Multiple Silent Infarcts Research Articles

A role of insomnia in the development of silent cerebral infarctions

To investigate the relationship between insomnia, hemostatic abnormalities and silent cerebral infarctions. A complex study of 76 male patients, aged 40-85, with vascular risk factors was carried out. Magnetic resonance imaging (MRI) data was used to verify presence of silent cerebral infarctions; the presence and severity of insomnia were determined using questionnaires and polysomnography. Laboratory diagnosis included a complete assessment of hemostatic system with thrombodynamics test. Patients were divided into 2 groups according the MRI data. The 1st group included 20 men with less than 4 silent cerebral infarctions, the 2nd group 56 men with multiple silent cerebral infarctions - from 5 to 25. Chronic insomnia was diagnosed in 35 (46%) of patients, more frequently in the second group (25% and 54% respectively, p<0.05). The group of patients with multiple silent infarctions demonstrated a loss of sleep efficiency and hypercoagulation with an increased rate of clot growth in thrombodynamics test. Correlation analysis confirmed the dependence between sleep efficiency and quantity of vascular sites, sleep efficiency and clot growth rate. The more severe plasma haemostasis disorder in patients with multiple silent infarctions and relation between insomnia severity and plasma haemostasis activation suggest that insomnia can be an additional risk factor of arteriole thrombosis.

Brief history of patent foramen ovale and stroke.

Lechat is usually credited with first calling attention to patent foramen ovale (PFO) and stroke in 1988.1 Previous studies of the role of echocardiography in stroke rarely, if ever, mentioned PFO and focused on now-almost-forgotten disorders, such as mitral valve prolapse.2 Interest in PFO has emerged for 3 main reasons: (1) renewed interest in cryptogenic stroke especially in younger patients; (2) technical advances, including bubble contrast transthoracic echocardiography, transesophageal echocardiography, and saline contrast transcranial doppler; and (3) perhaps most importantly, the emergence of endovascular device closure as a treatment option. Cryptogenic stroke is highly prevalent in stroke populations under the age of 55 years. Many of these patients have circumstantial evidence for embolism on MR, such as cortical infarct location or multiple silent infarcts in different vascular territories. Large PFO with a substantial shunt and atrial septal aneurysm has been identified in many (although not all) studies as anatomic comorbidities associated with stroke. However, as with PFO detection, new technology, including implantable cardiac monitors and MR plaque morphological analysis, has identified occult atrial fibrillation and acute rupture of benign atherosclerotic plaques as underdiagnosed causes of crytpogenic stroke.3 This suggests that in many patients with cryptogenic stroke, a PFO may be coincidental. The explosion of device technology has played a central role in the PFO renaissance. Reimbursement policies and an inherent bias in young patients with stroke to close the hole bolstered by numerous observational case series provided a strong incentive for endovascular device closure.4 With this background, 3 randomized clinical trials of the management of patients with cryptogenic stroke and PFO have recently been completed. Given the lingering controversy, it is important to review why the Evaluation of the STARFlex Septal Closure System in Patients With a Stroke and/or Transient Ischemic Attack Due to Presumed Paradoxical …

Pseudo-occlusion of the extracranial carotid artery caused by intracranial carotid artery stenosis

