Focal Hypoperfusion Research Articles

Tc99m HM-PAO single photon emission computed tomography in temporal lobe epilepsy

We present the results of single photon emission computed tomography (SPECT) in 40 patients with temporal lobe epilepsy and normal computed transmission tomography (CT). Abnormalities of regional cerebral blood flow were found in 26 patients. There was focal hypoperfusion alone in 14, focal hyperperfusion alone in 6, and both types of abnormality in 6. In 4 patients there were bilateral abnormalities. Repeat SPECT showed persistence of interictal hyperperfusion in 5/12 patients. There were no significant correlations between SPECT findings and clinical parameters, and no relation between the persistence of interictal hyperperfusion and time since last seizure or seizure frequency. Where SPECT and multiple surface EEG recordings were both lateralising, agreement between them was good. The results of this study support the usefulness of HMPAO SPECT in detecting lateralising abnormalities in temporal lobe epilepsy. Interictal hyperperfusion may be commoner than previous publications suggest, and may be persistent in some cases.

Ictal and interictal ECD-SPECT for focus localization in epilepsy

Forty-one ECD (Technetium-99m-ethyl cysteinate dimer) SPECT investigations were undertaken in the course of a presurgical diagnostic work-up in 23 patients with pharmacoresistant focal epilepsy. In 21 patients, both an ictal and interictal SPECT were conducted. In the patients receiving ictal SPECT the tracer was injected between 7 and 30 s after the seizure onset. Of the interictal SPECTs 17 of 23 showed focal hypoperfusion which was consistent in 17 cases (74%) with the area of the electrophysiological focus (EF) and 6 patients had a normal interictal SPECT. Of the ictal SPECTs 18 of 21 (86%) showed regional hyperperfusion, 18 of them in the same location as the EF. Ictal SPECT showed a hypoperfusion similar to that in interictal SPECT in another 3 patients. In these cases seizure duration was short (28-54 s), so that the tracer reached the brain postictally. Our results show that ictal ECD-SPECT is an effective method for demonstrating an epileptogenic focus. Possible reasons for false-negative ictal SPECT results are discussed.

P02-07 Neurobiological substrate of Autism Spectrum Disorder - Cerebral blood flow distribution of 11C-butanol as assessed by PET/CT

Background:Functional studies in Autism Spectrum Disorder (ASD) have shown localised focal hypoperfusion and abnormalities in the anatomo-functional connectivity of limbic-striatal “social” brain. However, no common regional abnormalities have been found across studies.The aim of this study was to investigate the cerebral blood flow (CBF) at rest in subjects with ASD as compared to a group of healthy controls.Methods:In this preliminary investigation six normal intelligence patients with ASD and 5 age and sex matched healthy controls (HC) were examined using PET/CT camera and, as CBF tracer, 11C-butanol, a radiopharmaceutical produced on-site. The combination of these two methodologies reduced the whole examination time to less than 10 minutes. Statistical Parametric Mapping was implemented to analyse the data.Results:As compared to HC, ASD showed a highly significant CBF increase (height threshold p=0.001, p< 0.0001 at voxel-level), bilaterally, in large portions of the cerebellum, of the visual associative cortex and of the posterior parietal lobe.Conclusions:This preliminary study was performed by the state-of-the-art neuroimaging methodologies that reduced considerably the examination time and resulted in less stress and more reliable investigations. The occipital and parietal associative cortex as well as the cerebellum showed an increased CBF in ASD, underscoring their involvement in the disease and raising methodological and diagnostic issues to be considered when exploring the neuroanatomy of ASD.

Neurodegeneration and cellular stress in the retina and optic nerve in rat cerebral ischemia and hypoperfusion models

