Diffusion-weighted magnetic resonance imaging in a case of cerebral venous thrombosis

BACKGROUND: Diffusion-weighted imaging (DWI) is the most sensitive MR sequence in acute arterial ischemic stroke but has not yet been evaluated in venous cerebral ischemia. We describe a patient with DWI performed at the acute phase of a venous ischemic stroke. CASE DESCRIPTION: A rapid cerebral MRI including DWI and fast fluid-attenuated inversion recovery (FLAIR) sequences was performed at the acute phase of a venous stroke confirmed by conventional angiography. DWI showed a slight decrease in apparent diffusion coefficient values 3 hours after onset (0.53+/-0.07x10(-3) mm2/s) and was normal 48 hours later (0.064+/-0.15x10(-3) mm2/s). Fast FLAIR sequences showed large left frontoparietal hyperintensities. The lack of a clear decrease in apparent diffusion coefficient values associated with marked FLAIR abnormalities may suggest prominent or early associated vasogenic edema. Physiopathological differences between arterial and venous ischemia may explain the different type of DWI FLAIR abnormalities during the acute phase as well as the better recovery of neurological deficit in venous stroke than in arterial ischemic stroke. CONCLUSIONS: In the context of an acute stroke, the contrast between marked FLAIR and subtle DWI abnormalities on MRI may reflect the venous mechanism of cerebral ischemia.     

A novel endothelin antagonist, A-127722, attenuates ischemic lesion size in rats with temporary middle cerebral artery occlusion: a diffusion and perfusion MRI study

BACKGROUND AND PURPOSE: Endothelins (ETs) are potent vasoconstrictors. Plasma ET levels increase during acute brain ischemia and may worsen the ischemic damage. Diffusion-weighted MRI (DWI) and perfusion imaging (PI) are powerful tools for evaluation of acute cerebral ischemia. We studied the effects of A-127722, a novel ET(A)-selective ET antagonist, on cerebral ischemic lesion size using 2,3,5-triphenyltetrazolium chloride (TTC) staining postmortem, on acute ischemic lesion development with DWI, and on the cerebral circulation using PI. METHODS: Twenty male Sprague-Dawley rats received either 5 mg/kg of A-127722 or vehicle (n=10 per group) intravenously 30 minutes and subcutaneously 4 hours after middle cerebral artery occlusion (MCAO). Whole-brain DWI and single-slice PI were done before initiation of treatment and repeated frequently thereafter up to 4 hours after MCAO. The animals were reperfused in the MRI scanner 90 minutes after the onset of MCAO. At 24 hours the animals were killed, and the brains were cut into six 2-mm-thick slices and stained with 2% TTC. Percent hemispheric lesion volume (%HLV) was calculated for each animal. RESULTS: Physiological parameters, body weight, neurological scores, and premature mortality (2 versus 2) did not differ between the two groups. No hypotension, abnormal behavior, or other adverse effects were seen. TTC-derived %HLV was 25.3+/-5.6% for controls and 16.2+/-9.6% for treated animals (36% reduction, P<.02). Six animals in each group had successful reperfusion as shown by PI. Among these animals, %HLV was 23.2+/-3.1% for controls and 9.3+/-4.4% for treated animals (60% reduction, P=.0001). The beneficial effect of A-127722 was limited to animals in which successful reperfusion was demonstrated. No difference in PI-detected perfusion deficit size was observed between the groups. DWI did not demonstrate significant in vivo lesion size differences. CONCLUSIONS: A-127722 significantly reduced ischemic lesion size in rats without observable adverse effects. It is not clear whether the effect was due to vasodilatation of collateral arterioles not detectable by PI or whether A-127722 has neuroprotective properties that are independent of vascular effects.     

