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Our objective was to investigate correlations between clinical motor scores and cerebral sensorimotor activation to demonstrate that this reorganization is the neural substratum of motor recovery. Correlation analyses identified reorganization processes shared by all patients. Nine patients with first-time corticospinal tract lacuna were clinically evaluated using the NIH stroke scale, the motricity index, and the Barthel index. Patients were strictly selected for pure motor deficits. They underwent a first fMRI session (E1) 11 days after stroke, and then a second (E2) 4 weeks later. The task used was a calibrated repetitive passive flexion/extension of the paretic wrist. The control task was rest. Six healthy subjects followed the same protocol. Patients were also clinically evaluated 4 and 12 months after stroke. All patients improved significantly between E1 and E2. For E1 and E2, the ipsilesional primary sensorimotor and premotor cortex, supplementary motor area (SMA), and bilateral Broadmann area (BA) 40 were activated. Activation intensity was greater at the second examination except in the ipsilesional superior BA 40. Magnitude of activation was lower than that of controls except for well-recovered patients. E1 clinical hand motor score and E1 cerebral activation correlated in the SMA proper and inferior ipsilesional BA 40. Thus, we demonstrated early functionality of the sensorimotor system. The whole sensorimotor network activation correlated with motor status at E2, indicating a recovery of its function when activated. Moreover, the activation pattern in the acute phase (E1) had a predictive value: early recruitment and high activation of the SMA and inferior BA 40 were correlated with a faster or better motor recovery. On the contrary, activation of the contralesional hemisphere (prefrontal cortex and BA 39-40) and of the posterior cingulate/precuneus (BA 7-31) predicted a slower recovery.

In order to determine the influence of a single dose of fluoxetine on the cerebral motor activation of lacunar stroke patients in the early phase of recovery, we conducted a prospective, double-blind, crossover, placebo-controlled study on 8 patients with pure motor hemiparesia. Each patient underwent two functional magnetic resonance imaging (fMRI) examinations: one under fluoxetine and one under placebo. The first was performed 2 weeks after stroke onset and the second a week later. During the two fMRI examinations, patients performed an active controlled motor task with the affected hand and a passive one conducted by the examiner with the same hand. Motor performance was evaluated by motor tests under placebo and under fluoxetine immediately before the examinations to investigate the effect of fluoxetine on motor function. Under fluoxetine, during the active motor task, hyperactivation in the ipsilesional primary motor cortex was found. Moreover, fluoxetine significantly improved motor skills of the affected side. We found that a single dose of fluoxetine was enough to modulate cerebral sensory-motor activation in patients. This redistribution of activation toward the motor cortex output activation was associated with an enhancement of motor performance.

The aim of the current study was to assess the reproducibility of functional magnetic resonance imaging (fMRI) brain activation signals in a sensorimotor task in healthy subjects. Because random or systematic changes are likely to happen when movements are repeated over time, the authors searched for time-dependent changes in the fMRI signal intensity and the extent of activation within and between sessions. Reproducibility was studied on a sensorimotor task called “the active task” that includes a motor output and a sensory feedback, and also on a sensory stimulation called “the passive task” that assessed the sensory input alone. The active task consisted of flexion and extension of the right hand. The subjects had performed it several times before fMRI scanning so that it was well learned. The passive task consisted of a calibrated passive flexion and extension of the right wrist. Tasks were 1 Hz-paced. The control state was rest. Subjects naïve to the MRI environment and non–MRI-naïve subjects were studied. Twelve MRI-naïve subjects underwent 3 fMRI sessions separated by 5 hours and 49 days, respectively. During MRI scanning, they performed the active task. Six MRI-naïve subjects underwent 2 fMRI sessions with the passive task 1 month apart. Three non–MRI-naïve subjects performed twice an active 2-Hz self-paced task. The data were analyzed with SPM96 software. For within-session comparison, for active or passive tasks, good reproducibility of fMRI signal activation was found within a session (intra-and interrun reproducibility) whether it was the first, second, or third session. Therefore, no within-session habituation was found with a passive or a well-learned active task. For between-session comparison, for MRI-naïve or non–MRI-naïve subjects, and with the active or the passive task, activation was increased in the contralateral premotor cortex and in ispsilateral anterior cerebellar cortex but was decreased in the primary sensorimotor cortex, parietal cortex, and posterior supplementary motor area at the second session. The lower cortical signal was characterized by reduced activated areas with no change in maximum peak intensity in most cases. Changes were partially reversed at the third session. Part of the test–retest effect may come from habituation of the MRI experiment context. Less attention and stress at the second and third sessions may be components of the inhibition of cortical activity. Because the changes became reversed, the authors suggest that, beyond the habituation process, a learning process occurred that had nothing to do with procedural learning, because the tasks were well learned or passive. A long-term memory representation of the sensorimotor task, not only with its characteristics (for example, amplitude, frequency) but also with its context (fMRI), can become integrated into the motor system along the sessions. Furthermore, the pattern observed in the fMRI signal changes might evoke a consolidation process.