Experimental cerebral ischemia induces a stress response in neuronal and non-neuronal cells. In the present study we aimed to evaluate detailed cellular stress responses and neurodegenerative changes in the retinas in rat focal cerebral ischemia and hypoperfusion models involving invasive vascular manipulations. Independent groups of adult male Wistar rats were subjected to i) transient middle cerebral artery occlusion (tMCAO), ii) permanent middle cerebral artery occlusion (pMCAO), iii) cortical photothrombosis of the sensorimotor cortex using Rose Bengal dye or iv) bilateral common carotid artery occlusion (BCCAO). Rats were killed, and their eyes with the optic nerves enucleated and processed for histology, immunohistochemistry for neuronal nuclei (NeuN), glial fibrillary acidic protein (GFAP), hypoxia-inducible factor 1α (HIF-1α), c-fos, αB-crystallin, heat shock protein (HSP) 27, HSP60 and HSP70, and detection of DNA defragmentation. The total number of the retinal ganglion cell layer (RGCL) neurons and GFAP-immunoreactive astrocytes located in the nerve fiber layer were estimated using unbiased stereological counting. Our findings indicate that although permanent and transient MCAO does not cause detectable morphological alterations in the retina or optic nerve, it evokes ischemic stress as revealed by HIF-1α and HSPs expression in the RGCL neurons and reactive gliosis in the Müller cells. Severe neurodegenerative changes in the retina and optic nerve of the BCCAO rats are accompanied by a significant increase in immunoreactivities for the c-fos, HSP27 and HSP70 as compared with the sham-operated animals. The retinas from the ipsilateral side of the Rose Bengal model showed a significant decrease in the total number of NeuN-positive neurons in the RGCL as compared with the contralateral ones. However, these eyes did not differ between each other in the HSPs and HIF-1α expression or in the GFAP-immunoreactivity of the Müller cells. In conclusion, our data suggest differential expression of various HSPs in the retina and possibly their distinct roles in the cerebral ischemia-mediated stress response and neurodegeneration.

Brain MRI and SPECT in the diagnosis of early neurological involvement in Wilson’s disease

To evaluate the impact of brain MRI and single-photon emission computed tomography (SPECT) in early detection of central nervous system abnormalities in patients affected by Wilson's disease (WD) with or without neurological involvement. Out of 25 consecutive WD patients, 13 showed hepatic involvement, ten hepatic and neurological manifestations, and twp hepatic, neurological, and psychiatric symptoms, including mainly movement disorders, major depression, and psychosis. Twenty-four healthy, age-gender matched subjects served as controls. All patients underwent brain MRI and (99m)Tc-ethyl-cysteinate dimer (ECD) SPECT before starting specific therapy. Voxel-by-voxel analyses were performed using statistical parametric mapping to compare differences in (99m)Tc-ECD brain uptake between the two groups. Brain MRI showed T2-weighted hyperintensities in seven patients (28%), six of whom were affected by hepatic and neurological forms. Brain perfusion SPECT showed pathological data in 19 patients (76%), revealing diffuse or focal hypoperfusion in superior frontal (Brodmann area (BA) 6), prefrontal (BA 9), parietal (BA 40), and occipital (BA 18, BA 39) cortices in temporal gyri (BA 37, BA 21) and in caudatus and putamen. Moreover, hepatic involvement was detected in nine subjects; eight presented both hepatic and neurological signs, while two exhibited WD-correlated hepatic, neurological, and psychiatric alterations. All but one patient with abnormal MRI matched with abnormal ECD SPECT. Pathologic MRI findings were obtained in six out of ten patients with hepatic and neurological involvement while abnormal ECD SPECT was revealed in eight patients. Both patients with hepatic, neurological, and psychiatric involvement displayed abnormal ECD SPECT and one displayed an altered MRI. These findings suggest that ECD SPECT might be useful in detecting early brain damage in WD, not only in the perspective of assessing and treating motor impairment but also in evaluating better the less investigated disorders in the cognitive domain.

Global Hemispheric CT Hypoperfusion May Differentiate Headache With Associated Neurological Deficits and Lymphocytosis From Acute Stroke