Do changes in oxygen metabolism in the unaffected cerebral hemisphere underlie early neurological recovery after stroke? A positron emission tomography study

BACKGROUND AND PURPOSE: Whether an initial depression of function in the unaffected hemisphere ("transcallosal diaschisis") plays a role in early neurological recovery after acute stroke remains controversial. Previous studies were confounded by lack of acute-stage assessment with follow-up and by the problem of defining a suitable control group, since preexisting stroke risk factors may influence prestroke cerebral metabolism. We evaluated with positron emission tomography (PET) the relationships between unaffected-hemisphere (ie, contralateral) oxygen consumption (cCMRO2) and quantitative neurological assessments (and their respective evolution over time) after ischemic stroke. METHODS: Among 30 consecutive patients with first-ever middle cerebral artery ischemic stroke studied with the (15)O equilibrium method, we selected all survivors (n=19; mean age, 74.6 years) who were investigated both within the first 18 hours after stroke onset (PET1; mean, 11 +/- 4 hours) and 15 to 30 days later (PET2; mean, 24 +/- 10 days), with each patient serving as his/her own control. Neurological deficits were quantified using Orgogozo's middle cerebral artery scale (N score) at each PET session. Neurological changes were calculated as changes in the N score. A late CT scan coregistered with PET provided infarct topography and volume index. RESULTS: At PET2, we observed the overall expected neurological recovery. There was a nearly significant trend for a decrease in cCMRO2 from PET1 to PET2, especially for the neocortex (P=.08, F test); in a subgroup of eight patients with large infarcts, this CMRO2 decline was significant (P<.05) in the mirror region to the infarct. There was no significant correlation (Spearman's tests) between acute-stage cCMRO2 and same-day N scores or between changes in cCMRO2 versus changes in N score from PET1 to PET2 (any region). There was a nearly significant trend for lower PET2 cCMRO2 in the subgroup of eight patients with large compared with small infarcts (P=.06). CONCLUSIONS: We found no evidence for an influence of cCMRO2 on acute-stage neurological deficit or for a role of the unaffected hemisphere in early recovery after acute MCA ischemic stroke. The decline in unaffected-hemisphere metabolism from the acute to the subacute stage in the face of overall clinical recovery appears clinically irrelevant. The fact that the neocortical cCMRO2 at PET2 tended to be lower, and declined significantly from PET1 to PET2 in the mirror region in the subgroup of patients with large infarcts, suggests that this delayed effect represents transcallosal fiber degeneration.     

How does brain MRI lesion volume change on serial scans in patients with multiple sclerosis?

Although lesion load changes on conventional T2-weighted brain magnetic resonance imaging (MRI) scans from patients with multiple sclerosis (MS) are used to monitor the effect of treatment, there is no clear definition of how lesion load changes over years according to the lesion load present at a baseline evaluation. In the present study, we evaluated the relationship between lesion load changes over time and lesion load at a baseline evaluation in a group of untreated patients with MS. We scanned nineteen patients on two separate occasions with a mean interval 16.4 months between the two examinations. In each scanning session, a scan with forty contiguous 3-mm-thick axial slices was acquired. We assessed MRI lesion loads using a semi-automated local thresholding technique. Both a linear (p < 0.0001) and a quadratic component (p = 0.0008) of the baseline volume were significant in describing the follow-up volume. The equation to model this finding was as follows: Vf = beta0 Vb + beta1 (Vb)2, where Vf is the lesion volume at follow-up, Vb is the lesion volume at baseline, beta0 = 0.834 (SE = 0.098), and beta1 = 0.014 (SE = 0.003) (mL)(-1). Our data indicate that lesion volume changes detectable on serial brain MRI studies from patients with MS are dependent on the extent of lesion burden present on the baseline MRI scans. This finding has to be considered when planning phase III trials.     

Microemboli during carotid angiography. Association with stroke risk factors or subsequent magnetic resonance imaging changes?

BACKGROUND AND PURPOSE: Carotid angiography is associated with a 1% risk of major stroke. Recently, transcranial Doppler ultrasonography (TCD) has shown cerebral microemboli during carotid angiography. To determine their significance, we correlated the number of microemboli during angiography with clinical characteristics, angiography findings, and preangiography and postangiography cerebral magnetic resonance imaging (MRI). METHODS: One middle cerebral artery was monitored with TCD in 24 patients during angiography for carotid territory ischemia. The number of microemboli was correlated with angiographic and clinical characteristics. T2-weighted cerebral MRI was performed before and < or = 48 hours after angiography, and the number of new ischemic lesions was determined in a blinded review. RESULTS: Microemboli were seen in all patients, with an average of 51 per procedure (range, 12 to 154). The majority of microemboli had signal characteristics typical of air. Sixteen of the 24 patients had both preangiography and postangiography MRI. One of 24 patients had an angiographic stroke, with a single new thalamic lesion on MRI. No other patient had a new lesion. The microembolus count correlated with the angiographic contrast volume (P < .001) but not with any other radiological or clinical characteristic. CONCLUSIONS: This study confirmed the presence of numerous cerebral microemboli during carotid angiography. The microembolic signal characteristics and the correlation with contrast volume indicate that introduced air is the cause. These microemboli are usually clinically silent and do not lead to new changes on cerebral MRI.     

