Growth advantage of chronic myeloid leukemia CFU-GM in vitro: survival to growth factor deprivation, possibly related to autocrine stimulation, is a more common feature than hypersensitivity to GM-CSF/IL3 and is efficiently counteracted by retinoids +- alpha-interferon.

Bcr/abl fusion gene, in experimental models, induces survival to growth factor deprivation and hypersensitivity to IL3. However, conflicting data were reported about chronic myeloid leukemia (CML) progenitors. We investigated the responsiveness of purified CML CFU-GM to GM-CSF/IL3 and their survival to growth factor deprivation. CFU-GM hypersensitivity to IL3 and/or GM-CSF was found in 3/11 CML cases only. CML CFU-GM survived well in stroma-free 'mass' culture (5 x 10(4) cells/ml) without cytokine addition, up to day 11, average recovery being around 95% in medium + 10% fetal bovine serum and 67-81% in serum-free medium. Conversely, normal progenitors declined steadily, particularly after extensive purification (18 +/- 10% recovery at the 7th day), and in serum-free medium (4 +/- 6% recovery). By contrast, normal and CML CFU-GM declined in a similar way in limiting dilution cultures (1-10 cells/50 microl). We also investigated the effects of retinoic acid and alpha-interferon on CFU-GM survival. Both all-trans- and 13-cis retinoic acid, particularly in combination with alpha-interferon, reduced CML CFU-GM recovery down to normal progenitors' values. In conclusion, hypersensitivity to CSFs is rare in CML, whereas resistance to growth factor deprivation has been confirmed in mass, but not in limiting, dilution cultures. Both stereoisomers of retinoic acid, at therapeutic concentrations and in combination with alpha-interferon, can overcome the survival advantage of CML progenitors.

Prediction of long-term outcome in the early hours following acute ischemic stroke. Italian Acute Stroke Study Group.

OBJECTIVE: To develop a model for predicting outcome in the first few hours after the onset of an ischemic stroke on the basis of the clinical findings obtained during a rapid bedside examination. DESIGN: Clinical records were retrieved from the data bank of a randomized multicenter trial. The resulting case series was split into two subgroups that served as a "training set" and a "test set." Logistic regression was applied to the training set to select the prognostic predictors among baseline clinical findings. The performances of the model based on independent prognostic predictors were then validated in the test set. SETTING: Eleven primary care institutions (either hospitals or university clinics) participating in the Italian Acute Stroke Study on the efficacy of hemodilution and monosialoganglioside in acute ischemic stroke. PATIENTS: Consecutive noncomatose patients (N = 300) observed within the first 6 hours after the onset of a first supratentorial ischemic stroke. MAIN OUTCOME MEASURE: Death or disablement 4 months after the index stroke. Disablement was defined as a score of 3 or higher on the Rankin Scale. RESULTS: Age and CNS score defined six risk groups with a predicted 4-month poor outcome rate ranging from 10% (patients aged 70 years or younger and with an initial CNS score of 7 or higher) to 89% (patients older than 70 years and with a CNS score of 4.5 or lower). When a risk of poor outcome of 60% was taken as a cutoff, the accuracy of the prediction was 78% +/- 6% in the training set and 72% +/- 9% in the test set. CONCLUSION: Long-term outcome can be predicted in the first few hours following an acute ischemic stroke by means of a simple model based on age and CNS score.

Progressing neurological deficit secondary to acute ischemic stroke. A study on predictability, pathogenesis, and prognosis.

