Cerebral Blood Flow Abnormalities Research Articles

Neocortical vasculature abnormalities in the Fragile X mental retardation syndrome

The Fragile X syndrome (FXS) is the leading form of inherited mental retardation. To date, the most prominent neuronal phenotype associated with the syndrome is an abundance of long thin spines exhibiting an immature morphology. However, in addition to synaptic abnormalities, recent case studies have demonstrated that Fragile X (FX) patients also exhibit abnormal cerebral blood flow (CBF). To examine the role of the Fragile X mental retardation protein (FMRP) in altering CBF, we examined blood vessel density (BVD) in the visual cortex of Adult and Middle-aged FX mice. Analysis of Middle-aged FX mice demonstrated elevated BVD compared to wildtype controls, suggesting that FX mice exhibit a lack of age-induced BVD plasticity. However, Adult FX and wildtype mice did not exhibit consistent differences in BVD. These data demonstrate that FMRP is required for age-induced neocortical vasculature plasticity. Furthermore, these data suggest a new role for FMRP in blood vessel regulation that would have profound implications towards appropriately timed delivery of neuronal nutrients, thus contributing to or exacerbating FX cognitive and neuronal abnormalities.

Regional Cerebral Blood Flow Abnormalities Associated With Apathy and Depression in Alzheimer Disease

The aim of this study was to identify brain areas related to apathy or depression in patients with Alzheimer disease (AD). Eighty-one AD patients were enrolled in this prospective study. (99m)Tc-HMPAO single photon emission computed tomography was performed to evaluate regional cerebral blood flow (rCBF). According to the Neuropsychiatric Inventory subscores of apathy and depression, 9 patients were classified as clinically significant (cs) depressed and non-cs-apathetic (D+) groups and 9 were classified as cs-apathetic and non-cs-depressed (A+) groups. In addition, 18 patients were classified as age-matched and Mini-Mental State Examination-matched disease control groups (D-, A-). The significance of rCBF differences between groups and the correlation between rCBF and subscores in 81 AD patients were estimated by SPM (uncorrected P < 0.005) analysis. D+ patients had significantly lower perfusion in the right orbitofrontal and inferior frontal gyri than D- patients, whereas A+ patients had this in the right amygdala, temporal, posterior cingulate, right superior frontal, postcentral, and left superior temporal gyri than A- patients. The negatively correlated areas with depression subscores included the left inferior frontal and the right middle frontal gyri and those with apathy subscores included the right temporal and right medial frontal gyri. We suggest that this finding may indicate that apathy and depression in AD patients involve distinct functional circuits.

Plasma BDNF and PDGF-AA levels are associated with high TCD velocity and stroke in children with sickle cell anemia

Sickle cell anemia (SCA) associated cerebrovascular disease includes vascular remodeling, abnormal cerebral blood flow (CBF) and infarction. We studied the relationships between plasma brain derived neurotropic factor (BDNF), platelet derived growth factors (PDGF-AA and -AB/BB) and high trans-cranial Doppler (TCD) velocity, an indication of CBF velocity. Baseline plasma samples from 39 children (19 SCA with abnormal/high TCD [SATCD], 13 SCA with normal TCD [SNTCD] and 7 healthy non-SCA), were assayed for BDNF, PDGF-AA and -AB/BB plus 11 other cytokines. The sensitivity, specificity and usefulness of these biomarkers for stroke prediction was investigated. All subject groups were of similar age and gender distribution. Mean BDNF was significantly higher among SATCD than SNTCD (p=0.004) as was mean PDGF-AA (p=0.001). Similarly, mean PDGF-AA was higher among SCA subjects who developed stroke than those who did not (p=0.012). Elevated BDNF and PDGF-AA were good predictors of the presence of abnormally high CBF velocity and were both associated with severity of anemia. Elevated PDGF-AA predicted risk for stroke development. Stroke incidence and high TCD velocity were associated with elevated BDNF and PDGF-AA. These findings suggest a role for BDNF and PDGF-AA in the patho-physiological mechanism of cerebrovascular disease in SCA.

