorferi was significantly elevated. A necropsy 4 years after her initial neurological signs revealed multifocal inflammatory change in the cerebral cortex, thalamus, superior colliculus, dentate nucleus, inferior olivary nucleus and spinal cord. The lesions showed spongiform change, neuronal cell loss, astrocytosis and proliferation of activated microglial cells. The internal capsule was partially vacuolated and the spinal cord, notably at the thoracic level, was demyelinated and cavitated in the lateral funiculus. Microglial cells aggregated within and around the spongiform lesions and microglial nodules were present in the medulla oblongata. Use of Warthin-Starry stain demonstrated silver-impregnated organisms strongly suggesting B. burgdorferi in the central nervous tissues. The dentate nucleus and inferior olivary nucleus showed the most advanced lesions with profound fibrillary gliosis. Occlusive vascular change was relatively mild, and fibrous thickening of the leptomeninges with lymphocyte infiltrates was localized in the basal midbrain. The ataxic symptoms were due to the dentate and olivary nucleus lesions and mental deterioration was attributable to the cortical and thalamic lesions. Spongiform change, neuronal cell loss, and microglial activation are characteristic pathological features in the present case. The cerebellar ataxia and subsequent mental deterioration are unusual clinical features of Lyme neuroborreliosis. Spirochete B. burgdorferi can cause focal inflammatory parenchymal change in the central nervous tissues and the present case may be an encephalitic form of Lyme neuroborreliosis.

PMID: 9370092
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