Headache with associated neurological deficits and lymphocytosis (HaNDL) is characterized by temporary recurrent neurological deficits, moderate–severe headache, cerebrospinal fluid lymphocytosis, elevated protein, and increased opening pressure.1 Although CT and MRI should be normal, single photon emission CT may indicate focal hypoperfusion and electroencephalogram may reveal slowing or even epileptiform activity2 resolving once the patient is symptom-free (3 months). Catheter angiography also yields normal results but may trigger an acute neurological episode.3,4 Because HaNDL is a benign, self-limited syndrome, it is important to differentiate it from cerebrovascular disease to avoid unnecessary interventions such as catheter angiography and thrombolysis. We present a case initially thought to be acute stroke in which the patient was considered for thrombolysis. CT perfusion changes atypical for stroke made stroke diagnosis questionable and thrombolysis was withheld. A 31-year-old man with hypertension, dyslipidemia, and sleep apnea (treated with continuous positive airway pressure), but no history of prior migraine, was brought into our emergency department by ambulance with suspected acute ischemic stroke. He had become aphasic at work so his coworkers called 911. On examination, he was globally aphasic without focal weakness or obvious sensory changes aside from questionable mild right facial paresis (National Institutes of Health Stroke Scale score 6). A noncontrast CT and CT angiogram (CTA) were normal, but CT perfusion revealed a striking pattern of …

Magnetic resonance angiography of carotid and cerebral arterial occlusion in rats using a clinical scanner

In rat models to induce both focal cerebral ischemia and chronic cerebral hypoperfusion, it is highly desirable to verify the success of vessel occlusion and reopening with non-invasive method. The contrast-agent free 3D time-of-flight magnetic resonance angiography (TOF-MRA), diffusion-weighted imaging (DWI) and T2-weighted imaging by 3.0-T MR clinical scanner were applied when unilateral middle cerebral artery (MCA) was occluded and reopened, and after bilateral common carotid arteries were in ligation. The arterial angiograms of the rat brain and neck were achieved successfully in all chosen directions by the 3D TOF-MRA. It was shown that MCA in occlusion presented no signal in MRA, and the parenchyma of the ipsilateral MCA territory hypointensity signal in maps of apparent diffusion coefficient (ADC). After reperfusion, the signal intensity of ipsilateral MCA was resumed in MRA, and the decreased ADC was restored simultaneously. However, after 5 h of reperfusion, it was found that the value of ADC deteriorated second time with high T2 value. In bilateral common carotid artery occlusion (BCCAO) rats, it can be confirmed by MRA that the effectively occluded BCCA presented the absent signal and the basilar artery became tortuous. As a result, MRA by clinical scanner was proved of a valuable method to validate transient middle cerebral artery occlusion (MCAO) and permanent BCCAO rat model.

Agreement of central venous saturation and mixed venous saturation in cardiac surgery patients

Comparison of the bias and the limits of agreement (LOA; 2 SD) of the central venous saturation (S(cv)O(2)) before, during and after coronary artery bypass graft surgery with a simultaneous measurement of the mixed venous saturation (S(v)O(2)). Prospective controlled study in a university hospital department of anaesthesiology. 60 patients with coronary artery bypass surgery, 300 paired measurements of S(v)O(2) and S(cv)O(2). S(cv)O(2) and S(v)O(2) were analysed after induction of anaesthesia 15 min after cardiopulmonary bypass and 1, 6 and 18 h after admission to the intensive care unit. Regression analysis for the pooled measurements of S(cv)O(2) and S(v)O(2) showed a correlation R (2) = 0.52. After induction of anaesthesia 15 min after weaning from cardiopulmonary bypass and 6 h after admission to the intensive care unit the correlation coefficient was R (2) = 0.46, on admission to the intensive care unit it was R (2) = 0.42, and at 18 h it was R (2) = 0.38. Bland-Altman analysis for the measurements of S(cv)O(2) and S(v)O(2) showed a mean bias and LOA of 0.3% and -11.9 to +12.4%. In patients with a low S(cv)O(2) there was a trend to overestimate the S(v)O(2) by using the S(cv)O(2). The only factor that influenced the DeltaS(v)O(2) - S(cv)O(2) was the oxygen extraction rate (R (2) = 0.16). In patients with S(cv)O(2) below 70% this association was more pronounced (R (2) = 0.60). Our findings demonstrate that oxygen extraction rate is the major factor in the difference between S(v)O(2) and S(cv)O(2). Under certain circumstances S(cv)O(2) differed substantially from S(v)O(2). Therefore in selected patients both parameters should be monitored to exclude general or focal hypoperfusion.