Prevalence of transcranial Doppler abnormalities in Nigerian children with sickle cell disease

Transcranial Doppler (TCD) ultrasonography helps to identify children with sickle cell disease (SCD) who are at an increased risk of stroke,making primary stroke prevention a reality. A cross-sectional study of145 Nigerian children aged ≥3 years with SCD was carried out to describe the pattern of cerebral blood flow (CBF) abnormalities. The mean time-averaged mean velocity (TAMV) was 152 ±27.0 cm/sec and122 ±22.0 cm/sec in Hb SS and Hb S1C group, respectively. Abnormal velocities were recorded in six (4.7%) of the Hb SS patients and none of the Hb S1C while conditional risk (CR) velocities were recorded in 19.7% of Hb SS (low conditional 11.0%, high conditional 8.7%) and low conditional in 5.6% of Hb S1C cases. Cerebral flow velocities showed a negative correlation with age and hematocrit. Compared with African-American children, Nigerian children with Hb SS disease have a considerably higher prevalence of CR velocities.

Pre-intervention cerebral blood volume predicts outcomes in patients undergoing endovascular therapy for acute ischemic stroke

BackgroundPre-intervention perfusion imaging is increasingly becoming part of stroke triage. Small studies supporting imaging based patient selection have been published. The goal of this larger study was to determine if...

Evaluation of Neurodegeneration in a Mouse Model of Infantile Batten Disease by Magnetic Resonance Imaging and Magnetic Resonance Spectroscopy

Neuronal ceroid lipofuscinoses (NCLs) represent a group of common hereditary childhood neurodegenerative storage disorders that have no effective treatment. Mutations in eight different genes cause various forms of NCLs. Infantile NCL (INCL), the most lethal disease, is caused by inactivating mutations in the palmitoyl-protein thioesterase-1 (PPT1) gene. The availability of Ppt1-knockout (Ppt1-KO) mice, which recapitulate virtually all clinical and pathological features of INCL, provides an opportunity to test the effectiveness of novel therapeutic strategies in vivo. However, such studies will require noninvasive methods that can be used to perform serial evaluations of the same animal receiving an experimental therapy. Thus, the development of noninvasive method(s) of evaluation is urgently needed. Here, we report our evaluation of the progression of neurodegeneration in Ppt1-KO mice starting at 3 months of age by MRI and MR spectroscopy (MRS) and repeating these tests using the same mice at 4, 5 and 6 months of age. Our results showed progressive cerebral atrophy, which was associated with histological loss of neuronal content and increase in astroglia. Remarkably, while the brain volumes in Ppt1-KO mice progressively declined with advancing age, the MRS signals, which were significantly lower than those of their wild-type littermates, remained virtually unchanged from 3 to 6 months of age. In addition, our results also showed an abnormality in cerebral blood flow in these mice, which showed progression with age. Our findings provide methods to serially examine the brains of mouse models of neurodegenerative diseases (e.g. Ppt1-KO mice) using noninvasive and nonlethal procedures such as MRI and MRS. These methods may be useful in studies to understand the progression of neuropathology in animal models of neurodegenerative diseases as they allow repeated evaluations of the same animal in which experimental therapies are tested.

Cerebral blood flow abnormalities in neurologically asymptomatic patients with primary antiphospholipid syndrome

To evaluate cerebral blood flow abnormalities in primary antiphospholipid syndrome (PAPS) patients without ongoing neurological manifestations. We included 28 PAPS patients and 28 healthy controls. Carotid Doppler ultrasound, and echocardiographic evaluation were done. Transcranial Doppler ultrasonography measured mean flow velocity (MFV) in the carotid siphon, middle, anterior, posterior, intracranial vertebral arteries, and basilar artery (11 cerebral arteries). Results were considered abnormal when the MFV was out of the normal range according to age and/or flow asymmetry and/or more than four arterial segments affected. The mean age of patients was 41.4 ± 11.2 and 39.3 ± 8.6 years in controls. Disease duration was 11 ± 2.7 years. A significant increase in MFV in 7/11 cerebral arteries in PAPS patients, mainly in the middle and anterior cerebral arteries was found compared with controls. A significant association between lupus anticoagulant, history of stroke and obesity with a greater number of affected arteries was found. We did not find an association between MFV and abnormal echocardiography, arterial hypertension and carotid intima-media thickness. Asymptomatic patients with PAPS can have significantly increased MFVs. These alterations may be the consequence of accelerated atherosclerosis, PAPS vasculopathy or both. Whatever the cause, these findings can represent a risk for stroke in PAPS patients that needs the trial of other therapeutic options.

