Investigation of risk factors, topographic location and stroke mechanisms of unilateral isolated and posterior cerebral ARTERY thalamic infarcts.

BACKGROUND AND PURPOSE: In this study, we aimed to examine the risk factors, topographic features and stroke mechanisms of acute ischemic unilateral infarcts of thalamus. METHODS: Patient with isolated thalamic infarct and those with posterior cerebral artery (PCA) infarction who were admitted to our hospital between January 2014 and January 2017 with acute unilateral thalamic infarction (TI) were included in this study (isolated thalamic infarction/ isolated TI; thalamic and posterior cerebral artery infarction/PCA+TI). Demographic characteristics and vascular risk factors of the patients were determined. Thalamic infarct areas were recorded topographically as anterior, posteromedial, ventrolateral, posterolateral, more than one area, and variant areas. Stroke mechanism was determined according to the criteria of "Trial of Org 10172 in Acute Stroke Treatment" (TOAST). Patients with isolated TI and PCA TI were compared according to risk factors, stroke mechanism and infarct topography. RESULTS: Forty-three patients with a mean age of 63.3 ± 14.5 years were included in the study. Twenty-eight patients (60.1%) were found to have isolated TI and the remaining 15 patients (34.9%) had PCA+TI. 32.1% of patients with isolated TI had sensory symptoms on presentation, and 60% of patients with PCA-TI had sensorimotor symptoms. The mean age, the mean score on National Institutes of Health Stroke Scale (NIHSS) and the mean frequency of atrial fibrillation were higher in PCA+TI patients than in isolated-TI patients (p: 0.04, p: 0.004, p: 0.02 respectively). 32.6% of the patients had ventrolateral, 30.2% had posteromedial involvement. Ventrolateral topography was seen in 46.7% of the PCA+TI patients, while posteromedial topography was seen in 39.3% of the isolated-TI patients. 53.6% of the isolated-TI had small vessel disease etiology, while 40% of the PCA+TI had cardioembolic etiology, and the other 40% had large artery atherosclerosis. CONCLUSION: Our study showed that the most ommon stroke mechanism in patients with thalamic infarction is the small vessel disease. Isolated TI and PCA+TI patients differ in terms of etiologic mechanism and infarct topography. Variant territorial involvement and multiple area involvements can be quite common in thalamic infarcts.

Supratentorial Cerebral Arterial Territories for Computed Tomograms: A Mapping Study in 1160 Large Artery Infarcts.

We recently generated a high-resolution supratentorial vascular topographic atlas using diffusion-weighed MRI in a population of large artery infarcts. These MRI-based topographic maps are not easily applicable to CT scans, because the standard-reference-lines for axial image orientation (i.e., anterior-posterior commissure line versus orbito-meatal line, respectively) are 'not parallel' to each other. Moreover, current, widely-used CT-based vascular topographic diagrams omit demarcation of the inter-territorial border-zones. Thus, we aimed to generate a CT-specific high-resolution atlas, showing the supratentorial cerebrovascular territories and the inter-territorial border-zones in a statistically rigorous way. The diffusion-weighted MRI lesion atlas is based on 1160 patients (67.0 ± 13.3 years old, 53.7% men) with acute (<1-week) cerebral infarction due to significant (>50%) stenosis or occlusion of a single large cerebral artery: anterior, middle, or posterior cerebral artery. We developed a software package enabling the transformation of our MR-based atlas into a re-oriented CT space corresponding to the axial slice orientations used in clinical practice. Infarct volumes are individually mapped to the three vascular territories on the CT template-set, generating brain maps showing the voxelwise frequency of infarct by the affected parent vessel. We then mapped the three vascular territories collectively, generating a dataset of Certainty-Index (CI) maps to reflect the likelihood of a voxel being a member of a specific vascular territory. Border-zones could be defined by using either relative infarct frequencies or CI differences. The topographic vascular territory atlas, revised for CT, will allow for easier and more accurate delineation of arterial territories and borders on CT images.

Oclusión de la arteria cerebral media en ataque cerebrovascular isquémico agudo / Middle cerebral artery occlusion in acute ischaemic cerebrovascular attack

El ataque cerebrovascular isquémico (ACV) es una de las principales causas de morbimortalidad a nivel mundial y nacional. Se estudiaron 35 pacientes identificándose que las arterias que presentaron mayor frecuencia de oclusión en el ACV isquémico agudo fueron la arteria cerebral media y la arteria cerebral posterior. Consideramos necesario que los especialistas puedan localizaran atómicamente los ACV para la aplicación de terapias neuroprotectoras mejorando las opciones de tratamiento y previniendo obstrucciones secundarias.