Anaphylactic shock: The advantages of intra aortic balloon counter pulsation for the treatment of heart failure

The authors report a patient with a history of angina pectoris who developed anaphylactic shock that was complicated by a heart failure due to focal heart ischaemia. Early coronary angiography confirmed the diagnosis of localised coronary hypoperfusion. Intra aortic balloon counter pulsation succeeded in the restoration of coronary blood flow and haemodynamic stability. The authors discuss the opportunity of such treatment when a focal coronary hypoperfusion is diagnosed.

Silent or non-clinical infarct-like lesions in the posterior circulation territory in migraine: brain hypoperfusion or hyperperfusion?

Kruit et al . (2005) described infratentorial predominantly cerebellar silent or non-clinical infarct-like lesions in a cohort of migraine patients with or without aura; these authors concluded that such discrete lesions represent the effects of episodic focal brain hypoperfusion coupled to embolic damage and elaborated upon a specific pathophysiological role for the cerebellum. While Kruit et al . (2005) attributed brain hypoperfusion to cortical spreading depression (CSD) there is a significant unbridged conceptual gap between CSD and cerebral oligaemia (Pearce, 1985; Blau, 1992; Vijayan, 1995). Conversely, a large, increasing body of evidence suggests that CSD has a neuronal protective influence (Thompson and Hakim, 2005; Yanamoto et al ., 2005). The case for a primary pathogenetic role for the cerebellum in migraine is far weaker than that for the occipital cortex. Nevertheless, several lines of pharmacological evidence do not support a central brain neuronal origin for migraine (Gupta, 2005 a ). In contrast to the relatively transient hypoperfusion that occurs in migraine, as reviewed by Kruit …

Sickle cell disease: Ischemia and seizures

Although the prevalence of seizures in children with sickle cell disease (SCD) is 10 times that of the general population, there are few prospectively collected data on mechanism. With transcranial Doppler and magnetic resonance imaging (MRI) and angiography, we evaluated 76 patients with sickle cell disease, 29 asymptomatic and 47 with neurological complications (seizures, stroke, transient ischemic attack, learning difficulty, headaches, or abnormal transcranial Doppler), who also underwent bolus-tracking perfusion MRI. The six patients with recent seizures also had electroencephalography. Group comparisons (seizure, nonseizure, and asymptomatic) indicated that abnormal transcranial Doppler was more common in the seizure (4/6; 67%) and nonseizure (26/41; 63%) groups than in the asymptomatic (10/29; 34%) group (chi2; p = 0.045), but abnormal structural MRI (chi2; p = 0.7) or magnetic resonance angiography (chi2; p = 0.2) were not. Relative decreased cerebral perfusion was found in all seizure patients and in 16 of 32 of the remaining patients with successful perfusion MRI (p = 0.03). In the seizure patients, the perfusion abnormalities in five were ipsilateral to electroencephalographic abnormalities; one had normal electroencephalogram results. These findings suggest that vasculopathy and focal hypoperfusion may be factors in the development of sickle cell disease-associated seizures.

Hemispheric asymmetries of hypometabolism associated with semantic memory impairment in Alzheimer's disease: a study using positron emission tomography with fluorodeoxyglucose-F18

Considerable disagreement exists about the neuroanatomical basis of conceptual–semantic impairments observed in a subgroup of patients with Alzheimer's disease (AD) at mild to moderate stages of the disease. Several studies of groups of patients have shown correlations between focal hypometabolism or hypoperfusion in left hemispheric areas and measures of verbal semantic memory impairment in AD patients. The question remains, however, whether left hemispheric hypometabolism is sufficient to produce such impairment in the single case and whether nonverbal semantic knowledge is also affected. We used positron emission tomography (PET) with fluorodeoxyglucose-F18 (FDG), statistical parametric mapping (SPM), and tests of verbal and nonverbal semantic memory in 11 AD patients with a mean score on the Mini-Mental State Examination of 22.6 (±2.8). Naming impairment was significantly associated with left hemispheric asymmetry of hypometabolism on a single-case basis. Our correlation analysis showed that metabolism in left anterior temporal, posterior inferior temporal, inferior parietal and medial occipital areas (Brodmann areas: 21/38, 37, 40 and 19) correlated with both verbal and nonverbal semantic performance. We conclude that left hemispheric synaptic dysfunction, as measured by regional glucose hypometabolism, was sufficient to produce semantic impairments in our patients. The majority of areas affected in our patients with semantic impairments were involved in multimodal or supramodal (verbal and nonverbal) semantic knowledge.

