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Background: Stressful life events are among the most reliable precipitants of major depressive disorder; yet, not everyone exposed to stress develops depression. It has been hypothesized that robust neural reactivity to reward and associated stable levels of positive affect (PA) may protect against major depressive disorder in the context of environmental adversity. However, little empirical data exist to confirm this postulation. Here, we test the hypothesis that individuals with relatively low ventral striatum (VS) reactivity to reward will show low PA levels in the context of recent life stress, while those with relatively high VS reactivity will be protected against these potentially depressogenic effects., Methods: Differential VS reactivity to positive feedback was assessed using blood oxygen level-dependent functional magnetic resonance imaging in a sample of 200 nonpatient young adults. Recent life stress, current depressive symptoms, and PA were assessed via self-report. Linear regression models were used to investigate the moderating effects of VS reactivity on the relationship between recent stress and state PA across participants., Results: Recent life stress interacted with VS reactivity to predict self-reported state PA, such that higher levels of life stress were associated with lower PA for participants with relatively low, but not for those with high, VS reactivity. These effects were independent of age, gender, race/ethnicity, trait PA, and early childhood trauma., Conclusions: The current results provide empirical evidence for the potentially protective role of robust reward-related neural responsiveness against reductions in PA that may occur in the wake of life stress and possibly vulnerability to depression precipitated by stressful life events., (Copyright © 2012 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.)

Background: Pediatric major depressive disorder (MDD) is associated with deficits in sustained attention, thought to be related to underlying motivation deficits. This hypothesis, however, has never directly been tested using functional magnetic resonance imaging. In this study, we investigated the neurofunctional correlates of the interplay between attention and motivation in medication-naive pediatric MDD using a rewarded sustained attention task., Methods: Functional magnetic resonance imaging was used to compare brain activation between 20 medication-naïve, noncomorbid, first-episode adolescents with MDD aged 13 to 18 years and 21 gender-, age-, and IQ-matched healthy adolescents. Participants performed a sustained attention task with and without a monetary reward to assess the impact of reward on sustained attention networks., Results: During nonrewarded sustained attention, adolescents with MDD showed reduced activation compared with healthy control subjects in occipital cortex. When sustained attention was rewarded, however, the underactivation in adolescents with MDD was in an extensive right hemispheric network of inferior fronto-striato-thalamic attention and limbic hippocampus-anterior cingulate reward processing areas. Major depressive disorder patients showed increased activation in cerebellum, which correlated with reduced frontal activation and depressive symptoms, suggesting compensatory response. Further analysis showed that reward upregulated fronto-striatal and hippocampal/temporal activation in control subjects but deactivated these regions in MDD, with opposite effects in the cerebellum., Conclusions: Medication-naïve MDD adolescents show abnormalities in the regulation in fronto-striato-cerebellar brain regions involved in attention and reward during motivated but not unmotivated attention. This suggests a dysfunctional interplay between motivation and cognition in pediatric MDD, where motivation appears less capable of upregulating attention networks relative to healthy youths., (Copyright © 2012 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.)

Churg-Strauss syndrome (CSS) is a rare systemic vasculitis, almost invariably accompanied by asthma, nasal polyposis, paranasal sinus abnormalities, and increased peripheral blood eosinophil count. Neurological involvement as peripheral neuropathy is a common feature, whereas cerebral involvement is extremely rare. Herein, we report the case of a young man who presented with sudden onset of right-side emiparesis and aphasia, whose head CT scan showed the presence of large haemorrhage in the left striatum nucleus involving part of the temporal lobe. Based on clinical and laboratory findings (asthma, eosinophilia >10%, paranasal sinus abnormalities and mononeuritis multiplex) a diagnosis of CSS was made. Cerebral angiography resulted normal, excluding the presence of vascular malformations or signs of vessel abnormalities. Pharmacotherapy with (intravenous and afterwards oral) corticosteroid and immunosuppressors (cyclophosphamide and then azathioprine) was initiated. The outcome was good with neurological follow-up showing a nearly complete recover. Our case points out that intracerebral haemorrhage can be, despite rare, a presenting feature of CSS. Previously reported patients affected by cerebral haemorrhage and CSS are summarized and briefly reviewed., (Copyright © 2010 Elsevier B.V. All rights reserved.)

