Dilek Evyapan

Acute Caudate Vascular Lesions

BACKGROUND AND PURPOSE We sought to evaluate demographic features, risk factors, clinical profiles, and behavioral abnormalities in patients with caudate lesion, either with infarct or with hemorrhage involving the caudate nucleus. METHODS We studied all patients with acute caudate stroke confirmed by CT or MRI who were admitted to our stroke unit over a 5-year period. A database containing risk factors, clinical features, type and mechanism of stroke, and caudate vascular territories was analyzed. RESULTS Thirty-one patients had acute caudate stroke (24 men and 7 women; mean age, 62.3 years). Caudate infarct was present in 25 patients and caudate hemorrhage in 6. The main risk factors for caudate infarct were hypertension (64%), hypercholesterolemia (32%), diabetes mellitus (28%), and previous myocardial infarct (20%). Hypertension was present in 4 patients (67%) with caudate hemorrhage, and arteriovenous malformation was present in 1 patient (17%). Small-artery disease was diagnosed in 14 patients (59%), cardiac embolism in 5 patients (20%), and large-artery disease in 2 patients (8%), and 2 patients (8%) had mixed etiology. The most frequent neurological abnormalities were abulia and psychic akinesia (48%), frontal system abnormalities (26%), speech deficits in patients with left-sided lesions (23%), and neglect syndromes in those with right-sided lesions (10%). Fifteen patients with caudate infarct (60%) and 3 patients with hemorrhage (50%) were able to return to normal daily life. Patients with infarct in the territory of the lateral lenticulostriate arteries extending to neighboring structures showed more frequent motor and neuropsychological deficits than those with infarct in the territory of the anterior lenticulostriate arteries. CONCLUSIONS The clinical presentation of patients with caudate hemorrhage mimicked subarachnoid hemorrhage with or without motor and neuropsychological signs. Caudate vascular lesions with concomitant neighboring structure involvement represent a specific stroke syndrome, usually caused by small-artery disease and in one fifth of the patients caused by cardiac embolism. The behavioral abnormalities were mostly due to medial, lateral, and ventral caudate subnuclei damage and coexisting lesion of the anterior limb of the internal capsule.

Bilateral thalamic infarction. Clinical, etiological and MRI correlates.

To determine clinical, behavioral, topographic and etiological patterns in patients with simultaneous bilateral thalamic infarction in varied thalamic artery territories, we studied 16 patients who were admitted to our stroke unit over a 7‐year period. Patients with bithalamic infarction represented 0.6% of our registry which included 2750 ischaemic stroke patients. On computed tomography and magnetic resonance imaging with gadolinium enhancement, there were 4 topographic patterns of infarction: 1) bilateral infarcts in the territory of paramedian artery (8 patients [50%]); 2) bilateral infarcts in the territory of thalamogeniculate arteries (3 patients [19%]); 3) bilateral infarcts involving territory of paramedian and thalamogeniculate arteries (3 patients [19%]); 4) bilateral infarcts involving territory of polar and thalamogeniculate arteries (2 patients [13%]). A specific clinical picture was found in up to 50% of the patients with bithalamic infarction. This included patients with bilateral paramedian infarction having disorder of consciousness, memory dysfunctions, various types of vertical gaze palsy and psychic changes. Bilateral sensory loss predicted accurately bilateral infarction in the territory of thalamogeniculate arteries. The main cause of bilateral thalamic infarction was small artery‐disease, followed by cardioembolism. Cognitive functions in patients with bilateral paramedian infarction did not change significantly during the follow‐up, in contrast to those with infarcts in varied arterial territories. Acute bilateral infarction involving both thalamus is uncommon, although they are often associated with specific neurologic–neuropsychological patterns, allowing diagnosis before radiological examination.