Ischaemic stroke (CVA) is one of the leading causes of morbidity and mortality at a global and national level. We studied 35 patients, determined the arteries that presented a higher frequency of occlusion in acute ischemic stroke and identified the middle cerebral artery and the posterior cerebral artery. We consider it necessary that specialists can locate anatomically strokes in order to apply neuroprotective therapies to improve treatment options and preventing secondary obstructions.

Beyond textbook neuroanatomy: The syndrome of malignant PCA infarction.

Given its limited vascular territory, occlusion of the posterior cerebral artery (PCA) usually does not result in malignant infarction. Challenging this concept, we present 3 cases of unilateral PCA infarction with secondary malignant progression, resulting from extension into what would classically be considered the posterior middle cerebral artery (MCA) territory. Interestingly, these were true PCA infarctions, not "MCA plus" strokes, since the underlying occlusive lesion was in the PCA. We hypothesize that congenital and/or acquired variability in the distribution and extent of territory supplied by the PCA may underlie this rare clinical entity. Patients with a PCA infarction should thus be followed closely and offered early surgical decompression in the event of malignant progression.

Sparing of the hippocampus indicates better collateral blood flow in acute posterior cerebral artery occlusion.

BACKGROUND: In acute posterior cerebral artery, occlusion involvement of the hippocampus is a common finding. Nevertheless, until today, infarction and ischemic lesion evolution in the hippocampus has not been studied systematically. AIM: Evaluation of hippocampal infarction patterns in posterior cerebral artery occlusion in the very early phase (≤six-hours) and ischemic lesion evolution on follow-up magnetic resonance imaging in relation to collateral blood flow assessed by a magnetic resonance imaging-based approach was conducted. METHODS: In 28 patients [mean age 69·4 ± 13·8 years, 19 (67·9%) males, 10 (32·1%) females] with proximal posterior cerebral artery occlusion, magnetic resonance imaging findings were analyzed, with emphasis on hippocampal infarction patterns on diffusion-weighted images and collateralization on dynamic 4D angiograms derived from perfusion-weighted raw images. RESULTS: On initial diffusion-weighted images, we identified all known hippocampal infarction patterns: type 1 (complete) in 6/18 (33·3%) patients, type 2 (lateral) in 10/18 (55·6%) patients, and type 3 (dorsal) and type 4 (circumscribed) in 1/18 (5·6%) patient respectively. On dynamic 4D angiograms, the grade of collateralization was classified as 1 in 9 (32·1%), 2 in 1 (3·6%), 3 in 10 (35·7%), and 4 in 8 (28·6%) patients. On follow-up diffusion-weighted images, we found new ischemic lesions in three and infarction growth in the hippocampus in five patients. Patients with better collateralization (grades 3 and 4) less often had hippocampal infarctions on initial (P = 0·003)/follow-up diffusion-weighted images (P = 0·046) as well as type 1 on initial (P = 0·007)/follow-up diffusion-weighted images (P = 0·005). CONCLUSIONS: Involvement of the hippocampus in proximal posterior cerebral artery occlusion is frequently but not obligatorily observed and highly dependent on the extent of collateralization. The same holds true for hippocampal infarction patterns.

Neural correlates of visual motion processing without awareness in patients with striate cortex and pulvinar lesions.

Patients with striate cortex lesions experience visual perception loss in the contralateral visual field. In few patients, however, stimuli within the blind field can lead to unconscious (blindsight) or even conscious perception when the stimuli are moving (Riddoch syndrome). Using functional magnetic resonance imaging (fMRI), we investigated the neural responses elicited by motion stimulation in the sighted and blind visual fields of eight patients with lesions of the striate cortex. Importantly, repeated testing ensured that none of the patients exhibited blindsight or a Riddoch syndrome. Three patients had additional lesions in the ipsilesional pulvinar. For blind visual field stimulation, great care was given that the moving stimulus was precisely presented within the borders of the scotoma. In six of eight patients, the stimulation within the scotoma elicited hemodynamic activity in area human middle temporal (hMT) while no activity was observed within the ipsilateral lesioned area of the striate cortex. One of the two patients in whom no ipsilesional activity was observed had an extensive lesion including massive subcortical damage. The other patient had an additional focal lesion within the lateral inferior pulvinar. Fiber-tracking based on anatomical and functional markers (hMT and Pulvinar) on individual diffusion tensor imaging (DTI) data from each patient revealed the structural integrity of subcortical pathways in all but the patient with the extensive subcortical lesion. These results provide clear evidence for the robustness of direct subcortical pathways from the pulvinar to area hMT in patients with striate cortex lesions and demonstrate that ipsilesional activity in area hMT is completely independent of conscious perception.