Hemispheric asymmetries of hypometabolism associated with semantic memory impairment in Alzheimer's disease: a study using positron emission tomography with fluorodeoxyglucose-F18

Considerable disagreement exists about the neuroanatomical basis of conceptual–semantic impairments observed in a subgroup of patients with Alzheimer's disease (AD) at mild to moderate stages of the disease. Several studies of groups of patients have shown correlations between focal hypometabolism or hypoperfusion in left hemispheric areas and measures of verbal semantic memory impairment in AD patients. The question remains, however, whether left hemispheric hypometabolism is sufficient to produce such impairment in the single case and whether nonverbal semantic knowledge is also affected. We used positron emission tomography (PET) with fluorodeoxyglucose-F18 (FDG), statistical parametric mapping (SPM), and tests of verbal and nonverbal semantic memory in 11 AD patients with a mean score on the Mini-Mental State Examination of 22.6 (±2.8). Naming impairment was significantly associated with left hemispheric asymmetry of hypometabolism on a single-case basis. Our correlation analysis showed that metabolism in left anterior temporal, posterior inferior temporal, inferior parietal and medial occipital areas (Brodmann areas: 21/38, 37, 40 and 19) correlated with both verbal and nonverbal semantic performance. We conclude that left hemispheric synaptic dysfunction, as measured by regional glucose hypometabolism, was sufficient to produce semantic impairments in our patients. The majority of areas affected in our patients with semantic impairments were involved in multimodal or supramodal (verbal and nonverbal) semantic knowledge.

Prise en charge des attaques cérébrales à l'aide du CT de perfusion

Given the high variability of stroke mechanisms, size, localisation and degree of the penumbra, clinicians treating acute stroke patients need tools in addition to clinical information to match the individual patient withdifferent available treatment strategies. Among the two types of perfusion CTs the dynamic perfusion CT is preferable over the whole-brain technique as it can generate truly quantitative regional cerebral blood volume and cerebral blood-flow values and threshold maps that may differentiate reversible from non-reversible ischaemia. Some drawbacks of perfusion CTs, such as the impossibility of serial examinations (amount of contrast, radiation) or failure to show lacunar or posterior fossa lesions, are counterbalanced by the availability of CTs in most emergency rooms, its easy accessibility, simple monitoring of patients and the possibility to quantify perfusion deficits. Perfusion CT has a sensitivity and positive predictive value above 90% for territorial infarcts in the supratentorial regions, even in the earliest phase of stroke. Dynamic perfusion CT reliably identifies and core tissue and closely predicts final stroke volume. The final stroke size is usually close to the initial core volume if early arterial recanalisation occurs, and close or equal to the initial core plus size if early recanalisation does not occur (with or without thrombolysis). TIAs or migraine, but not focal seizures or transient global amnesia, may rarely show minor focal hypoperfusion. In regard to information about supratentorial perfusion, it appears at least equivalent to MRI perfusion methods. Regarding treatment decisions, the degree of on perfusion CTs as well as an arterial occlusion on the angio CT could help to select between intraarterial and intravenous thrombolysis. Further studies might show that the current windows thrombolyses are too long for patients with little and too short for patients with a persistent penumbra. Therefore, perfusion imaging may allow to replace a rigid window for acute interventions and the saying time is brain might be replaced by penumbra is brain. Thus, even patients with unknown onset of stroke, waking up with a stroke or having an epileptic seizure at stroke onset may become candidates for treatment based on the demonstration of a significant on perfusion imaging. In case neuroprotective treatment becomes available, only patients with a significant involving the matter for which the substance is active (grey versus white matter) may be exposed to benefits, costs and side effects of these treatments. When testing new acute stroke therapies, a potential treatment effect may be better shown thanks to selecting patients with perfusion CTs who are more likely to respond to the treatment strategy. In such a study it could be the amount of salvage of the initial radiological on perfusion CTs that may be used as a surrogate marker to test the efficacy of a new intervention, rather than final infarct size.

Transient global amnesia -- not always a benign process.