OBJECTIVES: To identify predictors and possible pathogenetic mechanisms of early neurological deterioration in patients with acute ischemic strokes and to evaluate their impact on clinical outcome. DESIGN: Case series. SETTING: University hospital's stroke unit. PATIENTS: A continuous series of 152 patients with first-ever ischemic hemispheric strokes were hospitalized within 5 hours of onset, evaluated with the Canadian Neurological Scale, and underwent a computed tomographic (CT) scan. The initial subset of 80 patients also underwent angiography. A repeated CT scan or autopsy was performed within 5 to 9 days of a patient's stroke. Progressing neurological deficit was defined as a decrease of one point or more in the global neurological scale score during hospitalization, when compared with that at entry. RESULTS: The conditions of 39 patients (26%) deteriorated during the initial 4 days; 20 patients (51%) had an impaired level of consciousness, and 19 patients (49%) had impaired limb strength and/or speech. They had been hospitalized earlier and had higher serum glucose levels at admission; the baseline CT scans of these patients showed an early focal hypodensity and initial mass effect more frequently. On the repeated CT scan (144 patients) or at autopsy (eight patients), patients with a progressing course more frequently had large infarcts, severe mass effect, and hemorrhagic infarction. We found no differences with regard to demographic data, medical history, and treatments that were given; only subcutaneous heparin calcium was more frequently administered to patients with a progressing course. Twenty-two (27%) of the 80 patients who underwent angiography had a progressing course, of whom 20 (91%) had an intracranial and/or extracranial arterial occlusion, with collateral blood supply in seven patients (35%). Logistic regression analysis showed that the independent predictors of progression were the serum glucose levels at admission and the early focal hypodensity with cortical and corticosubcortical locations, with the positive predictive values of the latter being 34% (95% confidence interval [CI], 26% to 42%) and 57% (95% CI, 47% to 67%), respectively. Among patients who underwent angiography, logistic regression analysis showed a significant correlation between carotid siphon occlusion and a progressing course. The 30-day case-fatality ratio and disability (Barthel index, < 60) were higher in patients with a progressing course (36% and 54% vs 12% and 35%, respectively). CONCLUSIONS: Early stroke deterioration is still an event that is difficult to predict; it is largely determined by cerebral edema following an arterial occlusion, as indicated by an early focal hypodensity and initial mass effect on the baseline CT scan. Since early deterioration anticipates a bad outcome in 90% of patients, it might be used as an early surrogate end point in therapeutic trials.

Hemorrhagic transformation of brain infarct: predictability in the first 5 hours from stroke onset and influence on clinical outcome.

OBJECTIVE: To identify, in the first 5 hours of acute brain infarct, clinical and radiologic predictors of subsequent hemorrhagic transformation (HT), and to evaluate its influence on the clinical course. BACKGROUND: The identification of early predictors of HT might be important to plan antithrombotic or thrombolytic treatments. PATIENTS: One hundred fifty consecutive patients with cerebral anterior circulation infarct systematically underwent a first CT within 5 hours of onset. During the first week after stroke, we performed a repeat CT or autopsy to look for HT. Outcome measures were early neurologic deterioration within the first week of onset and 30-day case fatality rate and disability. RESULTS: HT was observed in 65 patients (43%): 58 (89%) had a petechial HT and seven (11%) a hematoma. Among initial clinical an CT findings, the only independent predictor of HT was early focal hypodensity. Its presence was associated with subsequent HT in 77% of cases (95% CI, 68 to 86%), whereas its absence predicted the absence of subsequent HT in 94% of cases (95% CI, 89 to 99%). No baseline clinical or CT characteristic differentiated patients with petechial HT from those with hematoma. Antithrombotic and antiplatelet agents did not influence the occurrence of either type of HT. The frequency of early neurologic deterioration and of 30-day death or disability in HT patients was twice as high as in those without HT. However, a large-sized infarct and the presence of mass effect at the repeat CT or autopsy were the only factors independently linked to both the outcome events, irrespective of the development of HT. Clinical evolution of HT patients given antithrombotics was comparable with that of HT patients not receiving these drugs. CONCLUSIONS: HT of a brain infarct is a common event that occurs independently of anticoagulation and can be reliably predicted as early as 5 hours from stroke onset by the presence of focal hypodensity at CT. Apart from the infrequent cases of massive hematoma, HT does not influence prognosis, whereas a poor outcome in HT patients is correlated with a higher frequency of large edematous infarcts in this subgroup. The clinical course and final outcome of HT in anticoagulated patients does not differ from that of non-anticoagulated HT patients.

Systemic hypertension as a treatable risk factor for cerebrovascular disease.

It has long been established that hypertension is the major risk factor for stroke. Three Italian studies have been reviewed in order to examine different aspects of the problem. In the first study, the role played by the systolic, diastolic and systodiastolic components of hypertension in causing atherosclerotic damage of extracerebral and intracerebral arteries was examined. At the extracranial level, a significant correlation between systolic hypertension and atherosclerotic lesions was evident. The second study evaluated the risk of major stroke, myocardial infarction and death in patients with transient ischemic attacks and reversible ischemic neurologic deficits. Possible prognostic predictors of these events were thoroughly considered: Cumulative survival with the multivariate Kaplan-Meier analysis was significantly lower in hypertensive than in normotensive subjects, particularly for cerebral deaths and for all deaths. The third study was aimed at assessing the risk factors for transient ischemic attacks and stroke in young adults. Again, hypertension emerged as a fundamental risk factor, significantly more frequent in the subgroup of older patients than in the younger subgroup.