Clinical spectrum of pontine infarction

Abstract. We sought clinical and radiological findings of 150 consecutive patients with acute isolated pontine infarct who were admitted to our Stroke Unit over 6 years. In all patients CT, MRI and magnetic resonance angiography (MRA) were performed during the hospitalization. On clinico-radiological analysis regarding the pontine lesion boundaries there were five main clinical patterns that depended on the constant territories of intrinsic pontine arteries: (1) anteromedial pontine syndrome (58 %) presented with motor deficit with dysarthria, ataxia, and mild tegmental signs in one third of patients; (2) anterolateral pontine syndrome (17 %) developed with motor and sensory deficits in half of the patients, and were associated with tegmental signs (56 %) more frequently than the anteromedial infarct syndrome; (3) tegmental pontine syndrome (10 %) presented with mild motor deficits and associated with sensory syndromes, eye movement disorders and vestibular system symptoms including vertigo, dizziness and ataxia; (4) bilateral pontine syndrome (11 %) consisted with transient consciousness loss, tetraparesis and acute pseudobulbar palsy; (5) unilateral multiple pontine infarcts (4 %) were rarely observed, and were always associated with severe sensory-motor deficits and tegmental signs. In our series, there was no infarct in the extreme dorsal and lateral tegmental pontine territories which have been mostly associated with cerebellar infarctions. The main etiology of stroke was basilar artery branch disease (BABD) in 59 patients (39 %), followed by small-artery disease (SAD) in 31 (21 %), large-artery disease of vertebrobasilar arteries in 27 patients (18 %), cardioembolism in 12 (8 %) and in 16 patients (11 %) no cause of stroke was found. Our findings suggest that it is possible to identify clinical subgroups of pontine infarction, in which BABD and SAD were the most common causes of stroke. After an acute onset, outcome is in general excellent except in those with bilateral pontine lesions.

Detection of Microembolic Signals in Patients with Neuropsychiatric Lupus erythematosus

The pathogenesis of central nervous system involvement in systemic lupus erythematosus (SLE) is not completely understood. In this study, we investigated the association of microembolic signals (MES) with a variety of neuropsychiatric SLE manifestations and compared our results with those from SLE patients without neuropsychiatric lupus and normal controls. Fifty-three patients with SLE (45 females and 8 males), all fulfilling the revised classification criteria for SLE, and 50 control subjects (44 females and 6 males) were enrolled in this study. All SLE patients were assessed by neuropsychological examination, including various neuropsychiatric tests. Twenty-five patients with SLE were found to have at least one of the neuropsychiatric syndromes defined by The American College of Rheumatology. The mean MES count in patients with neuropsychiatric lupus was significantly higher than those without (5.4 ± 1.1 vs. 0.3 ± 0.8/h; p < 0.005). We found a positive correlation between higher mean MES counts and the presence of neuropsychiatric syndromes in SLE. The mean MES count in the whole group of SLE patients was also significantly higher than that in healthy controls. The mean MES count of SLE patients with antiphospholipid (aPL) antibody positivity was significantly higher than those without aPL antibodies (3.6 ± 1.6 vs. 0.8 ± 0.1/h; p < 0.005). In conclusion, the association of MES with neuropsychiatric lupus may support the possible contribution of MES to the complex pathophysiology of this syndrome. More importantly, detection of MES on transcranial Doppler monitoring might suggest a high risk of involvement of the central nervous system in SLE, and could be used as a diagnostic tool.

Pontine anosognosia for hemiplegia

Article abstract Four patients had anosognosia for hemiplegia (AHP) as a manifestation of pontine infarction in the mediolateral region. Patients with AHP syndrome had no mental and neuropsychologic disturbances, and all had involvement of the medial or lateral part of the pons (medial or lateral pontine reticular nuclei). Brainstem lesions, which activate frontoparietosubcortical areas, may be a critical factor in the development of AHP syndrome.

Microembolic signal detection in patients with symptomatic and asymptomatic lone atrial fibrillation.

