Institut National de la Santé et de la Recherche Médicale, U 460, Batiment INSERM 13, 46 rue Henri Huchard, 75018 Paris, France. coutard@bichat.inserm.fr
The role of the arterial sympathetic innervation in cerebrovascular pathology was investigated in new experimental models using Brown Norway (BN) and Long-Evans (LE) rats. The BN rat is susceptible to intracerebral hemorrhage (ICH) within the cerebral cortex when rendered hypertensive whereas the LE rat is prone to cerebral aneurysms (CAs) in arteries of the circle of Willis with hypertension and carotid ligation. Noradrenaline (NA) content, determined by high performance liquid chromatography (HPLC), was lower both in the caudal and cerebral arteries in the BN than in the LE rat. Denervation of cerebral arteries by superior cervical ganglionectomy did not increase ICH lesion incidence in BN hypertensive rats. A possible link between the level of caudal artery NA content and the occurrence of ICH lesions and CAs was studied in rats from two distinct BNXLE crosses: back-cross (BC) rats (F1XBN) and F2 rats (F1XF1) which respectively display, with hypertension and carotid ligation, a high incidence of either ICH lesions or CAs. In BC rats, the level of caudal artery NA content was not related to ICH lesion occurrence. However, in F2 rats a low caudal artery NA content was associated with a high incidence of ruptured CAs. Thus, a low arterial sympathetic innervation may participate in mechanisms leading to rupture of CAs.
Cavernous carotid origin aneurysm rupture with intracerebral intraparenchymal hemorrhage after treatment of a traumatic Barrow type A cavernous carotid artery fistula.
This case report demonstrates delayed rupture of a cavernous carotid fistula and aneurysm into the temporal lobe 12 years after treating a direct cavernous carotid artery fistula using detachable silicon balloons. The ultimate treatment was performed using arterial endovascular sacrifice. Successful treatment of cavernous carotid fistulas may ultimately lead to formation of cavernous aneurysms. Although these lesions rarely cause intraparenchymal hemorrhage, the risk for such an event must be taken into consideration when patients are treated for the initial lesion.
Due to an increase in age of the patient population in cardiac surgery, cerebral complications are increasing in frequency, also as a cause of death. In order to reveal cerebral pathology associated with a fatal outcome after cardiac surgery, we re-evaluated the cast angiographs and medico-legal autopsy documents of 144 adult cardiac surgery subjects over a 7-year period. Special attention was paid to the ability of post-mortem cast angiography to aid in diagnosing cerebral pathology. The autopsy detected new ischemic cerebral lesions in 29 (20%) cases, of which 22 (15.3%) were recent infarcts, and 7 were cases of anoxic brain damage. Of the recent cerebral infarcts, 12 were associated with cerebral artery thrombosis, 4 showed multiple lesions, and the remaining 6 were small single infarcts. In addition, one subject had an intracerebral hemorrhage and 72 (50%) cerebral edema. By cast angiography, the leakage of contrast medium in the case of intracerebral hemorrhage and stenoses of intracranial and cervical arteries could be well demonstrated and also revealed 17 (77%) of the 22 recent cerebral infarcts. It was found to be suitable for detecting recent brain infarcts associated with main cerebral artery thrombosis, with a sensitivity of 92% (11 out of 12 cases), but was less sensitive in showing small recent infarcts with a sensitivity of 60% (6 out of 10 cases) and inferior for the older ones where none of the 6 cases were detected. Filling defects caused by cerebral edema were difficult to differentiate from technical errors and were encountered in 7 (4.8%) cases. A significant predictor for the 29 recent ischemic brain lesions was perioperative hypotension. The immediate cause of death was most often of cardiac (83%) and cerebral (14%) origin. In 14 cases, cerebral damage was considered to be an additional cause of death. The use of cerebral post-mortem cast angiography should be recommended, especially for its excellent ability to visualize intravascular pathology such as arterial stenoses and thromboses, with a 92% sensitivity in showing new main cerebral artery thromboses, before likely distortion of the vascular anatomy by dissection.
