Single Subcortical Infarction Research Articles

Single Subcortical Infarction Associated with Parental Arterial Disease: Important Yet Neglected Sub-Type of Atherothrombotic Stroke

Traditionally, single subcortical infarction has been considered to be caused by lipohyalinosis of small perforating arteries. However, atherosclerosis in the parental artery produces similar single subcortical infarction by blocking the orifice of branching arteries. The purpose of this paper is to review the evolving concepts, clinical characteristics, and classification issues of single subcortical infarction associated with parental artery disease. Single subcortical infarction associated with parental artery disease is an important cause of subcortical infarction, more so in the posterior than in anterior circulation stroke. It is one of the major causes of brainstem infarction. Single subcortical infarction associated with parental artery disease seems to be common in Asian population where intracranial atherosclerosis is prevalent. Although the clinical characteristics of single subcortical infarction associated with parental artery disease are similar to single subcortical infarction caused by small artery disease, single subcortical infarction associated with parental artery disease is more often associated with characteristics of atherosclerosis, and fluctuating and poorer outcomes. With advanced imaging techniques such as high-resolution cross-sectional magnetic resonance imaging, single subcortical infarction associated with parental artery disease emerges as an even more important stroke sub-type. Nevertheless, it has been neglected in previous stroke sub-type classifications, being erroneously classified as small artery disease or cryptogenic stroke. Prevention and treatment trials focusing on single subcortical infarction associated with parental artery disease are not available. Single subcortical infarction associated with parental artery disease is an important stroke sub-type, distinct from small artery disease, illustrating that greater efforts should be made in its accurate diagnosis. Studies are needed to investigate the prevalence of single subcortical infarction associated with parental artery disease in various parts of the world and to design a stroke classification system that includes single subcortical infarction associated with parental artery disease. Prevention and treatment trials should consider this important sub-group of stroke, so that tailored strategies can be applied in clinical practice.

Hidden ills May Underlie Parkinson's Signs

Parkinsonian signs such as motor slowing, gait disturbance, and tremor in old age may be caused by underlying cerebrovascular pathologies that cannot be detected by conventional brain imaging, according to findings from a clinical-autopsy study involving 418 cases. “Together these data suggest that a substantial portion of older people have brain tissue damage and small vessel disease that are unlikely to be detected before death and suggest that cerebrovascular disease may be an even larger public health challenge than currently estimated,” wrote Dr. Aron S. Buchman and his colleagues in Stroke: Journal of the American Heart Association. Macroscopic infarcts were found in 150 (36%) of the 418 brains that were autopsied for the study, and 110 of those also had evidence of pathologies that can’t be detected by conventional imaging, including microinfarcts, arteriolosclerosis, or both. Furthermore, those pathologies were detected in almost 30% of cases without macroscopic infarcts, according to Dr. Buchman, associate professor of neurological sciences at Rush University Medical Center, Chicago, and his coauthors. Of the 268 patients without macroinfarcts, 33 (7.9%) had microinfarcts, 62 (14.8%) had arteriolosclerosis, and 24 (5.7%) had both microinfarcts and arteriolosclerosis (Stroke doi:10.1161/ STROKEAHA.111.623462). Multiple cortical infarcts, or a single subcortical macroscopic infarct, was related to a higher global parkinsonian score, the investigators said. After the researchers controlled for macroscopic infarcts, they found an association between multiple microscopic infarcts and higher global parkinsonism. Cortical microinfarcts, but not subcortical microinfarcts, also were associated with a higher global parkinsonian score. Each type of pathology (arteriolosclerosis, microinfarcts, and macroinfarcts — particularly subcortical microinfarcts and macroinfarcts) was found to be independently and significantly associated with gait disturbance. This association was present for both single and multiple subcortical macroscopic infarcts, and for multiple subcortical microinfarcts. The brain autopsies used for this study were from deceased participants from the Religious Order Study, a longitudinal clinical-pathological study of aging in community-dwelling nuns and priests who had no known dementia at enrollment, and who were evaluated for parkinsonian signs with the 26-item modified version of the motor portion of the Unified Parkinson’s Disease Rating Scale prior to death. The study involved more women (61%) than men, and participants had a mean global parkinsonian score of 18.6 and a mean age of 88.5 years at death. The findings are important because mild parkinsonian signs affect up to 50% of people aged 85 and older without known neurological disease and are the source of significant morbidity and mortality, the investigators said. They also noted that the findings raise the question of whether improved public health strategies to increase prevention and treatment of vascular disease could decrease the burden of mild age-related parkinsonian signs. The researchers also suggested that the contribution of cerebrovascular disease to loss of motor function in old age is underestimated. “Further clinical-pathological-imaging studies will be needed to delineate antemortem imaging markers as well as the pathophysiology of both microinfarcts and small vessel disease in the development of motor impairment in old age,” they wrote. The study was funded by National Institutes of Health grants and the Illinois Department of Public Health. The authors disclosed no conflict of interest. CfA

Lesion volume increase is related to neurologic progression in patients with subcortical infarction

