Early carotid surgery in patients after acute ischemic stroke: is it safe? A retrospective analysis in a single center between early and delayed/deferred carotid surgery on 285 patients.

BACKGROUND: The early risk of stroke after transient ischemic attack (TIA)/stroke is of the order of 5-10% at 1 week and 10-20% at 3 months. Even if carotid endarterectomy (CEA) is the treatment of choice in symptomatic internal carotid artery stenosis, the timing of carotid intervention after acute stroke is not yet codified. The authors want to determinate whether early CEA is safely carried out in the first few hours (<48 hours) successive to the nondebilitating neurological event and whether the outcome (TIA/stroke/death) in these cases is comparable with the results of those treated by delayed/deferred surgery (range, 48 hours-24 weeks). METHODS: In 4 years, the authors performed 1,184 CEA (285 symptomatic). Five groups were formed from 285 symptomatic patients, according to interval between TIA/stroke onset and performance of CEA: G1, less than 48 hours; G2, 48 hours-2 weeks; G3, 2-4 weeks; G4, 4-8 weeks; G5, 8-24 weeks. Surgery was never performed on patients with disabling neurological deficit (modified Rankin Scale, 5) at the time of admittance, cerebral lesions greater than 3 cm at magnetic resonance/computed tomography scan, presence or suspect of parenchymal hemorrhage associated with ischemic damage, condition considered unfit for surgery (American Society of Anesthesiology classification grade V), and occlusion of the cerebral middle artery. Neurological and diagnostic examinations (duplex-scanning and computed tomography/magnetic resonance scan) were used in determining the selection for early CEA. RESULTS: Cumulative TIA/stroke/death rate after CEA was 3.8% (11/285) and at 30 days was 2.8% (8/285). The cumulative TIA rate after CEA and at 30 days was 0% (0/285). The cumulative stroke rate after CEA was 3.5% (10/285) and at 30 days was 2.4% (7/285). The cumulative death rate after CEA and at 30 days was 0.3% (1/285). Stroke rate after CEA in each group was: G1 4.2% (3/70); G2 3.2% (2/61); G3 0% (0/22); G4 3.4% (1/29); G5 3.8% (4/103). Any statistically significant difference between G1 and the other four groups was not detected with regard to postoperative stroke: G1 (4.2%) versus G2 (3.2%), p = 0.7641; G1 (4.2%) versus G3 (0%), p = 0.7648; G1 (4.2%) versus G4 (3.4%), p = 0.8473; G1 (4.2%) versus G5 (3.8%), p = 0.8952. No hemorrhagic stroke was detected after early CEA. The type of anesthesia and the use of a shunt didn't show any significant difference between the five groups. CONCLUSIONS: The analysis of these records suggests that early CEA in the acute post stroke phase, for patients clinically selected, does not result in greater complications than when performed delayed or deferred . Furthermore, the advantage of early CEA is the reduction of recurrent strokes, as untreated patients present a higher incidence of neurological events.

Carotid endarterectomy: comparison between general and local anesthesia. Revision of our experience with 428 consecutive cases.

BACKGROUND: This sequential retrospective monocentric study compares the results between general and local anesthesia for carotid endarterectomy (CEA). METHODS: Between November 2002 and October 2004, 428 CEAs were performed in our vascular unit. Two groups were formed: group GA (general anesthesia): 219 patients operated under general anesthesia; group LA (local anesthesia): 209 patients operated under local anesthesia. RESULTS: No mortality was found in both groups. After surgery, three strokes were detected in group GA and three in group LA (GA 1.36% vs. LA 1.43%, p = .9540); After CEA, there were three TIAs in GA group and none in LA group (GA 0.42% vs. LA 0%, p = .2634). CONCLUSION: The morbi-mortality was not influenced by the type of anesthesia used for carotid surgery. No statistical difference was detected in the perioperative neurological and cardiopulmonary complication rates between GA and LA.

Cluster headache attacks and multiple sclerosis.

We report the case of a patient who developed typical cluster headache attacks and was diagnosed as having multiple sclerosis (MS) at the same time. The headache attacks resolved after i.v. treatment with methylprednisolone. MR imaging showed a pontine demyelinating lesion involving the trigeminal nerve root inlet area, on the same side as the pain. The association between cluster headache and MS has been rarely described before. This case suggests that in patients with cluster headache neuroimaging is often useful in order to exclude structural lesions.

Endocrine function is altered in chronic migraine patients with medication-overuse.

OBJECTIVE: To evaluate the effects of analgesic overuse on endocrine function in patients with chronic migraine and medication-overuse headache (CM-MOH). BACKGROUND: Chronic migraine is frequently associated with an overuse of symptomatic medications. Drugs currently used in acute migraine attacks are associated with several endocrine effects. At present, the endocrine effects of medication overuse in chronic migraine patients are unknown. METHODS: Eighteen patients with CM-MOH, diagnosed according to the ICHD-II criteria, and 18 healthy controls received an intravenous administration of GHRH, hCRH, and TRH. Plasma concentrations of GH, TSH, ACTH, and cortisol were measured for a 90-minute period after administration of the specific releasing hormones. RESULTS: Hormonal basal concentrations were similar in both groups. GH response to GHRH was significantly reduced in patients with CM-MOH in comparison with controls. TRH induced a reduction of TSH concentrations only at the end of the test. After hCRH administration, ACTH and cortisol concentrations were significantly higher in cases than in controls. A significant correlation between duration of the disease and altered hormonal response was found. CONCLUSIONS: Our study shows that both corticotropic and somatotropic functions are significantly impaired in CM-MOH patients and suggests a role for hormones in the development of chronic migraine.

Absence of linkage between the interleukin-6 gene (-174 G/C) polymorphism and migraine.

To assess the role of interleukin-6 (IL-6) in migraine, we analyzed the -174 G/C IL-6 gene polymorphism in 268 patients with migraine and 305 controls. No significant difference in the distribution of IL-6 genotypes (chi(2)=0.601, P=0.74) and allelic frequencies (chi(2)=0.024, P=0.876) was found. When patients were subdivided into subgroups (migraine with aura, migraine without aura and mixed headaches), IL-6 alleles were similarly distributed. Comparison of the clinical features of the disease with the -174 G/C IL-6 genotypes showed no significant difference. In conclusion, we found no significant association between the -174 G/C IL-6 polymorphism and the occurrence or the clinical features of migraine.

A comparison of familial and sporadic migraine in a headache clinic population.

We compared the clinical, psychological and pharmacological characteristics of patients with familial migraine and patients with sporadic migraine. Five hundred and thirty consecutive new patients attending our Headache Center over a two-year period were involved in the study. The patients were divided into two groups: A. Familial migraine (famM)--at least one first-degree relative affected; B. Sporadic migraine (spoM)--no first-degree relative affected. Four hundred and twenty-four patients (80%) fulfilled the criteria for famM and 106 (20%) for spoM. The patients with famM showed a significantly (p<0.01) earlier age at onset of the disease. No significant difference in all the remaining features examined was found. Our data suggest that famM and spoM represent a single disease entity.