New England Medical Center Posterior Circulation Stroke Registry: I. Methods, Data Base, Distribution of Brain Lesions, Stroke Mechanisms, and Outcomes

Among 407 New England Medical Center Posterior Circulation Registry (NEMC-PCR) patients, 59% had strokes without transient ischemic attacks (TIAs), 24% had TIAs before strokes, and 16% had only posterior circulation TIAs. Embolism was the commonest stroke mechanism accounting for 40% of cases (24% cardiac origin, 14% arterial origin, 2% had potential cardiac and arterial sources). In 32%, large artery occlusive lesions caused hemodynamic brain infarction. Stroke mechanisms in the posterior and anterior circulation are very similar. Infarcts most often included the distal posterior circulation territory (rostral brainstem, superior cerebellum and occipital and temporal lobes), while the proximal (medulla and posterior inferior cerebellum) and middle (pons and anterior inferior cerebellum) territories were equally involved. Infarcts that included the distal territory were twice as common as those that included the proximal or middle territories. Most distal territory infarcts were attributable to embolism. Thirty day mortality was low (3.6%). Embolic stroke mechanism, distal territory location, and basilar artery occlusive disease conveyed the worst prognosis.     

Spectrum of superficial posterior cerebral artery territory infarcts

Posterior cerebral artery (PCA) territory infarction is not uncommon. Published series were concentrated either on isolated deep PCA territory infarcts or on incomplete calcarine artery territory infarcts. Although, correlations between clinical symptoms, causes of stroke and outcome at 6-months in patients with superficial PCA territory stroke are less well known. We sought prospectively stroke causes, infarct topography, and clinical findings of 137 patients with superficial PCA territory infarcts with or without mesencephalic/thalamic involvement, representing 11% of patients with posterior circulation ischemic stroke in our Stroke Registry. We analyzed patients by subdividing into three subgroups; (1). cortical infarct (CI) group; (2). cortical and deep infarcts (CDI) (thalamic and/or mesencephalic involvement) group; (3). bilateral infarcts (BI) group. We studied the outcomes of patients at 6-month regarding clinical findings, risk factors and vascular mechanisms by means of comprehensive vascular and cardiac studies. Seventy-one patients (52%) had cortical (CI) PCA infarct, 52 patients (38%) had CDI, and 14 patients (10%) had bilateral PCA infarct (BI). In the CDI group, unilateral thalamus was involved in 38 patients (73%) and unilateral mesencephalic involvement was present in 27% of patients. The presumed causes of infarction were intrinsic PCA disease in 33 patients (26%), proximal large-artery disease (PLAD) in 33 (24%), cardioembolism in 23 (17%), co-existence of PLAD and cardioembolism in 7 (5%), vertebral or basilar artery dissection in 8 (6%), and coagulopathy in 2. The death rate was 7% in our series and stroke recurrence was 16% during 6-month follow-up period. Features of the stroke that was associated with significant increased risk of poor outcome included, consciousness disturbances at stroke onset (RR, 66.6; 95% CI, 8.6-515.5), mesencephalic and/or thalamic involvement (RR, 3.79; 95% CI, 1.49-9.65), PLAD (RR, 2.71; 95% CI, 1.09-6.73), and basilar artery disease (RR, 5.94; 95% CI, 1.73-20.47). The infarct mechanisms in three different types of superficial PCA territory stroke were quite similar, but cardioembolism was found more frequent in those with cortical PCA territory infarction. Although, the cause of stroke could not reliably dictate the infarct topography and clinical features. Visual field defect was the main clinical symptom in all groups, but sensorial, motor and neuropsychological deficits occurred mostly in those with CDI. Outcome is good in general, although patients having PLAD and basilar artery disease had more risk of stroke recurrence and poor outcome rather than those with intrinsic PCA disease.     

