Anatomical variations in the posterior part of the circle of willis and vascular pathology in bilateral thalamic infarction.

BACKGROUND AND PURPOSE: Bilateral paramedian thalamic infarction is a rare subtype of stroke the etiology of which still remains undetermined in many patients. METHODS: From a computed tomography (CT)/magnetic resonance imaging report database, we identified and analyzed 48 patients with bilateral paramedian thalamic infarction on diffusion-weighted imaging. Vascular pathologies were noted on CT angiography (CTA)/magnetic resonance angiography (MRA) and the P1 segments of the posterior cerebral artery (PCA) described as normal, hypoplastic, or absent. RESULTS: Vascular imaging revealed top of the basilar artery (BA) occlusion in 6 (12.5%), BA occlusion in 4 (8.3%), BA stenosis in 1 (2.1%), and BA hypoplasia in 3 (6.3%), PCA occlusion in 4 (8.3%), and PCA stenosis in 4 (8.3%) patients. In 18 (37.5%) patients, one or both P1 segments of the PCA were hypoplastic or absent. Patients with hypoplastic/absent P1 segments were more likely to have exclusively bilateral paramedian thalamic lesions (P < .001). An embolic source could be identified in 25 (55.6%) patients; there were no significant differences between both groups. CONCLUSIONS: Vascular imaging is useful to determine underlying vascular pathologies and may support the diagnosis of small vessel disease in those patients with isolated bilateral paramedian thalamic infarction, hypoplastic/absent P1 segment of the PCA, and lack of vascular pathology.

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.

Design of the stenting and aggressive medical management for preventing recurrent stroke in intracranial stenosis trial.

BACKGROUND: Patients with recent transient ischemic attack (TIA) or stroke caused by 70% to 99% stenosis of a major intracranial artery are at high risk of recurrent stroke on usual medical management, suggesting the need for alternative therapies for this disease. METHODS: The Stenting and Aggressive Medical Management for Preventing Recurrent stroke in Intracranial Stenosis trial is an ongoing, randomized, multicenter, 2-arm trial that will determine whether intracranial angioplasty and stenting adds benefit to aggressive medical management alone for preventing the primary endpoint (any stroke or death within 30 days after enrollment or after any revascularization procedure of the qualifying lesion during follow-up, or stroke in the territory of the symptomatic intracranial artery beyond 30 days) during a mean follow-up of 2 years in patients with recent TIA or stroke caused by 70% to 99% stenosis of a major intracranial artery. Aggressive medical management in both arms consists of aspirin 325 mg per day, clopidogrel 75 mg per day for 90 days after enrollment, intensive risk factor management primarily targeting systolic blood pressure <140 mm Hg (<130 mm Hg in diabetics) and low density cholesterol <70 mg/dL, and a lifestyle modification program. The sample size required to detect a 35% reduction in the rate of the primary endpoint from angioplasty and stenting based on the log-rank test with an alpha of 0.05, 80% power, and adjusting for a 2% loss to follow-up and 5% crossover from the medical to the stenting arm is 382 patients per group. RESULTS: Enrollment began in November 2008 and 451 patients have been enrolled as of March 31, 2011. CONCLUSIONS: This is the first randomized stroke prevention trial to compare angioplasty and stenting with medical therapy in patients with intracranial arterial stenosis and to incorporate intensive management of multiple risk factors and a lifestyle modification program in the study design. Hopefully, the results of the trial will lead to more effective therapy for this high-risk disease.

Functional electrical stimulation (FES) of the upper limb alleviates unilateral neglect: a case series analysis.

We report the results of a new form of therapy for unilateral spatial neglect. Functional electrical stimulation (FES) applied to the left forearm extensor muscles reduced the symptoms of severe left unilateral visual neglect in three patients, with the benefits being measurable at 6 months post-treatment. We suggest that FES activates a proprioceptive map within the right parietal lobe whose level of activation is otherwise diminished by the lesion. This both increases awareness of the contralesional side and stimulates functional interactions with the environment.