Acute perfusion changes after spontaneous SAH: a perfusion CT study

Perfusion computed tomography (CT) is a rapid technique that allows the measurement of acute disturbances in local and global cerebral blood flow in patients suffering stroke and spontaneous subarachnoid haemorrhage (SAH). The purpose of this study was to establish the relationship between different measures of brain perfusion made on dynamic-contrast CT reconstructions performed as soon as SAH has been diagnosed and the severity of the bleeding determined by the clinical grade, the extent of the bleeding and the outcome of the patients. After the diagnosis of SAH by conventional CT, a perfusion CT was performed before CT angiography. All imaging studies were performed on a six-slice spiral CT scanner. All images were analysed using perfusion software developed by Philips, which produces perfusion CT quantitative data based on temporal changes in signal intensity during the first pass of a bolus of an iodinated contrast agent. Measurements of mean transient time (MTT), time to peak (TTP), cerebral blood volume (CBV) and cerebral blood flow (CBF) in volumes of interest corresponding to territories perfused by the major cerebral arteries were performed. Different data regarding severity of the bleeding-such as level of consciousness, amount of bleeding in conventional CT-were collected. All poor-grade patients received a ventriculostomy catheter so that ICP recordings were obtained. Also, the occurrence of delayed cerebral ischaemia (DCI) was recorded. Outcome was assessed by the Glasgow Outcome Scale 6 months after the bleeding. For statistical analysis, non-parametric correlations between variables were performed. Thirty-nine patients have been included in the study since January 2007. In SAH patients there are increasing perfusion abnormalities as the severity of the bleeding increases. The most affected perfusion parameters are TTP and MTT, as they significantly increase with the clinical severity of the bleeding and the total volume of bleeding (P < 0.01, Spearman's Rho). When average MTT time is increased over 5.9 s there is a 20-fold (95% CI = 2.1-182) risk of poor outcome. All patients presenting this MTT time suffered from DCI. This value has a positive predictive value of 100% for DCI and 90% for a poor outcome. SAH causes cerebral blood flow abnormalities even in the acute phase of the illness, consisting mainly of an increase in circulation times (TTP and MTT), which are correlated with the severity of the bleeding.

Intracranial Vasculopathy in a Patient with Systemic Sclerosis: Atherosclerotic or Moyamoya-Like Disease?

Intracranial Vasculopathy in a Patient with Systemic Sclerosis: Atherosclerotic or Moyamoya-Like Disease?

Place de l’évaluation de la quantité de liquide amniotique, du score biophysique et du doppler dans la surveillance des grossesses prolongées

To evaluate the role of ultrasound and doppler assessment in the management of prolonged pregnancies and to state its modalities.Medline, PubMed, embase and the Cochrane library were searched using terms prolonged pregnancy, post date pregnancy amniotic fluid, ultrasound assessment, doppler, biophysical profile.Single deepest vertical pool measurement is the method of choice of the assessment of amniotic fluid. Indeed, when this method was used, significantly fewer case of oligohydramnios were diagnosed and fewer women had inductions of labor. However, this method is not superior to the amniotic fluid index in the prevention of poor perinatal outcomes. There is a significant difference in the incidence of fetal distress, meconium stained fluid and caesarean section for fetal distress when the amniotic fluid is reduced as compared with normal amniotic fluid. However, sensibility and predictive positive value of oligohydramnios to predict poor perinatal outcomes is moderate. Similary, in most studies, diagnosis of an abnormal uterine, umbilical, aortic or cerebral blood flow doppler was associated with a weak prediction of a poor perinatal outcome. Therefore, we do not recommend its use in management of prolonged pregnancy. There were significantly more diagnosis of oligoamnios and more abnormal antenatal monitoring results in the modified biophysical profile group as compared with the group managed with only single deepest pool but no differences in cord blood gases, neonatal outcome, or in outcomes related to labour and delivery were noted between the two groups. Therefore, biophysical profile including AFI offers no advantage in detecting adverse outcomes and may cause more interventions.Close monitoring of fetal condition including assessment of amniotic fluid by single deepest pool twice a week from 41 weeks of gestation is recommended in the management of prolonged pregnancy. Induction of labor could be considered when oligohydramnios is diagnosed by single deepest pool less than 2 cm.

