Postictal Hypoperfusion Research Articles

Changes in postictal cerebral perfusion are related to the duration of electroconvulsive therapy-induced seizures.

Postictal symptoms may result from cerebral hypoperfusion, which is possibly a consequence of seizure-induced vasoconstriction. Longer seizures have previously been shown to cause more severe postictal hypoperfusion in rats and epilepsy patients. We studied cerebral perfusion after generalized seizures elicited by electroconvulsive therapy (ECT) and its relation to seizure duration. Patients with a major depressive episode who underwent ECT were included. During treatment, 21-channel continuous electroencephalogram (EEG) was recorded. Arterial spin labeling magnetic resonance imaging scans were acquired before the ECT course (baseline) and approximately 1 h after an ECT-induced seizure (postictal) to quantify global and regional gray matter cerebral blood flow (CBF). Seizure duration was assessed from the period of epileptiform discharges on the EEG. Healthy controls were scanned twice to assess test-retest variability. We performed hypothesis-driven Bayesian analyses to study the relation between global and regional perfusion changes and seizure duration. Twenty-four patients and 27 healthy controls were included. Changes in postictal global and regional CBF were correlated with seizure duration. In patients with longer seizure durations, global decrease in CBF reached values up to 28 mL/100 g/min. Regional reductions in CBF were most prominent in the inferior frontal gyrus, cingulate gyrus, and insula (up to 35 mL/100 g/min). In patients with shorter seizures, global and regional perfusion increased (up to 20 mL/100 g/min). These perfusion changes were larger than changes observed in healthy controls, with a maximum median global CBF increase of 12 mL/100 g/min and a maximum median global CBF decrease of 20 mL/100 g/min. Seizure duration is a key factor determining postictal perfusion changes. In future studies, seizure duration needs to be considered as a confounding factor due to its opposite effect on postictal perfusion.

Seizure-induced neutrophil adhesion in brain capillaries leads to a decrease in postictal cerebral blood flow

Cerebral hypoperfusion has been proposed as a potential cause of postictal neurological dysfunction in epilepsy, but its underlying mechanism is still unclear. We show that a 30% reduction in postictal cerebral blood flow (CBF) has two contributing factors: the early hypoperfusion up to ∼30min post-seizure was mainly induced by arteriolar constriction, while the hypoperfusion that persisted for over an hour was due to increased capillary stalling induced by neutrophil adhesion to brain capillaries, decreased red blood cell (RBC) flow accompanied by constriction of capillaries and venules, and elevated intercellular adhesion molecule-1 (ICAM-1) expression. Administration of antibodies against the neutrophil marker Ly6G and against LFA-1, which mediates adhesive interactions with ICAM-1, prevented neutrophil adhesion and recovered the prolonged CBF reductions to control levels. Our findings provide evidence that seizure-induced neutrophil adhesion to cerebral microvessels via ICAM-1 leads to prolonged postictal hypoperfusion, which may underlie neurological dysfunction in epilepsy.

Medication preventing postictal hypoperfusion and cognitive side-effects in electroconvulsive therapy: A retrospective cohort study.

Electroconvulsive therapy (ECT) is associated with postictal confusion and cognitive side-effects. In rats, acetaminophen, non-steroidal anti-inflammatory drugs (NSAIDs) and calcium antagonists decreased postictal cerebral hypoperfusion along with reduction in postictal symptoms. In this study, in ECT-patients, we explore associations between use of these potentially protective medications and occurrence of postictal confusion and cognitive outcome. In this retrospective, naturalistic cohort study, patient-, treatment-, and ECT-characteristics, were collected from medical files of patients treated with ECT for major depressive disorder (MDD) or bipolar depressive episode. To test for associations of use of these medications with occurrence of postictal confusion, 295 patients could be included. Cognitive outcome data were available in a subset of 109 patients. Univariate analyses and multivariate censored regression models were used to test for associations. Occurrence of severe postictal confusion was not associated with use of acetaminophen, NSAIDs or calcium antagonists (n = 295). Regarding the cognitive outcome measure (n = 109), use of calcium antagonists was associated with higher post-ECT cognitive scores (i.e., better cognitive outcome; β = 2.23; p = 0.047), adjusted for age (β = -0.02; p = 0.23), sex (β = -0.21; p = 0.73), pre-ECT cognitive score (β = 0.47; p < 0.0001), and post-ECT depression score (β = -0.02; p = 0.62), but use of acetaminophen (β = -1.55; p = 0.07) as well as NSAIDs (β = -1.02; p = 0.23) showed no associations. This retrospective study does not find arguments for protective effects of acetaminophen, NSAIDs or calcium antagonists against severe postictal confusion in ECT. As a preliminary finding, the use of calcium antagonists was associated with improved cognitive outcome after ECT in this cohort. Prospective controlled studies are necessary.

