Biomedical subjects
M G Bousser
Publications and source records attributed to M G Bousser.
The prevalence of ulcerated plaques in the aortic arch in patients with stroke.
BACKGROUND AND METHODS: The cause of cerebral infarction is obscure in up to 40 percent of patients with this disorder who are studied prospectively. In this investigation, we determined the frequency of ulcerated plaques in the aortic arch and explored the part they may play in the formation of cerebral emboli. Using an autopsy data bank, we studied the prevalence of ulcerated plaques in the aortic arch in 500 consecutive patients with cerebrovascular and other neurologic diseases who were studied at autopsy. RESULTS: Ulcerated plaques were present in 26 percent of the 239 patients with cerebrovascular disease but in only 5 percent of the 261 patients with other neurologic diseases (P less than 0.001). After we controlled for age and heart weight, the adjusted rates were 16.9 percent and 5.1 percent, respectively (adjusted odds ratio, 4.0; 95 percent confidence interval, 2.1 to 7.8; P less than 0.001). Among the patients with cerebrovascular disease, the prevalence of ulcerated plaques in the aortic arch was 28 percent in the 183 patients with cerebral infarcts and 20 percent in the 56 patients with brain hemorrhage. The prevalence of ulcerated plaques was 61 percent among the 28 patients with no known cause of cerebral infarction, as compared with 22 percent among the 155 patients with a known cause of cerebral infarction (P less than 0.001). After adjustment for covariates, the prevalence was 57.8 percent among patients with no known cause of cerebral infarction and 20.2 percent among those with a known cause (adjusted odds ratio, 5.7; 95 percent confidence interval, 2.4 to 13.6; P less than 0.001). The presence of ulcerated plaques in the aortic arch was not correlated with the presence of extracranial internal-carotid artery stenosis, suggesting that these were two independent risk factors for stroke. CONCLUSIONS: Ulcerated plaques in the aortic arch may play a part in causing cerebral infarction, especially in patients in whom cerebral infarction has no known cause.
Pain as the only manifestation of internal carotid artery dissection.
Internal carotid artery dissection is a major cause of ischemic stroke in the young. Pain is the leading symptom and is associated with other focal signs such as Horner's syndrome and painful tinnitus or with signs of cerebral or retinal ischemia. We report two patients with angiographically confirmed extracranial internal carotid artery dissection presenting with cephalic pain as the only manifestation. The first patient had a diffuse headache and a latero-cervical pain lasting for 12 days, reminiscent of carotidynia. The second patient experienced an exploding headache suggestive of subarachnoid hemorrhage, which was ruled out by computed tomography of the head and cerebrospinal fluid study. These patients demonstrate that recognition of carotid artery dissection as a cause of carotidynia and headache suggestive of subarachnoid hemorrhage may permit an earlier diagnosis and possibly the prevention of a stroke through the use of anticoagulation.
Ipsilateral cluster headache and chronic paroxysmal hemicrania: two case reports.
We report two patients with ipsilateral attacks of cluster headache and chronic paroxysmal hemicrania. The first patient, a 33-year-old man, started having attacks of chronic cluster headache at the age of 27. At 33, they were replaced by typical attacks of ipsilateral chronic paroxysmal hemicrania which showed a dramatic improvement with indomethacin 150 mg daily. After two days of complete remission, cluster headache attacks reappeared and persisted until verapamil, 360 mg a day, was added to indomethacin. The second patient, a 45-year-old man, first developed attacks of episodic cluster headache at the age of 35. At 44, he experienced ipsilateral typical attacks of chronic paroxysmal hemicrania, and two months later attacks of cluster headache. Under verapamil 240 mg daily, attacks of cluster headache disappeared, but those of chronic paroxysmal hemicrania increased in frequency until indomethacin 150 mg daily was added. These observations suggest a close relationship but not a similarity between cluster headache and chronic paraoxysmal hemicrania, and show the practical therapeutic interest of maintaining this distinction.
Headache following carotid endarterectomy: a prospective study.
The occurrence of headache in the 28 days following surgery was studied in 50 consecutive patients (14F and 36M, mean aged 70 years) who underwent carotid endarterectomy for atheromatous carotid stenosis. Thirty-one patients (62%) reported headache. Headache occurred in the first five days after surgery in 87% of cases. Its characteristics and temporal profile were highly variable but it was mostly bilateral (74%), mild or moderate (78%), requiring no treatment (77%). No correlation was found between the occurrence of headache and degree of stenosis, intraoperative characteristics and past history of headache. In none of our patients was severe ipsilateral headache, cerebral hyperperfusion syndrome, or cluster-like hemicrania encountered and only five patients met the IHS criteria for post-endarterectomy headache. Post-endarterectomy headache is frequent when specifically looked for and is therefore not a single entity. The present IHS criteria are unsatisfactory and should be modified accordingly.
Extracranial vertebral artery dissection.
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Transesophageal echocardiographic detection of aortic arch disease in patients with cerebral infarction.
BACKGROUND AND PURPOSE: Ulcerated plaques in the aortic arch are frequent autopsy findings in patients with cerebral infarctions, particularly those of unknown cause. It has been suggested that they could be a source of cerebral emboli. Using transesophageal echocardiography, we prospectively studied 12 consecutive patients with cerebral infarction of undetermined cause after noninvasive workup to evaluate the frequency of aortic plaques or mural thrombi that could embolize in cerebral arteries. SUMMARY OF REVIEW: Six patients (50%) had an intraluminal echogenic mass of the aortic arch, mainly located at the junction of the ascending aorta and arch. This material was pedunculated (in one patient) or broad based (in five patients) with a markedly irregular surface and intraluminal extension from 3 to 15 mm. In addition, we found cholesterol emboli in two of the four patients who underwent quadriceps biopsy. CONCLUSIONS: These results show that transesophageal echocardiography has capabilities in detecting such lesions and point to the aortic arch as a possible source of cerebral emboli in patients with cerebral infarction of unknown cause.