Background and Purpose —The hyperdense middle cerebral artery sign (HMCAS) is a marker of thrombus in the middle cerebral artery. The aim of our study was to find out the frequency of the HMCAS, its association with initial neurological severity and early parenchymal ischemic changes on CT, its relevance to clinical outcome, and the efficacy of intravenous recombinant tissue plasminogen activator (rtPA) in patients with the HMCAS. Methods —Secondary analysis of the data from 620 patients who received either rtPA or placebo in the European Cooperative Acute Stroke Study I (ECASS I), a double-blind, randomized, multicenter trial. The baseline CT scans were obtained within 6 hours from the onset of symptoms. Functional and neurological outcomes were assessed using the modified Rankin Scale and the Scandinavian Stroke Scale at day 90. Results —We found an HMCAS in 107 patients(17.7%). The initial neurological deficit was more severe in patients with the HMCAS than in those lacking this sign ( P P P P =0.0297). Conclusions —The HMCAS is associated with severe brain ischemia and poor functional outcome. However, it has no significant independent prognostic value when accounting for the effect of initial severity of neurological deficit and of early parenchymal ischemic changes on CT. Patients with the HMCAS may benefit from intravenous rtPA.

To determine whether the extent of subtle parenchymal hypoattenuation detected on computed tomographic (CT) scans obtained within 6 hours of ischemic stroke is a factor in predicting patients' response to thrombolytic treatment.The baseline CT scans of 620 patients, who received either recombinant tissue plasminogen activator (rt-PA) or a placebo, in a double-blind, randomized multicenter trial were prospectively evaluated and assigned to one of three categories according to the extent of parenchymal hypoattenuation: none, 33% or less (small), or more than 33% (large) of the middle cerebral artery territory. The association between the extent of hypoattenuation on the baseline CT scans and the clinical outcome in the placebo-treated and the rt-PA-treated groups after 3 months was analyzed.In 215 patients with a small hypoattenuating area, treatment increased the chance of good outcome. In 336 patients with a normal CT scan and in 52 patients with a large hypoattenuating area, rt-PA had no beneficial effect but increased the risk for fatal brain hemorrhage.The response to rt-PA in patients with ischemic stroke can be predicted on the basis of initial CT findings of the extent of parenchymal hypoattenuation in the territory of the middle cerebral artery.

Background Fou rire prodromique , described as pathological laughter preceding the onset of an apoplectic attack, is a rare phenomenon. Case Description A 61-year-old man manifested pathological laughter before a sudden right hemiplegia. MRI showed a left lenticular and caudate nucleus infarct with involvement of the external capsule and prerolandic area. MRA revealed a left internal carotid and middle cerebral artery occlusion. Conclusions The clinicoanatomic correlates of this phenomenon are discussed.

Background Ipsilateral sensory motor symptoms associated with carotid artery stenosis are rare, and few reports are available in the literature. Case Description We report the case of a 50-year-old man who presented with right hemiplegia that recurred 14 months later. A left hemisphere watershed infarction was detected. Repeated angiograms showed a left internal carotid occlusion and a right internal carotid stenosis that initially measured 50% and worsened to 80% after the second stroke. Conclusions Repeated quantitative measurements of cerebrovascular reserve demonstrated the hemodynamic mechanism of the strokes and the role of a right internal carotid lesion in causing the recurrence of right hemiplegia.