Identifying hypoxic tissue after acute ischemic stroke using PET and 18F-fluoromisonidazole

OBJECTIVE: To show that PET with 18F-fluoromisonidazole (18F-FMISO) can detect peri-infarct hypoxic tissue in patients after ischemic stroke. BACKGROUND: PET with (15)O-labeled oxygen and water is the only established method for identifying the ischemic penumbra in humans. We used PET with 18F-FMISO in patients after ischemic stroke to identify hypoxic but viable peri-infarct tissue likely to represent the ischemic penumbra, and to determine how long hypoxic tissues persist after stroke. METHODS: Patients with acute hemispheric ischemic stroke were studied using PET with 18F-FMISO either within 48 hours or 6 to 11 days after stroke onset. The final infarct was defined by CT performed 6 to 11 days after stroke. Tracer uptake was assessed objectively by calculating the mean activity in the contralateral (normal) hemisphere, then identifying pixels with activity greater than 3 SDs above the mean in both hemispheres. Positive studies were those with high-activity pixels ipsilateral to the infarct. RESULTS: Fifteen patients were studied; 13 within 48 hours of stroke, 8 at 6 to 11 days, and 6 during both time periods. Hypoxic tissue was detected in 9 of the 13 patients studied within 48 hours of stroke, generally distributed in the peripheries of the infarct and adjacent peri-infarct tissues. None of the 8 patients studied 6 to 11 days after stroke exhibited increased 18F-FMISO activity. All 6 patients studied both early and late exhibited areas of increased activity during the early but not the late study. CONCLUSIONS: PET with 18F-FMISO can detect peri-infarct hypoxic tissue after acute ischemic stroke. The distribution of hypoxic tissue suggests that it may represent the ischemic penumbra. Hypoxic tissues do not persist to the subacute phase of stroke (6 to 11 days).     

Serial neuropsychological assessment and magnetic resonance imaging analysis in multiple sclerosis

OBJECTIVE: To assess the correlation between cognitive dysfunction and disease burden in multiple sclerosis (MS) during a 1-year period. DESIGN: The Brief, Repeatable Battery of Neuropsychological Tests in Multiple Sclerosis was performed at entrance and 1 year. Patients underwent at least 20 proton density (range, 20-24) and T2-weighted axial magnetic resonance imaging (MRI) brain scans except for stable patients who were scanned monthly. Magnetic resonance imaging was evaluated using computer-automated, 3-dimensional volumetric analysis. SETTING: A research clinic of a university hospital. PATIENTS: Forty-four patients with MS of the following disease categories: relapsing-remitting (14), relapsing-remitting progressive (12), chronic progressive (13), and stable (5). MAIN OUTCOME MEASURES: The relationships between scores on the Brief, Repeatable Battery of Neuropsychological Tests in Multiple Sclerosis and 2 MRI measures (total lesion volume and brain to intracranial cavity volume ratio) were assessed using linear regression. These MRI measures were also compared with cognitive status at 1 year using analysis of variance. RESULTS: Overall, there was no decline in mean cognitive test performance during 1 year. Significant correlations were found between baseline neuropsychological test scores of nonverbal memory, information-processing speed, and attention and both MRI measures. Patients with chronic progressive MS demonstrated the strongest correlations. At 1 year, change in information-processing speed and attention correlated with change in total lesion volume. The mean increase in total lesion volume was 5.7 mL for 4 patients whose cognitive status worsened compared with 0.4 mL for 19 patients who improved and 0.5 mL for 21 patients who remained stable. CONCLUSIONS: During a 1-year period mean cognitive performance did not worsen. Automated volumetric MRI measures of total lesion volume and brain to intracranial cavity volume ratio correlated with neuropsychological performance, especially in patients with chronic progressive MS. Worsening MRI lesion burden correlated with cognitive decline.     