A 70-year-old female with hypertension and diabetes presented to the emergency room with sudden-onset drowsy mentation and disorientation. Her blood pressure was 130/80 mmHg, pulse rate was 70 beats per minute, respiratory rate was 18 breaths per minute, and body temperature was 36.7 C. Neurologic examination indicated confusion and generalized myoclonic jerks. Blood chemistry tests revealed an elevation of blood urea nitrogen and creatinine (83 and 3.5 mg/dl, respectively). Small deep infarcts on the right basal ganglia and corona radiata were visible on brain MRI (Fig. 1a), but a high signal intensity was not evident on the diffusion weighted image. In addition, her right proximal internal carotid artery (ICA) was invisible on contrast-enhanced magnetic resonance angiography (CE-MRA) (Fig. 1b). MRI was performed with a Signa Excite XI Twin Speed 1.5T system (GE Healthcare, Milwaukee, WI, USA). Her neurological symptoms resolved upon reduction of her blood urea nitrogen and creatinine levels, therefore, the patient was tentatively diagnosed with uremic encephalopathy. After improvement of her symptoms, we performed carotid duplex ultrasonography (CDUS, GE LOGIQ 7 PRO US machine, 12 MHz linear array transducer) to evaluate the right ICA on hospital day 6. There was no sonographic evidence of blood flow from the right carotid bifurcation to the proximal ICA (Fig. 1c). Transcranial Doppler could not be performed because she had a poor temporal window. Since MRI and CE-MRA showed multiple silent infarcts mainly in the right anterior circulation and string sign around the lacerum segment of the ipsilateral distal ICA, we planned further investigation including digital subtraction angiography (DSA) to assess her cerebral vascular reserve and vasculature and to determine how to prevent a stroke. DSA, performed on hospital day 8, revealed that the lacerum segment of the right ICA was severely stenotic, but the bulbous segment was not. Proximal to distal blood flow in the right ICA was significantly slower compared to the external carotid artery blood flow (Fig. 1d). The right anterior cerebral artery was filled by the left anterior cerebral and communicating arteries, but the right middle cerebral artery was only supplied by the ipsilateral ICA and was not visualized on vertebral or contralateral cerebral angiography. On hospital day 12, we decided to perform percutaneous transluminal balloon angioplasty (Fig. 2a). Since the diameters of the proximal and distal parent vessels adjacent to the stenotic lesion were 2.03 and 1.89 mm, respectively, we did not deploy a stent. On hospital day 14, follow-up CDUS showed normal configuration of the ICA and normal blood flow velocity (peak systolic velocity: 69.8 cm/s, end diastolic velocity: 33.2 cm/s; Fig. 2b). Since then she has been healthy and asymptomatic, and the blood flow velocity of the right proximal ICA (peak systolic: 69.1 cm/s, end diastolic: 34.8 cm/s; image not shown) was not reduced on 2-year follow-up CDUS. Pseudo-occlusion of the ICA was defined in previous studies as a collapsed distal ICA due to the reduced flow velocity caused by a severe stenotic lesion of the proximal ICA [1]. In this case, contrary to the classical definition of a D. Lee S. H. Heo D.-I. Chang (&) Departments of Neurology, College of Medicine, Kyung Hee University Hospital, Kyung Hee University, #1 Hoegi-dong, Dongdaemun-gu, Seoul 130-702, Korea e-mail: dichang@khmc.or.kr

Ischaemic stroke patients with heterozygous factor V Leiden present with multiple brain infarctions and widespread atherothrombotic disease

Factor V Leiden (FVL) mutation is a risk factor for venous and, to a degree, arterial thrombosis. It is unknown whether and how FVL affects the manifestations of ischaemic stroke (IS). We assessed the clinical, laboratory, radiological, and prognostic characteristics in an observational study with adult IS patients having FVL. We tested 860 patients with first-ever IS for FVL and found 48 FVL positive patients. Detailed clinical, laboratory, and radiological evaluation were compared with that of 144 (1:3) gender and age matched IS patients without FVL. All patients underwent a prognostic evaluation at an average of five years follow-up. Despite the relatively young age (mean 48.5 years, range 44-54 years) of the FVL positive IS patients, peripheral arterial occlusive disease (PAOD), coronary artery disease (CAD), and previous transient cerebrovascular event occurred more frequently compared with controls. Family history of cardiovascular disease (CVD) and multiple silent brain infarctions were revealed in half of the FVL positive patients, whereas these were seldom encountered among controls. Stroke severity, long-term recovery, and recurrence rates seemed similar irrespective of FVL status. Our findings indicate that the clinical profile of IS patients with FVL associated with wider manifestation of atherothrombosis, positive family history of arterial thrombosis, and presence of multiple silent infarctions on brain images.

Neuropsychological abnormalities associated with lacunar infarction

The objective of this study was to assess neuropsychological abnormalities in 40 patients with lacunar infarction. Topography of infarction, presence of isolated or multiple silent infarcts and white matter hyperintensities were correlated with results of neuropsychological tests and subtypes of lacunar infarction. Patients were studied within 1 month after stroke. A total of 21 patients were males and the mean age was 70.7 years; 30% had a single infarction (mean number of infarctions was 3.4). Twelve patients had pure motor hemiparesis, 9 pure sensory stroke, 8 dysarthria-clumsy hand/ataxic hemiparesis, 8 atypical lacunar syndrome, and 3 sensorimotor stroke. The mean score of the Mini-Mental State Examination was 28.4. Mild cognitive impairment of subcortical vascular features occurred in 23 patients and isolated executive disturbances in 4. Neuropsychological results showed that patients with atypical lacunar syndrome followed by pure motor hemiparesis showed significantly more cognitive executive disturbances. Patients with dysarthria-clumsy hand/ataxic hemiparesis accounted for the best scores in some tests of visuoconstructive function and visual memory. In summary, mild neuropsychological disturbances (57.5%) are not infrequent in acute lacunar infarcts especially in patients with atypical lacunar syndrome and pure motor hemiparesis. Neuropsychological impairment should be considered as common clinical feature in acute lacunar infarction.

