MR angiography is a reliable, noninvasive method for use in diagnosis and follow-up of extracranial internal carotid artery dissection. In vertebral artery dissection, however, conventional angiography remains useful.
The clinical course of dissecting aneurysms was benign, although spontaneous radiologic resolution occurred rarely. Medical management with antiplatelet therapy alone (after early anticoagulation) is generally sufficient, and surgical management was seldom required.
In order to assess the prevalence and characteristics of cephalic pain in internal carotid artery (ICA) dissection, and to compare clinical and angiographic features of patients with painful and non-painful dissections, we observed 65 patients with angiographically diagnosed extracranial ICA dissection from 1972 to 1990. Forty-eight patients (74%) complained of a cephalic pain which was inaugural in 38 (58.5%). It was homolateral to the dissection in 79% of cases and lasted from 1 h to 30 days, with a median of 5 days. Signs of cerebral or retinal ischemia were observed in 79% of patients, often delayed and occurring up to 29 days after the onset of pain. A painful Horner's syndrome was present in 31% of patients, and was the only manifestation of dissection in 16%. The clinical presentation of the dissections and angiographic findings were similar in patients with and without pain except for a past history of migraine which was more frequent in patients with painful dissections. Cephalic pain is frequent and often inaugural in carotid dissection. Its recognition is important for early diagnosis and treatment.
Positron emission tomography was used to study the effects of unilateral vascular thalamic lesions on cortical oxygen and glucose utilization in 10 patients. There was significant ipsilateral cortex hypometabolism in 9 of the 10 patients, affecting the whole cortical mantle diffusely. The only patient spared was free of neuropsychological deficit at the time of positron emission tomography. In 4 patients, the magnitude of ipsilateral cortical hypometabolism was significantly less at a follow-up PET study, when neuropsychological function had improved. When taken together, the 14 studies showed a significant tendency for the hypometabolism to improve with time after clinical onset. These data suggest that the ipsilateral cortical hypometabolism results from damage to the thalamocortical connections and reflect either loss of nonspecific activating afferences or a degenerative deafferentation-deafferentation process, or both. Its links with the concept of diaschisis are suggested by its tendency to recover. A causal relationship between cortical hypometabolism and neuropsychological deficit, however, although strongly suggested, cannot be firmly established from the present data.
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