Study of effect of nimodipine and acetaminophen on postictal symptoms in depressed patients after electroconvulsive therapy (SYNAPSE)

BackgroundPostictal phenomena as delirium, headache, nausea, myalgia, and anterograde and retrograde amnesia are common manifestations after seizures induced by electroconvulsive therapy (ECT). Comparable postictal phenomena also contribute to the burden of patients with epilepsy. The pathophysiology of postictal phenomena is poorly understood and effective treatments are not available. Recently, seizure-induced cyclooxygenase (COX)-mediated postictal vasoconstriction, accompanied by cerebral hypoperfusion and hypoxia, has been identified as a candidate mechanism in experimentally induced seizures in rats. Vasodilatory treatment with acetaminophen or calcium antagonists reduced postictal hypoxia and postictal symptoms. The aim of this clinical trial is to study the effects of acetaminophen and nimodipine on postictal phenomena after ECT-induced seizures in patients suffering major depressive disorder. We hypothesize that (1) acetaminophen and nimodipine will reduce postictal electroencephalographic (EEG) phenomena, (2) acetaminophen and nimodipine will reduce magnetic resonance imaging (MRI) measures of postictal cerebral hypoperfusion, (3) acetaminophen and nimodipine will reduce clinical postictal phenomena, and (4) postictal phenomena will correlate with measures of postictal hypoperfusion.MethodsWe propose a prospective, three-condition cross-over design trial with randomized condition allocation, open-label treatment, and blinded end-point evaluation (PROBE design). Thirty-three patients (age > 17 years) suffering from a depressive episode treated with ECT will be included. Randomly and alternately, single doses of nimodipine (60 mg), acetaminophen (1000 mg), or water will be given two hours prior to each ECT session with a maximum of twelve sessions per patient. The primary outcome measure is ‘postictal EEG recovery time’, expressed and quantified as an adapted version of the temporal brain symmetry index, yielding a time constant for the duration of the postictal state on EEG. Secondary outcome measures include postictal cerebral perfusion, measured by arterial spin labelling MRI, and the postictal clinical ‘time to orientation’.DiscussionWith this clinical trial, we will systematically study postictal EEG, MRI and clinical phenomena after ECT-induced seizures and will test the effects of vasodilatory treatment intending to reduce postictal symptoms. If an effect is established, this will provide a novel treatment of postictal symptoms in ECT patients. Ultimately, these findings may be generalized to patients with epilepsy.Trial registrationInclusion in SYNAPSE started in December 2019. Prospective trial registration number is NCT04028596 on the international clinical trial register on July 22, 2019.

Ictal hypoperfusion and iron deposition in the symptomatogenic zone of epilepsia partialis continua – A case report

Ictal hypoperfusion and iron deposition in the symptomatogenic zone of epilepsia partialis continua – A case report

Postictal brainstem hypoperfusion and risk factors for sudden unexpected death in epilepsy.

Since the strongest risk factor for sudden unexpected death in epilepsy (SUDEP) is frequent bilateral tonic-clonic seizures (BTCS), our aim was to determine whether postictal hypoperfusion in brainstem respiratory centers (BRCs) is more common following tonic-clonic seizures. We studied 21 patients with focal epilepsies who underwent perfusion imaging with arterial spin labeling MRI. Subtraction maps of cerebral blood flow were obtained from the postictal and baseline scans. We identified 6 regions of interest in the brainstem that contain key BRCs. Patients were considered to have postictal BRC hypoperfusion if any of the 6 regions of interest were significantly hypoperfused. All 6 patients who experienced BTCS during the study had significant clusters of postictal hypoperfusion in BRCs compared to 7 who had focal impaired awareness seizures (7/15). The association between seizure type studied and the presence of BRC hypoperfusion was significant. Duration of epilepsy and frequency of BTCS were not associated with postictal brainstem hypoperfusion despite also being associated with risk for SUDEP. Postictal hypoperfusion in brainstem respiratory centers occurs more often following BTCS than other seizure types, providing a possible explanation for the increased risk of SUDEP in patients who regularly experience BTCS.

