Borrelia and the Brain

Topics with information and discussion about published studies related to Lyme disease and other tick-borne diseases.
Joe Ham
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Borrelia and the Brain

Post by Joe Ham » Tue 8 Jan 2008 19:11

J Infect Dis. 1993 Jul;168(1):143-51.

Experimental infection of the mouse brain by a relapsing fever Borrelia species: a molecular analysis.

Cadavid D, Bundoc V, Barbour AG.

Department of Microbiology, University of Texas Health Science Center, San Antonio 78284-7758.

The spirochetal disease relapsing fever is notable not only for multiphasic antigenic variation but also for central neurologic manifestations.

To further characterize involvement of the brain in this disorder, immunocompetent and -deficient mice were infected with Borrelia hermsii. Immunodeficient mice were treated while spirochetemic with neutralizing IgM monoclonal antibodies to the infecting serotype. Blood, cerebrospinal fluid, and brain tissue were examined by culture and polymerase chain reaction.

In immunocompetent mice, antigenic variation occurred in the brain as well as in the blood.

In immunodeficient mice, the infecting serotype was still present in the brain after it had been eliminated from the blood by the administered antibodies.

These latter results cannot be accounted for by contamination of brain tissue and cerebrospinal fluid by blood and, hence, establish the direct involvement of the central nervous system in this experimental infection.


PMID: 8515101 [PubMed - indexed for MEDLINE]

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Clin Infect Dis. 1998 Jan;26(1):151-64.

Neuroborreliosis during relapsing fever: review of the clinical manifestations, pathology, and treatment of infections in humans and experimental animals.

Cadavid D, Barbour AG.

Department of Neurology, Georgetown University School of Medicine, Washington, D.C. 20007, USA.

The spirochetal disease relapsing fever is caused by different Borrelia species. Relapsing fever is well recognized as an infection of the blood, but little is known about its predilection for the nervous system and the eyes.
To investigate neurological and ocular involvement during relapsing fever, we reviewed the clinical manifestations, pathology, and treatment of relapsing fever of humans and experimental animals.

The results indicate that Borrelia turicatae and Borrelia duttonii, the agents of tick-borne relapsing fever in southwestern North America and sub-Saharan Africa, respectively, cause neurological involvement as often as Borrelia burgdorferi in Lyme disease.

Evidence of this is the frequent occurrence of lymphocytic meningitis and peripheral facial palsy in human disease; the identification of spirochetes in the brain and other nervous tissues of humans, animals, and arthropod vectors; and the persistence of brain infection after treatment with antibiotics that do not readily penetrate the blood-brain barrier.


PMID: 9455525 [PubMed - indexed for MEDLINE]


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J Infect Dis. 2006 May 15;193(10):1451-8. Epub 2006 Apr 4.

Residual brain infection in relapsing-fever borreliosis.
Cadavid D ,Sondey M ,Garcia E ,Lawson CL .

Department of Neurology and Neuroscience and Center for the Study of Emerging Pathogens, University of Medicine and Dentistry of New Jersey-New Jersey Medical School, Newark 07103, USA. cadavidi@umdnj.edu

BACKGROUND: Neurological involvement is common in the spirochetal infection relapsing fever (RF) in both humans and experimental animals.

RF is best known for antigenic variation caused by the sequential expression of variable outer membrane lipoproteins of 2 sizes, variable small (Vsp) and variable large (Vlp) proteins.

Less understood is the persistence of RF borreliae in the brain after they are cleared from the blood, referred to as residual brain infection (RBI). Our goal was to investigate the phenomenon of RBI in RF.

METHODS: We studied RBI in immunocompetent mice by culturing blood and perfused brain samples 1 month after intraperitoneal inoculation with Borrelia turicatae serotype 1 (Bt1). Mice deficient in Toll-like receptor 2 (TLR2-/-) or in B and T cells (scid) were included for comparison.

RESULTS: All scid mice had persistent infection in blood and brain. RBI was found in 3 (19%) of 16 immunocompetent and TLR2-/- mice.

RBI was caused by either persistence of the original serotype (Bt1) or newly emerged Vsp (n=1, renamed Bt3) or Vlp serotypes.

The Vsp of Bt1 (Vsp1) and Bt3 (Vsp3) were 75% identical.