Lesion patterns and etiology of ischemia in superior cerebellar artery territory infarcts

BACKGROUND AND PURPOSE: Infarcts in the territory of superior cerebellar artery (SCA) are uncommon. The clinical, and etiological mechanisms of different infarct patterns of SCA are not well known. Diffusion-weighted imaging (DWI) is superior to conventional magnetic resonance imaging for detecting acute small and multiple ischemic lesions. METHODS: We studied 60 patients with lesions involving SCA territory proved by DWI, which have been selected from 3,800 patients with first ischemic stroke consecutively admitted to our stroke unit over a period of 5 years. RESULTS: There are 7 distinctive SCA lesion patterns: (1) a lesion was found in the medial (m) branch territory of SCA (mSCA) in 14 patients; (2) a lesion in the lateral (l) branch territory of SCA (lSCA) was seen in 9 patients; (3) a coexisting lesion involving mSCA and lSCA was found in 9 patients; (4) a lesion in cortical borderzones between SCA and m/l branches of the posterior inferior cerebellar artery (PICA) was observed in 6 patients; (5) a lesion in deep borderzones between lSCA and mSCA, and lPICA and mPICA was present in 8 patients; (6) a lesion involving the medial rostral cerebellum between the right and left SCA was found in 4 patients; (7) multiple lesions involving SCA and other vertebrobasilar artery territories were present in 10 patients. The main cause was possible artery-to-artery embolism from atherosclerotic vertebrobasilar arteries to distal branches of SCA in 20 patients (33%). Fourteen patients had a source of cardioembolism (23%), and 6 patients (8%) had concomitant atherosclerotic vertebrobasilar artery disease and a source of cardioembolism. CONCLUSIONS: An acute ischemic lesion in the SCA territory is mainly multiple. The lSCA territory was the most involved area. Small territorial infarcts were frequently associated with large territorial SCA infarcts. Borderzone SCA infarcts occurred in one third of the patients with transient benign symptoms. Mass effects are unusual despite the large amount of SCA involvement. Our results supported the fact that embolism is the predominant stroke mechanism in the SCA territory infarction.     

New England Medical Center Posterior Circulation registry

Among 407 New England Medical Center Posterior Circulation registry patients, 59% had strokes without transient ischemic attacks (TIAs), 24% had TIAs then strokes, and 16% had only TIAs. Embolism was the commonest stroke mechanism (40% of patients including 24% cardiac origin, 14% intraarterial, 2% cardiac and arterial sources). In 32% large artery occlusive lesions caused hemodynamic brain ischemia. Infarcts most often included the distal posterior circulation territory (rostral brainstem, superior cerebellum and occipital and temporal lobes); the proximal (medulla and posterior inferior cerebellum) and middle (pons and anterior inferior cerebellum) territories were equally involved. Severe occlusive lesions (>50% stenosis) involved more than one large artery in 148 patients; 134 had one artery site involved unilaterally or bilaterally. The commonest occlusive sites were: extracranial vertebral artery (52 patients, 15 bilateral) intracranial vertebral artery (40 patients, 12 bilateral), basilar artery (46 patients). Intraarterial embolism was the commonest mechanism of brain infarction in patients with vertebral artery occlusive disease. Thirty-day mortality was 3.6%. Embolic mechanism, distal territory location, and basilar artery occlusive disease carried the poorest prognosis. The best outcome was in patients who had multiple arterial occlusive sites; they had position-sensitive TIAs during months to years.     

Neurovascular territory involved in different etiological subtypes of ischemic stroke in the Perugia Stroke Registry

We studied the correlation between the potential causes of stroke (TOAST etiological groups) and the involvement of different vascular territories seen on computed tomography (CT) scans in patients with ischemic stroke. Information from consecutive patients with a first-ever stroke have been prospectively coded and entered into a computerized data bank (Perugia Stroke Registry). A population of 1,719 patients were evaluated: 1,284 patients (74.7%) had ischemic stroke. Large artery disease was the main cause of entire middle cerebral artery (MCA) territory infarcts (40.9%), superficial MCA territory infarcts (35.7%), and watershed infarcts (68.2%). The highest presence of emboligenic heart disease was found in the entire MCA territory infarcts (28.8%) or superficial (29.4%) supratentorial infarcts and in cerebellar infarcts (36.8%). Small artery disease was the most common presumed cause of deep MCA infarcts (75.0%) and posterior cerebral artery (PCA) territory infarcts (52.1%). In conclusion: stroke location could depend on its etiology. Lacunar infarcts are the most prevalent (36.7%), being mostly localized in the deep MCA territory; large artery disease includes more than two-thirds of watershed infarcts; the most prevalent territories involved in cardioembolic stroke are the entire MCA and posterior fossa.     