Background and Purpose: There are few data on the occurrence of microembolic signals (MES) in patients with lone atrial fibrillation (LAF). The aim of this work was to systematically study the frequency of MES in patients with symptomatic and asymptomatic LAF and to compare it with that of nonvalvular atrial fibrillation (NVAF). Methods: 37 consecutive acute stroke patients with LAF, 10 asymptomatic patients with LAF and 100 age-matched healthy controls were studied. Another 92 stroke patients with known NVAF were included in the study to compare patients with LAF regarding the presence of MES. Both middle cerebral arteries were monitored by transcranial Doppler ultrasound for at least 30 min at admission and after 1 week in symptomatic and asymptomatic patients with LAF. All patients with LAF were followed up for a mean duration of 18 months, and recurrent strokes were registered. Results: MES was detected in 11 (29%) symptomatic patients with LAF but only in 1 asymptomatic patient with LAF (χ2 = 11.3; p = 0.0008) and in no control subjects (χ2 = 106; p = 0.00001). There was no difference in the frequency of MES-positive patients and the number of MES between subjects with symptomatic LAF and known NVAF (29% in both groups; mean count, 16 ± 4 vs. 17 ± 6; p = 0.73). In patients with symptomatic LAF and NVAF who underwent anticoagulant therapy, there was no difference in the frequency of MES after 1 week of hospitalization (χ2 = 1.53; p = 0.2). During a mean follow-up period of 18 months, 1 patient with symptomatic LAF and MES had a recurrent ischemic event 1 year after the first stroke and none of those with asymptomatic LAF had any events. Conclusion: Our study suggests that asymptomatic and paroxysmal LAF with a lower frequency of MES is a benign disorder compared to chronic and symptomatic LAF with a higher frequency of MES. Further studies need to justify whether MES has a predictive value in patients with chronic LAF who are prone to ischemic stroke.

Visuospatial stimulus-bound automatic writing behavior: A right hemispheric stroke syndrome

Three cases of visuospatial stimulus-bound automatic writing behavior were identified among 80 patients (4%) with acute right cerebral hemispheric stroke. All cases had similar clinical characteristics and writing behavior, and visuospatial stimulus-bound automatic writing was related to visually perceived letters. This syndrome might be specific for right hemispheric stroke and might be included among other hypergraphic syndromes attributable to right hemispheric damage.

Association of baseline dyslipidemia with stroke recurrence within five‐years after ischemic stroke

Background and purpose The association between dyslipidemia (DL) and stroke recurrence is unclear, but may be influenced by different subtypes of stroke. This study aims to explore whether DL contributes to the recurrence of certain subtypes of ischemic stroke. Methods Data from the Ege Stroke Registry was examined, and five-years follow-up data for stroke recurrence was analyzed. Trial of Org 10172 in Acute Stroke Treatment criteria was used to classify the subtypes of all stroke. Recurrent stroke was defined as a new neurological deficit compatible to ischemic stroke or intracerebral hemorrhage. The association between DL and stroke recurrence in patients with different sroke subtypes was analyzed using univariable and multivariable logistic regression models. Survival curves were estimated with Kaplan–Meier methods, and survival analyses were undertaken using Cox proportional hazards models. Results Of the 9940 patients with ischemic stroke, 5838 (58·7%) had DL and 2202 (22·2%) experienced a stroke recurrence within five-years. The frequency of stroke recurrence of patients with DL was unsignificantly higher than those without at five-years of follow-up (18·0% vs. 17·0%; P = 0·21). After stratification by Trial of Org 10172 in Acute Stroke Treatment subtypes, multivariable analysis revealed a significant association between DL and stroke recurrence in all ischemic stroke at five-years (odds ratio, 1·2; 95% confidence interval, 1·02–1·42), and in the large-artery disease subtype (odds ratio, 1·46; 95% confidence interval, 1·12–1·91), but not in the other stroke subtypes (cardioembolic: odds ratio, 1·18; 95% confidence interval, 0·84–1·65; small-artery disease: odds ratio, 1·24; 95% confidence interval, 0·87–1·76; other subtype: odds ratio, 0·79; 95% confidence interval, 0·48–1·31). The probability of stroke recurrence increased in patients with large-artery disease and DL, compared with other subtypes of stroke [log rank test (Mantel–Cox) P < 0·013]. Conclusions Our results showed that DL is related to the recurrent strokes in patients with ischemic stroke within five-years after ischemic stroke, specifically to the large-artery disease subtype.

