Here's a few particularly relevant results from about 5 minutes of browsing, using first "brain lesion borreliosis" then "white matter lesion Lyme."
Neurol Sci. 2004 Apr;25(1):30-3.
Isolated monolateral neurosensory hearing loss as a rare sign of neuroborreliosis.
Iero I, Elia M, Cosentino FI, Lanuzza B, Spada RS, Toscano G, Tripodi M, Belfiore A, Ferri R.
Department of Neurology, Oasi Institute for Research on Mental Retardation and Brain Aging, Via Conte Ruggero 73, I-94018 Troina (EN), Italy. [email protected]
Lyme disease, or borreliosis, is a zoonosis transmitted by Borrelia burgdorferi which also involves the central nervous system (CNS), in 15% of affected individuals, with the occurrence of aseptic meningitis, fluctuating meningoencephalitis, or neuropathy of cranial and peripheral nerves.
Encephalopathy with white matter lesions revealed by magnetic resonance imaging (MRI) scans in late, persistent stages of Lyme disease has been described.
In this report, we describe a patient with few clinical manifestations involving exclusively the eighth cranial nerve, monolaterally and diffuse bilateral alterations of the white matter, particularly in the subcortical periventricular regions at cerebral MRI.
This single patient study shows that the search for antibodies against Borrelia burgdoferi should always be performed when we face a leukoencephalopathy of unknown origin. An isolated lesion of the eighth cranial nerve can be the only neurologic sign in patients with leukoencephalopathy complicating Lyme disease.
Regional cerebral blood flow and cognitive deficits in chronic lyme disease.
Fallon BA, Keilp J, Prohovnik I, Heertum RV, Mann JJ.
The NYS Psychiatric Institute, New York, New York 10032, USA.
This study examined brain functioning in patients with Lyme encephalopathy. Eleven patients underwent neuropsychological tests and Xenon(133)-regional cerebral blood flow (rCBF) studies, using an external detector system. Each rCBF scan was age- and sex-matched to two archival, normal controls. While few differences were noted on gray-matter flow indices (ISI, fg), Lyme patients demonstrated significant flow reductions in white matter index (k(2)) (p=.004), particularly in the posterior temporal and parietal lobes bilaterally (p=.003). Flow reductions in white matter areas were significantly associated with deficits in memory (r=.66, p=.027) and visuospatial organization (r=.62, p=.041). Results suggest that Lyme encephalopathy may be a disease primarily affecting the cerebral white matter.
PMID: 12928508 [PubMed - indexed for MEDLINE]
Neurology. 2001 Dec 11;57(11):1980-5.
FLAIR and magnetization transfer imaging of patients with post-treatment Lyme disease syndrome.
Morgen K, Martin R, Stone RD, Grafman J, Kadom N, McFarland HF, Marques A.
Neuroimmunology Branch, National Institute of Neurological Disorders and Stroke, NIH, Bethesda, MD 20892-1400, USA.
OBJECTIVE: To determine patterns of abnormalities on cerebral MRI that may characterize subgroups of patients with post-treatment Lyme disease syndrome (PTLDS) and to help identify pathomechanisms of disease.
METHODS: The authors analyzed the distribution of cerebral lesions in a cohort of 27 patients with PTLDS. A subgroup of eight patients with PTLDS was further studied using whole-brain magnetization transfer ratio measures to identify abnormalities not seen on T2-weighted images.
RESULTS: Four patients had focal neurologic deficits, relapsing-remitting disease, and lesions in a distribution typical of MS. Twenty-three patients presented with nonfocal symptoms such as fatigue, subjective memory deficits, and mood disturbance. Twelve of these patients had normal MRI, including the more sensitive fluid-attenuated inversion recovery sequence, 10 had primarily punctate and subcortical lesions, and one patient had multiple periventricular lesions.
CONCLUSIONS: In a portion of patients with post-treatment Lyme disease syndrome, white-matter hyperintensities tend to occur in subcortical arteriolar watershed areas and are not specific. Magnetization transfer ratio analysis did not provide evidence for structural abnormalities of the brain parenchyma in patients with nonfocal disease.
PMID: 11739813 [PubMed - indexed for MEDLINE]
Neurol Neurochir Pol. 2001 Sep-Oct;35(5):803-13.
[Neuroborreliosis: CT and MRI findings in 14 cases. Preliminary communication]
[Article in Polish]
Tarasow E, Ustymowicz A, Zajkowska J, Hermanowska-Szpakowicz T.
Zakladu Radiologii Akademii Medycznej w Bialymstoku.
Since 1987 when Januszkiewicz and Kieda first described borreliosis, it is commonly recognized as infection of the nervous system in Poland, especially in north-east region.
The diagnosis of the disease is mainly based on typical clinical signs, supported by serological testing.