Conventional indices of the utilization of FDOPA in living human brain have not consistently revealed important declines in dopamine function with normal aging. However, most methods of kinetic analysis have assumed irreversible trapping of decarboxylated FDOPA metabolites in brain, an assumption that is violated even in PET recordings of short duration. Therefore, we have developed methods for the calculation of steady-state storage of FDOPA together with its decarboxylated metabolites (V(d), mlg(-1)), based upon improved kinetic analysis of 120-min emission recordings. In a group of 28 normal male subjects, of age ranging from 23 to 73 years, the magnitude of V(d) in the striatum and in extrastriatal regions declined by approximately 10% with each decade. The utilization of FDOPA was also calculated by several conventional methods assuming irreversible trapping, i.e. the net blood brain clearance (K(in)(app), mlg(-1)min(-1)), the DOPA decarboxylase activity relative to a reference tissue input (k(3)(S), min(-1)), and relative to the arterial input (k(3)(D), min(-1)). None of these methods revealed an age-related decline in FDOPA utilization in the extended striatum, although the magnitude of K(in)(app) did decline in cerebral cortex. Thus, the capacity to synthesize [(18)F]fluorodopamine remained largely intact in striatum of the elderly subjects, but in the presence of a substantially increased rate of washout (k(loss)), which was evident in all brain regions examined. Consequently, the magnitude of V(d) declined with healthy aging, possibly reflecting impaired vesicular storage capacity, resulting in enhanced exposure of cytosolic [(18)F]fluorodopamine to monoamine oxidase., (Copyright 2008 Elsevier Inc. All rights reserved.)

Aims: To investigate the expression of P-gp and caveolins in brain striatum capillaries in inbred mice with type 2 diabetes., Main Methods: Inbred mice with type 2 diabetes (male New Zealand obese; NZO) were compared with related mice without diabetes (female NZO and New Zealand White). Protein expression of P-gp and caveolins in capillaries of the brain striatum was examined by immunohistochemical analysis. P-gp efflux pump activity in the blood-brain barrier (BBB) was measured by in vivo brain microdialysis. Regulation of P-gp and caveolin expression was examined in cultured adult rat brain endothelial cells (ARBEC)., Key Findings: In capillaries in the brain striatum, expression of P-gp and caveolins was higher and lower, respectively, in mice with type 2 diabetes compared with non-diabetic mice. Brain extracellular concentrations of intravenously injected rhodamine 123 were more than 50-60% lower in type 2 diabetic mice. Insulin and PMA treatments significantly increased P-gp expression, whereas the same treatments decreased caveolin expression in ARBEC., Significance: Protein expression of P-gp and caveolins can be regulated in animals with type 2 diabetes. These changes may be important in modulating P-gp activity in the BBB in type 2 diabetes.

Studies of Parkinson's disease (PD) suggest that cognitive deficits accompany the classically recognized motor symptoms, and that these cognitive deficits may result from damage to frontal-basal ganglia circuits. PD patients are impaired on ordering events and action components into coherent sequences. In this study, we examined early-stage, nondemented, medicated PD subjects and matched control subjects during a semantic event sequencing task using functional MRI (fMRI). The task required subjects to examine four pictures of meaningful events, determine the correct temporal relationship between each picture, and re-order the pictures into a coherent sequence. There were two main findings. First, we found abnormal activation within the prefrontal cortex (PFC) and the "default" network in the PD group. Distinct areas of the PFC showed both hypoactivation and hyperactivation, whereas the "default" network showed reduced levels of resting activation in PD. Secondly, we observed left caudate hyperactivation in the PD group. The findings are discussed in relationship to how more activation may be compensatory, but does not necessarily mean efficient and correlated brain function.