Overweight as an adverse prognostic factor for non-Hodgkin's lymphoma patients receiving high-dose chemotherapy and autograft.

Despite detailed evaluation of disease-associated prognostic factors, little is known about the impact of overweight in autograft programs for non-Hodgkin's lymphoma (NHL) patients. In order to address this issue, 121 NHL patients were retrospectively evaluated. They had been upfront (92 patients) or in relapse (29 patients) and received high-dose sequential (HDS) chemotherapy including peripheral blood progenitor cell (PBPC) autograft. Body mass index (BMI) was calculated as weight in kilograms divided by the square of the height in meters; overweight was defined as BMI > or = 28. Univariate and multivariate analyses were used to determine the prognostic implication of overweight and other known prognostic indicators on overall (OS) and event-free (EFS) survival for the entire group and overweight and non-overweight (reference) subgroups. With a median follow-up of 3 years, the estimated 5-year OS and EFS for the entire group were 58% and 49%, respectively. Twenty-eight patients (23%) had BMI > or = 28. Their median OS and EFS were 2.2 and 1.4 years, respectively, whereas median OS and EFS for the reference group have not been reached, with a 5-year projection of 65 and 55%, respectively (P < 0.002). On multivariate analysis, the risk of death among overweight patients was 2.9 (CI, 1.3-6.2) times that of the reference group; using EFS as the end point, a similar association between overweight and survival was observed. In conclusion, in high-risk NHL patients undergoing intensive chemotherapy and PBPC autografting overweight is associated with a poorer outcome.

Does hyperglycaemia play a role on the outcome of acute ischaemic stroke patients?

A consecutive series of 327 patients (188 males, 139 females; mean age 68.4, SEM 1.33) were hospitalized within 12 h of the onset of their first-ever hemispheric infarct. Three groups of patients were identified: diabetics (n = 70), non-diabetic hyperglycaemics (n = 93) and normoglycaemics (n = 164). Case-fatality ratios at 30 days after stroke were 38.6%, 22.6% and 9.2% (P less than 0.001) respectively, whereas the causes of death and functional outcome of survivors were not significantly different between the groups. Mean admission serum glucose levels (SGLs) of decreased, impaired/unchanged and improved patients within each one of the three groups, were also not significantly different as opposed to their mean Canadian Neurological Scale (CNS) scores at entry (P less than 0.01). Among patients with less severe initial neurological deficit (i.e., CNS score greater than or equal to 7.0), 82.6% of non-diabetic hyperglycaemic subjects fared well, in comparison with 56.5% of diabetic and 70.1% of normoglycaemic individuals. The size of the infarcted areas at the second CT correlated with mean CNS scores (P less than 0.01) but not with mean SGLs on admission. The site of the ischaemic areas did not correlate with mean SGLs at entry. Therefore the influence of initial SGLs on the clinical course of the present series of patients is questionable or, alternatively, varied probably according to the pattern of residual cerebral blood flow after arterial occlusion.

Ischaemic supratentorial stroke: angiographic findings in patients examined in the very early phase.

Eighty patients were studied by angiography within 6 h of an ischaemic stroke. Angiography was carried out with digital equipment and was usually limited to the vascular territory responsible for the neurological deficits. In 12 of 19 patients with internal carotid occlusion, the contralateral side was also studied. The angiographic abnormalities were classified as extracranial, intracranial, and combined extra and intracranial. The data show a high incidence (66%) of occlusive pathology of intracranial arteries, either isolated or associated with a significant presence of a potential embolic source (85%), and a high incidence of carotid occlusions located at the cervical segment (8 of 19). These observations suggest that most strokes are occlusive in origin.

Correlation of angiographic and sequential CT findings in patients with evolving cerebral infarction.