A reproducible and translatable model of focal ischemia in the visual cortex of infant and adult marmoset monkeys.

Models of ischemic brain injury in the nonhuman primate (NHP) are advantageous for investigating mechanisms of central nervous system (CNS) injuries and testing of new therapeutic strategies. However, issues of reproducibility and survivability persist in NHP models of CNS injuries. Furthermore, there are currently no pediatric NHP models of ischemic brain injury. Therefore, we have developed a NHP model of cortical focal ischemia that is highly reproducible throughout life to enable better understanding of downstream consequences of injury. Posterior cerebral arterial occlusion was induced through intracortical injections of endothelin-1 in adult (n = 5) and neonatal (n = 3) marmosets, followed by magnetic resonance imaging (MRI), histology and immunohistochemistry. MRI revealed tissue hyperintensity at the lesion site at 1-7 days followed by isointensity at 14-21 days. Peripheral macrophage and serum albumin infiltration was detected at 1 day, persisting at 21 days. The proportional loss of total V1 as a result of infarction was consistent in adults and neonates. Minor hemorrhagic transformation was detected at 21 days at the lesion core, while neovascularization was detected in neonates, but not in adults. We have developed a highly reproducible and survivable model of focal ischemia in the adult and neonatal marmoset primary visual cortex, demonstrating similar downstream anatomical and cellular pathology to those observed in post-ischemic humans.

A systematic study of topographical memory and posterior cerebral artery infarctions.

OBJECTIVE: To estimate the prevalence of topographical memory impairment following posterior cerebral artery infarctions (PCAI) and define its anatomical correlations. METHODS: We recruited 15 patients (mean duration of 4 months postinfarct). We administered 2 sets of experimental tests to assess topographical memory: one set included 5 computerized tasks (CompT) and the other set consisted of one ecological topographical orientation test (EcolT) that included 4 tasks (i.e., map drawing, picture recognition and ordering, backward path). Fifteen healthy participants served as controls. Patients and controls underwent a volumetric T1 MRI brain scan. Brain lesions in patients were segmented, normalized, and correlated with performance. RESULTS: Topographical memory impairments were evidenced in patients with PCAI using both group and individual analyses (50%), with more severe outcomes in patients with PCAI in the right hemisphere. CompT and EcolT were highly correlated, but the ecological test was more sensitive in revealing topographical memory impairments. Voxel-based lesion-symptom mapping demonstrated that 2 regions located in the cuneus and the calcarine sulcus correlated significantly with behavioral performance. CONCLUSIONS: Topographical memory disorders following PCAI are reported in 50% of the patient population. Our results demonstrate the importance of developing and using dedicated batteries of topographical memory tests, in particular real-life tests, to identify such deficits.

False-negative diffusion-weighted imaging in acute stroke and its frequency in anterior and posterior circulation ischemia.

OBJECTIVE: We aimed to investigate the location and size of ischemic stroke lesions that were frequently overlooked by diffusion-weighted imaging (DWI). MATERIALS AND METHODS: We retrospectively reviewed the medical records of 162 patients who had symptoms suggesting ischemic stroke. National Institutes of Health Stroke Scale and Modified Rankin Scale scores, lesion size, magnetic resonance imaging (MRI) findings, delay between onset of symptoms and initial MRI (MRI latency), and vascular distribution of the stroke lesions were analyzed in patients with false-negative DWI findings. RESULTS: Of the 116 patients with a final diagnosis of acute ischemic stroke, 11 patients (9.48%) had false-negative DWI findings in the initial period. The mean (SD) MRI latency was 4.3 (1.2) hours. There was no statistically significant difference in point of lesion size, the National Institutes of Health Stroke Scale, and the Modified Rankin Scales scores. CONCLUSIONS: False-negative DWI findings in acute stroke can be observed both in association with the posterior circulation/small lesions and the anterior circulation/large lesions.

The frequency and severity of extinction after stroke affecting different vascular territories.