Since serotonin (5-HT) stimulates motor function, pharmacological potentiation of 5-HT neurotransmission may improve motor function in healthy subjects and, possibly, recovery in post-stroke patients. Indeed, fluoxetine, a selective serotonin reuptake inhibitor (SSRI), increased activation in executive motor areas of healthy subjects as fenozolone, a releaser of monoamines (including noradrenaline, dopamine, and serotonin) from intracellular stores. This study is intended to test the hypothesis that paroxetine can likewise modulate brain motor activity in a dose-dependent manner in healthy subjects. In a double-blind counterbalanced study, six subjects underwent functional MRI examinations on three sessions 1 week apart (E1, E2, and E3) at the time of peak plasma concentrations (5 h after drug intake, i.e., either 20 or 60 mg of paroxetine or placebo) with a complex sequential opposition task. Rest and activation alternated in a block design. During activation, subjects performed, with the right hand, a 1-Hz-paced task that alternated two fist closings with a sequential opposition task. Paroxetine elicited effects similar to those reported for fluoxetine; notable changes were hyperactivation in the contralateral S1/M1, and posterior SMA and widespread hypoactivation of basal ganglia and cerebellum. There was an inverse correlation between dose and effect: significantly greater effects were observed with the 20-mg dose compared with 60 mg. Paroxetine dose-dependently modulates activation of the entire motor pathway in a way that favors motor output. Thus, a single dose of the SSRI paroxetine reorganized motor processing.

To assess the capability of computed tomography (CT) in the prediction of irreversible ischemic brain damage and its association with the clinical course within 6 hours of stroke onset.Serial CT scans obtained within 6 hours of stroke onset, at 22-96 hours (median, 1 day), and at 2-36 days (median, 7 days) after symptom onset in 786 patients with ischemic stroke were prospectively studied, and follow-up CT scans were used as the reference. Clinical variables were assessed prospectively and independently of CT evaluation.The specificity and positive predictive value of ischemic edema at baseline CT for brain infarcts were 85% (95% CI: 77%, 91%) and 96% (95% CI: 94%, 98%), respectively. Sensitivity and negative predictive values were 64% (95% CI: 60%, 67%) and 27% (95% CI: 23%, 32%), respectively. Patients without early CT findings were less severely affected (P.001), developed smaller infarcts (P.001), had fewer intracranial bleeding events (P.001), and had a better clinical outcome at 90 days (P.001) compared with patients with hypoattenuating brain tissue at early CT.After ischemic stroke, x-ray hypoattenuation at CT is highly specific for irreversible ischemic brain damage if detection occurs within the first 6 hours. Patients without hypoattenuating brain tissue have a more favorable clinical course.

Background and Purpose —The clinical correlates of the varying degrees of early hemorrhagic transformation of a cerebral infarct are unclear. We investigated the cohort of a randomized trial of thrombolysis to assess the early and late clinical course associated with different subtypes of hemorrhagic infarction (HI) and parenchymal hematoma (PH) detected within the first 36 hours of an ischemic stroke. Methods —We exploited the database of the European Cooperative Acute Stroke Study I (ECASS I), a randomized, placebo-controlled, phase III trial of intravenous recombinant tissue plasminogen activator in acute ischemic stroke. Findings on 24- to 36- hour CT were classified into 5 categories: no hemorrhagic transformation, HI types 1 and 2, and PH types 1 and 2. We assessed the risk of concomitant neurological deterioration and of 3-month death and disability associated with subtypes of hemorrhagic transformation, as opposed to no bleeding. Risks were adjusted for age and extent of ischemic damage on baseline CT. Results —Compared with absence of hemorrhagic transformation, HI1, HI2, and PH1 did not modify the risk of early neurological deterioration, death, and disability, whereas, in both the placebo and the recombinant tissue plasminogen activator groups, PH2 had a devastating impact on early neurological course (odds ratio for deterioration, 32.3; 95% CI, 13.4 to 77.7), and on 3-month death (odds ratio, 18.0; 95% CI, 8.05 to 40.1). Risk of disability was also higher, but not significantly, after PH2. Conclusions —Risk of early neurological deterioration and of 3-month death was severely increased after PH2, indicating that large hematoma is the only type of hemorrhagic transformation that may alter the clinical course of ischemic stroke.