The usefulness of CT and angiography for predicting the final ischemic brain damage resulting from supratentorial ischemic stroke was evaluated in 36 patients. CT was performed within 4 hr and angiography within 6 hr after the onset of symptoms. CT was used to assess the site and size of parenchymal brain damage and angiography was used to evaluate the cerebral circulation. A 3-month follow-up CT study was used to determine the site and size of final ischemic damage. Angiography was normal in six patients and showed complete occlusion in 30. Angiographic findings in patients with arterial occlusion were classified as either internal carotid artery occlusion or middle cerebral artery (MCA) occlusion. MCA occlusions were subdivided into occlusion before the origin of internal lenticulostriate arteries (type 1), occlusion beyond the origin of these branches (type 2), occlusion at the bifurcation of the main trunk (type 3), and occlusion of the peripheral branches (type 4). Collateral blood supply was also studied. Early CT findings were positive in 25 of 36 patients; the lentiform nucleus alone, the lentiform nucleus and the cortex, or only the cortex were involved. In all patients with positive early CT findings, angiography showed an arterial occlusion, often located in the main trunk of the MCA. Involvement of the lentiform nucleus on early CT was always seen in patients with internal carotid artery or type 1 MCA occlusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Relationship between vascular enhancement, cerebral hemodynamics, and MR angiography in cases of acute stroke.

BACKGROUND AND PURPOSE: The use of MR angiography and contrast-enhanced T1-weighted MR imaging in cases of acute cerebral ischemia may be helpful in the evaluation of middle cerebral artery (MCA) occlusion and leptomeningeal collaterals, respectively. The aim of our work was to investigate the relationship between MCA occlusion, T1-weighted vascular contrast enhancement, hemodynamic alterations, and tissue damage in cases of acute ischemic stroke. METHODS: We studied the MCA territory in 15 patients with acute ischemic stroke within 8 hr of symptom onset. The first MR imaging study (<8 hr after onset) comprised diffusion-weighted imaging, MR angiography, perfusion-weighted imaging, and contrast-enhanced T1-weighted MR imaging sequences. Follow-up MR imaging, performed 1 week later, consisted of MR angiography and T2-weighted fluid-attenuated inversion recovery MR imaging. RESULTS: Early MR angiography showed MCA stem occlusion in nine of 15 patients. Patients with MCA occlusion had significantly larger areas of abnormality on early diffusion-weighted images, significantly larger areas of altered hemodynamics, larger final lesion volumes, and poorer clinical outcome. Among the nine patients with MCA stem occlusion, vascular enhancement was marked in seven and absent in two who had complete MCA infarcts and poor clinical outcome. Among patients with MCA patency, vascular enhancement was marked in only one, mild in four, and absent in one. Patients with marked vascular enhancement had significantly larger regions of altered hemodynamics and significantly higher asymmetries in both regional cerebral blood volume and mean transit time because of increased values in the affected hemisphere. CONCLUSION: Among patients with stroke with MCA occlusion, marked vascular enhancement and increased blood volume indicate efficient leptomeningeal collaterals and compensatory hemodynamic mechanisms.

Clinical and instrumental evaluation of patients with ischemic stroke within the first six hours.

The development of fibrinolytic agents such as streptokinase and recombinant tissue type plasminogen activator (r-TPA) and other modalities of treatment in acute ischemic stroke, has raised the need for a more precise knowledge of the pathophysiology of the acute phases of ischemic stroke as it pertains to prediction of clinical outcome. In a prospective analysis, 80 patients were studied within less than 6 h from the onset of symptoms by means of a detailed protocol including clinical evaluation, cerebral computed tomography, digital angiography and ultrasound transcranial Doppler sonography. Early angiography revealed a complete arterial occlusion in 76% of cases, the majority of which were intracranial (66%). Seventy percent of the occlusions that were retested were removed within 1 week. Potential embolic sources were found in more than 80% of cases. Patients with documented intracranial occlusion and scarce or absent collateral filling at early angiography, had the worst clinical outcome (P less than 0.05), based on mortality data and the Canadian Neurological Scale. The 30-day mortality rate was 25%. Survival was significantly better (P less than 0.01) in patients with a Canadian Neurological Score on entry of greater than or equal to 6.5 than in patients with a less than 6.5 value. Our data indicate that early pathophysiological studies augment the clinical information and should be taken into account in the design and analysis of therapeutic trials of acute ischemic stroke.

Influence of hyperglycaemia on infarct size and clinical outcome of acute ischemic stroke patients with intracranial arterial occlusion.

