Neuronal loss or dysfunction in patients with early Lyme neuroborreliosis

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Sproetje
Berichten: 3121
Lid geworden op: Di 28 Okt 2014, 20:33

Neuronal loss or dysfunction in patients with early Lyme neuroborreliosis

Berichtdoor Sproetje » Wo 14 Aug 2019, 18:09

Neuronal loss or dysfunction in patients with early Lyme neuroborreliosis: a proton magnetic resonance spectroscopy study of the brain

Adam Garkowski Bożena Kubas Marcin Hładuński Joanna Zajkowska Olga Zajkowska Dorota Jurgilewicz Radosław Zawadzki Ewa Garkowska Sławomir Pancewicz Urszula Łebkowska
10 Mei 2019

https://link.springer.com/article/10.10 ... 19-09359-0

Abstract

Background
We hypothesized that since Borrelia burgdorferi causes systemic inflammation and infects the brain, it may lead to alterations in cerebral metabolism, as measured by 1H-magnetic resonance spectroscopy (1H-MRS). The purpose of our study was to determine whether 1H-MRS could detect brain metabolite alterations in patients with early Lyme neuroborreliosis (LNB) in normal-appearing brain tissue on the conventional magnetic resonance imaging (MRI).

Methods
Twenty-six patients diagnosed with early LNB and twenty-six healthy volunteers as a control group have been involved in the study. All of them underwent routine MRI protocol using 3.0-T MRI scanner. 1H-MRS examinations were performed with repetition time (TR) = 2000 ms, and echo time (TE) = 135 ms. Single voxels were positioned in the anterior and posterior parts of the right and left frontal lobes.

Results
We found a statistically significant decrease of the N-acetylaspartate/creatine ratio within the anterior part of the right and left frontal lobes (p ≤ 0.001 and p = 0.001 respectively) and in the posterior part of the right and left frontal lobes (p ≤ 0.001 and 0.031) in the patients with LNB.

Conclusion
A significant reduction in NAA/Cr ratio in comparison with the controls suggests the presence of diffuse neuronal loss in patients with early LNB.

Introduction

Lyme borreliosis (or Lyme disease) is a tick-transmitted multisystem inflammatory disease caused by the spirochete Borrelia burgdorferi sensu lato genospecies complex, and is the most common arthropod-borne disease in temperate regions of the northern hemisphere.
In Europe, this disease affects approximately 65,500 patients annually.
Lyme neuroborreliosis (LNB) is a disease of the nervous system, occurring in 10–15% of all Lyme borreliosis cases, and can occur at any stage of the disease, and may affect both the central (CNS) and peripheral nervous system.
LNB is more common in Europe than in the United States, and typically manifests as Bannwarth’s syndrome including lymphocytic meningitis, cranial neuritis, and radiculoneuritis.These manifestations can occur separately or together [1, 2].
The direct symptoms of CNS involvement vary widely, and may result, e.g., in symptoms such as a headache, difficulty with concentration, mood swings, disturbance of consciousness or Parkinson-like symptoms, and cerebrovascular complications like stroke caused by cerebral vasculitis [2, 3].

It is known that B. burgdorferi has a tropism for the meninges in the CNS and for connective tissues elsewhere in the body.
Autopsy brain studies on patients with LNB are limited to single case reports or small case series. These studies showed, inter alia, diffuse demyelination of the cerebral and cerebellar white matter with diffuse astrocytosis [4], and rhombencephalopathy with microgliosis and obliterative inflammatory vasculitis associated with ischemic strokes [5].
In a recent study of an animal model of systemic inflammation, Ramesh et al., conducted an investigation to examine the role of inflammation on the CNS of Rhesus macaques infected intrathecally with B. burgdorferi.
Histological studies of brain tissue from R. Macaques at necropsy performed early after infection, revealed, inter alia, leptomeningitis in the brain and spinal cord, vasculitis in the brainstem, focal inflammation in the CNS, and inflammation with neurodegeneration in the dorsal root ganglia that was concomitant with significant neuronal and glial cell apoptosis [6]. Neuroimaging studies are relatively insensitive in detecting the primary changes of B. burgdorferi-associated encephalitis.
On conventional magnetic resonance imaging (MRI), the positive neuroimaging findings of patients with LNB are comparatively unusual. These findings are usually focal hyperintense lesions on T2-weighted images in the white matter of the brain or the nerve root or meningeal enhancement [7]. Sometimes imaging features may mimic primary demyelinating disease [8].

We hypothesized that since B. burgdorferi causes systemic inflammation and infects the brain, leading to impaired CNS function, it may lead to alterations in cerebral metabolism, as measured by in vivo 1H-magnetic resonance spectroscopy (1H-MRS).

1H-MRS is a non-invasive feasible method for in vivo quantification of several brain metabolites including N-acetylaspartate (NAA), choline-containing compounds (Cho), creatine (Cr), myo-inositol (mI) and glutamate–glutamine. Until now, 1H-MRS has been used as a research and clinical tool for detecting pathological changes visible or not yet visible on conventional MRI. The advantage of this method is the possibility to provide information about metabolite alterations in the brain, while MRI fails to reveal any morphological abnormalities [9].

The purpose of our study was to determine whether 1H-MRS could detect brain metabolite alterations in patients with early LNB in normal-appearing brain tissue on the conventional MRI study compared with healthy controls. We decided to use the long echo time (TE) of 135 ms for a more precise evaluation of changes in the NAA/Cr ratio.
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