Cerebral stroke is a serious complication related to carotid endarterectomy (CEA), being most frequently caused by thromboembolic events and less frequently on account of cerebral haemorrhage. The present series comprised five out of 857 (0.6%) patients who had undergone CEA at Oulu University Hospital between the years 1974 and 1993 and suffered a postoperative stroke four to 13 days after surgery due to intracerebral haemorrhage (IH). Preoperatively, all these patients were neurologically intact, with transient ischaemic attacked (TIA) as the main indication for CEA. All five patients had a history of arterial hypertension treated adequately preoperatively, and one patient had high blood pressure levels after surgery. Critical ipsilateral stenosis of the internal carotid artery (> 90%) was detected in the preoperative angiogram in all five cases. The primary outcome after CEA was uneventful in every case, without any signs of neurological deficiency. The symptoms, comprising severe headache, convulsions and/or hemiparesis occurred suddenly four to 13 days (mean seven days) after CEA. The diagnosis of IH was based on computed tomography (CT) findings. All five patients were treated conservatively. Three of them died. We conclude that even normotensive, neurologically intact patients without demonstrable cerebral infarction or postoperative hypertension may suffer cerebral haemorrhage after the relief of high-grade carotid stenosis. The role of possible insufficiency of the autoregulatory mechanisms of the cerebral vasculature on account of long-standing critical stenosis of the internal carotid artery and subsequent uncontrolled hyperperfusion following CEA are discussed.
We report results of clinical examinations, computed tomography, quantitative electroencephalography (QEEG), and cerebral blood flow measurements performed on a series of 56 consecutive brain injury patients including 15 alcohol abusers and 41 non-alcoholic subjects. Greater volumes of intracranial haemorrhage were noted in the alcoholics for a similar severity of injury and local brain atrophy became more pronounced in them during a follow-up of 1 year. After this time, the third ventricle width, distance between frontal horns, the sum of lateral ventricle dimensions and cortical sulci were all markedly larger in the alcoholics. The QEEG results also indicated a weaker improvement in the alcoholics. The cerebral blood flow at the site of the injury was initially slow in the alcoholics when compared to the contralateral region of the other hemisphere, although these differences disappeared during the follow-up. Permanent occupational disability was also found to be associated with pretraumatic alcohol abuse. The findings indicate that ethanol abuse is not only commonly associated with cerebral trauma but is also a risk factor for a more severe brain damage following the injury.
Combined surgical and endovascular access of the superficial middle cerebral vein to occlude a high-grade cavernous dural arteriovenous fistula: case report.
High-grade cavernous sinus (CS) dural arteriovenous fistulae with cortical venous drainage often have a malignant presentation requiring urgent treatment. In the absence of a venous access to the lesion, transarterial embolization can potentially cure these lesions; however, the high concentration of eloquent arterial territories adjacent to the fistula creates a precarious risk of arterial-arterial reflux. In such cases, a combined surgical and endovascular approach may provide the least invasive option.
We describe a patient presenting with a venous hemorrhagic infarct caused by a high-grade CS dural arteriovenous fistula (Barrow type D caroticocavernous fistula) with isolated drainage via the superficial middle cerebral vein into engorged perisylvian cortical veins. No transfemoral or ophthalmic strategy was angiographically apparent, and the posterior location of the involved CS compartment mitigated a direct puncture. The patient underwent direct puncture of the superficial middle cerebral vein via an orbitozygomatic craniotomy and the CS was catheterized under fluoroscopic guidance. The CS was coil-embolized back into the distal superficial middle cerebral vein with complete obliteration of the fistula. The patient did well with no new deficits and made an uneventful recovery.
This novel combined open surgical and endovascular approach enables obliteration of a CS dural arteriovenous fistula with isolated cortical venous drainage and avoids the additional manipulation with direct dissection and puncture of the CS itself.