CONCLUSIONS: RBI in RF is relatively frequent and can occur by persistence of the original or newly emerged serotypes.

PMID: 16619194 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov/entrez/quer ... s=16619194

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Microbes Infect. 2006 Jul;8(8):2213-9. Epub 2006 May 30.

Persistent brain infection and disease reactivation in relapsing fever borreliosis.
Larsson C ,Andersson M ,Pelkonen J ,Guo BP ,Nordstrand A ,Bergstrom S .

Department of Molecular Biology, Umea University, SE-901 87 Umea, Sweden.

Relapsing fever, an infection caused by Borrelia spirochetes, is generally considered a transient, self-limiting disease in humans.

The present study reveals that murine infection by Borrelia duttonii can be reactivated after an extended time as a silent infection in the brain, with no bacteria appearing in the blood and spirochete load comparable to the numbers in an infected tick.

The host cerebral gene expression pattern is indistinguishable from that of uninfected animals, indicating that persistent bacteria are not recognized by the immune system nor cause noticeable tissue damage.

[SAY WHAT?
Are a few weeks in a mouse brain equivalent to decades in the human brain?]


Silent infection can be reactivated by immunosuppression, inducing spirochetemia comparable to that of initial densities. B. duttonii has never been found in any host except man and the tick vector.

We therefore propose the brain to be a possible natural reservoir of the spirochete.

The view of relapsing fever as an acute disease should be extended to include in some cases prolonged persistence, a feature characteristic of the related spirochetal infections Lyme disease and syphilis.

PMID: 16782384 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov/entrez/quer ... s=16782384

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Microbes Infect. 2006 Nov-Dec;8(14-15):2832-40. Epub 2006 Sep 22.

Invasion of human neuronal and glial cells by an infectious strain of Borrelia burgdorferi.

Livengood JA, Gilmore RD Jr.
Centers for Disease Control and Prevention, Division of Vector-borne Infectious Diseases, 3150 Rampart Road, CSU Foothills Campus, Fort Collins, CO 80522, USA.

Human infection by Borrelia burgdorferi, the etiological agent for Lyme disease, can result in serious acute and late-term disorders including neuroborreliosis, a degenerative condition of the peripheral and central nervous systems.

To examine the mechanisms involved in the cellular pathogenesis of neuroborreliosis, we investigated the ability of B. burgdorferi to attach to and/or invade a panel of human neuroglial and cortical neuronal cells. In all neural cells tested, we observed B. burgdorferi in association with the cell by confocal microscopy. Further analysis by differential immunofluorescent staining of external and internal organisms, and a gentamicin protection assay demonstrated an intracellular localization of B. burgdorferi.

A non-infectious strain of B. burgdorferi was attenuated in its ability to associate with these neural cells, suggesting that a specific borrelial factor related to cellular infectivity was responsible for the association.

Cytopathic effects were not observed following infection of these cell lines with B. burgdorferi, and internalized spirochetes were found to be viable.

Invasion of neural cells by B. burgdorferi provides a putative mechanism for the organism to avoid the host's immune response while potentially causing functional damage to neural cells during infection of the CNS.

PMID: 17045505 [PubMed - indexed for MEDLINE]

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Microb Pathog. 2007 Nov 19 [Epub ahead of print]

Residual brain infection in murine relapsing fever borreliosis can be successfully treated with ceftriaxone.
Larsson C, Lundqvist J, Bergström S.

Department of Molecular Biology, Laboratory for Molecular Infection Medicine Sweden (MIMS), Umeå University, SE-901 87 Umeå, Sweden.

Like several other spirochetes, relapsing fever Borrelia can cause persistent infection of the central nervous system (CNS). By treating mice harboring residual Borrelia duttonii brain infection with the bacteriocidal, cell wall inhibiting antibiotic ceftriaxone, bacteria were cleared from the brain. This shows that the residual infection is not latent but actively growing.

PMID: 18083325 [PubMed - as supplied by publisher]


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LymeEnigma
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Re: Borrelia and the Brain

Post by LymeEnigma » Tue 8 Jan 2008 19:36

GREAT articles, JoeHam!!! I'm going to have to borrow some of those! 8-)

Joe Ham
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Re: Borrelia and the Brain

Post by Joe Ham » Wed 5 Nov 2008 19:51

Interleukin 10 Protects the Brain Microcirculation From Spirochetal Injury.
October 2008.