Plasma Brain Derived Neurotropic Factor and Platelet Derived Growth Factor Levels Are Elevated in Children with Sickle Cell Anemia and Abnormal Transcranial Doppler and/or Stroke

Abstract 516Children with sickle cell anemia (SCA) are at increased risk for stroke due to abnormal cerebral blood flow (CBF). The Stroke Prevention (STOP I) study showed that abnormal CBF could be detected using Trans-cranial Doppler (TCD), and may predict the risk for stroke. High TCD may be an indicator of main or branch cerebral artery vascular dysfunction, stenosis or fibrosis. Abnormal CBF is associated with cerebral ischemia and ultimately stroke. Brain derived neurotropic factor (BDNF) is a nerve growth factor with anti-apoptotic and neuro-protective properties. It is released in the central nervous system in response to ischemia. Platelet derived growth factor (PDGF) is an endothelial and smooth muscle mitogen. We hypothesized that circulating BDNF and PDGF levels will be elevated and may be associated with abnormal CBF as indicated by high TCD velocity measurements.Three groups of children, i.e. 1) SCA with abnormal TCDs (SATCD) - abnormal TCD ≥200 cm/sec, 2) SCA with normal TCDs (SNTCD) -normal TCD ≤170 cm/sec and 3) healthy controls were investigated. Stored, baseline plasma samples from the Stroke Prevention (STOP I) study and from an ongoing study of nutritional effects on inflammation in SCA children (NUTSCD) were analyzed in duplicate, using a multiplex antibody immobilized bead assay. Plasma levels of BDNF, PDGF AA and AB/BB and 10 other pro- and anti-inflammatory cytokines were assessed. A total of 39 samples (11 SATCD, 21 SNTCD and 7 controls) were analyzed. Of the 11 SATCD, 8 were eventually randomized to the standard care (SC), while 3 were in the transfusion (Tx) arm of STOP I. Since some of the SCA patients subsequently developed stroke, the levels of BDNF and PDGF in those who did vs. did not develop stroke were compared. Except where not applicable, values are presented as mean±SD. Chi-square was used to access distribution, while means were compared using t-test and analysis of variance (ANOVA). A Receiver Operator Characteristic (ROC) curve was used to access the sensitivity of BDNF and PDGF in predicting abnormal CBF as indicated by abnormal TCD measurement.The TCD velocity for SATCD group was 250±32 cm/s. There was no statistically significant difference in age or gender distribution among the groups. The mean body mass index was significantly lower for SCA subjects compared with controls (15±1kg/m2 vs. 23±7 kg/m2, p= 0.026). There was a statistically significant difference in mean BDNF levels, which was highest in SATCD compared with SNTCD (234±53 vs. 166±110 pg/ml, p=0.036) and controls (34±20 pg/ml, p<0.001). Difference in the BDNF levels between SNTCD and controls was also statistically significant, p=0.006. PDGF AA levels were significantly higher in SATCD compared with SNTCD (356±147pg/ml vs. 227±156 pg/ml, p = 0.045) and controls (34±32pg/ml, p<0.001). Also, PDGF AA levels were significantly higher for SNTCD vs. controls (p = 0.014). Six of the 7 patients who developed stroke had abnormal TCD, while one had conditional TCD (186cm/s, F, 3yo). However, all SCA patients who subsequently developed stroke had significantly higher PDGF AA levels than those who did not (350±180pg/ml vs. 249±154pg/ml, p=0.039). The BDNF levels, were not significantly different for SCA who subsequently developed stroke vs. those who did not (201±69pg/ml vs. 186±106pg/ml). Of the 3 patients receiving Tx, one who eventually had stroke, had very high (pre-Tx) PDGF AA level (312pg/ml); almost as high as those on SC who developed stroke (358±197pg/ml, n=6), and higher than the remaining 2 Tx patients who did not develop stroke (233±0.5pg/ml). The ROC curve showed that both BDNF and PDGF were sensitive (AUC=0.8, p<0.05) predictors of abnormal CBF as indicated by high TCDs velocity measurement.High TCD velocity in children with SCA was associated with elevated BDNF and PDGF AA levels. Moreover, PDGF AA levels were significantly higher in the SCA patients who developed stroke. Further study is warranted to determine whether BDNF and/or PDFG AA, alone or with abnormal TCD, will better predict future stroke risk. [Display omitted] [Display omitted] Disclosures:No relevant conflicts of interest to declare.