Objectives: About one in five patients with atrial fibrillation have significant carotid artery disease, but not all strokes are cardioembolic in origin in these patients., Purpose: We investigated stroke sub-types based mainly on clinical, carotid ultrasonographic, and neuroimaging findings in ischemic stroke patients with non-valvular atrial fibrillation (NVAF)., Patients and Methods: The etiology of stroke was classified as definite or probable cardioembolic, possible lacunar, or possible atherothrombotic, as proposed by Hart et al. and the TOAST criteria. Clinical features and risk factors (gender, age, diabetes mellitus, hypertension, hyperlipidemia, cigarette smoking, and alcohol consumption) were designated as clinical variables., Results: One hundred and six of 1938 patients (5.5%) had NVAF. In patients with and without NVAF, hyperlipidemia was more common in patients without NVAF (p<0.001), while the prevalence of other risk factors was not statistically different. On the basis of the TOAST criteria, none of the patients with NVAF could be classified as having had an atherothrombotic stroke. According to the classification by Hart et al., of the patients with NVAF, 49 patients (46.3%) had a definite embolic stroke, 17 (16.0%) had a probable embolic stroke, 12 (11.3%) had a possible atherothrombotic stroke, 17 (16.0%) had a possible lacunar infarction, and 11 (10.4%) had a stroke of undetermined etiology. Besides the presence of significant carotid stenosis (p<0.001), none of the variables related to stroke were different among the sub-groups., Conclusion: Patients with significant carotid stenosis were more likely to develop atherothrombotic stroke, while other risk factors associated with stroke failed to point to an etiologic cause. It should also be emphasized that the conventional classification system failed to aid in the correct diagnosis and risk stratification in patients with multiple confounding risk factors.

We investigated the effect of minocycline on neuronal damage in the hippocampus and striatum in a mouse model of transient global forebrain ischemia. Male C57BL/6 mice were anesthetized with halothane and subjected to bilateral occlusion of the common carotid artery (BCCAO) for 30 min. Minocycline (90 mg/kg, i.p., qd) or saline was injected immediately after BCCAO and daily for the next two days (45 mg/kg, i.p., bid). In order to reduce the variability in ischemic neuronal damage, we applied selection criteria based on regional cerebral blood flow (rCBF), evaluated using laser Doppler flowmetry, and the plasticity of the posterior communicating artery (PcomA), evaluated using India ink solution. In animals with rCBF that was less than 15% of the baseline value and with a smaller PcomA, of diameter less than one-third that of the basilar artery, we consistently observed neuronal damage in the striatum and hippocampal subfields, including medial CA1, CA2, and CA4. When the effect of minocycline was assessed with cresyl violet staining, neuronal damage in the medial part of the CA1 subfield and the striatum was found to be significantly attenuated, although minocycline did not protect against neuronal damage in the remaining hippocampal subfields. Immunohistochemistry for NeuN, adenosine A1 receptor, and SCIP/Oct-6 confirmed the region-specific effect of minocycline in the hippocampus. In summary, our results suggest that minocycline protects neurons against global forebrain ischemia in a subregion-specific manner.

Background: Schizophrenia has been frequently associated with impaired inhibitory control. Such control is known to involve the striatum. Here, we investigate whether impaired inhibitory control is associated with abnormal striatal activation in schizophrenia. First-degree relatives of patients were also tested to examine whether striatal abnormality is associated with schizophrenia, or with the risk for the illness., Methods: Both functional MRI and behavioral data were acquired during a task designed to invoke inhibitory control in 21 patients, 15 unaffected siblings, and 36 matched controls. Subjects must refrain from responding to designated stop cues occurring within a series of motor cues. Subjects could anticipate the occurrence of stop cues as the likelihood of these cues increased in a linear fashion throughout the task., Results: Control subjects showed striatal activation while responding to motor cues. This activation increased in a linear fashion when the likelihood of having to inhibit the response was increased. Both patients siblings did not show anticipation-related increase in either striatal activation. However, only patients showed behavioral impairments., Conclusions: Striatal abnormalities occur in schizophrenia patients and unaffected siblings. Thus striatal abnormalities may be related to an increased (genetic) risk to develop schizophrenia.