Journal of Neuropathology & Experimental Neurology. 67(10):976-983,

http://www.jneuropath.com/pt/re/jnen/ab ... 28!8091!-1

Londono, Diana MD; Carvajal, Jenny MD; Arguelles-Grande, Carolina MD; Marques, Adriana MD; Cadavid, Diego MD

Abstract:
Spirochetal infections are an important cause of neurological disease. In previous studies of the pathogenesis of spirochetal brain infection, mice inoculated with Borrelia turicatae, an agent of tick-borne relapsing fever in North America, developed mild meningitis and parenchymal activation/infiltration by interleukin 10 (IL-10)-producing microglia/macrophages.

Here, we investigated the neuroprotective effects of IL-10 during spirochetal infection by comparing the outcomes of B. turicatae infection in wild-type and IL-10-deficient RAG2-deficient mice.
Mice were infected with either serotype 1 (Bt1), which causes more brain infection but lower bacteremia, or
Bt2, which causes less brain infection but higher bacteremia.

Interleukin 10 deficiency resulted in early death from subarachnoid/intraparenchymal brain hemorrhage in Bt2-infected mice. These mice had marked apoptosis of brain microvascular endothelial cells as assessed by terminal transferase-mediated DNA nick end-labeling staining. In contrast, Bt1 infection caused milder subarachnoid hemorrhage.
Neuronal apoptosis was observed in mice infected with both serotypes and was prominent in the cerebellum.

Neutralization of tumor necrosis factor prevented death and reduced morbidity and brain injury in mice infected by both serotypes.
We conclude that IL-10 plays a critical role protecting the cerebral microcirculation from spirochetal injury possibly by inhibition effects of tumor necrosis factor.

(C) 2008 American Association of Neuropathologists, Inc

Joe Ham
Posts: 489
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Re: Borrelia and the Brain

Post by Joe Ham » Wed 5 Nov 2008 20:23

The Journal of Infectious Diseases 2007;195:1686–1693
© 2007 by the Infectious Diseases Society of America. All rights reserved.
http://www.journals.uchicago.edu/doi/abs/10.1086/516783
0022-1899/2007/19511-0018$15.00
DOI: 10.1086/516783

Coinfection with Borrelia turicatae Serotype 2 Prevents the Severe Vestibular Dysfunction and Earlier Mortality Caused by Serotype 1

Diego Cadavid, Edwin Garcia,a and Harald Gelderbloma
Department of Neurology and Neuroscience and the Center for the Study of Emerging Pathogens, University of Medicine and Dentistry of New Jersey–New Jersey Medical School, Newark

Background. Relapsing fever (RF) is a multisystemic spirochetal infection caused by different Borrelia species. Studies in our laboratory have shown that disease severity varies depending on the infecting serotype. However, the relative contribution of each serotype to pathogenesis during mixed infections is not known. To investigate this, we compared the outcome of infection with isogenic serotypes 1 (Bt1) or 2 (Bt2) of the RF agent B. turicatae alone or in combination.

Methods. B cell–deficient mice were used for these experiments, to avoid serotype clearance by the host's variable membrane protein–specific antibodies. Observers masked to infection status examined infected and uninfected control mice for clinical disease and functional impairment for up to 65 days.

Results. All mice developed persistent infection with the serotypes with which they were originally inoculated. Severe vestibular dysfunction developed in mice infected with Bt1 alone and was associated with increased morbidity and mortality. However, coinfection with Bt2 significantly reduced the severity of vestibular dysfunction and prevented earlier mortality. In contrast, coinfection with Bt1 had little effect on the severe arthritis caused by Bt2 infection.

Conclusions. The manifestations of infection with B. turicatae are significantly influenced by the combination of serotypes present during mixed infection.

Received 1 June 2006; accepted 17 December 2006; electronically published 17 April 2007.
Reprints or correspondence: Dr. Diego Cadavid, UMDNJ–New Jersey Medical School, 185 S. Orange Ave., MSB H506, Newark, NJ 07103 (cadavidi@umdnj.edu).
Note that this was published by IDSA. What do you want to bet that it will be referenced in the next issue of the Guidelines?

Will B.turicatae read positive on a test for B. burgdorferi?