Basilar artery occlusive disease in the New England Medical Center Posterior Circulation Registry

BACKGROUND: Most reports on basilar artery (BA) occlusive disease have retrospectively described single cases or small patient series. OBJECTIVE: To assess clinical and vascular features, stroke mechanisms, etiologies, and outcome of moderate to severe BA occlusive disease among 407 patients in the New England Medical Center Posterior Circulation Registry, the largest prospective series of consecutively collected patients with posterior circulation ischemia to date. RESULTS: We studied 87 patients and identified 3 patient groups with distinct vascular, clinical, etiological, and prognostic characteristics: isolated BA disease (39 patients [44.8%]), BA involvement as part of widespread posterior circulation atherosclerosis (36 patients [41.4%]), and embolism to the BA (12 patients [13.8%]). Vascular risk factors were common and often multiple. Most patients (54 [62.1%]) had involvement of the midportion of the BA. Fifty-eight patients (66%) initially had transient ischemic attacks, of whom 34 (58.6%) progressed to stroke. Transient ischemic attacks were usually multiple, lasted for several months, and increased in frequency as the stroke approached. When an infarct was present, the middle posterior intracranial territory was most often involved (66 patients [75.9%]). Outcome was much better than previously assumed. The mortality rate was 2.3%, and 62 patients (almost 75%) had minor or no deficits at follow-up. Outcome was best among patients with widespread atherosclerotic disease and worst in 7; (58.3%, with major disability) of 12 patients with embolism to the BA. Distal territory involvement, embolism, BA occlusion, decreased level of consciousness, tetraparesis, and abnormal pupils were significant predictors of poor outcome. CONCLUSION: Inclusion of patients into 1 of the BA groups and early identification of predictive outcome factors guide diagnostic evaluation and treatment.     

Posterior cerebral artery territory infarcts: clinical features, infarct topography, causes and outcome. Multicenter results and a review of the literature

Only a few large series of posterior cerebral artery (PCA) stroke exist, and clinical features and causes have not been studied as extensively as in other vascular territories. The PCA syndrome includes more clinical signs than the well-known visual field deficits. Concomitant findings are frequently sensory, slight motor and neuropsychological deficits. Unilateral headaches are the common presenting symptom making complicated migraine an important differential diagnosis. Combined deep and superficial PCA territory infarcts involving the lateral thalamus are more frequent than commonly assumed and are mostly associated with sensory and reversible slight motor deficits. Occlusion of the precommunal PCA segment with associated paramedian midbrain infarction causes severe motor deficits, oculomotor signs, and decreased consciousness and has a poorer outcome than other PCA territory infarcts. Embolism from a cardiac or undetermined source is the leading mechanism accounting for up to half of the cases, whereas arterial embolism from significant proximal vertebrobasilar disease is less frequent. Local atherothrombotic stenosis or occlusion of the PCA is uncommon. In spite of thorough diagnostic evaluation, the etiology of PCA territory infarction cannot be determined in at least one quarter of patients. Among the rare causes of PCA territory infarction carotid artery disease is important while the significance of migraine remains controversial.     

Long‐term outcome in posterior cerebral artery stroke

Introduction: Previous studies on posterior cerebral artery (PCA) strokes focused mainly on topography and underlying pathophysiology. However, there are no data on long‐term prognosis and its association with the localization of the infarct. Methods: All consecutive PCA strokes registered in the Athens Stroke Outcome Project between 01/1998 and 12/2009 were included in the analysis. The New England Posterior Circulation Registry criteria were applied to classify them in relation to topography: (i) pure PCA infarcts, including pure cortical‐only and combined cortical/deep PCA infarcts (groups A and B respectively), and (ii) PCA‐plus strokes, including cortical‐only and combined cortical/deep PCA strokes with ≥1 concomitant infarcts outside PCA territory (groups C and D respectively). Patients were prospectively followed up to 10 years after stroke. Results: Amongst 185 (8.1%) PCA patients that were followed up for 49.6 ± 26.7 months, 98 (53%), 24 (13%), 36 (19.5%), and 27 (14.6%) were classified in group A, B, C, and D, respectively. Infections and brain edema with mass effect were more frequently encountered in PCA‐plus strokes compared to pure PCA (P < 0.05 and <0.01 respectively). At 6 months, 56% of cortical‐only PCA patients had no or minor disability, compared to 37%, 36%, and 26% in the other groups (P = 0.015). The 10‐year probability of death was 55.1% (95%CI: 42.2–68.0) for pure PCA compared to 72.5% (95%CI: 58.8–86.2) for PCA‐plus (log‐rank 14.2, P = 0.001). Long‐term mortality was associated with initial neurologic severity and underlying stroke mechanism. Conclusions: Patients with pure PCA stroke have significantly lower risk of disability and long‐term mortality compared to PCA strokes with coincident infarction outside the PCA territory.     