[Thalamic dementia secondary to acute bilateral paramedian thalamic infarcts after occlusion of the artery of Percheron]. / Demencia talámica secundaria a infarto agudo paramediano talámico bilateral por oclusión de la arteria de Percheron.

INTRODUCTION: The anterior and medial part of the thalamus is the responsible of multiples cognitive functions through the thalamus-cortical connections. A bilateral thalamic infarction can cause a secondary dementia and these are related to a thalamocortical deafferentation with a partial recovery. We report a case of sudden onset dementia caused by bilateral thalamus lesions. CASE REPORT: A 42 smoker male, that suddenly had an acute confusional syndrome with altered language, bradypsychia, right hemiparesis and right hemisensory loss. Cranial magnetic resonance imaging showed a bilateral thalamic stroke probably due to a variant talamus irrigation (artery of Percheron type 2). From this date, in three months, the patient had attention deficit, impairment of memory retention, apathy, initiative deficit, depressive syndrome and mood changes. All these symptoms improving partially in the following six months. CONCLUSIONS: The thalamic stroke can cause a thalamic dementia, commonly bilateral and preferable located in the anterior and medial nuclei. In our case, cranial SPECT showed frontal hypocaptation for diaschisis phenomenon.

Neuroprotective effect of hyperbaric oxygen therapy monitored by MR-imaging after embolic stroke in rats.

The potential neuroprotective effects of hyperbaric oxygen (HBO) were tested in an embolic model of focal cerebral ischemia with partially spontaneous reperfusion. Rats (n = 10) were subjected to embolic middle cerebral artery occlusion (MCAO) and diffusion weighted MRI (DWI) was performed at baseline, 1, 3, and 6 h after MCAO to determine the ADC viability threshold yielding the lesion volumes that best approximated the 2,3,5-triphenyltetrazolium chloride (TTC) infarct volumes at 24 h (experiment 1). For assessment of neuroprotective effects, rats were treated with 100% oxygen at 2.5 atmospheres absolute (ATA, n = 15) or normobaric room air (n = 15) for 60 min beginning 180 min after MCAO (experiment 2). DWI-, perfusion (PWI)- and T2-weighted MRI (T2WI) started within 0.5 h after MCAO and was continued 5 h, 24 h (PWI and T2WI only), and 168 h (T2WI only). Infarct volume was calculated based on TTC-staining at 24 h (experiment 1) or 168 h (experiment 2) post-MCAO. ADC-lesion evolution was maximal between 3 and 6 h. In experiment 2, the relative regional cerebral blood volume (rCBV) of both groups showed similar incomplete spontaneous reperfusion in the ischemic core. HBO reduced infarct volume to 145.3 +/- 39.6 mm3 vs. 202.5 +/- 58.3 mm3 (control, P = 0.029). As shown by MRI and TTC, HBO treatment demonstrated significant neuroprotection at 5 h after embolic focal cerebral ischemia that lasted for 168 h.

Neuroimaging determinants of cognitive performances in stroke associated with small vessel disease.