Transient global amnesia (TGA) is an episodic dysfunction of declarative memory, which is assumed to be a benign disorder. Brain perfusion single photon emission computed tomography (SPECT) was shown to be abnormal during the acute stage and to become normal with normalization of memory function. No data are known about the brain perfusion pattern among these patients with recurrent TGA. Sixteen patients with TGA were studied with an initial brain imaging during the acute stages of their attack, and a second imaging was performed after 3 months. In the event of a patients having a second abnormal brain perfusion HMPAO SPECT, a third imaging was performed after 1 year. Hypofusion perfusion was demonstrated in all cases during the acute stage. In all patients who had a first TGA, a normal SPECT was demonstrated after 3 months. In three patients with recurrent TGA, the brain perfusion remained abnormal after 3 months and after 1 year. A normal perfusion in TGA after 3 months can be expected in a patient with a first attack. In patients with recurrent TGA attacks, a persistent focal hypoperfusion can be expected. This subgroup of patients may demonstrate a non-benign type of TGA, eventually due to a different etiology of event.

Validation of ictal single photon emission computed tomography with depth encephalography and epilepsy surgery.

Many centers have reported that ictal single photon emission computed tomography (SPECT) localizes regions of seizure onset with greater sensitivity and specificity than interictal SPECT. Here we report interictal and ictal SPECT scan results in both lesional and nonlesional cases. Using technetium hexamethyl propylamenamine oxide (HMPAO) or ethyl cysteinate dimer (ECD), these scans were done in 52 patients with partial and secondarily generalized seizures. Twenty-five had normal MRI and 27 showed structural lesions. None had mesial temporal sclerosis clearly identified on MRI. All 52 subsequently had interictal and ictal intracranial EEG studies that appeared to localize the seizure focus. Thirty-nine patients had surgery and have been followed for 2 or more years. Interictal SPECT scans showed focal hypoperfusion consistent with intracranial EEG localization of the seizure focus in 29% of patients. In another 13%, there was correct lateralization but not localization. Ictal SPECT scans showed focal hyperperfusion consistent with intracranial EEG localization of the seizure focus in 52% of patients. In another 25%, there was correct lateralization but not localization. The presence or absence of structural lesions on MRI did not affect ictal hyperperfusion or its correlation with intracranial EEG. Thirty-nine patients had resective surgery, of whom 62% had class I outcomes. There was a trend towards better outcome when ictal SPECT data were concordant with intracranial EEG data. The presence or absence of structural lesions on MRI did not affect the likelihood of class I outcome. Ictal SPECT is superior to interictal SPECT in localizing and lateralizing seizure foci. Its results correlate well with intracranial EEG, but in more than one third of cases, the latter shows focal seizure onset in areas that do not show focal hyperperfusion. Surgical outcome tends to be better when the two modalities give concordant results.

Cerebral perfusion and haemodynamics measured by SPET in symptom-free patients with transient ischaemic attack: clinical implications.

Transient ischaemic attacks (TIAs) are heterogeneous from the clinical, physiopathological, aetiological and prognostic points of view. Single-photon emission tomography (SPET) may influence patient management by helping to define the vascular topography and by suggesting the probable mechanism (embolic or haemodynamic). However, the variables predicting focal regional cerebral blood flow (rCBF) and cerebrovascular reserve (CVR) abnormalities on SPET and their clinical correlation are poorly known. Our objective in this study was to assess the value of rCBF and CVR measured by SPET in a prospective series of 42 patients with recent (within the preceding 30 days) first-ever TIA Two SPET examinations [baseline and post-acetazolamide (ACZ)] were consecutively performed, and region/reference ratios were obtained using an irregular region of interest (ROI) method. Percentages of interhemispheric asymmetry between homologous brain regions were used to identify abnormalities on baseline SPET, and the percentage changes in asymmetry between the baseline and post-ACZ SPET studies were used to identify abnormal responses to the vasodilator stimulus. Mean baseline and test-retest values previously obtained in normals were used as a reference. The relationship of SPET findings with clinical data and results of complementary examinations was assessed. Most patients (98%) had abnormal findings on either baseline (43%), post-ACZ (19%) or both SPET studies (36%). Thus, 33 patients had hypoperfusion on baseline SPET (78.5%, symptom related in 45%). In 23 patients, a poor response to ACZ was found (55%, symptom related in 21.5%). No predictors for rCBF or CVR impairment were found. Most patients with a first-ever TIA episode present focal hypoperfusion on SPET, either with or without correlation with TIA symptoms. Post-ACZ SPET increases the probability of finding cerebrovascular abnormalities, and orients attention towards an haemodynamic compromise. Focal hypoperfusion on SPET should not be viewed as clinically insignificant because it probably reflects previous or ongoing clinical and/or subclinical episodes of cerebral ischaemia.