Background: Frontostriatal dysfunction is a primary hypothesis for the neurocognitive changes of depression in late life. The aim of the present study was to test this hypothesis with the use of functional magnetic resonance imaging (fMRI) tasks that are known to engage the prefrontal and neostriatal cognitive circuits., Methods: Twenty-three elderly subjects (mean age, 69.9 years) participated: 11 subjects with a current major depressive episode and 12 nondepressed elderly control subjects. Subjects underwent fMRI while performing a concurrent implicit and explicit sequence learning task. Region of interest (ROI)-based analyses were conducted, focusing on the dorsal anterior cingulate cortex, the dorsolateral prefrontal cortex, and the neostriatum., Results: As expected, both the control and depressed subjects learned the sequence during both implicit and explicit conditions. During explicit learning, decreased prefrontal activation was found in the depressed subjects, along with increased striatal activation. The increased striatal activity in the depressed subjects was due to increased activity on the trials that violated the sequence. During implicit learning, no significant differences were found between the groups in the identified ROIs., Conclusions: The increased striatal activation on trials that violated the sequence demonstrates a greater response to negative feedback for depressed compared with control subjects. Our observations of significant differences in both prefrontal and striatal regions in the depressed elderly subjects relative to elderly control subjects supports the frontostriatal dysfunction hypothesis of late-life depression.

Background: Emotional information can facilitate or interfere with cognitive processes. In this study, we examined the influence of emotional information in biasing performance and the biological basis underlying this influence., Methods: Ten human subjects (five female) were scanned with functional magnetic resonance imaging while performing an emotional go/nogo task., Results: Subjects were slower to approach fearful target expressions and had more difficulty avoiding happy nontarget expressions. The amygdala was recruited most for negative emotional context, and activity in this region was positively correlated with response time when detecting negative expressions. Increased signal in the right caudate nucleus was observed when avoiding nontargets and was negatively correlated with the number of false alarms subjects made., Conclusions: Emotional context can alter behavioral and biological responses when approaching or avoiding a stimulus. We showed that recruitment of the amygdala, a region implicated in evaluating emotional significance, was associated with longer response latencies when approaching negative information, whereas recruitment of the caudate nucleus, a structure previously implicated in reward and impulse control, was most active when avoiding positive information. Our findings have significant implications for exaggerated and inhibited emotional responses that are characteristic of a number of psychiatric disorders.

Objectives: If the pattern of neonatal lenticulostriate vasculopathies (NLSV) is well-known, the prognosis is unknown except in TORCH syndromes. This study was aimed to describe the short, mid and long-term outcome of NLSV of various origins., Population and Methods: Of 9138 neonates (1981-2000) which were submitted to an early brain ultrasound study, 70 presented with a pattern of minor (35), moderate (27) or severe (8) NLSV, a single finding in 42 cases and in association with minor peri-intraventricular haemorrhage and/or leukomalacias in 28. The maternal and neonatal charts were reviewed, and the survivors were followed according to our usual policy., Results: Of nine deaths, eight cases included severe congenital defects (metabolic or malformations or acquired: transfused monochorial twins). Of 61 survivors, eight were lost to follow-up within the first year, 53 were followed for 21 months to 9 years and 7 months (median 4 years 5 months). Of 53 children, 35 (66%) were strictly normal, eight had minor deviations, four had moderate and six had major neurodevelopmental deficits. Of 34 survivors with isolated NLSV and known follow-up, 27 were normal (79%) versus 8/19 (42%) in associated NLSV., Conclusions: Minor or moderate isolated NLSV generally have a good long-term prognosis. Associated forms of any severity depend mainly upon the severity of periventricular leukomalacias. Major forms of NLSV must be a warning sign of a possible underlying congenital anomaly which will rule the vital and functional prognosis.