Joe Ham
Posts: 489
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Re: Borrelia and the Brain

Post by Joe Ham » Fri 28 Nov 2008 21:18

Am J Pathol. 2008 Nov;173(5):1415-27. Epub 2008 Oct 2.
Interaction of the Lyme disease spirochete Borrelia burgdorferi with brain parenchyma elicits inflammatory mediators from glial cells as well as glial and neuronal apoptosis.

http://www.ncbi.nlm.nih.gov/pubmed/18832582

Ramesh G, Borda JT, Dufour J, Kaushal D, Ramamoorthy R, Lackner AA, Philipp MT.
Division of Bacteriology and Parasitology, Tulane National Primate Research Center, Tulane University, Covington, LA 70433, USA.

Lyme neuroborreliosis, caused by the spirochete Borrelia burgdorferi, often manifests by causing neurocognitive deficits. As a possible mechanism for Lyme neuroborreliosis, we hypothesized that B. burgdorferi induces the production of inflammatory mediators in the central nervous system with concomitant neuronal and/or glial apoptosis.

To test our hypothesis, we constructed an ex vivo model that consisted of freshly collected slices from brain cortex of a rhesus macaque and allowed live B. burgdorferi to penetrate the tissue. Numerous transcripts of genes that regulate inflammation as well as oligodendrocyte and neuronal apoptosis were significantly altered as assessed by DNA microarray analysis. Transcription level increases of 7.43-fold (P = 0.005) for the cytokine tumor necrosis factor-alpha and 2.31-fold (P = 0.016) for the chemokine interleukin (IL)-8 were also detected by real-time-polymerase chain reaction array analysis. The immune mediators IL-6, IL-8, IL-1beta, COX-2, and CXCL13 were visualized in glial cells in situ by immunofluorescence staining and confocal microscopy.

Concomitantly, significant proportions of both oligodendrocytes and neurons undergoing apoptosis were present in spirochete-stimulated tissues. IL-6 production by astrocytes in addition to oligodendrocyte apoptosis were also detected, albeit at lower levels, in rhesus macaques that had received in vivo intraparenchymal stereotaxic inoculations of live B. burgdorferi.

These results provide proof of concept for our hypothesis that B. burgdorferi produces inflammatory mediators in the central nervous system, accompanied by glial and neuronal apoptosis.

PMID: 18832582 [PubMed - indexed for MEDLINE]

[apoptosis: cell death]

Joe Ham
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Re: Borrelia and the Brain

Post by Joe Ham » Fri 28 Nov 2008 21:54

Double post, sorry

Joe Ham
Posts: 489
Joined: Fri 27 Jul 2007 6:15
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Re: Borrelia and the Brain

Post by Joe Ham » Wed 17 Dec 2008 3:19

Arthritis Rheum. 2008 Dec 15;59(12):1742-9.

Role of psychiatric comorbidity in chronic Lyme disease.
http://www.ncbi.nlm.nih.gov/pubmed/19035409

Hassett AL, Radvanski DC, Buyske S, Savage SV, Gara M, Escobar JI, Sigal LH.
University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School, New Brunswick.

ABSTRACT:
OBJECTIVE: To evaluate the prevalence and role of psychiatric comorbidity and other psychological factors in patients with chronic Lyme disease (CLD).

METHODS: We assessed 159 patients drawn from a cohort of 240 patients evaluated at an academic Lyme disease referral center. Patients were screened for common axis I psychiatric disorders (e.g., depressive and anxiety disorders); structured clinical interviews confirmed diagnoses.
Axis II personality disorders, functional status, and traits like negative and positive affect and pain catastrophizing were also evaluated. A physician blind to psychiatric assessment results performed a medical evaluation.

Two groups of CLD patients (those with post-Lyme disease syndrome and those with medically unexplained symptoms attributed to Lyme disease but without Borrelia burgdorferi infection) were compared with 2 groups of patients without CLD (patients recovered from Lyme disease and those with an identifiable medical condition explaining symptoms attributed to Lyme disease).

RESULTS: After adjusting for age and sex, axis I psychiatric disorders were more common in CLD patients than in comparison patients (P = 0.02, odds ratio 2.64, 95% confidence interval 1.30-5.35), but personality disorders were not.