Posterior cerebral artery infarction from middle cerebral artery infarction

BACKGROUND: While it is known that posterior cerebral artery (PCA) infarction may simulate middle cerebral artery (MCA) infarction, the frequency and localization of this occurrence are unknown. OBJECTIVE: To determine the frequency of PCA infarction mimicking MCA infarction and the territory of the PCA most commonly involved in this simulation. DESIGN: We studied 202 patients with isolated infarction in the PCA admitted to our stroke center to determine the frequency of PCA infarction simulating MCA infarction, the involved PCA territory, and the patterns of clinical presentation. RESULTS: We found 36 patients (17.8%) with PCA ischemic stroke who had clinical features suggesting MCA stroke. The PCA territory most commonly involved was the superficial PCA territory (66.7%), followed by the proximal PCA territory (16.7%) and both the proximal and the superficial PCA territories (16.7%). The principal stroke mechanism was cardioembolic (54.1%) in the superficial PCA territory, lacunar (46.2%) in the proximal PCA territory, and undetermined (40.2%) in both the proximal and the superficial territories. Among the 36 patients, the most common clinical associations were aphasia (13 patients), visuospatial neglect (13 patients), and severe hemiparesis (7 patients). CONCLUSIONS: Posterior cerebral artery infarction simulating MCA infarction is more common than previously thought. Early recognition of the different stroke subtypes in these 2 arteries may allow specific management.     

Posterior cerebral artery stenosis

We analyzed the clinical features of symptomatic posterior cerebral artery (PCA) stenosis in 6 patients selected from 15 patients with angiographically documented PCA atherostenosis occurring during a 7-year period. Transient ischemic attacks (TIAs) were the major presentation in 5 patients. A homonymous visual field defect was present in 2 patients. TIA symptoms were predominantly visual or sensory, or both. The most common visual symptom was difficulty seeing to one side. One patient saw flashing lights. Sensory spells were always paresthetic, usually involving the arm and hand and occasionally the face and leg. Three patients had visual and sensory spells together. Two patients with a visual field defect had calcarine infarcts found by computed tomography. All patients were treated with warfarin. During follow-up (4 months to 4 years), no patient had a new stroke in the PCA territory, and only one continued to have TIAs. PCA atherostenosis is rarer then PCA embolic occlusion. In contrast to those with PCA embolism, our patients with PCA atherostenosis had more TIAs and fewer infarcts. The clinical features of PCA stenosis--preponderance of visual and sensory TIAs--distinguish this vascular lesion from stenosis of the middle cerebral artery.     

Multiple large and small cerebellar infarcts

To assess the clinical, topographical, and aetiological features of multiple cerebellar infarcts,18 patients (16.5% of patients with cerebellar infarction) were collected from a prospective acute stroke registry, using a standard investigation protocol including MRI and magnetic resonance angiography. Infarcts in the posterior inferior cerebellar artery (PICA)+superior cerebellar artery (SCA) territory were most common (9/18; 50%), followed by PICA+anterior inferior cerebellar artery (AICA)+SCA territory infarcts (6/18; 33%). One patient had bilateral AICA infarcts. No infarct involved the PICA+AICA combined territory. Other infarcts in the posterior circulation were present in half of the patients and the clinical presentation largely depended on them. Large artery disease was the main aetiology. Our findings emphasised the common occurrence of very small multiple cerebellar infarcts (<2 cm diameter).These very small multiple cerebellar infarcts may occur with (13 patients/18; 72%) or without (3/18; 22%) territorial cerebellar infarcts. Unlike previous series, they could not all be considered junctional infarcts (between two main cerebellar artery territories: 51/91), but also small territorial infarcts (40/91). It is suggested that these very small territorial infarcts may be endzone infarcts, due to the involvement of small distal arterial branches. It is possible that some very small territorial infarcts may be due to a microembolic process, but this hypothesis needs pathological confirmation.     