Glioma, the most common form of brain tumor, has been shown mostly by in vitro studies to utilize matrix metalloproteinase (MMP) for invasive growth through degradation of the extracellular matrix. In order to examine the in vivo role of MMP, we established a rodent model of glioma progression using C6 rat glioma cells and analyzed the effect of tissue inhibitors of metalloproteinases (TIMPs). TIMP-2 rather than TIMP-1 caused significant reduction of the tumor size accompanied by the presence of degenerated blood vessels and ischemic necrosis. Because TIMP-2 inhibits MMP-2 preferentially, we then examined glioma growth in MMP-2-deficient mice and observed essentially identical consequences. While MMP-2 activity was present in the tumor and adjacent tissues of the wild-type mice, no MMP-2 activity was detected even in the tumor of the null mice, although C6 cells are known to express MMP-2. These observations suggest that glioma induces MMP-2 and utilizes its activity in the host tissue to support angiogenesis and to maintain angioarchitecture.

The blood-brain barrier (BBB) controls the exchange of regulatory substances, including tumor necrosis factor-alpha (TNF), between the brain and the blood. Transport across the BBB of some regulatory substances is altered with aging. Here, we measured the blood to brain unidirectional influx rate (Ki) for whole brain and 10 brain regions for radioactively labeled TNF in three groups of mice: young (2 mo old) ICR (the standard outbred albino laboratory mouse also termed CD-1), young SAMP8 (a strain which develops impaired learning and memory with aging that correlates with an age-related increase in brain levels of amyloid beta protein), and aged (17 mo) SAMP8 mice. In ICR mice, the hypothalamus had the fastest (1.73 microl/g-min) and the parietal cortex the slowest (0.189 microl/g-min) rates of uptake, a regional difference of about 9 fold. No differences in transport into whole brain or brain regions occurred between the ICR and young SAMP8, showing a lack of differences between strains. Transport was higher for the occipital cortex, midbrain, and striatum in aged SAMP8 mice. These results show blood-borne TNF enters some regions of the brain much more readily than others and TNF transport is increased into some brain regions of the SAMP8 mice at an age when learning and memory are impaired.

Neuroimaging studies of major depression have identified neurophysiologic abnormalities in multiple areas of the orbital and medial prefrontal cortex, the amygdala, and related parts of the striatum and thalamus. Some of these abnormalities appear mood state-dependent and are located in regions where cerebral blood flow increases during normal and other pathologic emotional states. These neurophysiologic differences between depressives and control subjects may thus implicate areas where physiologic activity changes to mediate or respond to the emotional, behavioral, and cognitive manifestations of major depressive episodes. Other abnormalities persist following symptom remission, and are found in orbital and medial prefrontal cortex areas where postmortem studies demonstrate reductions in cortex volume and histopathologic changes in primary mood disorders. These areas appear to modulate emotional behavior and stress responses, based upon evidence from brain mapping, lesion analysis, and electrophysiologic studies of humans and/or experimental animals. Dysfunction involving these regions is thus hypothesized to play a role in the pathogenesis of depressive symptoms. Taken together, these findings implicate interconnected neural circuits in which pathologic patterns of neurotransmission may result in the emotional, motivational, cognitive, and behavioral manifestations of primary and secondary affective disorders.

Increasing evidence has accumulated for structural brain changes associated with unipolar recurrent major depression. Studies of neuroanatomic structure in early-onset recurrent depression have only recently found evidence for depression-associated structural change. Studies using high-resolution three-dimensional magnetic resonance imaging (MRI) are now available to examine smaller brain structures with precision. Brain changes associated with early-onset major depression have been reported in the hippocampus, amygdala, caudate nucleus, putamen, and frontal cortex, structures that are extensively interconnected. They comprise a neuroanatomic circuit that has been termed the limbic-cortical-striatal-pallidal-thalamic tract. Of these structures, volume loss in the hippocampus is the only consistently observed change to persist past the resolution of the depression. Possible mechanisms for tissue loss include neuronal loss through exposure to repeated episodes of hypercortisolemia; glial cell loss, resulting in increased vulnerability to glutamate neurotoxicity; stress-induced reduction in neurotrophic factors; and stress-induced reduction in neurogenesis. Many depressed patients, particularly those with late-onset depression, have comorbid physical illnesses producing a high rate of hyperintensities in deep white matter and subcortical gray matter and brain damage to key structures involved in the modulation of emotion. Combining MRI studies with functional studies has the potential to localize abnormalities in blood flow, metabolism, and neurotransmitter receptors and provide a better integrated model of depression.

