Acute carotid dissection in an adult caused by pertussis.

We present a 57-year-old man who worked in a pediatric setting who, after a strong coughing attack caused by a pertussis infection, presented with an internal carotid dissection and a consequent ischemic cerebral lesion. This case suggests the importance of vaccination for subjects who belong to high-risk categories.

Cerebrovascular reactivity and cognitive decline in patients with Alzheimer disease.

BACKGROUND AND PURPOSE: The aim of this study was to explore the possible contribution of alterations in cerebral hemodynamics to the evolution of cognitive impairment in patients with Alzheimer disease (AD). METHOD: Fifty-three patients with AD were investigated. The evolution of cognitive decline over 12 months was evaluated by means of changes in Mini Mental State Examination (MMSE) and AD Assessment Scale for Cognition (ADAS-Cog) scores. Demographic characteristics, vascular risk profile, pharmacological treatment, and presence of white matter lesions were assessed at entry. Further, a basal evaluation of cerebrovascular reactivity to hypercapnia was measured with transcranial Doppler ultrasonography using the breath-holding index (BHI). RESULTS: Of all the variables considered, both MMSE and ADAS-Cog changes had the highest correlation with BHI, followed by age and diabetes. After subdividing both cognitive measures reductions into bigger and smaller-than-average decline (2 points for MMSE; 5 points for ADAS-Cog), multiple logistic regression indicated BHI as the sole significant predictor of cognitive decline. CONCLUSIONS: These results show an association between impaired cerebral microvessels functionality and unfavorable evolution of cognitive function in patients with AD. Further research is needed to fully establish whether altered cerebral hemodynamics may be considered an independent factor in sustaining cognitive decline progression or an effect of pathological processes involved in AD.

Markers of lacunar stroke in patients with moderate internal carotid artery stenosis.

The benefits of surgical correction of moderate internal carotid artery stenosis have been demonstrated only in symptomatic subjects. It is debatable whether patients with lacunar infarct ipsilateral to a moderate carotid stenosis may be considered symptomatic like those with large-artery stroke. The aim of the study was to seek markers capable of differentiating patients with lacunar or non-lacunar stroke ipsilateral to a moderate internal carotid artery stenosis. We enrolled 95 patients with a first stroke ipsilateral to a moderate (50-69 %) stenosis of the internal carotid artery and divided them into lacunar and non-lacunar stroke based on clinical presentation and neuroradiological findings; 34 subjects with asymptomatic moderate carotid stenosis and 31 normal individuals were also studied. Baseline characteristics; risk factors, cerebrovascular reactivity to hypercapnia evaluated by means of the breath-holding index (BHI), the presence and severity of carotid stenosis and intimamedia thickness (IMT) of the common carotid arteries were determined. There were 36 patients with lacunar and 59 with non-lacunar stroke. Degree of stenosis, and IMT and BHI ipsilateral to symptomatic stenosis were found to be significant independent predictors as each 10 % increase of stenosis carried a 4.3 higher probability of non-lacunar stroke (95 % CI: 1.91-9.51); each decimillimeter increment in IMT increased this probability by 1.45 (95 % CI: 1.10-1.92); and the risk odds ratio associated with each 0.1 increase in BHI was 1.88 (95 % CI: 1.33-2.66). A decrease in BHI of 0.1 thus carried a 90% greater probability of having a lacunar stroke. The results show that patients with moderate internal carotid artery stenosis and lacunar stroke can be differentiated from those with non-lacunar stroke on the basis of distinctive ultrasonographic findings. Further studies are needed to clarify whether our findings have pathogenetic implications and may be of help for the planning of different therapeutic strategies in patients with moderate internal carotid stenosis and lacunar or non-lacunar ipsilateral stroke.

Cerebral blood flow changes in the different phases of migraine.

The haemodynamic changes that take place in migraine are reviewed focusing on cerebral blood flow (CBF) data measured with different techniques in patients suffering from migraine with and without aura during the different phases of attacks and in interictal periods. Special attention is paid to the factors underpinning the conflicting cerebral blood flow data and to pathophysiological implications of the CBF changes detected in migraineurs.