The mechanism of ischemic stroke in patients with dolichoectatic basilar artery

Basilar artery dolichoectesia (BD) may cause brainstem ischemia by multiple mechanisms, including thrombosis, embolism, occlusion of deep penetrating arteries. The objective of this study was to determine and characterize clinical, imaging findings and hemodynamic mechanisms in patients with cerebrovascular event associated with BD and compare these data with those for patients with BD who did not have stroke. We studied 29 consecutive stroke, two transient ischemic attack (TIA) patients with BD who have been admitted to our stroke unit. We sought the diameter of ectasia, height of the bifurcation, lateral displacement, shape deformities, and blood flow velocity of the basilar artery (BA) by transcranial Doppler. Imaging and hemodynamic findings were compared with those found in a group of 18 patients without stroke or TIA. The main infarct localization was pons, eight (28%) with restricted single lesion, 10 (32%) with multiple lesions involving thalamus, midbrain, posterior cerebral artery (PCA) territory. Patients with BD were more probably to have had stroke fitting a clinical and imaging patterns of multiple infarcts than those with restricted infarct in territories supplied by branches of the BA (60% vs. 40%). Hypertension and atherosclerotic changes of the posterior circulation were more frequent in patients with stroke than those without (P = 0.004 and P = 0.028, respectively), whilst the incidence of other vascular risk factors were not significantly different in two groups. Patients with stroke/TIA had more often low blood flow velocity but not significant in the BA when compared with those for BD patients without cerebrovascular event (71% vs. 39%; P = 0.1). Reduced blood flow velocity in the BA was correlated significantly with distal lesions involving thalamus, midbrain and PCA territory rather than those located in the territory supplied by branches of the BA (P = 0.02). In conclusion, it seems probably that BD may cause vertebrobasilar system ischemia by multiple mechanisms, especially reduced blood flow in the BA and atheromatous changes in the vertebrobasilar system may precipitate thromboembolic stroke.     

The clinical and topographic spectrum of cerebellar infarcts: A clinical—magnetic resonance imaging correlation study

We studied 34 consecutive patients with non–mass-producing cerebellar infarcts using a standard protocol of investigations including magnetic resonance imaging (MRI). We analyzed the topography of infarcts to determine the involved arterial territories and we correlated the findings with neurological dysfunction and potential causes of stroke. Sixteen patients had an infarct in the territory of the posterior inferior cerebellar artery (PICA); 2, in the territory of the anterior inferior cerebellar artery (AICA); 13, in the territory of the superior cerebellar artery (SCA); and 8 had junctional infarcts between the territories of the medial and lateral branches of the PICA or PICA/SCA territories. PICA or medial PICA territory infarcts were manifested by acute vertigo and truncal ataxia, while the patients with lateral PICA territory infarcts presented with unsteadiness, limb ataxia and dysmetria without dysarthria. Patients with infarcts in the AICA territory were characterized by limb and trunk ataxia associated with signs of lateropontine involvement. Patients with SCA territory infarcts presented with dysarthria, unsteadiness and/or vertigo, limb ataxia, and dysmetria. Cardiac embolism was the main cause of large infarcts in the territories of the PICA (8/16) or SCA (4/7). Multiple small infarcts were associated with vertebrobasilar atherosclerosis (8/12). These clinical–MRI correlations allow better definition of the topographic and etiological spectrum of cerebellar infarction, which was previously based on pathological studies in subjects with severe infarction.     

Thalamic infarcts in young adults: relationship between clinical-topographic features and pathogenesis.

BACKGROUND: Most reports on thalamic infarcts have focused on clinicoanatomical correlations while the mechanisms of stroke have rarely been investigated. Moreover, most series have included mainly elderly stroke patients, whereas scarce information is available about the etiology of thalamic infarcts in the young. OBJECTIVE: To investigate the mechanisms of thalamic infarcts according to vascular territory in a series of young adults. METHODS: A sample of 24 consecutive patients with thalamic infarcts were found in an unselected series of 129 patients with cerebral infarction aged 18-45 years. Diagnostic investigation included computed tomography and magnetic resonance imaging scans, ultrasonic scanning of the extracranial and intracranial arteries, conventional angiography and magnetic resonance angiography, transthoracic and transesophageal echocardiography and extensive thrombophilic studies. The affected vascular territory within the thalamus was determined using standard templates. RESULTS: Thalamic infarcts constituted almost one fifth of the ischemic strokes in our series. Ten patients (42%) had infarct in the territory of the thalamogeniculate pedicle (group 1), 10 (42%) in the territory of the paramedian thalamosubthalamic artery (group 2) and 3 (12%) in the territory of the tuberothalamic artery (group 3). In 1 patient (4%), the lesion involved more than one vascular thalamic territory. A significant association between cardioembolism and paramedian infarcts was found when comparing the mechanisms of stroke of group 2 with those of the group including infarcts in other thalamic territories (p = 0.002) and with those of group 1 (p = 0.02). CONCLUSIONS: Our findings provide information about the epidemiology of thalamic infarcts in young adults and point to a differential association between the distribution of infarcts in specific vascular territories and the mechanism of stroke.     