In 14 patients with clinical symptoms of neuroborreliosis CT and MR were performed to evaluate CNS changes. MR examinations were abnormal in 36%.
Most patients (60%) presented cerebral atrophy. In 2 cases areas of abnormal signal were identified within cerebral white matter as well as within the brain stem. In the first case it was, recognized as demyelination focus, in second one MR showed evidence of or were suggestive of vascular involvement. In one case symmetrical calcifications were also found in internal capsules. Neuroradiological signs in Lyme disease are not specific. Neuroborreliosis has to be considered when patients present foci of hyperintense signal (T2-weighted images) in white matter and brain stem.
Publication Types: Case Reports
PMID: 11873593
Neurol Sci. 2004 Apr;25(1):30-3.
Isolated monolateral neurosensory hearing loss as a rare sign of neuroborreliosis.
Iero I, Elia M, Cosentino FI, Lanuzza B, Spada RS, Toscano G, Tripodi M, Belfiore A, Ferri R.
Department of Neurology, Oasi Institute for Research on Mental Retardation and Brain Aging, Via Conte Ruggero 73, I-94018 Troina (EN), Italy. [email protected]
Lyme disease, or borreliosis, is a zoonosis transmitted by Borrelia burgdorferi which also involves the central nervous system (CNS), in 15% of affected individuals, with the occurrence of aseptic meningitis, fluctuating meningoencephalitis, or neuropathy of cranial and peripheral nerves.
Encephalopathy with white matter lesions revealed by magnetic resonance imaging (MRI) scans in late, persistent stages of Lyme disease has been described.
In this report, we describe a patient with few clinical manifestations involving exclusively the eighth cranial nerve, monolaterally and diffuse bilateral alterations of the white matter, particularly in the subcortical periventricular regions at cerebral MRI.
This single patient study shows that the search for antibodies against Borrelia burgdoferi should always be performed when we face a leukoencephalopathy of unknown origin. An isolated lesion of the eighth cranial nerve can be the only neurologic sign in patients with leukoencephalopathy complicating Lyme disease.
Publication Types: Case Reports
PMID: 15060815 [PubMed - indexed for MEDLINE]
Presse Med. 2003 Oct 18;32(34):1607-9.
[Acute severe leukoencephalitis with posterior lesions due to Borrelia burgdorferi infection]
[Article in French]
Drouet A, Meyer X, Guilloton L, Mullet JP, Dusseau JY, Denoyel GA, Felten D.
Service de neurologie, HIA Desgenettes Lyon (69).
INTRODUCTION: Central nervous system manifestations represent 0.54 to 8% of neurological complication in Lyme disease.
OBSERVATION: A 78-year-old woman presented a severe meningo-encephalitis with visual disorders (agnosia, alexia) progressing towards coma.
Cranial magnetic resonance imaging revealed large areas of hypersignal T2 in the white matter of the lower, parieto-occipital lobes and left temporal lobe.
The cerebrospinal fluid (CSF) contained 16 then 293 white corpuscles/mm3 of lympho-monocytes, increased protein level from 2.67 to 5.83 g/l and an increase in IgG index with oligoclonal distribution of IgG.
Serological Elisa analysis for Lyme disease was slightly positive in blood (confirmed by western blot) but clearly in the CSF (IgG and IgM). Treatment with ceftriaxone followed by methylprednisolone provided clinical improvement 3 months later.
DISCUSSION: Acute meningo-encephalitis is often benign, protein-like and of good prognosis: the gnosic visual disorders with posterior leukoencephalopathy are unusual. A blood level of specific antibodies slightly positive on Elisa at the early stage of the infection warrants confirmation by Western blot in the blood and by Elisa in the CSF. Additional corticosteroid therapy may be required in the severe forms that evoke acute disseminated encephalomyelitis.
Publication Types: Case Reports
PMID: 14576583
Brain. 1996 Dec;119 ( Pt 6):2143-54.
Inflammatory brain changes in Lyme borreliosis. A report on three patients and review of literature.
Department of Internal Medicine, Turku University Central Hospital, Finland.
Despite a rapid increase in the number of patients with Lyme neuroborreliosis (LNB), its neuropathological aspects are poorly understood.
The objective of this study was evaluation of neuropathological, microbiological, and magnetic resonance imaging (MRI) findings in three patients with the Borrelia burgdorferi infection and neurological disease from whom brain tissue specimens were available.
Perivascular or vasculitic lymphocytic inflammation was detected in all specimens. Large areas of demyelination in periventricular white matter were detected histologically and by MRI in one patient. The disease had a fatal outcome in this patient. Brain MRI suggested malignancies in two patients before histopathological studies were carried out. One of these two patients was a child with sudden hemiparesis. Another was a 40-year-old man presenting with epileptic seizures and MRI-detected multifocal lesions, which disappeared after repeated courses of antibiotics.