BACKGROUND AND PURPOSE: Controversies still exist as to the neuroimaging determinants of cognitive impairment in cerebral small vessel disease (SVD). The authors studied the neuroimaging correlates of cognitive performances among patients with stroke associated with SVD. METHODS: The authors per formed cerebral computed tomography, magnetic resonance imaging, and diffusion-weighted imaging among 74 consecutive patients admitted to the acute stroke unit because of stroke associated with SVD. They examined the association between cognitive performances and the following neuroimaging features: volume of white matter changes (WMC), multiplicity of lacunae, location of lacunae, total cerebral atrophy, and frontal and medial temporal lobe atrophy. RESULTS: Apart from age and education, univariate linear regression analyses revealed that WMC volume, presence of thalamic lacunae, cerebral atrophy, and left frontal lobe atrophy predicted performance on the Mini-Mental State Examination while WMC volume, presence of thalamic infarcts, cerebral atrophy, and frontal lobe atrophy of both sides predicted performance on the Mattis Dementia Rating Scale-Initiation/Preservation subscale. In the multivariate analyses, education (R2=0.22, P<.001), left frontal lobe atrophy (R2=0.10, P=.004), and presence of thalamic lacunae (R2=0.04, P=.049) were found to predict performance on the Mini-Mental State Examination while age (R2=0.23, P<.001) and presence of thalamic lacunae (R2=0.08, P=.011) were found to predict performance on the Mattis Dementia Rating Scale-Initiation/Preservation. CONCLUSIONS: Among patients with stroke associated with SVD, thalamic lacunae and frontal lobe atrophy are key determinants of cognitive performances.

[The efficacy of treating cerebral ischemia due to changes in the major cerebral arteries by using the preparation Tanakan (EGB 761)]. / Effektivnost' lecheniia ishemii mozga, obuslovlennoi izmeneniiami v magistral'nykh arteriiakh golovy, s ispol'zovaniem preparata "Tanakan" (EGB 761).

Cerebrovascular pathology is one of the chief causes of death. Effects were studied of the drug preparation "Tanakan" on the process of the rehabilitation of those patients (n = 150) operated on for abnormalities and deformity of brain major arteries. Two groups were identified: pathologies of the vertebral arteries (n = 50), carotid abnormalities (n = 51), control groups (n = 24 and 25 respectively). The drug was administered in a dose of 40 mg on a three-times daily schedule. Clinical approaches were used as were the dopplerographic, electroencephalographic, biochemical, micromorphological, neuropsychological methods of investigation. Determined in the study was a positive dynamics of clinical indices, which was more apparent for vertebrobasilar discirculations. EEG-investigation revealed differences in the course of changes in left- and right-hemispheric location of carotidogenous discirculations. Increase in blood serum antioxidant activity was recorded as was a positive transformation of vegetative indices and improvement of cognitive functions. Thus, the use of the above drug is indicated in the postoperative complex of rehabilitative measures in patients with cerebrovascular ischemia secondary to developmental anomalies and deformities of brain major arteries.

[Evaluation of the treatment of aneurysmal meningeal hemorrhage with antifibrinolytic agents, calcium inhibitors and maintenance of effective blood volume]. / Bilan du traitement des hémorragies méningées anévrysmales par antifibrinolytique, inhibiteur calcique et maintien d'une volémie efficace.

To prevent and treat the ischemic complications due to the vasospasm, this report suggest the management of aneurysmal subarachnoid haemorrhage by the association of antifibrinolytics (tranexamic acid) to lower the risk of rebleeding, calcium channel blockers (nimodipine), and the keeping of an effective total blood volume (thanks to volume expansion and dopamine). From 88 patients aged from 4 to 73, two thirds were admitted at latest 48 h after the aneurysmal rupture Emergency surgery was carried out in the case of a compressive hematoma, early surgery (between the first and the third day) on the grades I, II and III of Hunt and Hess without any signs of angiographic vasospasms (40% of this series), delayed surgery for the others (27.5%), 10% didn't undergo any surgery. Only three patients (3.4%) presented rebleeding leading to death. The features of the whole series are: 51% recovered without any after effects, 22% had mild neurological deficiency, 10% had severe neurological deficiency and 17% died after their release from hospital. This protocol allowed a decrease in the ischemic complications due to the vasospasm and in the rate of rebleeding during the waiting interval when an angiographic or a clinical vasospasm allowed no surgery.

Cerebral energy metabolism measured in vivo by 31P-NMR in middle cerebral artery occlusion in the cat--relation to severity of stroke.