HMPAO Single-Photon Emission Computed Tomography in Posterior Circulation Infarcts

The sensitivity of single-photon emission computed tomography (SPECT) in evaluating posterior mculation infarcts compared with that of computed tomography (CT) or magnetic resonance imaging (MRI) remains unknown. In a hospital-based population, the authors studied SPECT, CT, and MRI in 35 consecutive patients presentmg with acute infarction clinically localized in the thalamus (7), posterior cerebral artery (PCA) territory (15), bramtem (19), and cerebellum (3) Multiple infarcts were noted m 8 patients. Overall, the SPECT sensitivity was lower than that of MRI (21% vs 93%, p ~ 0 004) and CT (42% vs 65%, p = 0 046) The SPECT and CT sensitivities were not Significantly different (67% vs 73%) for PCA Infarcts. Performed within 24 hours, SPECT showed a relevant hypoperfusion in all PCA mfarcts. For brainstem infarcts, CT (33%, p = 0 074) and MRI (91 %, p = 0.004) were more sensitive than SPECT, which showed no hemispheric hypoperfusion. The sensitivity of the three imaging techniques was 100% for large cerebellar infarcts. For the small group of thalamic infarcts, the SPECT, CT, and MRI sensitivities were 14, 71, and 100%, respectively. Thus, SPECT compared to CT and MRI is not helpful in the subacute phase to localize PCA and cerebellar infarcts and is of limited value for thalamic infarcts. In the first hours, the absence of cerebral hypoperfusion in brainstem mfarcts may help to differentiate them from hemispheric infarcts usually associated with profound hypoperfusion.     

Mechanisms of infarction in the superficial posterior cerebral artery territory

Numerous reports have described a variety of clinical syndromes resulting from posterior cerebral artery (PCA) infarction, whereas only a few pathoanatomical and retrospective clinical studies have investigated the underlying mechanisms. Therefore we attempted to determine the causes of infarction in the superficial posterior cerebral artery (PCA) territory by means of a more comprehensive, modern vascular and cardiac study. During a 4-year period 74 consecutive patients (49 men, 25 women) with acute PCA infarction documented on CT (n = 74) and MRI (n = 41) were included in the study. Patients had a neurological examination, vascular studies [extra- and transcranial Doppler (n = 74), magnetic resonance (n = 31) or intra-arterial (n = 22) angiography], cardiac evaluation [ECG (n = 74), transthoracic (n = 74) and transoesophageal echocardiography (n = 30)], and coagulation tests. A cardiac source of embolism was established in 31%, significant vertebrobasilar artery disease in 22%, and PCA stenosis or occlusion in 8% of the patients. Rare causes, such as hypercoagulopathy or paradoxical embolism via a patent foramen ovale, were present in 15%. However, in spite of the comprehensive diagnostic evaluation, the cause of the stroke remained undetermined in 24% of the cases. Apart from complete infarcts of the posterior branches of the PCA, which occurred more frequently in cardioembolic strokes (18%, P < 0.05), the topographical patterns of infarct extension and the coincidence of infarction in the deep territories of the PCA, the cerebellum and brainstem were not significantly different among the causal subgroups. The frequency of haemorrhagic transformation (18%) was highest among cardioembolic strokes (44%, P < 0.001). This prospective study of PCA infarction demonstrated embolism from cardiac and vascular sources as the predominant cause. In contrast to previous studies, we found no evidence of migraine as a cause of PCA infarction, whereas paradoxical embolism was the presumed cause in a considerable number of cases. Whereas the cause of stroke could not reliably be derived from infarct topography, haemorrhagic transformation indicated there had been cardioembolism in most cases. Received: 9 January 1997 Received in revised form: 24 June 1997 Accepted: 24 July 1997     

Presentation and prognosis of bilateral infarcts in the territory of the superior cerebellar artery.