Relation between MR abnormalities and patterns of cognitive impairment in multiple sclerosis

OBJECTIVE: This study correlated the extent of abnormalities detected by different magnetic resonance imaging (MRI) techniques [proton density (PD)-weighted, T1-weighted, and magnetization transfer imaging (MTI)] with the overall cognitive, frontal lobe, and memory impairments in patients with MS. PATIENTS: There were 30 clinically definite MS patients, with different disease courses. Exclusion criteria: psychoactive/steroid treatments, mood disorders, acute relapse phase. MAIN OUTCOME MEASURES: Neuropsychological test results. Total (TLL) and frontal (FLL) lesion loads assessed from PD-weighted, T1-weighted (22 patients), and MTI (22 patients) MRI scans. Average lesion MT ratios (MTR) and analysis of the MTR histograms from brain tissue axial slabs on MTI scans. RESULTS: Patients with frontal lobe deficits (n=15) or memory impairment (n-17) had a higher TLL on PD scans (p=0.04 and p=0.01, respectively). Patients with frontal lobe deficits had higher FLL on PD scans (p=0.01) and TLL on MTI (p=0.03) scans. No significant relationships between the extent of T1-weighted lesion loads and the presence of any neuropsychological impairment. Mean MTR of both MS lesions and whole brain tissue was lower in patients with frontal lobe impairment (p=0.04). MRI lesion loads correlated significantly with some neuropsychological test scores. CONCLUSIONS: Lesion loads on PD-weighted MRI and MTI-derived measures are associated with cognitive decline in MS patients. Overall macroscopic and microscopic brain damage is more important than the corresponding regional brain disease in determining deficits of selective cognitive domains.     

Posterior leukoencephalopathy without severe hypertension: utility of diffusion-weighted MRI

OBJECTIVE: Standard MRI confirms the diagnosis of posterior leukoencephalopathy syndrome (PLES), recently associated with an increasing number of medical conditions. In PLES, T2-weighted MRI demonstrates hyperintensity spreading out from posterior brain regions; the pathophysiology remains mysterious. In the acute setting, diffusion-weighted imaging (DWI), but not standard MR imaging, can distinguish ischemic injury from those conditions known to cause vasogenic brain edema. DWI is potentially valuable in understanding the pathophysiology of PLES and in diagnosing patients who do not have previously known risk factors. METHODS: Serial CT and MRI studies (including DWI, apparent diffusion coefficient [ADC] maps, and, in one instance, perfusion-weighted imaging) were performed in three female patients with a neurologic syndrome consistent with PLES while hospitalized for treatment of other conditions. RESULTS: None of the patients had previously described risk factors for PLES; all had only mild elevations in blood pressure. MRI showed large, abnormal, T2 hyperintense regions in the posterior cerebrum with corresponding hyperintensity on ADC maps-signal characteristics predominantly consistent with vasogenic edema. There were also smaller patchy posterior cortical regions with decreased ADC and bright DWI consistent with infarction in one, and dramatic conversion of a large region to an ischemic pattern in another. CONCLUSIONS: ADC maps and DWI can successfully differentiate PLES from early cerebral ischemia, thus playing a pivotal role in treatment decisions. PLES is associated with a wider variety of conditions than has been previously reported and is not always reversible. Hyperintense DWI signal in patients with the syndrome likely marks a tissue stage of permanent brain injury.     

Utility of repeat brain imaging in stroke

PURPOSE: To determine the utility of repeat brain imaging in patients with stroke. METHODS: We reviewed the medical records of 98 consecutive patients in whom stroke was diagnosed between January 1 and December 31, 1991. We noted the number of brain scans performed, the indications cited, and whether repeat imaging changed the therapeutic decisions or final diagnosis. RESULTS: Ninety-eight patients underwent 221 procedures, with 123 repeat imaging studies (98 CT scans and 25 MR images). Sixteen patients had only one scan; 51 had two, and 31 had three or more. Indications for repeat imaging were explicitly documented in 62 (50%) of 123 repeated scans and inferred in another 41 (33%). In 20 (16%), no definite indication could be determined. Indications included lack of acute abnormal imaging findings on the initial scan (n = 48, 39%); compliance with stroke research protocol (n = 11, 9%). In none of the 82 patients did the repeated scan change the diagnosis; therapy was changed in only two (2%) of 82 patients (aspirin was discontinued). CONCLUSIONS: Repeat imaging in patients rarely results in changes in the initial diagnosis or the therapeutic plan; indications for repeat imaging are frequently not clearly stated; in certain groups of patients with stroke, repeat imaging may not be useful.     