Localizing the seizure onset zone by comparing patient postictal hypoperfusion to healthy controls.

Arterial spin labeling (ASL) MRI can provide seizure onset zone (SOZ) localizing information in up to 80% of patients. Clinical implementation of this technique is limited by the need to obtain two scans per patient: a postictal scan that is subtracted from an interictal scan. We aimed to determine whether it is possible to limit the number of ASL scans to one per patient by comparing patient postictal ASL scans to baseline scans of 100 healthy controls. Eighteen patients aged 20-55years underwent ASL MRI <90min after a seizure and during the interictal period. Each postictal cerebral blood flow (CBF) map was statistically compared to average baseline CBF maps from 100 healthy controls (pvcASL; patient postictal CBF vs. control baseline CBF). The pvcASL maps were compared to subtraction ASL maps (sASL; patient baseline CBF minus patient postictal CBF). Postictal CBF reductions from pvcASL and sASL maps were seen in 17 of 18 (94.4%) and 14 of 18 (77.8%) patients, respectively. Maximal postictal hypoperfusion seen in pvcASL and sASL maps was concordant with the SOZ in 10 of 17 (59%) and 12 of 14 (86%) patients, respectively. In seven patients, both pvcASL and sASL maps showed similar results. In two patients, sASL showed no significant hypoperfusion, while pvcASL showed significant hypoperfusion concordant with the SOZ. We conclude that pvcASL is clinically useful and although it may have a lower overall concordance rate than sASL, pvcASL does provide localizing or lateralizing information for specific cases that would be otherwise missed through sASL.

CT perfusion measurement of postictal hypoperfusion: localization of the seizure onset zone and patterns of spread.

Seizures are often followed by a period of transient neurological dysfunction and postictal alterations in cerebral blood flow may underlie these symptoms. Recent animal studies have shown reduced local cerebral blood flow at the seizure onset zone (SOZ) lasting approximately 1h following seizures. Using arterial spin labelling (ASL) MRI, we observed postictal hypoperfusion at the SOZ in 75% of patients. The clinical implementation of ASL as a tool to identify the SOZ is hampered by the limited availability of MRI on short notice. Computed tomography perfusion (CTP) also measures blood flow and may circumvent the logistical limitations of MRI. Thus, we aimed to measure the extent of postictal hypoperfusion using CTP. Fourteen adult patients with refractory focal epilepsy admitted for presurgical evaluation were prospectively recruited and underwent CTP scanning within 80min of a habitual seizure. Patients also underwent a baseline scan after they were seizure-free for > 24h. The acquired scans were qualitatively assessed by two reviewers by visual inspection and quantitatively assessed through a subtraction pipeline to identify areas of significant postictal hypoperfusion. Postictal blood flow reductions of > 15ml/100g-1/min-1 were seen in 12/13 patients using the quantitative method of analysis. In 10/12 patients, the location of the hypoperfusion was partially or fully concordant with the presumed SOZ. In all patients, additional areas of scattered hypoperfusion were seen in areas corresponding to seizure spread. CTP can reliably measure postictal hypoperfusion which is maximal at the presumed SOZ.

Quantitatively detecting postictal hypoperfusion in patients with focal epilepsy using CT perfusion: Determining cross-modality comparisons and electrode artifacts

BackgroundWe previously showed that CT perfusion (CTP) and arterial spin labelled (ASL) MRI can localize the seizure onset zone in humans via postictal perfusion patterns. As a step towards improving the feasibility/ease of collecting postictal CBF data, we determined whether EEG electrodes need to be removed for CTP data collection and whether a cross-modality comparison between baseline ASL and postictal CTP data is possible. New methodFive patients with epilepsy underwent postictal CTP scanning. Three patients had an interictal ASL scan; one patient had both an ASL and CTP interictal scan. Postictal CTP maps were quantitatively compared to 1) ASL maps averaged from 100 healthy controls, 2) each patient’s baseline ASL map and 3) each patient’s baseline CTP map. To assess for electrode artifacts, a phantom and one patient underwent CTP scanning with EEG electrodes in place. The acquired scans were assessed for artifacts and for postictal hypoperfusion. ResultsFocal postictal hypoperfusion was observable only in intra-modality comparisons (CTP to CTP) and not in cross-modality comparisons (CTP to ASL). EEG electrodes produced streaking artifact that decreased image quality and precluded quantitative analysis. Comparison with existing methods(s)An intra-modality comparison of baseline CTP to postictal CTP was the only comparison method that showed localized hypoperfusion. ConclusionsQuantitative comparison between postictal CTP and baseline ASL scans is not feasible. Postictal hypoperfusion can be detected by CTP only when two CTP scans are collected and when metallic EEG electrodes are removed.

