Carotid endarterectomy vs carotid angioplasty.
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Biomedical subjects
Publications and source records attributed to A Clifton.
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The N-methyl-d-aspartate (NMDA) receptor has been implicated in the pathophysiology of schizophrenia. We administered subanesthetic doses of the NMDA receptor antagonist ketamine in a double-blind, placebo-controlled design to 13 neuroleptic-free schizophrenic patients to investigate if schizophrenics will experience an exacerbation of psychotic symptoms and cognitive impairments with ketamine. We also examined whether schizophrenics experienced quantitative or qualitative differences in ketamine response in comparison to normal controls. Schizophrenics experienced a brief-ketamine-induced exacerbation of positive and negative symptoms with further decrements in recall and recognition memory. They also displayed greater ketamine-induced impairments in free recall than normals. Qualitative differences included auditory hallucinations and paranoia in patients but not in normals. These data indicate that ketamine is associated with exacerbation of core psychotic and cognitive symptoms in schizophrenia. Moreover, ketamine may differentially affect cognition in schizophrenics in comparison to normal controls.
BACKGROUND AND PURPOSE: There has been concern about carotid percutaneous transluminal angioplasty (PTA) carrying a greater risk of cerebral ischemia than carotid endarterectomy. We set out to compare cerebral hemodynamics and microembolization during carotid PTA and CEA. METHODS: We used transcranial Doppler to monitor the middle cerebral artery of 28 patients undergoing carotid PTA (n = 14) or carotid endarterectomy (CEA) with a shunt (n = 14). Each period during which the internal carotid artery was occluded by PTA balloon or by clamp when the shunt was not in place was timed. Individual periods were summated to give a total occlusion time. Ischemic time was defined as the period for which mean middle cerebral artery velocity fell to a third or less of baseline. Microembolic signals were counted during each procedure. RESULTS: CEA resulted in significantly longer individual and total occlusion time than PTA (mean individual occlusion time, seconds), CEA, 168 +/- 51; PTA, 20 +/- 7; P < .001; mean total occlusion time; CEA, 337 +/- 70; PTA, 26 +/- 10; P < .001. Ischemic time was also significantly longer during CEA than during PTA (CEA, 165 +/- 40; PTA, 17 +/- 5; P = .001). There were significantly more microembolic signals during PTA than during CEA (mean number of microembolic signals during CEA, 52 +/- 64; during PTA, 202 +/- 119; P = .001). There was no correlation between any of the parameters measured and periprocedural stroke, which occurred in one patient in each group. CONCLUSION: PTA results in less hemodynamic ischemia but more cerebral microembolism than CEA. In this small series, however, it is not possible to comment on the relations between ischemic time, microembolism, and stroke.
BACKGROUND AND PURPOSE: Carotid percutaneous transluminal angioplasty (PTA) is a new method of treating carotid artery stenosis. There has been concern about restenosis after carotid PTA. This study was performed to ascertain the change in percent stenosis 1 year after carotid PTA. METHODS: Twelve patients with symptomatic carotid stenosis were treated by PTA, and the anatomic result was studied by digital subtraction angiography at 1 year, supplemented by duplex ultrasound examinations at 1 month and 6 months. RESULTS: The mean severity of stenosis treated, measured by the common carotid method, was 82% (range, 69% to 98%). The immediate result of PTA was a reduction in the severity of stenosis in all patients to a mean of 51% (P<.005). Six of the 12 patients showed a further improvement in lumen diameter of > or = 14% at 1-year angiographic follow-up from a mean stenosis of 47% (range, 24% to 76%) immediately after PTA to 28% (range, 0% to 52%) at 1 year. This indicates an active process of remodeling in response to carotid PTA. PTA initially reduced the stenosis by > or = 20% in 9 of the 12 arteries, and 8 of these remodeled or remained largely unchanged compared with only 1 of the 3 with a suboptimal initial dilation. In 3 patients the lumen diameter improved by < 5%. Three other patients restenosed with an increase in stenosis after PTA of 9%, 16%, and 66% at 1 year, but all were asymptomatic. The duplex findings showed that remodeling occurred at variable times between PTA and 1 year. CONCLUSIONS: Remodeling of the carotid artery after PTA has not been described before. Our results confirm that carotid angioplasty has an acceptable patency rate at 1 year. It has been suggested that endovascular treatment of carotid stenosis should include placement of a stent. Our results indicate that this may not be necessary unless the initial PTA result is a reduction in stenosis of < 20%.