Cognitive Decline in Patients with Leukoaraiosis Within 5 Years after Initial Stroke.

BACKGROUND Leukoaraiosis (LA) is closely associated with cognitive deficits. The association between LA and cognitive disorders, such as mild cognitive impairment (MCI) and dementia, after initial stroke has not been systematically studied. In this study, we sought to identify whether LA contributes to the occurrence of certain type of cognitive disorders after initial stroke. METHODS Data from our Stroke Registry were examined, and 5-year follow-up data for LA and cognitive disorders were analyzed. We performed Kaplan-Meier analysis and log-rank test to assess the predictive value of LA for risk of cognitive decline and the Cox proportional hazards model to test the risk factors studied as independent determinants of cognitive impairment. RESULTS The frequency of patients with normal cognitive function decreased significantly at 5 years compared with initial stroke (78% vs 70%; odds ratio, 1.51; 95% confidence interval, 1.41-1.62). Of 8784 patients, 1659 (19%) had dementia and 964 (11%) had MCI at the final analysis. After 5 years of follow-up, survival analysis showed that all patients with LA had an increased probability of MCI compared with those without LA (P < .0001). Patients with LA had an increased chance of dementia compared with those without LA (P < .0001) at the end of follow-up. Cognitive decline probability was significantly higher in patients with severe LA compared with those with mild/moderate LA (P < .0001). Cox regression analyses showed that recurrence of stroke (hazard ratio [HR], 3.92 [95% CI, 3.26-4.72]), hypertension (HR, 1.11 [95% CI, 1.0-1.22]), LA (HR, 1.15 [95% CI, 1.05-1.25]), age (HR, 1.05 [95% CI, 1.04-1.06]), hypercholesterolemia (HR, .86 [95% CI, .77-.95]), higher LDL cholesterol (HR, 1.21 [95% CI, 1.11-1.32]), lower HDL cholesterol (HR, .90 [95% CI, .83-.98]), coronary heart disease (HR, .85 [95% CI, .77-.94]), and National Institutes of Health Stroke Scale score at admission (HR, .77 [95% CI, .72-.82]) were also significantly associated with cognitive impairments. CONCLUSIONS Our findings suggest that patients with LA may be at risk of developing new cognitive impairments at long-term period after initial stroke. The evaluation of the concomitant risk factors, besides providing insights about the possible mechanisms behind the cognitive dysfunction present in LA, may be of help for the prevention of cognitive impairments.

Transcranial Doppler detection of microembolic signals in patients with Behçet’s disease

Abstract We evaluated the prevalence of microembolic signals (MES) in patients with Behçet’s disease (BD). We also attempted to determine the frequency of MES in BD patients with or without neurological involvement. This study enrolled 55 patients fulfilling the diagnostic criteria of International Study Group for BD. Bilateral transcranial Doppler ultrasound of the middle cerebral arteries was performed. MES were identified based on the criteria of International Consensus group on Microembolus Detection. Patients with BD were divided into two groups in respect of the presence of neurological involvement (n = 10) or not (n = 45), and counts of MES in the two were compared with each other and with normal subjects. We found MES in 16 patients (29%) with BD. The frequency was higher in patients with neurological involvement than in those without (80% vs. 17%, P < 0.001). In patients with neurological involvement there was a positive correlation in regression analysis between the prevalence of MES and disease duration (P = 0.025). There was a significantly higher prevalence of MES in BD patients than in control subjects. The frequency of MES was higher in patients with neurological involvement than in those without. TCD detection of MES may allow the recognition of subset of patients at high risk for the appearance of neurological involvement.