Patients with CLD had higher negative affect, lower positive affect, and a greater tendency to catastrophize pain (P < 0.001) than comparison patients.
All psychological factors except personality disorders were related to level of functioning.
A predictive model based on these psychological variables was confirmed.
Fibromyalgia was diagnosed in 46.8% of CLD patients.


CONCLUSION: Psychiatric comorbidity and other psychological factors distinguished CLD patients from other patients commonly seen in Lyme disease referral centers, and were related to poor functional outcomes.

Joe Ham
Posts: 489
Joined: Fri 27 Jul 2007 6:15
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Re: Borrelia and the Brain

Post by Joe Ham » Sun 4 Jan 2009 23:35

J Neuroinflammation. 2008; 5: 40. PMCID: PMC2564911
Published online 2008 September 25. doi: 10.1186/1742-2094-5-40.

Persisting atypical and cystic forms of Borrelia burgdorferi and local inflammation in Lyme neuroborreliosis
http://www.pubmedcentral.nih.gov/articl ... d=18817547

Miklossy, et al
ABSTRACT
Background
The long latent stage seen in syphilis, followed by chronic central nervous system infection and inflammation, can be explained by the persistence of atypical cystic and granular forms of Treponema pallidum. We investigated whether a similar situation may occur in Lyme neuroborreliosis.


Method
Atypical forms of Borrelia burgdorferi spirochetes were induced exposing cultures of Borrelia burgdorferi (strains B31 and ADB1) to such unfavorable conditions as osmotic and heat shock, and exposure to the binding agents Thioflavin S and Congo red. We also analyzed whether these forms may be induced in vitro, following infection of primary chicken and rat neurons, as well as rat and human astrocytes. We further analyzed whether atypical forms similar to those induced in vitro may also occur in vivo, in brains of three patients with Lyme neuroborreliosis. We used immunohistochemical methods to detect evidence of neuroinflammation in the form of reactive microglia and astrocytes.


Results
Under these conditions we observed atypical cystic, rolled and granular forms of these spirochetes. We characterized these abnormal forms by histochemical, immunohistochemical, dark field and atomic force microscopy (AFM) methods. The atypical and cystic forms found in the brains of three patients with neuropathologically confirmed Lyme neuroborreliosis were identical to those induced in vitro. We also observed nuclear fragmentation of the infected astrocytes using the TUNEL method. Abundant HLA-DR positive microglia and GFAP positive reactive astrocytes were present in the cerebral cortex.


Conclusion
The results indicate that atypical extra- and intracellular pleomorphic and cystic forms of Borrelia burgdorferi and local neuroinflammation occur in the brain in chronic Lyme neuroborreliosis. The persistence of these more resistant spirochete forms, and their intracellular location in neurons and glial cells, may explain the long latent stage and persistence of Borrelia infection. The results also suggest that Borrelia burgdorferi may induce cellular dysfunction and apoptosis. The detection and recognition of atypical, cystic and granular forms in infected tissues is essential for the diagnosis and the treatment as they can occur in the absence of the typical spiral Borrelia form.

The full version contains 74 references, most of them linked, but some are not available electronically including this provocative title. Note the date.

48.MacDonald, AB. Concurrent neocortical borreliosis and Alzheimer's disease: Demonstration of a spirochetal cyst form. Ann New York Acad Sci. 1988;539:468–470

Joe Ham
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Re: Borrelia and the Brain

Post by Joe Ham » Wed 14 Jan 2009 3:35

Mol Med. 2008 Mar–Apr; 14(3-4): 205–212.

The Pathogenesis of Lyme Neuroborreliosis: From Infection to Inflammation

Tobias A Rupprecht, et al
Department of Neurology, Ludwig-Maximilians University, Munich, Germany
http://www.pubmedcentral.nih.gov/articl ... l14_3p0205
...
Major clinical findings of the neurological manifestation of acute Lyme neuroborreliosis (LNB) include painful meningoradiculitis with inflammation of the nerve roots and lancinating, radicular pain (Bannwarth’s syndrome), lymphocytic meningitis, and various forms of cranial or peripheral neuritis (5). ...

The clinical picture of painful meningoradiculitis was first described in 1922 (6), but the etiology was unknown till the description of the causative spirochetes by Burgdorfer et al. in 1982 (7) and the isolation of spirochetes from the CSF of a patient with Bannwarth’s syndrome in 1984 (8). ...