Cerebrovascular reactivity and subcortical infarctions.

To investigate the association between different kinds of ischemic lesions and cerebrovascular reactivity (CR) and to evaluate their relationships with the major risk factors for stroke. We evaluated CR using the breath-holding index technique during bilateral transcranial Doppler monitoring of flow velocity in the middle cerebral arteries of 41 consecutive patients attending our clinic for a recent, first-ever, ischemic stroke and in 15 control subjects. Based on the location of the lesion determined by computed tomography, the following 3 types of infarctions were identified: cortical (or territorial), single subcortical, and subcortical with multiple silent subcortical infarctions. Patients with a condition of severe carotid artery stenosis or occlusion, which in itself could account for altered CR, were excluded from this study. All physiological and pathologic conditions that could possibly cause an impairment in CR were recorded. The breath-holding index was significantly lower in the multiple subcortical infarctions group than in the control subjects (P < .001), single subcortical infarctions group (P < .01), and cortical infarctions group (P < .01). In all of the groups male sex (P < .05) and a history of hypertension (P < .05), regardless of whether hypertension was treated, correlated with low CR. The multiple regression analysis indicated that the only significant factor able to influence the breath-holding index was the type of lesion. Nonstenotic patients with first-ever stroke who had a recent symptomatic subcortical infarction associated with multiple silent infarctions seem to have an impaired cerebrovascular reserve capacity. The strong association of subcortical infarctions with multiple silent infarctions with low CR indicates the role of small vessel vasculopathy and hypoperfusion as possible pathogenetic mechanisms of subcortical infarctions with multiple silent infarctions.

Silent brain infarcts in 755 consecutive patients with a first-ever supratentorial ischemic stroke. Relationship with index-stroke subtype, vascular risk factors, and mortality.

We wanted to establish independent associations of various clinical variables, computed tomographic (CT) scan features, presenting stroke subtypes, and outcome with the presence of silent infarcts on CT. We studied 755 consecutive patients in a prospective registration of patients with first-ever supratentorial atherothrombotic, cardioembolic, or lacunar stroke or stroke of undetermined cause by multiple logistic regression analysis. Two hundred six patients (27%) with a first symptomatic territorial or small deep ischemic stroke had one or more silent infarcts on CT. Of all silent lesions, 169 (82%) were small and deep. Silent infarcts were significantly more strongly associated with a lacunar than atherothrombotic (odds ratio [OR], 1.59; 95% confidence interval [CI], 1.02 to 2.47; P = .039) or cardioembolic (OR, 1.89; 95% CI, 1.2 to 2.99; P = .005) index stroke. Silent territorial lesions were more strongly associated with cardioembolic than with lacunar stroke but not with atherothrombotic stroke. In this respect, no differences were found between the atherothrombotic and undetermined-cause group. Advanced age and hypertension were the only risk factors that were significantly associated with silent infarcts (OR, 1.76; 95% CI, 1.14 to 2.71; P = .011; and OR, 1.58; 95% CI, 1.13 to 2.21; P = .007; respectively), mainly because of a strong independent association of these risk factors with silent small deep infarcts (OR, 1.75; 95% CI, 1.10 to 2.79; P = .018; and OR, 1.57; 95% CI, 1.09 to 2.24; P = .014; respectively). A cardioembolic source or atrial fibrillation in specific was not independently associated with any type or number of silent infarcts. Significant carotid stenosis (diameter reduction > 50%) was not significantly associated with any type of silent lesion. Initial severe handicap (Rankin Scale score > 3), 30-day case fatality rate, and 1-year mortality were not affected by the presence of silent infarcts. The strong association of silent small deep lesions with first symptomatic small deep infarcts suggests a common underlying mechanism (presumably small-vessel vasculopathy), whereas cardiogenic embolism and large-vessel thromboembolism are the most likely causes in both silent and first symptomatic territorial infarcts. Single or multiple silent infarcts do not predict a cardioembolic stroke mechanism in first symptomatic supratentorial brain infarcts. As silent infarcts do not predict the cause of carotid embolic stroke in first symptomatic brain infarcts, their presence should not influence the decision on carotid surgery. Silent infarcts do not affect the degree of initial handicap, 30-day case fatality, or 1-year mortality. The significance of silent infarcts for predicting possible future cognitive decline and risk of recurrent stroke deserves further study.