The aim of this study was to analyze the spectrum of clinical presentations of internal carotid artery dissection. Twenty-two patients with internal carotid artery dissection, mean age 39.02, were evaluated over the past ten years. Magnetic resonance imaging and magnetic resonance angiography were used to establish the diagnosis. Facial and neck pain and Horner's syndrome were the only presenting symptoms in 4 patients (without brain infarction); facial pain, Horner's syndrome and contralateral sensorimotor deficit in 6; headache and contralateral sensorimotor deficit in 2; contralateral sensorimotor deficit with or without speech impairment in 10. Internal carotid artery dissection was triggered by a trauma in 7, whereas it was spontaneous in 15. Magnetic resonance imaging revealed infarction in 18 patients. A good outcome (modified Rankin score 0-2) was seen in 20 patients. The spectrum of clinical presentations of internal carotid artery dissection is variable. Internal carotid artery dissection is not necessarily accompanied by infarction on magnetic resonance imaging.
Introduction. Cerebral vasomotor reactivity (VMR) represents an autoregulatory response of the arterial trunks on the specific vasoactive stimuli, most commonly CO2. Objective. The aim of this retrospective study was to compare VMR in high-grade symptomatic (SCAS) and asymptomatic carotid stenosis (ACAS), using the apnea test to evaluate the hemodynamic status. Methods. The study included 50 patients who were hospitalized at the neurology and vascular surgery departments as part of preparation for carotid endarterectomy. We evaluated VMR by calculating the breath holding index (BHI) in 34 patients with SCAS and 16 patients with ACAS, with isolated high-grade carotid stenosis. We evaluated the impact of risk factors and collateral circulation on BHI, as well as the correlation between the degree of carotid stenosis and BHI. Results. A pathological BHI was more frequent in the SCAS group (p<0.01). There was no difference in the range of BHI values between the groups, both ipsilaterally and contralaterally. Only male gender was associated with pathological BHI in both groups (p<0.05). Collateral circulation did not exist in over 60% of all subjects. We confirmed a negative correlation between the degree of carotid stenosis and BHI. Conclusion. SCAS and ACAS patients present with different hemodynamics. While ACAS patients have stable hemodynamics, combination of hemodynamic and thromboembolic effects is characteristic of SCAS patients.
A 32-year-old white woman presented with acute onset of right limb weakness, 3 days before hospitalization. She had non-regulated hyperthyreoidism and a history of smoking. Brain computed tomography (CT) showed a several occipital and high parietal ischemic lesions of the left hemisphere [ Figure 1a and b]. Duplex ultrasonography scan (DUS) showed the existence of fibrolipid plaque located on the back wall of the common carotid artery, that extended to the external as well as internal carotid artery making an uneven plaque, a part of which moved up and down with the heart beat, creating stenosis of 80-90% [ Figure 1c and d]. CT angiography revealed unstable plaque in left internal carotid artery that protrudes into the lumen as well as moderate stenosis in the proximal segment of the external carotid artery [ Figure 2]. She underwent total carotid endarterecotomy of symptomatic left internal carotid artery, 25 days after being admitted. Histopathological finding indicated that the plaque was atherosclerotic. In the prevention of stroke recurrence, the patient was given 75 mg of clopidogrel and 100 mg of aspirin daily. The patient did well, with residual discrete right-sided weakness and no recurrent strokes. Follow-up DUS was done and it showed no signs of plaque or restenosis.Mobile carotid plaques are unstable and associated with recurrent stroke, [1] with the estimated prevalence of 1 in 2000. [2] They bear high risk of embolic cerebrovascular incidents, as was the case in our patient. This type of plaque usually represents degenerated atherosclerotic flap, ruptured plaque with mobile thrombus or intimal dissection plaque. The only method that can show the mobility of the plaque is ultrasonography. [1] Mobile floating carotid plaques can be treated with urgent carotid endarterectomy, delayed carotid endarterectomy and carotid angioplasty and stenting. [2,3] Beside surgery, patients are treated with antiplatelet therapy. [2] Neuroimage Figure 1: Brain computed tomography showed several occipital and high parietal ischaemic leasions of the left hemisphere (a, b). Duplex ultrasonography scan revealed fibrolipid plaque located on the back wall of the common carotid artery, that extended to the external as well as internal carotid artery making an uneven plaque (c, d) d c b a Figure 2: Computed tomographic angiography of the neck showed unstable plaque in left internal carotid artery that protrudes into the lumen as well as moderate stenosis in the proximal segment of external carotid artery. Axial source imaging (a, b) and 3D reconstruction imaging (c, d) d c b a
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