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Brain abscesses are associated with high mortality and morbidity even in the antibiotic era and with complex imaging techniques, mainly because of delayed diagnosis. Several reasons can be identified: (1) the incidence of abscesses is low, about 1.1/100 000 person-year1; (2) clinical features may be non-specific without evidence of infection and with neurological signs similar to tumours, which are 50 times more frequent; (3) neuroradiological imaging may be confusing specially in the early stages.
The only way to improve the outcome of this pathology is to consider an abscess when faced with a space occupying lesion and to perform a stereotactic biopsy even in elderly or severely deteriorated patients.
Recently, in vivo 1H MR spectroscopy (MRS) was reported to give metabolic information on brain abscesses very different from that of brain tumours, permitting a non-invasive differential diagnosis between these two diseases.2
We report a case in which the diagnosis of an abscess was made on the basis of in vivo 1H MRS resulting in complete recovery.
A 50 year old woman with headache and increasing confusion over the previous 3 days was transferred to our institution. Brain CT was inconclusive and MRI showed a focal contrast enhancement near the right ventricle on T1 weighted images, after gadolinium injection. This region appeared heterogeneous on T2 and a diagnosis of glioblastoma was evoked (figure A). At the time of admission, the patient was confused and agitated. Neurological examination disclosed a left hemiparesis. There was no evidence of infection, with white blood cells at 9000/mm3 and only a slight rise in C reactive protein, despite a temperature of 37.8°C. The family reported benign dental cares 2 weeks earlier. Intravenous methylprednisolone resulted in clinical improvement and a stereotactic biopsy was planned after the performance of an in vivo 1H MR spectroscopy, applied for brain tumours at our institution. This procedure was performed on a Magnetom Vision 1.5T imager (Siemens, Erlangen, Germany) with the patient mildly sedated for 30 minutes. The volume of interest (VOI) was 20 mm×20 mm×20 mm. Two types of sequences were used: a STEAM sequence with TR 1500 ms and a short TE of 20 ms which enables many metabolites to be visualised including those with short T2 and a spin echo sequence with TR 1500 ms and a TE of 135 ms for lactate identification. Each sequence was taken from the lesion and the controlateral area. This spectrum was very unusual for a tumour, with large amounts of amino acids (0.9 ppm), lactate (1.35 ppm, inverted with TE 135 ms), and unexpected signals at 1.85 and 2.4 ppm attributed respectively to acetate and succinate. With respect to a 1H MRS spectrum of glioblastoma, N-acetyl-aspartate (NAA 2.0 ppm), creatine, and choline were present in smaller quantities (figure B). The clinical status of the patient was worsening rapidly, the possibility of an abscess was considered, and an emergency biopsy was performed. Pus (20 ml) was drawn off stereotactically and Gram stain with bacterial cultures isolated multiple organisms with an anaerobic streptococcus and haemophilus.
The pus was analysed with in vitro 1H NMR (figure C). The resonances were assigned by spiking samples with authentic standards. The main signals in the complex spectrum were those of lactate (1.33 ppm), alanine (1.48 ppm), acetate (1.92 ppm), succinate (2.41 ppm), and glycine (3.56 ppm), thus confirming the in vivo 1H NMR study.
The status of the patient improved rapidly with a 3 week intravenous antibiotic therapy with cefotaxime and metronidazole, then ceftriaxone and metronidazole for another 6 weeks. At the end of this period, in vivo 1H MRS showed amino acids remaining but no lactate present, and the NAA signal rose. The steady increase of the choline and creatine peaks expressed a process of slow recovery. Six months later, the patient had totally recovered, MRI only showed a punctiform gadolinium uptake, and the general aspect of the in vivo 1H MR spectrum was nearly normal.
The clinical diagnosis of brain abscess is difficult because barely half the patients exhibit the four main groups of symptoms: (1) increased intracranial pressure; (2) focal neurological signs; (3) systemic indication of infection; (4) known extracranial infection. Despite improvements in neuroimaging, CT guided stereotaxy,3 and newer antibiotics, this so called benign pathology kills one patient out of four, sometimes only because of delayed diagnosis. Radiologically, an abscess can mimic a brain tumour whether it be in the collected stage or, even more so, in the early stages of cerebritis.4 Misdiagnosis as a brain tumour can lead to inappropriate corticotherapy, resulting in a clinical worsening as happened in our patient, or in a dramatic intraventricular rupture with mortality as high as 80%.5 Thus diagnosis cannot rely only on clinical and radiological features; stereotactic aspiration is mandatory.
In vivo 1H MRS can provide metabolic information on the development of a brain abscess. Actually, a metabolic degradation due to bacteria is responsible for the appearance of characteristic compounds such as acetate and succinate, end products of carbohydrate metabolism, and an amino acid peak linked with the reaction of polynuclear leucocytes against bacterial aggression. Lactate was also found but its bacterial origin was not certain. Moreover, a decrease of neuron density, energy metabolism failure, and phosphomembrane breakdown were expressed respectively by loss of NAA, creatine, and choline. The brain tumour spectra are different as acetate, succinate, and amino acids have never been reported.2 High levels of succinate and acetate have been detected in the 1H NMR spectrum of aspirated abscess material.2
After 3 weeks of intravenous antibiotic therapy, succinate, acetate, and lactate were absent, indicating a return to an aseptic condition. Nevertheless, aminoacids were still present. As they are only indirect consequences of bacterial development, they were not modified sooner by antibiotic treatment. The increases in NAA, choline, and creatine indicated a progressive return to a normal metabolism. Six months later, MRI and the brain spectrum were normal.
This work was supported by grant No 6635 from the Association pour la Recherche sur le Cancer.
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