The influence of chronic cerebral hypoperfusion on cerebral energy metabolism was studied. The bilateral common carotid arteries of Wistar rats were occluded for 0, 2, 7, and 28 days. Cerebral energy metabolism was evaluated by assaying adenosine triphosphate (ATP), phosphocreatine (PCr), and lactate levels and measuring pyruvate dehydrogenase (PDH) activity (each time point, n = 6). Pathological changes were assessed light-microscopically by Klüver-Barrera staining and immunohistochemical labeling for astroglia (each time point, n = 3). There were no changes in ATP and PCr levels or PDH activity; there was slight but significant transient lactate accumulation at 2 days. Myelin pallor and increase in immuno-reactive astroglia were only observed at 28 days. These results indicate that chronic cerebral hypoperfusion induces delayed white matter changes in the corpus callosum of rat brain, but does not affect energy production.

The purpose of this study is to evaluate in a rat model if the early removal of an experimental intracerebral mass mimicking an extensive subcortical hematoma improves neurological outcome. Fifty six male Wistar rats were studied. A balloon was placed sterotactically at the level of the striatum. The balloon was inflated to 100 microl for periods of 10, 60 or 120 min (with 10 animals in each group). In 10 animals the balloon was not deflated and there were four sham operated cases. Neurological deficit was evaluated by a blinded observer by means of a clinical scale from 0 to 8 points at 24 and 72 h after inflation. Three additional animals at each inflation period were sacrificed after 6 h for pathological study with hematoxylin-eosin staining. Death rate was 9/10 animals who had permanent inflation, 4/10 in those with 2 h inflation, 2/10 for 1 h inflation and 0/10 for 10 min inflation (P<0.01 in chi square test). Many animals developed a particular clinical syndrome not previously described. Mean 72 h clinical scores (0-8 points) were 7.6 (S.D.: 1. 2) for the permanent inflation group, 4.4 (S.D.: 3.2) for 2 h of inflation, 2.3 (S.D.: 3.2) for 1 h and 0.4 (0.9) for 10 min of inflation (P<0.01 in Kruskal Wallis test). In the pathological study the rate of damaged neurons was significantly higher in the permanent than in transient inflation groups. In conclusion, in this balloon model evacuation of an extensive acute expanding subcortical (hematoma-like) mass must be performed within a limited time window to prevent the development of irreversible neurological deficits or death.

A case of hemichorea in a patient with poorly controlled diabetes is reported. T1-weighted magnetic resonance imaging (MRI) showed an unusual homogeneous high-intensity area in the corpus striatum. Of interest in the case was the fact that the globus pallidus, which was enhanced with gadolinium at the onset of hemichorea, showed homogeneous high-intensity on a subsequent T1-weighted image. This indicated that blood brain barrier destruction preceded the signal intensity change in the basal ganglia. As far as the authors could determine, this is the first reported case showing such enhancement during the course of diabetic hemichorea.

