Bacterial DNA findings in ruptured and unruptured intracranial aneurysms.

OBJECTIVE: Chronic inflammation has earlier been detected in ruptured intracranial aneurysms. A previous study detected both dental bacterial DNA and bacterial-driven inflammation in ruptured intracranial aneurysm walls. The aim of this study was to compare the presence of oral and pharyngeal bacterial DNA in ruptured and unruptured intracranial aneurysms. The hypothesis was that oral bacterial DNA findings would be more common and the amount of bacterial DNA would be higher in ruptured aneurysm walls than in unruptured aneurysm walls. MATERIALS AND METHODS: A total of 70 ruptured (n = 42) and unruptured (n = 28) intracranial aneurysm specimens were obtained perioperatively in aneurysm clipping operations. Aneurysmal sac tissue was analysed using a real-time quantitative polymerase chain reaction to detect bacterial DNA from several oral species. Both histologically non-atherosclerotic healthy vessel wall obtained from cardiac by-pass operations (LITA) and arterial blood samples obtained from each aneurysm patient were used as control samples. RESULTS: Bacterial DNA was detected in 49/70 (70%) of the specimens. A total of 29/42 (69%) of the ruptured and 20/28 (71%) of the unruptured aneurysm samples contained bacterial DNA of oral origin. Both ruptured and unruptured aneurysm tissue samples contained significantly more bacterial DNA than the LITA control samples (p-values 0.003 and 0.001, respectively). There was no significant difference in the amount of bacterial DNA between the ruptured and unruptured samples. CONCLUSION: Dental bacterial DNA can be found using a quantitative polymerase chain reaction in both ruptured and unruptured aneurysm walls, suggesting that bacterial DNA plays a role in the pathogenesis of cerebral aneurysms in general, rather than only in ruptured aneurysms.

The connection between ruptured cerebral aneurysms and odontogenic bacteria.

BACKGROUND: Patients with ruptured saccular intracranial aneurysms have excess long-term mortality due to cerebrovascular and cardiovascular diseases compared with general population. Chronic inflammation is detected in ruptured intracranial aneurysms, abdominal aortic aneurysms and coronary artery plaques. Bacterial infections have been suggested to have a role in the aetiology of atherosclerosis. Bacteria have been detected both in abdominal and coronary arteries but their presence in intracranial aneurysms has not yet been properly studied. OBJECTIVE: The aim of this preliminary study was to assess the presence of oral and pharyngeal bacterial genome in ruptured intracranial aneurysms and to ascertain if dental infection is a previously unknown risk factor for subarachnoid haemorrhage. METHODS: A total of 36 ruptured aneurysm specimens were obtained perioperatively in aneurysm clipping operations (n=29) and by autopsy (n=7). Aneurysmal sac tissue was analysed by real time quantitative PCR with specific primers and probes to detect bacterial DNA from several oral species. Immunohistochemical staining for bacterial receptors (CD14 and toll-like receptor-2 (TLR-2)) was performed from four autopsy cases. RESULTS: Bacterial DNA was detected in 21/36 (58%) of specimens. A third of the positive samples contained DNA from both endodontic and periodontal bacteria. DNA from endodontic bacteria were detected in 20/36 (56%) and from periodontal bacteria in 17/36 (47%) of samples. Bacterial DNA of the Streptococcus mitis group was found to be most common. Aggregatibacter actinomycetemcomitans, Fusobacterium nucleatum and Treponema denticola were the three most common periodontal pathogens. The highly intensive staining of CD14 and TLR-2 in ruptured aneurysms was observed. CONCLUSIONS: This is the first report showing evidence that dental infection could be a part of pathophysiology in intracranial aneurysm disease.

Long-term MRI findings of patients with embolized cerebral aneurysms.

BACKGROUND: Long-term follow-up studies after endovascular treatment for intracranial aneurysm are still rare and inconclusive. Parenchymal infarctions related to aneurysms have mostly been studied in patients with subarachnoidal hemorrhage (SAH) but infarction rates in patients with endovascularly treated unruptured aneurysms have been little studied. PURPOSE: To determine the frequency of permanent parenchymal lesions as detected in magnetic resonance imaging (MRI) in patients treated with endovascular coiling and to assess aneurysm-related infarctions after the initial treatment period. MATERIAL AND METHODS: A total of 64 patients (32 with primarily ruptured aneurysms) with 69 embolized aneurysms were examined neurologically and by MRI and magnetic resonance angiography (MRA) more than 9 years after the initial endovascular treatment. RESULTS: A total of 14 out of 32 (44%) SAH patients and 11 (34%) patients with unruptured aneurysms had parenchymal lesions in MRI. Infarctions were detected in 10 (31%) SAH patients and the majority (9/10, 90%) of them were aneurysm-related. All aneurysm-related infarctions were detected at the acute hospitalization stage. A total of six (55%) out of 11 infarctions in patients with unruptured aneurysms were aneurysm-related and two of them appeared after the treatment period. Patients with infarction had poorer clinical outcome than patients with no ischemic lesions in MRI. CONCLUSION: Nineteen percent of patients with unruptured and 41% with ruptured aneurysms had aneurysm-related parenchymal lesions in MRI. Most of these were detected during acute treatment period. Aneurysm-related infarctions after treatment period are uncommon.

Long term outcome after subarachnoid haemorrhage of unknown aetiology.

BACKGROUND AND PURPOSE: The aim of this study was to assess the long term outcome after non-aneurysmal subarachnoid haemorrhage (SAH). METHODS: 1154 patients with SAH were treated in our hospital between 1989 and 1999. From this patient population, 97 patients had a non-aneurysmal SAH. All hospital records and death certificates were studied and 33 patients were examined by MRI and MR angiography more than 9 years (mean 12 years) after the initial bleeding. RESULTS: The cohort consisted of 97 patients. Mean follow-up time was 9 years (range 0-19). During the follow-up period, 13 patients (13%) died. Four (4%) died from the initial bleeding less than 5 weeks after the initial haemorrhage. There was no delayed mortality due to SAH or subsequent bleedings. MR angiography revealed no new findings in 33 surviving patients. CONCLUSIONS: Excess mortality during the first year after SAH was higher than 4%, and remained thereafter comparable with the general population. There were no rebleedings and MR imaging did not reveal any vascular pathology that could explain the earlier SAH.