It remains unknown whether subacute lesion volume increase is related to neurologic progression (NP) and clinical outcome (CO) in patients with single subcortical infarct (SSI) in the middle cerebral artery (MCA) territory. We studied 77 patients who underwent diffusion-weighted MRI (DWI) within 48 h after stroke onset, which revealed unilateral SSI in the MCA territory, and follow-up DWI and MR angiography within 7 days of onset. Neurologic progression was defined as the increase of the National Institutes of Health Stroke Scale (NIHSS) score by ≥2 during the first week. Clinical outcome was dichotomized as good (≤2) and poor (≥3) according to the modified Rankin Scale at 1 month after the onset. Lesion volume increase was defined when the infarct volume in the follow-up MRI exceeds the initial one by either ≥30% or 50%. Fourteen patients (18.2%) had NP, and 17 (22.1%) had poor CO. Increase in lesion volume, found in 42 patients (54.5%) when defined by 50% increase and in 51 (66.2%) by 30%, was significantly associated with NP (50%, p=0.010; 30%, p=0.027) and poor CO (50%, p=0.040; 30%, 0.111). Multivariate logistic analyses revealed that lesion volume increase was independently related to NP (odd ratio, 8.48; 95% CI, 1.55–46.46) and that NP was the important predictor for poor CO (odd ratio, 39.69; 95% CI, 3.44–458.68). We conclude that subacute lesion volume growth is closely related to the NP and that the NP predicts subsequent poor CO.

Location of single subcortical infarction due to middle cerebral artery atherosclerosis: proximal versus distal arterial stenosis

Background: Atherosclerotic middle cerebral artery (MCA) disease may produce subcortical infarction either in the upper part (corona radiata, CR) or in the lower area (internal capsule, IC) of the pyramidal...

The cognitive pattern of vascular dementia and its assessment

Prevailing definitions of dementia are based on the Alzheimer disease (AD) model, which places major emphasis on memory impairment. In other dementias, such as vascular dementia (VaD), several other cognitive dysfunctions predominate over the memory disorder. The cognitive pattern changes according to the type of VaD. In multi-infarct dementia (MID), cortical lesions may cause loss of instrumental functions manifested by aphasia, amnesia, apraxia, or agnosia. Language in MID patients has shorter phrase length, restricted lexical variability, simplified syntax, and low verbal fluency; dysarthria or mechanical impairment of speech with abnormal pitch, melody, or articulation rate also occur. The latter are rare in degenerative dementias. Compared with AD, patients with MID demonstrate superior performance on verbal learning and memory, better delayed recall, and lower rates of forgetting, intrusions, and false positives. Subcortical ischemic dementia, subcortical hemorrhages, or single subcortical strategic infarcts frequently impair executive functions, attention, and speed of information processing; anterograde memory is generally less impaired than in AD patients. The two main problems of batteries used for evaluation of dementia such as those recommended by CERAD (verbal fluency test, a brief naming test such as the Modified Boston Naming Test, free recall of a word list, with immediate and delayed recall, followed by a recognition task of the same words, and line drawings of figures), as well as the Mini-Mental State Examination (MMSE), are (1) their strong emphasis on memory, temporal and spatial orientation, calculation, language, and constructional praxis, and (2) their failure to assess executive functions. Simple tests of executive function include the Trail Making Test, the Wisconsin Card Sorting Test, and the EXIT-25. A simple and effective test is the CLOX, an executive variation of the clock-drawing task. Depressive symptoms and other psychiatric disturbances are particularly common in VaD and become sources of cognitive and functional disability. Several questionnaires assess the neuropsychiatric manifestations of dementia including the Neuro-Psychiatric Inventory (NPI), the BEHAVE-AD test, the Cohen-Mansfield Scale, and the CERAD Behavioral Rating Scale for Dementia. Finally, development of dementia after a stroke may represent true VaD in patients with intact cognition before the stroke, or AD + CVD when the dementia occurs in patients that already had memory problems before the ictus. The diagnosis of VaD is a challenging clinical problem that encompasses the fields of medicine, neurology, psychiatry, and psychology.

Constraint-Induced Therapy in Stroke: Magnetic-Stimulation Motor Maps and Cerebral Activation

Constraint-induced movement therapy (CI), a standardized intensive rehabilitation intervention, was given to patients a year or more following stroke. The goal was to determine if CI was more effective than a less-intensive control intervention in changing motor function and/or brain physiology and to gain insight into the mechanisms underlying this recovery process. Subjects were recruited and randomized more than 1 year after a single subcortical infarction. Clinical assessments performed before and after the intervention and at 6 months postintervention included the Wolf Motor Function Test (WMFT), the Motor Activity Log (MAL), and the Assessment of Motor and Process Skills (AMPS). Transcranial magnetic stimulation was used to map the motor cortex. Positron emission tomography was used to measure changes in motor task-related activation due to the intervention. MAL increased by 1.08 after CI therapy and decreased by 0.01 after control therapy. The difference between groups was significant (P < 0.001). Changes in WMFT and AMPS were not significantly different between groups. Cerebral activation during a motor task decreased significantly, and motor map size increased in the affected hemisphere motor cortex in CI patients but not in control patients. Both changes may reflect improved ability of upper motor neurons to produce movement.

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.