Seizure onset zone localization using postictal hypoperfusion detected by arterial spin labelling MRI.

Neurological dysfunction following epileptic seizures is a well-recognized phenomenon. Several potential mechanisms have been suggested to explain postictal dysfunction, with alteration in cerebral blood flow being one possibility. These vascular disturbances may be long lasting and localized to brain areas involved in seizure generation and propagation, as supported by both animal and human studies. Therefore, measuring perfusion changes in the postictal period may help localize the seizure onset zone. Arterial spin labelling is a non-invasive, rapid and reproducible magnetic resonance imaging technique that measures cerebral perfusion. To this end, we measured postictal perfusion in patients with drug resistant focal epilepsy who were admitted to our seizure-monitoring unit for presurgical evaluation. Twenty-one patients were prospectively recruited and underwent arterial spin labelling scanning within 90 min of a habitual seizure. Patients also underwent a similar scan in the interictal period, after they were seizure-free for at least 24 h. The acquired scans were subtracted to identify the areas of significant postictal hypoperfusion. The location of the maximal hypoperfusion was compared to the presumed seizure onset zone to assess for concordance. Also, the localizing value of this technique was compared to other structural and functional imaging modalities. Postictal perfusion reductions of >15 units (ml/100 g/l) were seen in 15/21 patients (71.4%). In 12/15 (80%) of these patients, the location of the hypoperfusion was partially or fully concordant with the location of the presumed seizure onset zone. This technique compared favourably to other neuroimaging modalities, being similar or superior to structural magnetic resonance imaging in 52% of cases, ictal single-photon emission computed tomography in 60% of cases and interictal positron emission tomography in 71% of cases. Better arterial spin labelling results were obtained in patients in whom the seizure onset zone was discernible based on non-invasive data. Thus, this technique is a safe, non-invasive and relatively inexpensive tool to detect postictal hypoperfusion that may provide useful data to localize the seizure onset zone. This technique may be incorporated into the battery of conventional investigations for presurgical evaluation of patients with drug resistant focal epilepsy.

Various pathophysiological states of acute symptomatic seizures immediately after ischemic stroke, namely “onset seizures,” shown by complementary use of peri‐ictal magnetic resonance imaging and electroencephalography

AbstractBackground“Onset seizures” are acute symptomatic seizures occurring within 24 h after the onset of ischemic stroke, and their pathophysiological states are unknown. Electroencephalography is commonly used to diagnose epileptic activities; however, it is limited for use with acute stroke. Magnetic resonance imaging, including diffusion‐weighted imaging and perfusion imaging with arterial spin labeling, are applied mainly in an emergency. Ictal hyperperfusion on arterial spin labeling and cortical hyperintensity of cytotoxic edema on diffusion‐weighted imaging, peri‐ictally, can be obtained from an epileptically activated cortex.AimWe aimed to show pathophysiological states of onset seizures by complementary use of peri‐ictal magnetic resonance imaging and electroencephalography.MethodsFour patients diagnosed as onset seizures underwent an initial magnetic resonance imaging and subsequent electroencephalography.ResultsIn case 1, having persistent non‐convulsive status epilepticus after control of onset seizures, ictal magnetic resonance imaging and electroencephalography findings clearly showed the topographical relationship between the acute atherothrombotic infarction and the peri‐infarction activated cortex. In case 2, with multiple embolic strokes in the bifrontal lobes, prolonged arterial spin labeling hyper signals were observed in the perirolandic area of the right leg; cortical hyperintensity on diffusion‐weighted imaging and paroxysmal activities on electroencephalography were not shown. In cases 3 and 4, postictal hypoperfusion was shown in the large extent involving the multiple embolic infarctions. Because the epileptic cortex was located in the convexity, electroencephalography clearly showed inter‐ictal paroxysms in case 3, and localized slow wave in case 4.ConclusionThe present study shows that the complementary use of peri‐ictal arterial spin labeling/diffusion‐weighted imaging and electroencephalography potentially offers the ability to document the various pathophysiological states of onset seizure.