We investigated the effects of hyperglycaemia on infarct size of 82 acute ischaemic stroke patients with angiographically diagnosed intracranial occlusion in middle cerebral artery territory. There were 9 diabetics, 40 non-diabetic hyperglycaemics and 33 non-diabetic normoglycaemics (mean age 67 +/- 8 SD years, male/female ratio 1:1). For each patient the infarct at CT was compared to that predicted from the location of the arterial occlusion. The extent of the infarct was then classified as equal to, smaller than and larger than estimated, taking a standard anatomical template of arterial territories as reference. The results were analysed separately according to the presence or absence of a collateral blood supply (CBS) at angiography. The clinical outcome at 30 days was also evaluated. The 35 patients lacking CBS had a high frequency of equal to estimated lesions (75%), without substantial differences among the three subgroups (72% of hyperglycaemics, 82% of normoglycaemics and 67% of diabetics; Fisher's exact test not significant for any of the pairwise comparisons). On the contrary, the 47 patients with CBS exhibited an overall predominance of smaller than estimated lesions (66%) but with a very uneven distribution among hyperglycaemics, normoglycaemics and diabetics (82%, 64% and 0%, respectively; p < 0.05 at Fisher's exact test for diabetics vs hyperglycaemics). Finally, the clinical outcome was bad (death and neurological impairment) in 89% of diabetics, 72% of hyperglycaemics and 54% of normoglycaemics (p < 0.05). These results suggest that in patients with intracranial arterial occlusion associated with CBS the effects of hyperglycaemia might be beneficial in non-diabetics and harmful in diabetics.(ABSTRACT TRUNCATED AT 250 WORDS)

Computed tomography findings in the first few hours of ischemic stroke: implications for the clinician.

In order to evaluate the clinical usefulness of emergency computed tomography (CT) in acute ischemic stroke, we assessed whether CT findings within the first few hours of stroke onset reliably predict type, site and size of the index infarction, and risk of death or disability. For this reason we reviewed clinical and CT findings in a cohort of unselected consecutive patients referred to the stroke unit of a large urban hospital because of a presumed ischemic stroke in the anterior circulation (AC), and submitted to CT within 5 h from onset. Out of 158 total patients, emergency CT revealed parenchymal changes compatible with AC focal ischemia in 77 (49%) and a hyperdense middle cerebral artery (MCA) in 41 (26%). Parenchymal changes and hyperdense MCA predicted an AC territorial infarction respectively in 97% of cases (95% C.I. 93% to 100%) and in 95% of cases (95% C.I. 88% to 100%). Site and size of early changes coincided with those of final lesions in 79% of patients with cortical changes and in 95% of patients with cortico-subcortical changes, but only in 37% of patients with initial subcortical changes, the remainder of whom developed a cortico-subcortical infarction. At logistic regression parenchymal changes were the only independent predictor of an AC territorial infarction. Negative predictive power, however, was only 40% (95% C. I. 29% to 51%) for parenchymal changes, and 35% for hyperdense MCA (95% C.I. 26% to 44%). The odds for death or disability at 1 month associated with parenchymal changes were thrice as high as with negative CT, even after adjustment for clinical severity on admission. These results indicate that CT scan adds significantly to the prediction of outcome made on clinical grounds. The frequent development of a territorial infarction in patients with initially negative CT and the subsequent recruitment of the cortex in those initially exhibiting only subcortical changes suggest that the transition from ischemia to infarction often occurs after the first five h following stroke.

No differences in corpus callosum size by sex and aging. A quantitative study using magnetic resonance imaging.

To identify normal variations in the magnetic resonance imaging appearances of the corpus callosum with regard to sex and age, a prospective study was performed in 130 normal subjects. Callosal measurements were calculated by morphometric analysis. There were no significant sex differences in corpus callosum area or the callosal subregions. The absolute area did not decrease significantly with aging in normal males or females. However, age-related changes of callosal configuration were shown by a decrease in the ratio of the rostrum and genu to the splenium.

Circadian variation in the onset of acute cerebral ischemia: ethiopathogenetic correlates in 80 patients given angiography.

In a continuous series of 80 acute ischemic hemispheric strokes, the onset of symptoms was between 6:01 a.m. and noon in 45% of cases, between noon and 6:00 p.m. in 22.5%, between 6:01 p.m. and midnight in 31.25%, and between midnight and 6:00 a.m. in 1.25% (p less than 0.0001). By means of angiography and computerized tomography, and by detection of arterial and cardiac sources of emboli, four stroke subtypes were identified. Embolic and thrombotic strokes had their most frequent onset between 6:01 a.m. and noon (45% and 71%, respectively), whereas strokes of unknown origin and lacunar strokes were randomly distributed between 6:01 p.m. and midnight. The morning activation of the catecholaminergic system can account for this pattern of circadian onset of ischemic stroke.