We describe the successful relief of compression of the spinal cord due to a vertebral haemangioma by transcatheter embolisation using cyanoacrylate compounds before operation, and provide a brief review of the literature.
The presence of the 5HT2C receptor allele, Ser23, has recently been reported to predict favorable response to the antipsychotic drug, clozapine. This finding is of interest as Ser23, compared with the more abundant Cys23, alters pharmacological characteristics of the receptor and therefore may provide insights into the mechanism of action of antipsychotic drugs. We determined 5HT2C receptor genotype at the Cys23Ser locus in 66 subjects participating in double-blind studies of clozapine. There was no relationship between Ser23 and clozapine response (p = 0.30, Fisher's exact) nor was there any effect of Ser23 upon absolute levels of psychiatric symptoms after 10 weeks of clozapine treatment (t = -0.57, p = 0.57). These data suggest that this 5HT2C receptor polymorphism is not associated with clozapine response.
BACKGROUND AND PURPOSE: Carotid percutaneous transluminal angioplasty ( PTA) may offer an alternative treatment to carotid endarterectomy. However, in contrast to carotid endarterectomy, which has been shown to normalize impaired cerebral hemodynamics, the effects of carotid PTA are unknown. Therefore, we prospectively studied the effect of carotid PTA on both perioperative and postoperative cerebral hemodynamics. METHODS: Eleven patients undergoing carotid PTA for symptomatic carotid artery stenosis were prospectively studied. Transcranial Doppler recordings from the ipsilateral middle cerebral artery (MCA) were performed during the procedure. In addition, MCA blood flow velocity and CO2 reactivity were determined before PTA and at 2 days, 1 month, and 6 months after procedure. The results were compared with those in 11 similar patients undergoing carotid endarterectomy in whom measurements were performed before and 1 month after the operation. RESULTS: During carotid PTA, in 2 of 11 patients during passage of the balloon catheter through the stenosis, MCA blood flow velocity fell transiently. In 6 of 11 patients there was a reduction in flow velocity (>50%) during balloon deflation, but this lasted only a few seconds. After the procedure there was a significant improvement in ipsilateral hypercapnic reactivity: preoperative value, 59.8+/-42.2% (mean+/-SD); 2 days, 77.9+/-31.4%; 1 month, 88.7+/-45.0%; 6 months, 89.8+/-33.9%; and (ANOVA P=.003) preoperative value versus 1 month, P<.02; versus 6 months, P<.02. In all cases in which reactivity was significantly impaired preoperatively, it returned to the normal range. Pulsatility index also increased significantly: preoperative value, 0.827+/-0.251 (mean+/-SD); 2 days, 0.992+/-0.262 (P=.002). Contralateral MCA hypercapnic reactivity also improved after carotid PTA. There was a similar improvement in ipsilateral hypercapnic reactivity after carotid endarterectomy. CONCLUSIONS: Carotid PTA results in a normalization of impaired hemodynamics, as assessed by CO2 reactivity. The degree of improvement is similar to that seen after carotid endarterectomy.
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A 42-yr-old woman with hypertension and renal involvement due to systemic lupus erythematosus (SLE) developed unilateral headache followed by the sudden onset of confusion and a grand mal convulsion. Cerebral computed tomography was normal. A magnetic resonance imaging angiogram revealed cerebral venous thrombosis and a venous infarct. Nephrotic syndrome had resulted in an acquired protein S deficiency. A review of previous cases suggests that either renal disease with proteinuria or features of the antiphospholipid syndrome are prerequisites for the development of cerebral venous thrombosis in SLE. Low free-protein S levels may be an additional risk factor. Furthermore it is likely that this condition is underdiagnosed.