We examined the frequency and severity of visual versus tactile extinction based on data from a large group of sub-acute patients (n=454) with strokes affecting different vascular territories. After right hemisphere damage visual and tactile extinction were equally common. However, after left hemisphere damage tactile extinction was more common than visual. The frequency of extinction was significantly higher in patients with right compared to left hemisphere damage in both visual and tactile modalities but this held only for strokes affecting the MCA and PCA territories and not for strokes affecting other vascular territories. Furthermore, the severity of extinction did not differ as a function of either the stimulus modality (visual versus tactile), the affected hemisphere (left versus right) or the stroke territory (MCA, PCA or other vascular territories). We conclude that the frequency but not severity of extinction in both modalities relates to the side of damage (i.e. left versus right hemisphere) and the vascular territories affected by the stroke, and that left hemisphere dominance for motor control may link to the greater incidence of tactile than visual extinction after left hemisphere stroke. We discuss the implications of our findings for understanding hemispheric lateralization within visuospatial attention networks.

The artery of Percheron: an anatomic study with potential neurosurgical and neuroendovascular importance.

BACKGROUND: One variant branch of the P1 segment of the posterior cerebral artery (PCA) is the artery of Percheron (AOP). This unilateral trunk supplies thalami and potentially mesencephalic structures. As studies of this vessel are scant in the literature and damage to this artery can have catastrophic results, the authors performed this study to better elucidate its morphology. MATERIALS AND METHODS: Twenty-five adult latex-injected cadaveric heads underwent brain removal and microdissection with specific attention to the presence of the AOP. When identified, measurements were made and observations given to the origin and course of this vessel. A case illustration is also presented that demonstrates bilateral thalamic and midbrain infarctions most likely due to thrombosis of the AOP. RESULTS: An AOP was identified in three specimens (12%)-2 right and 1 left side (1 male and 2 female specimens) and arose, on average, 8 mm lateral to the basilar artery bifurcation. The average diameter was 2.1 mm, and the length between the origin and brain penetration had a mean distance of 1.5 cm. In all specimens, the AOP had a coiled appearance, especially in its proximal extraparenchymal segment. The contralateral P1 segment of the PCA was not absent or hypoplastic in any of the three specimens. All arteries supplied small branches to the ipsilateral and contralateral thalami and midbrain. CONCLUSIONS: Knowledge of the AOP may be important during surgical or neuroendovascular approaches to the basilar bifurcation or during interpretation of imaging, especially in patients presenting with bilateral thalamic and midbrain infarctions.

QTc-prolongation in posterior circulation stroke.

BACKGROUND AND PURPOSE: To evaluate the relationship between infarct location and QTc-prolongation in patients with posterior circulation strokes. METHODS: Admission electrocardiograms (ECG) of 131 patients among a prospective sample of 407 consecutive adult patients in the New England Medical Center Posterior Circulation Registry were retrospectively analyzed. The QT interval (ms) was measured and corrected using Bazett's formula (QTcBazett) as well as linear regression functions (QTcLinear). QTcBazett > 440 ms and QTcLinear ≥ 450 ms for men (≥460 ms for women) were considered prolonged. Multivariable linear and logistic regression analyses were used to identify independent predictors of the QTc. RESULTS: Overall, 34% of patients had a prolonged QTcBazett and 7% had a prolonged QTcLinear noted on the admission ECG. There was a significant association between temporal lobe infarction and QTcBazett and QTcLinear (p < 0.001 for both) in multivariable linear regression analyses adjusting for demographics, ECG parameters, and preadmission medication use. In multivariable logistic regression analysis, temporal lobe infarction emerged as an independent predictor of prolonged QTcBazett (p = 0.009) and QTcLinear (p = 0.008), respectively. Sensitivity analyses excluding patients with transient ischemic attack yielded similar results. Exploratory analyses indicated that patients with temporal lobe infarction had worse functional 30-day outcomes in multivariable logistic regression (p = 0.022). However, there was no significant association between QTc and 30-day functional outcome. CONCLUSIONS: QTc-prolongation is common after posterior circulation stroke and associated with temporal lobe infarction. Prospective studies are needed to confirm these preliminary findings and to examine potential long-term consequences.

Posterior cerebral artery territory infarctions.