Importance of fats as energy supply, membrane building blocks and immunomodulators in parenteral nutrition

We assessed the use of cranial computed tomography (CT) in elderly patients with acute neurological deficit and its influence on patient management. Clinical notes from 100 consecutive CT referrals from geriatric admissions presenting with acute neurological deficit were reviewed and categorized according to clinical presentation. CT results and subsequent therapy were recorded. Twenty of the patients had treatable lesions (in 6 out of 14 patients with signs atypical of stroke and 7 out of 19 patients with acute confusion). These two groups contained 68% of all treatable lesions found. Forty-four scans yielded no new diagnostic information; these included all scans for transient ischaemic attacks and for progression of stroke. The remaining scans yielded information regarding pathology but did not alter patient management. CT is a valuable first-line investigation in elderly patients presenting with signs atypical of stroke and unexplained confusion but may be less useful in patients with other presentations.     

Duration of glutamate release after acute ischemic stroke

BACKGROUND AND PURPOSE: High levels of glutamate in plasma and cerebrospinal fluid (CSF) have been demonstrated in patients with acute ischemic stroke. The duration of this excitatory amino acid release has not been studied, and therefore the window of opportunity of treatment with glutamate antagonists is unknown. The aim of this investigation was to study the duration of the glutamate increase in patients with stable and progressing ischemic stroke. METHODS: Glutamate in CSF was measured by high-performance liquid chromatography in 184 patients with an acute cerebral infarction of less than 24 hours' duration and in 43 control subjects. RESULTS: Among the 120 patients with stable ischemic stroke, median glutamate levels were significantly lower- and within the reference range of control subjects-in those patients studied 6 to 24 hours from onset of symptoms than in patients studied in the first 6 hours (3 [range, 2 to 10] versus 5 mumol/L [range, 2 to 17]; P < .0001). In 64 patients with progressing ischemic stroke, glutamate concentrations measured at any time interval during the first 24 hours from onset were significantly higher than in the stable stroke and control groups. CONCLUSIONS: The presence of glutamate increase in the CSF cannot be documented for greater than 6 hours in stable ischemic stroke. The sustained elevation of glutamate observed in progressing stroke suggests that the window to prevent neurological deterioration may be wider.     

Further evolution toward effective therapy for acute ischemic stroke

The effective treatment of acute ischemic stroke remains an important goal of modern medicine and substantive advances are occurring. Recently, thrombolytic therapy with tissue-type plasminogen activator was approved for selected patients with acute ischemic stroke when therapy is started within 3 hours of onset. Streptokinase therapy for acute ischemic stroke has not been shown to be effective and is associated with an increased risk of hemorrhage, although it was not evaluated as early after stroke onset as tissue-type plasminogen activator. Various types of neuroprotective interventions are effective in animal models, but none has yet been proven effective in patients. In the future, combinations of thrombolytic and neuroprotective drugs may be used to attempt maximum rates of recovery after acute ischemic stroke. For combination therapy to achieve its maximum potential, patients with acute ischemic stroke will have to be carefully selected and treated.     

Intravenous thrombolysis with recombinant tissue plasminogen activator for acute hemispheric stroke. The European Cooperative Acute Stroke Study (ECASS)