One hundred and two consecutive patients with cerebral haematoma were prospectively allocated to one of two groups according to their CT on admission. Group 1 patients were thought to have a high probability of an underlying structural lesion and underwent cerebral angiography acutely. If normal, this was repeated at three months. Group 2 patients were thought not to have such a lesion and underwent angiography at three months. Patients older than the mean age of the study population, and hypertensive patients were much less likely to harbour an aneurysm or arteriovenous malformation than younger or normotensive patients (p < 0.01; sensitivity 87.9%, specificity 88.6%). An aneurysm or arteriovenous malformation was the cause of haemorrhage in 12.8% of hypertensive patients, in 30.9% of patients with haematoma involving the basal ganglia, and 18.2% of those with posterior fossa haemorrhage. Features of CT in isolation give a sensitivity of 77.2% and a specificity of 84.2%. Follow up angiography in group 1 showed an arteriovenous malformation in one of seven patients in whom the original study was normal. These results contrast sharply with data from previous retrospective studies. The decision to investigate a patient with cerebral haematoma should be primarily based on the patient's clinical condition, rather than on the site of haemorrhage.
BACKGROUND AND PURPOSE: Carotid angioplasty may offer an effective treatment for carotid stenosis, but there has been concern about the incidence and clinical consequences of distal embolization. Transcranial Doppler monitoring in carotid endarterectomy has demonstrated embolic signals during this procedure. We used this technique in patients undergoing carotid angioplasty. METHODS: Transcranial Doppler ultrasound was used to monitor for embolic signals in the ipsilateral middle cerebral artery before and during 10 technically successful carotid angioplasties and at various standardized times in the following month. RESULTS: In the month before angioplasty asymptomatic embolic signals were detected in 3 of 10 patients. During angioplasty multiple embolic signals were detected immediately after balloon inflation in 9 of 10 subjects. A minor ipsilateral cerebral ischemic event occurred in 1 of these 9, but the other 8 were asymptomatic. Embolic signals were common immediately after the procedure and intra-arterial femoral catheter removal (8 of 10 subjects) but thereafter became less frequent and were present in 1 of 5 at 4 hours, 2 of 10 at 48 hours, 1 of 6 at 7 days, and 1 of 10 at 1 month. CONCLUSIONS: Embolization at the time of carotid angioplasty is very common but usually asymptomatic; monitoring by means of Doppler ultrasound will allow the effectiveness of measures to reduce this embolization to be studied. Late embolization occurs in a minority of patients and may account for the small but significant risk of delayed stroke. Doppler monitoring may allow identification of patients at risk and assessment of the effectiveness of prophylactic therapy.
Cerebral angiography is associated with a risk of neurological complications and air embolism may contribute towards this risk. To test this hypothesis, transcranial doppler ultrasonography was used to monitor the presence of air emboli in the middle cerebral arteries of 7 patients undergoing cerebral angiography. Doppler signals consistent with numerous air emboli were noted during each injection of radiographic contrast. This phenomenon was studied further in sheep. Radiographic contrast medium was injected into the carotid artery while a major carotid branch was insonated transorbitally. Embolic signals similar to those seen in patients were noted. Air was introduced at two points. First, at the time of drawing up the contrast into the syringe, especially with more viscous media. Standing the media before injection resulted in a highly significant reduction of air embolism, reducing the total mean duration of emboli from 1.32 (SD 0.60) s after immediate injection to 0.04 (0.05) s after ten minutes standing for iohexol 340 mg/mL (p < 0.001). Second, air was introduced at the time of injection, possibly by the formation of cavitation bubbles under pressure. This occurred most prominently with the less viscous contrast media and with saline, and was significantly reduced by slow injection (mean duration of emboli for saline 2.85 [2.43] s with fast injection compared with 0.32 [0.37] s with slow injection, p = 0.004). Air embolism may contribute towards neurological dysfunction after angiography. Measures should be taken to reduce this by allowing contrast media to stand prior to injection, and by flushing catheters with saline injected slowly.
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