Thrombolysis acute ischemic stroke.

Thrombolysis is an attractive but potentially dangerous they for cerebral ischemia: it is capable of dissolving an arterial thrombus, but can also transform a pale infarct into a hematoma and/or may cause severe oedema and herniation. The safety and efficacy of the treatment critically depend on the timing of intervention ad on patient selection. In recent studies on ischemic stroke, spontaneous hemorrhagic transformation of an infarct seems to be related to the size of the lesion, and can be reliably predicted as early as five hours from stroke onset by the presence of focal hypodensity in the CT scan. That is why in the European Co-operative Acute Stroke (ECASS), a randomised, double blind trial on intravenous rt-PA in hemispheric stroke, patients showing, on the admission CT scan, extended early hypodensity, involving more than one third of the territory of the middle cerebral artery, were excluded from the day. Other ongoing trials on thrombolytic agents are expected to provide further indications on how to identify those patients most likely to benefit and least likely to experience adverse effects from this treatment.

Emergency and early carotid endarterectomy in patients with acute ischemic stroke selected with a predefined protocol. A prospective pilot study.

AIM: The appropriateness of early carotid endarterectomy (CEA) in patients with acute ischemic stroke is still unsettled. The aim of this study was to verify the safety and feasibility of early CEA in a consecutive series of patients with acute ischemic stroke observed in an emergency Department Stroke Unit. METHODS: During a 24-month study, out of 756 patients with acute ischemic stroke 33 (4.4%) were scheduled for early CEA. Endarterectomy procedures were distinguished according to the time between the onset of stroke and operation as emergency (within 8 hours), early CEA (1-18 days). Patients with impaired consciousness or an infarct larger than 2.5 cm on computed tomographic (CT) or magnetic resonance (MR) scans or both were excluded from surgery. All patients underwent spiral CT, echo-color-Doppler (ECD) sonography, transcranial Doppler (TCD) sonography and, when necessary, MR angiography within 6 hours of admission. No patient underwent conventional angiography. Most patients were operated on under cervical block (CB) anesthesia; general anesthesia (GA) was used only for those with an unstable neurological deficit. Selective shunting was used on the basis of intra-operative transcranial Doppler in patients under GA and the onset or worsening of neurological deficit under CB anesthesia. RESULTS: Of the 6 patients operated on within a median 6 hours after the onset of stroke, 1 (16.5%) had a fatal hemorrhagic transformation of the infarct, while the remaining 5 (83.5%) stopped fluctuating or progressing and had a favourable neurological outcome. Of the 16 patients operated on within a median 36 hours and of the 11 patients operated on within 7 days, none deteriorated after operation. CONCLUSION: Emergency CEA is feasible for acute ischaemic stroke provided that strict selection criteria are applied and the door-to-surgery interval is kept short (within 8 hours). Early CEA for secondary prevention is feasible and safe, confirming that a delayed operation is in most cases unwarranted. Large randomized trials are warranted before implementing emergent and early CEA in routine clinical practice.

Quantitative assessment of cerebral blood flow in partial epilepsy using Xe-133 inhalation and SPECT.

The Xe-133 inhalation method was used to study rCBF in 12 patients with partial epilepsy during the interictal phase. SPECT images evidenced a focal CBF defect in 10 out of 12 patients, while quantitative analysis showed CBF abnormalities in all the patients. The focal CBF defect corresponded to the site of EEG abnormalities in nine patients. Additional low-flow areas beyond the EEG focus were found. Five patients presented a significant CBF decrease in the cerebellar hemisphere contralateral to the EEG focus. In five patients with unilateral EEG abnormalities, a CBF reduction was found in the contralateral cerebral hemisphere, mirror to the EEG focus. Finally, a widespread CBF decrease involving one or both cerebral hemispheres was observed in seven patients. Global and rCBF values were not correlated with age, duration of disease, frequency of seizures, secondary generalization, or specific therapy. SPECT may be useful in evaluating EEG epileptic foci, and quantitative SPECT allows the detection of functional effects of the epileptic focus on anatomically connected remote areas, probably due to the decrease of afferent inputs (diaschisis phenomenon).