One reason for our incomplete understanding of the mechanisms that lead to LNB is the limited availability of an adequate animal model. The only induction of reliable, clinically manifest LNB in an animal model so far was in a primate model involving the rhesus macaque, where for example, spirochetes could be demonstrated at the nerve roots (9). ...

The borrelia possess several mechanisms that enable them to escape (Figure 1) including (1) downregulation of immunogenic surface proteins, (2) inactivation of effector mechanisms, or (3) hiding in less accessible compartments like the extracellular matrix. ...

[There is no mention in this article of evasion by alternate morphologies (cysts etc).]

The most prominent clinical manifestation of Bannwarth’s syndrome is lancinating radicular pain (5), whereas patients with meningitis suffer mainly from headache and facial nerve palsy (2,95). Besides these symptoms, focal abnormalities like paresis or paresthesias are frequently observed in patients with polyradiculoneuritis or cranial neuritis (5). These symptoms are the result of a focal or diffuse neural dysfunction, but the pathophysiology is far from clear. ...

Borrelia adhere to neuronal cells. ... The adherent borrelia can be cytotoxic for the neural cells (97), and OspA induces apoptosis and astrogliosis (99). ...

[There is no mention that Bb can and does invade neurons. See Cadavid Barbour, Miklossy, above, and Livengood, Gilmore, MacDonald elsewhere. ]

On the other hand, secreted substances could injure the neural cells. Although B.b. do not possess any known endotoxin (100), cells of the host could secret neurotoxic products in response to the spirochetes. ...

Although B.b. do not possess any known endotoxin (100), cells of the host could secret neurotoxic products in response to the spirochetes. Schwann cells, for example, appear to produce nitric oxide (NO) in the rhesus monkey model of LNB (101) ...

Joe Ham
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Re: Borrelia and the Brain -- Vasculitis, Ischaemia

Post by Joe Ham » Wed 11 Feb 2009 20:43

Dev Med Child Neurol. 2009 Feb;51(2):155-8.

Local intra-arterial thrombolysis in a 4-year-old male with vertebrobasilar artery thrombosis.
http://www.ncbi.nlm.nih.gov/pubmed/19191847

Janmaat M, Gravendeel JP, Uyttenboogaart M, Vroomen PC, Brouwer OF, Luijckx GJ.
Department of Neurology, University Medical Center, University of Groningen, The Netherlands. m.janmaat@neuro.umcg.nl

We report the case of a 4-year-old male with vertebrobasilar artery thrombosis for which he was treated with local intra-arterial urokinase 60 hours after onset of symptoms. Initially the patient had dysarthria and dysphagia.

Brain magnetic resonance imaging (MRI) in a community hospital showed abnormalities in the pons, and vertebrobasilar artery thrombosis was suspected.

The patient was transferred to the university hospital because of neurological deterioration. Just before thrombolysis, his physical examination revealed a downward ocular deviation, stretching of the arms, and spontaneous movements of the legs.

Brain MRI showed recent ischaemia in the pons and caudal part of the mesencephalon, and magnetic resonance angiography showed occlusion of the basilar artery.

Intra-arterial thrombolysis with urokinase (total dose 36 000U/kg) was performed 60 hours after onset of symptoms. After thrombolysis he was treated with heparin for 10 days, followed by aspirin. The patient recovered well. After 1 year he had only minor ataxia and performed all activities at school.

Local vasculitis due to an infection with Borrelia burgdorferi was thought to be the cause of the local thrombosis.

A review of the literature revealed 11 other case reports of successful local intra-arterial thrombolysis in children and adolescents with ischaemic stroke. This suggests that intra-arterial thrombolysis is feasible and safe in selected paediatric patients with ischaemic stroke.
I don't see anything about the treatment of Bb in this abstract; it seems to focus exclusively on clearing the clot. Maybe it's mentioned in the full text but that is secured to subscribers by Wiley.

dysarthria
n : impaired articulatory ability resulting from defects in the
peripheral motor nerves or in the speech musculature

dysphagia
n : condition in which swallowing is difficult or painful

thrombolysis
n : the process of breaking up and dissolving blood clots

ischaemia
n : local anemia in a given body part sometimes resulting from
vasoconstriction or thrombosis or embolism [syn: ischemia]

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