Regional Cerebral Blood Flow Abnormalities in Patients With Kawasaki Disease

Kawasaki disease (KD) is an acute febrile disorder of unknown etiology. Brain single-photon emission computed tomography (SPECT) and magnetic resonance imaging (MRI) help in detecting regional cerebral blood flow abnormalities and brain damage. The usefulness of SPECT and MRI in patients with KD was evaluated. All 22 patients with KD underwent brain SPECT using Tc-99m-hexamethyl propylene amine oxime from 6 days to 3 years after onset, and 8 patients underwent brain MRI. Of the 22 patients, 4 had neurologic symptoms. Case 1 showed prolonged apnea; case 2, prolonged disturbance of consciousness; and cases 3 and 4 generalized tonic-clonic seizures. Initial brain SPECT showed localized hypoperfusion in 4 and 13 patients with and without neurologic symptoms, respectively. All patients with neurologic symptoms underwent follow-up SPECT; localized hypoperfusion was detected between 1- and 6-month follow-up in 3 of these patients. Six patients without neurologic symptoms underwent follow-up SPECT. Localized hypoperfusion was detected at approximately 1- to 11-month follow-up in 4 of these patients. Diffusion-weighted imaging revealed abnormal high-intensity areas in the corpus callosum in case 1. Case 2 showed a bilateral chronic subdural hematoma with decreased size and ischemic changes, and case 3 showed bilateral hippocampal atrophy and left hippocampal sclerosis. Because the occurrence of localized hypoperfusion is possibly not restricted to only the acute phase in KD, brain SPECT and MRI should also be performed in KD patients with neurologic symptoms.

The relationship between serum iron deficiency and the pathogenesis of vasovagal syncope

Vasovagal syncope is the most common cause of syncope in children. Its pathogenesis is related to hemodynamics, vasodilation, cerebral blood flow abnormalities, nerve and changes in humoral factors. Body iron deficiency also cause these changes. This paper summarizes the intrinsic link between serum iron deficiency and these changes. Key words: Serum iron; Vasovagal syncope

Correlation of defects in regional cerebral blood flow determined by 99mTc SPECT with residual neurocognitive testing abnormalities during and 3 months post exposure in acutely poisoned patients with organophosphates

Introduction. Following acute organophosphate exposure, morphological changes in certain regions of the brain have been reported to develop within a few hours and involve neuronal degeneration. Single photon emission computed tomography (SPECT) has been used to determine changes in the regional cerebral blood flow and attempts have been made to correlate these changes with long-term neurological sequelae. Purpose of study. The aim of the study was to determine changes in the regional cerebral blood flow by 99mTc-ECD SPECT following acute organophosphate poisoning and to correlate these defects with abnormalities in neurocognitive testing carried out during admission and at 3 months post exposure, in order to determine whether any changes in the cerebral blood flow could help in predicting future development of neurocognitive deficit. Patients and methods. Twenty-eight patients with acute organophosphorous poisoning were included in the study. The inclusion criteria were a history of ingestion or accidental exposure, clinical features of cholinergic crises, and low serum acetylcholinesterase (AChE). Twenty age- and sex-matched patients from a previous study were used as controls for the neurocognitive tests. There were no controls for SPECT. Results. Of the 28 patients studied, 27 had abnormalities in the regional cerebral blood flow on SPECT with men having significantly higher abnormalities than women (p < 0.05). The right side of the brain had more defects than the left, with the occipital lobes being the most commonly involved. Of seven neurocognitive function tests carried out on patients who had regional cerebral blood flow defects during admission, abnormalities were observed in six tests. In 18 of 26 patients who could be tested at 3 months post exposure, improvement was observed in Trail B and Visual retention tests. However, others tests remained significantly abnormal. Conclusion. We conclude that a single episode of clinically significant organophosphate intoxication can lead to persistent residual neurocognitive deficits. Detection of regional cerebral blood flow defects on 99mTc-ECD SPECT can possibly help in predicting long-term deficits in neurocognitive functions in such patients.