Cerebral venous thrombosis in Behçet's disease: clinical study and long-term follow-up of 25 cases.
Among 250 patients with Behcet's disease, we describe 25 cases of angiographically proven cerebral venous thrombosis. Intracranial hypertension was the most frequent manifestation. Two initially untreated patients relapsed. Treatment of cerebral venous thrombosis consisted of combined heparin and steroids in 19 patients, steroids alone in three, and heparin alone in three others. Neurologic symptoms improved rapidly in all. Nineteen patients received long-term anticoagulation, and two received aspirin. Relapse of cerebral venous thrombosis or development of optic atrophy did not occur in treated patients. Partial or total recanalization of the occluded sinus was frequent. After more than 3 years of follow-up, the prognosis of dural sinus thrombosis is satisfactory.
[Pathology of cranial nerves: diagnostic orientation and aphorisms].
Despite the remarkable progress of Neuroradiology, the etiologic diagnosis of cranial nerve disorders remains, because of the numerous potential causes, one of the most difficult clinical problems in Neurology. It requires a perfect collaboration between neurologists, ophthalmologists, and ENT specialists, and also between clinicians and radiologists. First of all however, it is based on a rigorous clinical analysis in order to determine the site of the lesion and to guide complementary investigations. The purpose of this short paper is to provide a brief outline of this clinical approach and to recall some aphorisms which are essential to keep in mind when dealing with this pathology.
[Management of migraine].
When considering treatment for migraine patient, the physician should bear in mind how little is known about this remarkably complex and diverse condition with no miracle cure or single uniform method of treatment. Experience suggests that adherence to a number of principles based on a combination of common sense, modesty, and open-mindedness is essential to effective management of migraine. The patient needs to be both reassured and taken seriously, and should be told that the cause of migraine is unknown and that performing multiple investigations would be unhelpful. The difference between acute treatments and maintenance prophylactic treatments should be clearly explained. The patient should participate in therapeutic decisions such as whether or not to use prophylaxis and whether pharmacologic or nonpharmacologic treatment is most appropriate. Finally, and most importantly, both the physician and patient must be aware that much patience is needed but that this patience will usually be rewarded, not by complete resolution of the disease, but by an often dramatic improvement in the migraine patient's quality of life.
[Beta-blockers and migraine].
Five beta-blocking agents are effective as long-term prophylactic treatment of migraine: propranolol, metoprolol, timolol, atenolol and nadolol. Propranolol has been most extensively studied and proved effective in 19 of 21 controlled trials. The optimal dose should be determined on a case-by-case basis, by increasing the daily dosage gradually. Among the properties of beta-blockers, the only one which appears to be correlated--albeit negatively--with effectiveness on migraine is intrinsic sympathomimetic activity (ISA): drugs without ISA are effective against migraine whereas partial agonists are not. The mode of action of beta-blockers in migraine is still poorly understood; one of the most cogent current hypotheses involves reduction of brain catecholaminergic hyperactivity.
Clinical pharmacology of migraine.
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[Methodology of clinical trials in migraine: a rating system].
Several problems confront trials of drugs for migraine: no clinical or biological markers for objective diagnosis are available, severity of the attack cannot be readily evaluated, the placebo effect is significant, and both compliance with therapy and patient follow-up may be difficult to ensure. No statistical method is capable of solving these problems and it is the clinicians' role to minimize them by consistent efforts at establishing good communication with their patients during the trial. Because of these significant intrinsic difficulties, trials of drugs for migraine require especially stringent data collection and analysis protocols in order to minimize the risk of errors which exist in any drug trial. The protocol used have not always been satisfactory with this respect. A rating system for helping non-specialists to evaluate the reliability of migraine drug trials is proposed.
[Physiopathogenesis of migraine].
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Cerebral venous thrombosis.
Neuroimagining facilities allow early recognition of cerebral venous thrombosis (CVT), which now appears far more common than previously assumed. The diagnosis remains difficult because of a wide spectrum of clinical presentation and a highly variable mode of onset. Numerous conditions (presently mostly noninfectious) can cause or predispose to CVT, which therefore requires an extensive etiologic work-up. The functional and vital prognosis is much better than classically thought with, in noninfectious CVT, a fatality rate of less than 10% and a complete recovery in over 70%. Although spontaneous recovery is possible, the efficacy of heparin is now well established.
[Neurosarcoidosis].
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Penicillamine in amyotrophic lateral sclerosis.
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Perhexiline maleate and peripheral neuropathy.
Peripheral neuropathy has been noted as a complication of therapy with perhexiline maleate, a drug widely used in France (and in clinical trials in the United States) for the prophylactic treatment of angina pectoris. In 24 patients with this complication, the marked slowing of motor nerve conduction velocity and the electromyographic changes imply mainly a demyelinating disorder. Improvement was noted with cessation of therapy. In a few cases the presence of active denervation signified a poor prognosis, with only slight improvement. The underlying mechanism causing the neuropathy is not yet fully known, although some evidence indicates that it may be a lipid storage process.