We conclude that cerebral lymphocytic vasculitis and multifocal encephalitis may be associated with B. burgdorferi infection. The presence of B. burgdorferi DNA in tissue samples from areas with inflammatory changes indicates that direct invasion of B. burgdorferi may be the pathogenetic mechanism for focal encephalitis in LNB.
Publication Types: Case Reports
PMID: 9010017
Posted by seibertneurolyme (Member # 6416) on :
An easier to remember address for the same website given above is http://www.pubmed.com
Search here on LymeNet under either lesions or MRI for lots of discussion of this topic.
Bea Seibert
Posted by welcome (Member # 7953) on :
Thanks for the response.
A note. For several years I've been a regular on many boards (various discussion topics). I've noticed a tendency for some to "remind" posters to do their own searches.
Being perfectly capable of, and having actually performed hundreds if not thousands of searches, when I post to a board, I consider it speaking live to those who are there, which I consider different than putting up a note and waiting for someone to read it later. Please don't construe me asking for other information as a lack of ability or laziness. It's more of a real-time thing for me. I'm merely looking to utilize the power of the collective. Posted by bpeck (Member # 3235) on :
I have 2 friends, both documented Lyme patients by conventional testing, both had severe neuro symptoms, and both had NUMEROUS MRIs showing lesions changing over time.
Both had all the research papers indicating lesions can be produced by Lyme.
Long story short- one of them ended up have the head nero at Mt Siani argue with the head neuro at Darmouth Hitchcock about whether it was Lyme causing the results seen in the MRI or 'some other disorder" or both.
Basically - it was a unbelievable waste of money time and emotion.
So, I never even went down the MRI road.
Barb
Posted by Michelle M (Member # 7200) on :
Hello, Welcome. I have brain lesions; fierce headaches were my first clue to Lyme. My neuro duck refused to consider Lyme, insisting I had MS or possibly even just migraines. However, my radiologist is MUCH smarter than my neurologist. When he read my MRI films, he thought that my lesions were too big to be the "spots" that occur with migraines. (Some up to 5 mm). Also, he felt they were in the wrong place for MS (mainly frontal lobe.)
So while location and characteristics of lesions don't absolutely rule out other things (like MS, etc), they can sure POINT to certain things.
My neuro duck hates to be wrong. He refused me a western blot following my negative ELISA. When I got a CDC positive IGeneX Western Blot through an LLMD and faxed it to him, he was very annoyed. He refused to tell me how many lesions I had. He said, "That's not my job." So I talked to the radiologist, who was very kind, and told me I had 11.
I believe there are several others on LymeNet with lesions. Wish your post title had been more specific to the subject -- they may miss it!
I've read (though don't have links) that brain lesions can be reversed or disappear. I've also read that some may not get better, but at least might not get worse. Seems like it's about a 50/50 thing. Wish there was more known in that regard.
Good luck to your friend!
Michelle
Posted by Lymetoo (Member # 743) on :
You can also go to the search function and type in MS and Lyme. There should be plenty of references to the brain lesions.
Posted by Marnie (Member # 773) on :
White matter lesions (WMLs) and blood-brain barrier (BBB) dysfunction are common in dementia.
J Alzheimers Dis. 2004 Dec;6(6):639-649. Borrelia burgdorferi persists in the brain in chronic lyme neuroborreliosis and may be associated with Alzheimer disease.
University Institute of Pathology, Division of Neuropathology, University Medical School (CHUV), 1011, Lausanne, Switzerland. and University of British Columbia, Department of Psychiatry, Kinsmen Laboratory of Neurological Research, Vancouver, B.C. V6T 1Z3, Canada.
The cause, or causes, of the vast majority of Alzheimer's disease cases are unknown. A number of contributing factors have been postulated, including infection.
It has long been known that the spirochete Treponema pallidum, which is the infective agent for syphilis, can in its late stages cause dementia, chronic inflammation, cortical atrophy and amyloid deposition.
Spirochetes of unidentified types and strains have previously been observed in the blood, CSF and brain of 14 AD patients tested and absent in 13 controls.
In three of these AD cases spirochetes were grown in a medium selective for Borrelia burgdorferi. In the present study, the phylogenetic analysis of these spirochetes was made.
Positive identification of the agent as Borrelia burgdorferi sensu stricto was based on genetic and molecular analyses. Borrelia antigens and genes were co-localized with beta-amyloid deposits in these AD cases.
The data indicate that Borrelia burgdorferi may persist in the brain and be associated with amyloid plaques in AD. They suggest that these spirochetes, perhaps in an analogous fashion to Treponema pallidum, may contribute to dementia, cortical atrophy and amyloid deposition.
Further in vitro and in vivo studies may bring more insight into the potential role of spirochetes in AD.
PMID: 15665404 [PubMed
Now...want Alzheimers and MS files and a brain damage file...how to arrest?
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