Decreased regional cerebral blood flow in medial prefrontal cortex during trauma-unrelated stressful imagery in Vietnam veterans with post-traumatic stress disorder

Neuroimaging research has demonstrated medial prefrontal cortex (mPFC) hyporesponsivity and amygdala hyperresponsivity to trauma-related or emotional stimuli in post-traumatic stress disorder (PTSD). Relatively few studies have examined brain responses to the recollection of stressful, but trauma-unrelated, personal events in PTSD. In the current study, we sought to determine whether regional cerebral blood flow (rCBF) abnormalities in mPFC and amygdala in PTSD could be observed during the recollection of trauma-unrelated stressful personal events. Participants were 35 right-handed male combat veterans (MCVs) and female nurse veterans (FNVs) who served in Vietnam: 17 (seven male, 10 female) with current military-related PTSD and 18 (nine male, nine female) with no current or lifetime PTSD. We used positron emission tomography (PET) and script-driven imagery to study rCBF during the recollection of trauma-unrelated stressful versus neutral and traumatic events. Voxelwise tests revealed significant between-group differences for the trauma-unrelated stressful versus neutral comparison in mPFC, specifically in the anterior cingulate cortex (ACC). Functional region of interest (ROI) analyses demonstrated that this interaction in mPFC represented greater rCBF decreases in the PTSD group during trauma-unrelated stressful imagery relative to neutral imagery compared to the non-PTSD group. No differential amygdala activation was observed between groups or in either group separately. Veterans with PTSD, compared to those without PTSD, exhibited decreased rCBF in mPFC during mental imagery of trauma-unrelated stressful personal experiences. Functional neuroanatomical models of PTSD must account for diminished mPFC responses that extend to emotional stimuli, including stressful personal experiences that are not directly related to PTSD.

Brain perfusion and markers of neurodegeneration in rapid eye movement sleep behavior disorder

Potential early markers of neurodegeneration such as subtle motor signs, reduced color discrimination, olfactory impairment, and brain perfusion abnormalities have been reported in idiopathic rapid eye movement sleep behavior disorder, a risk factor for Parkinson's disease and Lewy body dementia. The aim of this study was to reproduce observations of regional cerebral blood flow abnormalities in a larger independent sample of patients and to explore correlations between regional cerebral blood flow and markers of neurodegeneration. Twenty patients with idiopathic rapid eye movement sleep behavior disorder and 20 healthy controls were studied by single-photon emission computerized tomography. Motor examination, color discrimination, and olfactory identification were examined. Patients with rapid eye movement sleep behavior disorder showed decreased regional cerebral blood flow in the frontal cortex and in medial parietal areas and increased regional cerebral blood flow in subcortical regions including the bilateral pons, putamen, and hippocampus. In rapid eye movement sleep behavior disorder, brain perfusion in the frontal cortex and occipital areas was associated with poorer performance in the color discrimination test. Moreover, a relationship between loss of olfactory discrimination and regional cerebral blood flow reduction in the bilateral anterior parahippocampal gyrus, a region known to be involved in olfactory functions, was found. This study provides further evidence of regional cerebral blood flow abnormalities in rapid eye movement sleep behavior disorder that are similar to those seen in Parkinson's disease and Lewy body dementia. Moreover, regional cerebral blood flow anomalies were associated with markers of neurodegeneration.

HIV and chronic methamphetamine dependence affect cerebral blood flow.