Carotid artery wall thickness in patients with obstructive sleep apnea syndrome.

BACKGROUND AND PURPOSE: Epidemiological studies have suggested a pathophysiological link between sleep apnea syndrome and cerebrovascular diseases. The mechanism by which sleep disturbance can affect the predisposition to developing stroke is not clear. The aim of this study was to investigate whether patients with obstructive sleep apnea syndrome have an increase in atherosclerosis indicators at the carotid artery level. METHODS: We included 23 male patients with severe obstructive sleep apnea syndrome (respiratory disturbance index >30). Intima-media thickness and the presence of steno-occlusive lesions in the common carotid arteries were investigated with B-mode high-resolution ultrasonography. Results of the ultrasonographic examination were compared with those of a group of 23 subjects without obstructive sleep apnea syndrome who were matched for age and comorbid factors. RESULTS: The intima-media thickness of the common carotid arteries of patients with obstructive sleep apnea syndrome was significantly higher (P<0.0001) than that of control subjects (1.429+/-0.34 versus 0.976+/-0.17 mm). CONCLUSIONS: Results of the present study show that carotid wall thickness is increased in patients with severe sleep apnea syndrome. There is strong evidence that an increase in the thickness of the carotid artery wall is a valid marker of the risk of stroke. For this reason, our finding seems to further strengthen the hypothesis that patients with obstructive sleep apnea syndrome are at risk of developing cerebrovascular diseases regardless of the association with other vascular risk factors.

Carotid atherosclerosis and cognitive decline in patients with Alzheimer's disease.

Aim of the study was to explore the correlation between the progression of carotid atherosclerosis and the evolution of cognitive impairment in 66 patients with Alzheimer's disease (AD). They underwent cognitive status evaluation and ultrasonography (US) to investigate carotid arteries intima-media thickness (IMT) and plaque index (PI). After a 12-month follow-up period, neuropsychological and US examinations were repeated to assess the progression of carotid atherosclerosis and of cognitive decline [in terms of changes in Mini Mental State Examination (MMSE) scores]. MMSE score changes were related to baseline IMT (p=0.018), changes in IMT (p<0.001) and PI (p=0.006), and "antihypertensive drug intake" (p<0.001). While the first three variables correlated with increased cognitive impairment, the last one was associated with a reduced extent of MMSE score decline. Results show a link between progression of carotid wall changes and of cognitive decline, and suggest a possible protective role of antihypertensive therapy. Given the potential clinical implications, our preliminary findings could stimulate further investigations into the role of vascular impairment in patients with AD.

Basilar and middle cerebral artery reactivity in patients with migraine.

BACKGROUND: Migraine has been reported as a possible risk factor for ischemic stroke. The mechanisms underlying this association are unknown. OBJECTIVES: To evaluate cerebrovascular reactivity to hypercapnia in the anterior and posterior circulation of patients with migraine, as reduced cerebrovascular reactivity is associated with a predisposition to stroke in various clinical conditions. METHODS: Using transcranial Doppler ultrasonography, changes in flow velocity during apnea were measured in both middle cerebral arteries and in the basilar artery of 15 control subjects and 30 patients with migraine (15 with aura and 15 without aura) during an attack-free period. Cerebrovascular reactivity was evaluated using the breath-holding index, which is calculated by dividing the percent increase in mean flow velocity recorded during a breath-holding episode by its duration (in seconds) after a normal inspiration. RESULTS: Vascular reactivity in the middle cerebral arteries was similar in patients and controls and significantly lower in the basilar artery of patients with migraine with aura compared with the other 2 groups (P <.0001). CONCLUSIONS: These findings show that in patients with migraine with aura, there is an impairment in the adaptive cerebral hemodynamic mechanisms in the posterior circulation. This fact could have pathogenetic implications since the association between migraine and stroke frequently regards patients with migraine with aura, and cerebral infarcts occur more commonly in the vertebrobasilar district.