P 87 The perfusion changes in temporal and parietal lobe epilepsy

Purpose The aim of this study was to assess the regional relative interictal and postictal perfusion changes in temporal and parietal lobe epilepsy. Methods We investigated interictal and postictal magnet resonance perfusion changes in five patients with temporal lobe epilepsy either with hippocampal sclerosis (n = 3) or without (n = 2), and in one patient with extratemporal (parietal lobe) epilepsy. T(2)∗-weighted single-shot echo-planar images were acquired after bolus application of 0.2 mmol/kg gadolinium-diethylene triamine pentaacetic acid (GD-DTPA) at baseline and after intervals of 2–12 min, 15–23 min, 28–50 min, 63–72 min, and 180–240 min. The bolus-peak ratio was calculated in regions of interest in the hippocampus (HIP), parahippocampal gyrus (PHG), thalamus (THA), cortex (COR), and white matter (WM), yielding relative perfusion changes. Results Interictally, we found relative hyperperfusion of the ictogenic side in five of six patients in the HIP. Postictally, the perfusion decreased in the HIP by 25–39% as compared to baseline, whereas the PHG showed a reverse pattern. In the late postictal phase, perfusion increased in the HIP again and decreased in the PHG. In the THA, the inter- and postictal changes were small (5–19%). COR and WM showed equivocal results. Conclusion Postictal relative hypoperfusion in the HIP appears to be associated with the cessation of neuronal ictal discharge, whereas postictal hyperperfusion in the PHG lags behind and may reflect increased metabolism to restore the interictal state of neuronal excitability.

Focal and Generalized Patterns of Cerebral Cortical Veins Due to Non-Convulsive Status Epilepticus or Prolonged Seizure Episode after Convulsive Status Epilepticus – A MRI Study Using Susceptibility Weighted Imaging

ObjectiveThe aim of this study was to investigate variant patterns of cortical venous oxygenation during status epilepticus (SE) using susceptibility-weighted imaging (SWI).MethodsWe analyzed magnetic resonance imaging (MRI) scans of 26 patients with clinically witnessed prolonged seizures and/or EEG-confirmed SE. All MRI exams encompassed SWI, dynamic susceptibility contrast perfusion MRI (MRI-DSC) and diffusion-weighted imaging (DWI). We aimed to identify distinct patterns of SWI signal alterations that revealed regional or global increases of cerebral blood flow (CBF) and DWI restrictions. We hypothesized that SWI-related oxygenation patterns reflect ictal or postictal patterns that resemble SE or sequelae of seizures.ResultsSixteen patients were examined during nonconvulsive status epilepticus (NCSE) as confirmed by EEG, a further ten patients suffered from witnessed and prolonged seizure episode ahead of imaging without initial EEG. MRI patterns of 15 of the 26 patients revealed generalized hyperoxygenation by SWI in keeping with either global or multifocal cortical hyperperfusion. Eight patients revealed a focal hyperoxygenation pattern related to focal CBF increase and three patients showed a focal deoxygenation pattern related to focal CBF decrease.ConclusionsSWI-related hyper- and deoxygenation patterns resemble ictal and postictal CBF changes within a range from globally increased to focally decreased perfusion. In all 26 patients the SWI patterns were in keeping with ictal hyperperfusion (hyperoxygenation patterns) or postictal hypoperfusion (deoxygenation patterns) respectively. A new finding of this study is that cortical venous patterns in SWI can be not only focally, but globally attenuated. SWI may thus be considered as an alternative contrast-free MR sequence to identify perfusion changes related to ictal or postictal conditions.