Human immunodeficiency virus (HIV) and methamphetamine (METH) dependence are independently associated with neuronal dysfunction. The coupling between cerebral blood flow (CBF) and neuronal activity is the basis of many task-based functional neuroimaging techniques. We examined the interaction between HIV infection and a previous history of METH dependence on CBF within the lenticular nuclei (LN). Twenty-four HIV-/METH-, eight HIV-/METH+, 24 HIV+/METH-, and 15 HIV+/METH+ participants performed a finger tapping paradigm. A multiple regression analysis of covariance assessed associations and two-way interactions between CBF and HIV serostatus and/or previous history of METH dependence. HIV+ individuals had a trend towards a lower baseline CBF (-10%, p = 0.07) and greater CBF changes for the functional task (+32%, p = 0.01) than HIV- subjects. Individuals with a previous history of METH dependence had a lower baseline CBF (-16%, p = 0.007) and greater CBF changes for a functional task (+33%, p = 0.02). However, no interaction existed between HIV serostatus and previous history of METH dependence for either baseline CBF (p = 0.53) or CBF changes for a functional task (p = 0.10). In addition, CBF and volume in the LN were not correlated. A possible additive relationship could exist between HIV infection and a history of METH dependence on CBF with a previous history of METH dependence having a larger contribution. Abnormalities in CBF could serve as a surrogate measure for assessing the chronic effects of HIV and previous METH dependence on brain function.

Precuneus hypoperfusion plays an important role in memory impairment of patients with systemic lupus erythematosus

The present study was designed to identify regional cerebral blood flow (rCBF) abnormalities in systemic lupus erythematosus (SLE) patients with memory impairments. Nineteen SLE patients (mean age 36.1 ± 8.6years, range 17-47) with subjective memory complaints underwent brain single-photon emission computed tomography (SPECT). The Korean Wechsler Adult Intelligence Scale (K-WAIS) and the Rey-Kim Memory Test (RKMT) were used objectively to evaluate cognitive functions in these patients. On the basis of the Intelligence Quotient-Memory Quotient (IQ-MQ) difference score, patients were classified into two groups: those with below one standard deviation (SD) from the mean for normal subjects of comparable age and education (memory impairment, n = 6) and those with without memory impairment (non-memory impairment, n = 13). Their brain SPECT images were analyzed by statistical parametric mapping (SPM) for group comparisons. The group of SLE patients with memory impairment showed significant hypoperfusion in the right precuneus compared with those with non-memory impairment (p < 0.001). Hypoperfusion of the precuneus may play a significant role in the memory function of SLE patients. SPM analysis of brain SPECT images could be a useful and objective tool for identifying abnormal rCBF in SLE patients with memory impairment.

Quantitative and Noninvasive Assessment of Prenatal X-Ray-Induced CNS Abnormalities Using Magnetic Resonance Imaging

Our purpose was to noninvasively assess formation of the microvasculature, blood-brain barrier (BBB) and blood-CSF barrier formation of prenatal X-ray-induced CNS abnormalities using quantitative MRI. Eight pregnant female Sprague-Dawley rats were divided into two groups consisting of control and X-irradiated animals. After birth, 20 neonatal male rats were divided into four groups of five rats. To evaluate the development of the BBB, changes in T(1) induced by Gd-DTPA were compared quantitatively in normal and prenatally irradiated animals in the formative period 1 to 2 weeks after birth. To assess the abnormalities of the microvasculature, quantitative perfusion MRI and MR angiography were also used. Histology was also performed to evaluate the BBB (albumin) and vascular endothelial cells (laminin). Decreased cerebral blood flow (CBF) and angioarchitectonic abnormalities were observed in the prenatally irradiated rats. However, abnormalities of the BBB and blood-CSF barrier were not observed using Gd-enhanced MRI and albumin staining. Quantitative perfusion MRI, MR angiography and Gd-enhanced T(1) mapping are useful for assessing CNS disturbance after prenatal exposure to radiation. These techniques provide important diagnostic information for assessing the condition of patients during the early stages of life after accidental or unavoidable prenatal exposure to radiation.

Do abnormalities in regional cerebral blood flow in anorexia nervosa resolve after weight restoration?

Previous studies have demonstrated localised abnormalities of cerebral blood flow in anorexia nervosa, suggesting reduction of cerebral activity and function in specific regions. There is debate as to whether such findings are secondary to starvation or indicative of a primary abnormality predating the illness, representing an underlying biological substrate. This small study, the first in early onset anorexia nervosa, reports findings of regional cerebral blood flow (rCBF) at both baseline and follow up. Nine participants who had previously undergone rCBF studies at the start of treatment, had a repeat scan at an average of 4.2 years later. Seven out of the nine had persisting reduced cerebral blood flow in one area of the brain, predominantly the medial temporal region. These data suggest that in the majority of cases rCBF does not return to normal following weight restoration. The implications for future research are explored.