The view that CT is negative within the first 24–48 h after stroke has been handed down over the past 20 years. However, even with the first generation of CT scanners the prevalence of CT findings was not low during this time period. Using the 80 × 80 or 160 × 160 matrix of the early EMI scanner, Yock and Marshall observed five infarctions with “patchy low-density areas with irregular margins” less than 1 day old [45]. Aulich et al. described positive signs of cerebral infarctions in 54% of 41 patients examined within 48 h of symptom onset. In two patients they observed an area of low density within 3–4 h after the onset of symptoms [2]. Inoue et al. observed hypodense areas in three of 14 patients within the first 6 h and in eight of nine patients between 6 and 24 h [16]. Wall et al. found 79% CT scans positive within 24 h after onset of symptoms, and 65% of the positive scans were obtained at or less than 12 h after stroke [42]. More recent work has shown higher incidences of positive CT scans during the first 6 h after stroke: Tomura et al. studied 25 patients with embolic cerebral infarction between 40 and 340 min after the onset of symptoms. Twenty-three CT scans (92%) were positive, with obscuration of the lentiform nucleus [35]. Bozzao et al. observed parenchymal hypodensity in 25 of 36 patients (69%) [5]. Truwit et al. reported 23 of 27 patients (85%) with hypodensity on CT scan after stroke, the insular cortex being involved in all instances [37]. Horowitz et al. reported on hypodensity and mass effect in 56% of 50 scans [14]. When MR versus CT imaging were compared for identical patients within 3 h of acute hemispheric stroke, CT was found positive for 19 (53%) and MRI for 18 (50%) patients [21]. Von Kummer et al. reported 17 positive CT scans (68%) performed in a series of 25 patients with MCA trunk occlusion during the first 2 h. The incidence of positive CT findings increased to 89% in the third hour after symptom onset and to 100% thereafter [40]. In another series of patients with hemispheric stroke the incidence of early CT signs of infarction was 82% [41]. The initial CT of the ECASS population (620 patients) showed hypodense areas in 46%, less than or equal to 33% of the MCA territory in 35%, and areas exceeding 33% (exclusion criterion) in 8%.

We selected the following 20 patients from the ECASS to show the variety of early CT signs of hemispheric infarction. Each patient is presented by four continuous axial slices (5–10 mm thickness) through a representative volume of the brain. All CT scans are unenhanced. To reflect the real world, we did not exclude scans with artifacts or those of low technical quality. You will find the CT scans first with a short description of clinical symptoms, but without mention of aphasia or indication of the side of pathology. Try to delineate the region of parenchymal hypodensity and swelling, to differentiate between acute and old ischemic tissue alterations, and to describe the density of basal brain arteries. Thereafter, you can read our neurological description of the findings. You may realize that you have missed something. Then go back to the undescribed scans and find out whether you can see the pathological phenomena with your own eyes. The relevance of your finding is demonstrated by the follow-up scans, most of which were performed the next day. You will see that, except for severe swelling, almost every pathological tissue alteration is already be present on the first scan. Having studied all 20 patients, it is unlikely that you will oversee the CT signs of early hemispheric infarction in the future.

✓ The authors report their experience with 240 cases with lumbar phlebography in the diagnosis of lumbar disc herniations. The normal radiological anatomy and the radiological signs of disc herniations are described. Indications for phlebography are given, and the reliability of this test is compared with that of myelography performed with water-soluble agents.

The diagnosis and treatment involving the mesencephalic region are particularly challenging. Deeply located, and containing vital functions, the mesencephalic region regroups most of the problems that can be encountered in CNS vascular malformations (Smith and Rolla 1982): “cortical” lesions (temporal lobe—cerebellum) “deep” lesions (diencephalon—brain stem) dural structures (tentorium—falx) involvement cranial nerves (IIIrd, IVth and Vth) involvement

The authors describe the angio-architecture of intracranial vascular malformations. Several patterns can be identified thanks to the intracranial superselective angiograms that can now be performed. Schematically, the following features can be seen: 1. Direct arterial supply, 2. Indirect arterial supply, 3. Flow-related arterial ectasia (aneurysm), 4. Dysplastic aneurysm, 5. Direct arteriovenous fistula, 6. Intralesional arterial ectasia (aneurysm), 7. Intralesional venous ectasia (aneurysm), 8. Venous ectasia. Each of these elementary arrangements are illustrated and their clinical significance outlined whenever possible. Finally, the dural AVM drainage into the cortical venous system serves as an almost experimental model for the appreciation of the role played by the venous congestive phenomenon in brain AVM symptoms.

The authors report their experience with the endovascular approach of AVMs. Although the follow-up is short, the approach to the lesion and the morbidity related to the technique is low. 41 patients are reviewed. The most important feature of this series is that only 17 patients had previously bled. 27 had seizures and the remaining intractable headaches or progressive deficits. Only 4 patients were operated on following embolization. Clinical results are good, although few "anatomic" cures have been obtained by embolization alone (5 cases). However, the morbidity was moderately important (19%) per patient, 2/3 of which were totally regressive within a month. One death occurred during the procedure for a young male with a non-surgical posterior fossa brain AVM which had bled two times prior to the endovascular treatment. Topographic presentation of our results is the following: Pure cortical (13 cases), cortico-ventricular (17 cases), deep-seated (without vein of Galen) (2 patient), Posterior fossa (3 cases).