Functional imaging in the work-up of childhood epilepsy.

In children with medically intractable lesional epilepsy, surgery is deemed successful if the epileptogenic focus can be removed while major neurological functions are spared. Current techniques rely on invasive intracranial recordings. The new developments in functional imaging offer the possibility of localizing the epileptogenic focus noninvasively (PET/SPECT) and mapping cognitive functions (fMRI). Ictal SPECT shows hyperperfusion in the focus and has proved to have better localizing value than interictal PET or SPECT, which show focal hypometabolism or hypoperfusion. Ictal SPECT is useful for deciding on the placement of intracranial electrodes in extratemporal epilepsies, particularly in young children. Functional MRI has proved highly accurate for localizing motor and language networks, thus offering the possibilities of replacing the Wada test (language hemispheric lateralization) and studying postlesional brain plasticity. Despite the difficulties of functional imaging in children owing to the limited cooperation that can be expected, ethical constraints, and poor normative data, SPECT/PET and fMRI provide clinically useful information for presurgical work-up of childhood epilepsies.

Evidence of cerebral hypoperfusion in scleroderma patients.

To investigate regional cerebral blood flow by (99m)Tc-hexamethylpropylenamineoxime (HMPAO) single photon emission computed tomography (SPECT) in a series of 40 patients (mean age 58.5+/-11.5 yr) affected by systemic sclerosis (SSc) in comparison with age-matched healthy controls. Subjects affected by concomitant severe pathologies that might interfere with the interpretation of the SPECT results were excluded. SPECT findings were correlated with the severity of peripheral microvascular involvement, as assessed by nailfold videocapillaroscopy (NVC). Whenever possible, patients underwent magnetic resonance imaging (MRI) of the brain. Twenty-one SSc patients (52%) showed hypoperfusion in two or more regions of interest (ROIs) at the SPECT analysis. MRI was available in 14 of these patients, and was shown to be altered in eight of them (57%). One patient with both abnormal SPECT and abnormal MRI was affected by mild cognitive impairment. Transcranial Doppler sonography was normal in all but one of these patients with hypoperfusion. Nineteen patients exhibited a normal brain SPECT scan, but the MRI was shown to be altered in 3/12 of them (25%). No significant differences were found between the group of SSc patients showing hypoperfusion and those showing a normal SPECT scan regarding age, the duration of disease, the presence of vascular risk factors or damage of other organs typically involved in the disease, and the severity of peripheral microvascular involvement (NVC). Focal or diffuse cerebral hypoperfusion was found in more than half of the neurologically asymptomatic SSc patients studied, paralleling the incidence of altered brain MRI. The hypoperfusion was not linked to ageing and possibly reflects the cerebral location of the microangiopathic process characterizing the disease.

SPECT in focal enterovirus encephalitis: evidence for local cerebral vasculitis

We report a 4-year-old, left-handed male with focal coxsackievirus A3 encephalitis who presented with seizures and acquired aphasia. Electroencephalography exhibited focal spike discharges over the right frontal regions, but cranial magnetic resonance imaging did not reveal any structural abnormalities. However, brain single-photon emission computed tomography performed during the acute phase disclosed focal hypoperfusion in the right frontal lobe, consistent with decreased regional cerebral blood flow in the territory of some branches of the right cerebral anterior artery. Without specific treatment, the patient recovered completely within 1 month, when brain single-photon emission computed tomography images returned to normal and cranial magnetic resonance imaging still demonstrated no abnormalities. The present case suggests the possible role of transient local cerebral vasculitis in the pathogenesis of focal enterovirus encephalitis.