The energy metabolism of the brain has been measured in a middle cerebral artery (MCA) occlusion model in the cat utilizing 31P-nuclear magnetic resonance (NMR). 31P-NMR spectra were serially obtained during 2 h of ischemia and a subsequent 4-h recovery period. The ratio of creatine phosphate (PCr) to inorganic phosphate (Pi) (PCr/Pi) showed a precipitous decrease in parallel with changes in electroencephalographic (EEG) amplitude in severe strokes during ischemia as well as during recirculation. Animals with mild strokes, as determined by EEG criteria, exhibited a much smaller decrease in PCr/Pi during ischemia. In the severe strokes, there was a splitting and significant shift of the Pi peak immediately after occlusion. In addition, the shifted Pi peak rapidly increased and remained elevated throughout the study. In the mild strokes, Pi also increased, but not as markedly. Intracellular pH determination by chemical shift of the Pi peak revealed a decrease from 7.1 to 6.2-6.3 during ischemia and the subsequent recovery period in the animals with severe strokes, whereas the pH in the animals with mild strokes did not show a significant change. A gradual decrease in adenosine triphosphate (ATP) to 57-79% of the control was exhibited in severely stroked animals during both the ischemia and the recovery period, whereas there was no change in ATP in the mild stroked animals. These results suggest that the dynamic process of pathophysiological changes in an MCA occlusion model in the cat leads to significant differences in cerebral metabolism between animals with mild and severe strokes.

Delayed ischemic deterioration in patients with early aneurysm operation and intravenous nimodipine.

A consecutive series of 100 individuals with aneurysmal subarachnoid hemorrhage were subjected to early aneurysm operation followed by subsequent intravenous administration of the calcium antagonist nimodipine during the critical period for symptomatic vasospasm. A total of 85 patients were in Hunt and Hess neurological Grades I through III, and 15 were in Grade IV or V before operation. In 39 individuals the aneurysm was located in the anterior cerebral artery complex (ACA), in 29 it originated from the internal carotid artery complex (ICA), and in 32 individuals the ruptured aneurysm arose from the middle cerebral artery (MCA). Of the patients, 71% made a good neurological recovery; the morbidity was 22%, and the mortality was 7%. Of the Grade I-III patients, 79% made a good neurological recovery, and the mortality was 6%. Delayed ischemic cerebral deterioration with permanent dysfunction occurred in five patients, all with ruptured ACA aneurysms. No single patient in the ICA or MCA populations developed delayed ischemic deterioration with fixed neurological deficit despite the presence of several potential risk factors, especially among the MCA aneurysm patients.

Vasospasm following transsphenoidal tumor removal associated with the arterial changes of oral contraception.

A case of fatal cerebral vasospasm after transsphenoidal removal of a pituitary macroadenoma with suprasellar extension is reported. On the second postoperative day the patient developed headache, lethargy, and cardiorespiratory arrest. Five days later, after recovery from this episode, she developed signs of involvement of the left hemisphere. At that time she demonstrated severe cerebral vasospasm, which was worse in the left supraclinoid segment of the internal carotid artery, and she died 19 days postoperatively. Postmortem examination showed left hemispheric and hypothalamic infarction with subsequent herniation. In addition, pathologic arterial changes usually related to use of oral contraceptives were present.

Transient global amnesia.

Transient global amnesia (TGA) was found in 41 of 76 patients admitted to the North Carolina Baptist Hospital with temporary disturbances of memory. Risk factors for stroke were present in 26 (63%) of these 41 patients, and additional risk factors developed in 9 (27%) of the 33 patients available for follow-up. Follow-up evaluation in 33 patients (80%) for periods ranging from 1 to 17 years (mean, 60.3 months) revealed a low rate of recurrence (18%) and a still lower rate of progression to stroke (6%). No transient ischemic attacks were reported during this period. In 2 patients, multiple recurrences of TGA ceased after treatment of the underlying condition (polycythemia in 1 case and myxomatous degeneration of the mitral valve in the other.