Unilateral cerebellar infarcts in the territory of the superior cerebellar artery (SCA) have been studied in recent years to delineate the clinical presentation and stroke mechanism, but most studies excluded bilateral infarctions. We have studied patients with bilateral SCA infarctions to provide data on clinical findings, stroke distribution and outcome. We collected data of 8 patients with bilateral SCA infarctions recognized by computed tomography and/or magnetic resonance imaging. The most common clinical presentation of patients with bilateral SCA infarctions were nausea, vomiting or vertigo (6 patients), often associated with ataxia and dysarthria (5 patients). Further symptoms were variable and depended on additional infarcts in other vascular territories. Infarcts were often partial or scattered with equal distribution between the medial and lateral branches of the SCA. Complete infarction within the SCA area occurred in less than half of the cases. Clinical outcome was either benign (full recovery in 3 patients) or fatal (5 patients). Predictors for a good clinical recovery were young age, few vascular risk factors, only partial involvement of the SCA territory without involvement of other vascular territories, and absent limb weakness on clinical presentation.     

Brachiofacial pure motor stroke.

Pure motor stroke is the commonest lacunar syndrome, but it may be associated with nonlacunar mechanisms of infarction. Pure motor brachiofacial weakness has been considered as a partial syndrome depending on a lacunar mechanism. We studied the correlations between stroke type, topography of infarction and etiology in 22 patients with pure motor brachiofacial weakness who were consecutively admitted to our stroke unit during a 10-year period. Seventeen patients had a small deep infarct, 4 had a cortical infarct in the superficial MCA territory and 1 had no specific lesion. The part of the cardiovascular risk factors was about 36% for smoking, 13% for diabetes mellitus, 60% for dyslipidemia and 40% for heart disease. Hypertension was present in 75% of our cases. None of the patients had a large artery stenosis on Doppler ultrasonography. We concluded that brachiofacial pure motor stroke is not always correlated to lacunar infarcts and may be due to a cortical infarct. MRI should be performed when brain CT is normal because of the implications it may have in management and therapy.     

Mechanisms involved in large subcortical infarcts]

Large subcortical infarcts(maximum diameter of infarct > or = 20 mm) result from various stroke patterns, including striatocapsular infarcts (SCI), corona radiata infarcts, centrum semiovale infarcts, and internal borderzone infarcts. A systematic investigation of stroke pathogenesis involved in large subcortical infarcts, however, has not been performed. This study attempted to clarify the stroke mechanisms involved in large subcortical infarcts, by examining 50 patients with large subcortical infarcts out of 430 ischemic stroke patients consecutively registered in our department. The subjects were divided into two groups according to the vascular territories involved on the MRI: 1) the lenticulostriate arteries group for 39 patients whose infarcts were restricted to within the vicinity of the lenticulostriate arteries; 2) the internal borderzone group for 11 patients whose infarcts mainly involved the internal borderzone (the upper part of the corona radiata and the centrum semiovale) between the territories of the deep perforating branches from the basal cerebral arteries and the medullary branches from the superficial pial arteries. Stroke pathogenesis were classified into the following 6 categories: A) cardiogenic embolism, 9 patients; B) artery-to-artery embolism, 6 patients; C) cryptogenic embolism, 2 patients; D) thrombotic MCA (M1) occlusion, 9 patients; E) thrombotic ICA occlusion, 10 patients; F) undetermined cause, 14 patients. The lenticulostriate arteries group consisted of 9 patients with cardiogenic embolism, 6 with artery-to-artery embolism, 2 with cryptogenic embolism, 8 with thrombotic M1 occlusion, and 14 with undetermined cause. The internal borderzone group consisted of 10 patients with thrombotic ICA occlusion and 1 patient with thrombotic M1 occlusion. The stroke pathogenesis of the undetermined cause is considered to be thrombotic occlusion at the orifice of the lateral lenticulostriate artery, a so-called "branch atheromatous disease (BAD)". The patients in this group experienced a gradual onset, and did not have a cardiac source of the embolism or proximal large artery disease. Among the patients reported as having SCI, BAD may play a role in some cases, especially in those whose the cause was classified as "undetermined". In conclusion, the lenticulostriate arteries group exhibited a higher frequency of cerebral embolisms (cardiogenic embolism, artery-to-artery embolism, and cryptogenic embolism) and thrombotic M1 occlusion, whereas the internal borderzone group had a higher frequency of thrombotic ICA occlusion.     

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 2,750 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.