Multimodal CT to Differentiate Acute Ischemic Stroke From Stroke Mimics

A 64-year-old man was evaluated in the emergency department after reportedly being found unconscious and “stiff.” A “stroke alert” was called from the field prior to arrival. At the time of initial evaluation, collateral history was not available. On examination, the patient was agitated, did not follow commands, and had a left gaze preference. There were symmetric and semipurposeful movements of the limbs. The patient was sedated and intubated to facilitate additional testing. Head computed tomography (CT) showed no hemorrhage. Computed tomography angiography (CTA) demonstrated diminished flow in the left hemispheric convexity branches without the evidence of proximal occlusion. CT Perfusion (CTP) showed reduced cerebral blood volume, cerebral blood flow, and increased time to peak perfusion involving the left cerebral hemisphere diffusely. The urine toxicology was positive for methamphetamine and cannabis. No thrombolytic therapy was administered and the patient recovered over the subsequent 24 hours. Multimodal CT has been adopted by many stroke centers as the neuroimaging modality of choice to guide acute stroke treatment. In this patient, the absence of proximal vascular occlusion and the diffusely reduced left-hemisphere blood flow and blood volume were suggestive of postictal hypoperfusion rather than focal cerebral ischemia.1 The CTP images for this patient are shown in Figure 1 (A-C), and they demonstrate the typical findings for postictal hypoperfusion, which includes holo-hemispheric involvement, crossing of multiple vascular distributions, sparing of the basal ganglia, and predilection for the smaller cortical vessels.2 This patient’s left gaze preference is therefore explained in the context of loss of cortical function in the hypoperfused hemisphere postictally. In acute ischemic stroke, the CTP would show an area of decreased relative cerebral blood flow (CBF) and relative cerebral blood volume (CBV) with increased time to peak (TTP) at the site of focal stenosis or occlusion surrounded by an area of decreased rCBF, increased rCBV, and increased TTP due to autoregulation. Additionally, there would be no sparing of any structures within the affected vascular distribution. Figure 1. Demonstrated is reduced cerebral blood flow (A) on the order of 10-30 mL/100 mg tissue per minute in the entire left hemisphere across the anterior, middle, and posterior cerebral artery territories with relative sparing of the basal ganglia. Likewise, ... This case illustrates the diagnostic utility of CTP in differentiating between stroke and stroke mimic when collateral history is limited or the examination is confounded.

Clinical Neurophysiology: EEG–Video Monitoring

Clinical Neurophysiology: EEG–Video Monitoring

Ictal SPECT

The localizing value of ictal single-photon emission computed tomography (SPECT) performed with cerebral blood flow agents in patients with epilepsy is based on cerebral metabolic and perfusion coupling. Ictal hyperperfusion is used to localize the epileptogenic zone noninvasively, and is particularly useful in magnetic resonance (MR)-negative partial epilepsy and focal cortical dysplasias. Subtraction ictal SPECT coregistered with MRI (SISCOM) improves the localization of the area of hyperperfusion. Ictal SPECT should always be interpreted in the context of a full presurgical evaluation. Early ictal SPECT injections minimize the problem of seizure propagation and of nonlocalization due to an early switch from ictal hyperperfusion to postictal hypoperfusion during brief extratemporal seizures. The degree of thresholding of SISCOM images affects the sensitivity and specificity of ictal SPECT. Ictal hypoperfusion may reflect ictal inhibition or deactivation. Postictal and interictal SPECT studies are less useful to localize the ictal-onset zone. Statistical parametric mapping analysis of groups of selected ictal-interictal difference images has the potential to demonstrate the evolution of cortical, subcortical, and cerebellar perfusion changes during a particular seizure type, to study seizure-gating mechanisms, and to provide new insights into the pathophysiology of seizures.

Typical and atypical perfusion patterns in periictal SPECT of patients with unilateral temporal lobe epilepsy.

To characterize perfusion patterns of periictal single-photon emission tomography (SPECT) in patients with unilateral temporal lobe epilepsy (TLE) and to determine their relationship to the epileptogenic zone (EZ). We studied periictal SPECT scans of 53 patients after anterior mesial temporal lobectomy who had good seizure outcome after surgery. Ictal SPECT scans were performed during video-EEG monitoring. Typical SPECT patterns consisted of ipsilateral ictal hyperperfusion or ipsilateral postictal hypoperfusion. Atypical ictal patterns included normal scans, bilateral temporal hyperperfusion, or contralateral patterns. These perfusion patterns were retrospectively analyzed searching for concordance rate with the EZ. We obtained 51 ictal and two early postictal scans. In the typical group, 40 (75.4%) patients had ipsilateral ictal temporal lobe hyperperfusion, and one (1.9%) patient had ipsilateral postictal temporal lobe hypoperfusion. Twelve (22.7%) patients exhibited atypical perfusion patterns: seven (13.2%) patients had bitemporal ictal hyperperfusion (four cases showed asymmetric temporal lobe changes), four (7.6%) patients had contralateral hyperperfusion, and one (1.9%) patient had a normal SPECT scan. All four patients with bitemporal asymmetric hyperperfusions showed greater perfusion lateralized to the side of the EZ. Three of the four patients who had contralateral hyperperfusion also had a complex postictal-like pattern in the ipsilateral temporal lobe consisting of anteromesial hyperperfusion with adjacent lateral hypoperfusion. This study analyzed typical and atypical perfusion patterns in unilateral TLE, and suggested that not only typical, but also some atypical perfusion patterns may contribute to the lateralization of EZ.