Gender differences in the vulnerability of the lateral striatal artery (1STR artery) to systemic intoxication with 3-nitropropionic acid (3-NPA, succinate dehydrogenase inhibitor) were studied. Subcutaneous injection of 3-NPA (20 mg/kg once a day for 2 days) induced striatal selective lesions in half of male rats associated with motor symptoms (rolling, paddling, recumbency, etc) while female rats were resistant. Lesions were located in the lateral striata and characterized by astroglial necrotic cell death, enhanced immunoreaction to factor VIII-related antigen, edema, extravasation of IgG and sometimes bleeding. The motor and histological disturbances were highly sex-dependent and modulated by changes in hormonal levels. Males were more susceptible than females. Castration had little effect but ovariectomy enhanced the vulnerability. Replacement therapy with testosterone increased while estradiol or tamoxifen suppressed the vulnerability in ovariectomized females. Investigation of the arterial architecture of the brain often revealed rectangular and acute angled branchings in the centrolateral striatum where the ISTR artery feeds. A parallel in vitro toxicity study demonstrated that an extreme Ca++ overload and a strong cellular swelling resulted in astrocytic cell death. Data suggest that 1STR artery and astrocytes are highly vulnerable to 3-NPA intoxication in males. The greater vulnerability of the ISTR artery may contribute to the pathogenesis of neurodegenerative diseases, striatal bleeding, etc. Protective effects of estrogen and tamoxifen may mediate gender differences often observed in these disorders and suggest their potential use as therapeutic agents for these disorders.

The aim of this work was to follow the evolution of striatal dopamine D1 and D2 receptors after hypoxic-ischemic (H/I) insult in immature rats. SPET imaging of these receptors could be used as an index to assess brain dysfunctions after perinatal H/I without change in cerebral blood flow or neuronal loss. We submitted 1-week-old rat pups to unilateral ligation of the left carotid artery plus 2h exposure to 8% O2. After recovery periods of 1, 2 or 9 weeks, ex vivo and in vitro autoradiographic studies of dopamine receptors were performed on normal appearing brains using specific ligands usable in human SPET imaging. Striatal dopamine D2 receptors tended to decrease bilaterally after one week's recovery. The decrease then reached 40% at 3 weeks of age and at 10 weeks of age the level of receptors had returned to normal values. By contrast, no change in dopamine D1 receptors was seen, whatever the age studied. In conclusion, changes in dopamine D2 receptors could be a valuable index for SPET imaging to evaluate H/I brain damage in the absence of anatomical lesions.

Controversies exist concerning factors that contribute to the occurrence of epileptic seizures after stroke. Therefore, we studied prospectively the occurrence of seizures in 322 patients with a first-ever CT-confirmed symptomatic territorial brain infarct involving the cortex. We also studied potential risk factors for seizures, and gave special attention to cortical infarct location. Fifty-four patients developed post-stroke seizures. We distinguished between early- and late-onset seizures, occurring within two weeks following stroke-onset, or later than two weeks, respectively. We found that patients of 65 years or older with a cardioembolic brain infarct involving the middle temporal or post-central gyrus, had an almost eight times increased risk of early-onset seizures, whereas patients with a large brain infarct involving the supramarginal or superior temporal gyrus, had a five times increased risk of late-onset seizures. We conclude that risk factors and epileptogenic cortical areas for post brain infarct seizures can be identified, which however, differ between early- and late-onset seizures. These two seizure types may also differ in terms of seizure mechanism. Our findings may influence the decision on prophylactic treatment with antiepileptic drugs in stroke patients.

During 30 minutes of global forebrain ischemia in rats, striatal intracellular levels of dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) increase at the same time extracellular levels, measured by microdialysis, decrease. If DOPAC and HVA were free to diffuse out of cells, these changes in opposite directions should not occur. These data support the theory that a membrane potential-dependent active transport system is required for DOPAC and HVA to leave striatal cells. During ischemia and subsequent to ATP depletion, neurons and glia depolarize and active transport systems fail. DOPAC and HVA, which are still being produced inside neurons and possibly glia, can not be transported out of these cells and accumulate intracellularly.

We report 4 cases of acute hemiplegia and a small low-density lesion on computerized tomography (CT) after varicella infection. In 3 of them, CT in the acute hemiplegic stage, and later, reveals the development of lacunar infarct around the internal capsule. Focal low density may be caused by occlusive vascular lesions of the penetrating arteries. Varicella infection may play an important role as one of the causes of acute hemiplegia in childhood producing lacunar infarct, as well as delayed hemiplegia, reported previously in herpes zoster ophthalmicus.