Infarctions in the territory of the posterior cerebral artery (PCA) occur in about 5-10% of all ischemic strokes. The PCA can be divided into 'deep' (P1 and P2 segments) and 'superficial' (P3 and P4) segments. Occlusion of paramedian perforating arteries arising from P1 causes rostral midbrain infarction with or without thalamic lesion. The classical clinical triad after thalamomesencephalic infarcts is hypersomnolence, cognitive deficits and vertical oculomotor paresis. Two main arterial groups arise from P2: infarction in the territory of the thalamogeniculate arteries causes severe contralateral hypesthesia and ataxia, whereas infarction in the territory of the posterior choroidal arteries results in sectoranopia with involvement of the lateral geniculate body. After superficial PCA infarcts, visual field defects and somatosensory deficits are the most frequent signs. Additionally, disorders of reading may be seen after unilateral left infarction and disorientation for place and visual neglect after right lesion. After bilateral PCA infarcts, amnesia, cortical blindness (the patient cannot see but pretend he can) may occur. Acute thrombolysis is as useful after PCA infarctions as after anterior circulation strokes. Mortality after PCA strokes is low, but long-term behavioral and cognitive deficits are underestimated.

Visual agnosia and posterior cerebral artery infarcts: an anatomical-clinical study.

BACKGROUND: To evaluate systematically the cognitive deficits following posterior cerebral artery (PCA) strokes, especially agnosic visual disorders, and to study anatomical-clinical correlations. METHODS AND FINDINGS: We investigated 31 patients at the chronic stage (mean duration of 29.1 months post infarct) with standardized cognitive tests. New experimental tests were used to assess visual impairments for words, faces, houses, and objects. Forty-one healthy subjects participated as controls. Brain lesions were normalized, combined, and related to occipitotemporal areas responsive to specific visual categories, including words (VWFA), faces (FFA and OFA), houses (PPA) and common objects (LOC). Lesions were located in the left hemisphere in 15 patients, in the right in 13, and bilaterally in 3. Visual field defects were found in 23 patients. Twenty patients had a visual disorder in at least one of the experimental tests (9 with faces, 10 with houses, 7 with phones, 3 with words). Six patients had a deficit just for a single category of stimulus. The regions of maximum overlap of brain lesions associated with a deficit for a given category of stimuli were contiguous to the peaks of the corresponding functional areas as identified in normal subjects. However, the strength of anatomical-clinical correlations was greater for words than for faces or houses, probably due to the stronger lateralization of the VWFA, as compared to the FFA or the PPA. CONCLUSIONS: Agnosic visual disorders following PCA infarcts are more frequent than previously reported. Dedicated batteries of tests, such as those developed here, are required to identify such deficits, which may escape clinical notice. The spatial relationships of lesions and of regions activated in normal subjects predict the nature of the deficits, although individual variability and bilaterally represented systems may blur those correlations.

Isolated lateral thalamic infarction: the role of posterior cerebral artery disease.

BACKGROUND AND PURPOSE: Lateral thalamic infarction (LTI) is usually caused by small vessel disease (SVD), i.e., occlusion of the deep perforator. However, focal atherosclerotic posterior cerebral artery disease (PCAD) may produce LTI via thrombotic occlusion of the perforator. We aimed to investigate the prevalence of PCAD in LTI and differences in clinical and imaging findings between LTIs associated with PCAD and SVD. METHODS: We retrospectively evaluated 58 consecutive patients with isolated LTI who underwent diffusion-weighted imaging (DWI) and MR angiography (MRA) within 7 days after stroke onset. Patients were divided into two groups: those with PCAD and those with SVD. Clinical syndromes were divided into pure sensory stroke (PSS) and sensory stroke plus (SS-plus), i.e., the concomitant presence of motor dysfunction or ataxia. Clinical and imaging findings were compared between these two groups. RESULTS: Of the 58 patients, 13 (22.4%) had PCAD. PSS was more frequently associated with SVD than with PCAD (57.8% vs. 23.1%, P=0.032). Initial DWI lesion volume (cm³) was significantly larger in PCAD than in patients with SVD (0.38±0.13 vs. 0.33±0.22, P=0.025). Among the 23 patients (39.7%) who underwent follow-up DWI, patients with PCAD showed a significantly greater increase in subacute lesion volume than those with SVD (P=0.019). Although National Institutes of Health Stroke Scale scores did not differ at admission (P=0.185), they were significantly higher at discharge in PCAD than in patients with SVD (P=0.012). CONCLUSIONS: Our data suggest that PCAD is an important cause of LTI, being related to SS-plus, larger lesion volume, and worse clinical outcomes.