OBJECTIVE: To evaluate the efficacy and safety of intravenous thrombolysis using recombinant tissue plasminogen activator (rt-PA) in patients with acute ischemic stroke. DESIGN: Randomized, prospective, multicenter, double-blind, placebo-controlled clinical trial. SETTING: A total of 75 hospitals in 14 European countries. PATIENTS: A total of 620 patients with acute ischemic hemispheric stroke and moderate to severe neurologic deficit and without major early infarct signs on initial computed tomography (CT). INTERVENTION: Patients were randomized to treatment with 1.1 mg per kilogram of body weight of rt-PA (alteplase) or placebo within 6 hours from the onset of symptoms. OUTCOME MEASURES: Primary end points included Barthel Index (BI) and modified Rankin Scale (RS) at 90 days. Secondary end points included combined BI and RS, Scandinavian Stroke Scale (SSS) at 90 days, and 30-day mortality. Tertiary end points included early neurologic recovery (SSS) and duration of in-hospital stay. Safety parameters included mortality and incidence of intracranial or extracranial hemorrhage. RESULTS: The distribution of demographic variables was similar among patients in the rt-PA and placebo treatment arms in both the intention-to-treat (ITT) analysis and the explanatory analysis for the target population (TP). A total of 109 patients (17.4%) were included in the trial despite major protocol violations but excluded from the TP. There was no difference in the primary end points in the ITT analysis, while the TP analysis revealed a significant difference in the RS in favor of rt-PA-treated patients (P = .035). Of the secondary end points, the combined BI and RS showed a difference in favor of rt-PA-treated patients in both analyses (P < .001). Neurologic recovery at 90 days was significantly better for rt-PA-treated patients in the TP (P = .03). The speed of neurologic recovery assessed by the SSS was significantly better up to 7 days in the ITT analysis and up to 30 days for the TP in the rt-PA treatment arm. In-hospital stay was significantly shorter in the rt-PA treatment arm in both analyses. There were no statistically significant differences in the mortality rate at 30 days or in the overall incidence of intracerebral hemorrhages among the rt-PA and placebo treatment arms in either analysis. However, the occurrence of large parenchymal hemorrhages was significantly more frequent in the rt-PA-treated patients. CONCLUSIONS: Intravenous thrombolysis in acute ischemic stroke is effective in improving some functional measures and neurologic outcome in a defined subgroup of stroke patients with moderate to severe neurologic deficit and without extended infarct signs on the initial CT scan. However, the identification of this subgroup is difficult and depends on recognition of early major CT signs of early infarction. Therefore, since treating ineligible patients is associated with an unacceptable increase of hemorrhagic complications and death, intravenous thrombolysis cannot currently be recommended for use in an unselected population of acute ischemic stroke patients.     

Diffusion-weighted MR imaging of acute cerebral ischemia

Diffusion-weighted MR imaging has been used in studies on experimental animal models and on patients with acute cerebral ischemia. Compared with CT and conventional MR techniques, diffusion-weighted imaging can provide earlier and more precise detection of the location and the extent of an ischemic lesion during the critical first few hours after the onset of stroke. Quantitative apparent diffusion coefficient (ADC) mapping of the brain water can also be carried out by recording a series of diffusion-weighted images with different amplitudes of the displacement encoding gradients. ADC maps can provide important information about the extra- and intracellular water homeostasis. ADC reduction of the tissue water is one of the early signals of the pathophysiological cascade resulting from ischemic tissue injury. Diffusion MR imaging has become a valuable tool in stroke research. It may also prove a valuable tool in monitoring the efficiency of therapeutic effects in stroke patients. It is our intention to provide an overview of the recent development in this area with emphasis on the diffusion-weighted MR techniques, and to discuss the possible underlying biophysical mechanisms responsible for the contrast of diffusion-weighted imaging.     

Diffusion, perfusion, and T2 magnetic resonance imaging of anti-intercellular adhesion molecule 1 antibody treatment of transient middle cerebral artery occlusion in rat

The effect of anti-intercellular adhesion molecule-1 (anti-ICAM-1) antibody treatment of transient (2 h) middle cerebral artery (MCA) occlusion in the rat was measured using diffusion (DWI)-, T2 (T2I)- and perfusion (PWI)-weighted magnetic resonance imaging. Rats were treated upon reperfusion with an anti-ICAM-1 monoclonal antibody (n=11) or a control antibody (n=7). DWI, T2I and PWI were performed before, during, and after induction of focal cerebral ischemia from 1 h to 7 days. In both groups, the apparent diffusion coefficient of water (ADCw) and cerebral blood flow (CBF) values in the ischemic region significantly declined from the preischemic ADCw values (p<0. 05). The post ischemic increase in T2 of the control group was significantly higher at 48 h than in the anti-ICAM-1 treated group (p<0.05). CBF was not significantly different between the two groups. The temporal profiles of MRI cluster analysis, which combines ADCw and T2 maps into a single image, was significantly different between groups. These data suggest that the neuroprotective effect of anti-ICAM-1 antibody treatment is reflected in reductions of T2 and lesion growth during reperfusion and may not be associated with increased cerebral perfusion.     

The Sunnybrook Stroke Study: a prospective study of depressive symptoms and functional outcome

BACKGROUND AND PURPOSE: To assess the prevalence of depressive symptoms, their clinical correlates, and the effects of depressive symptoms on stroke recovery, a relatively unselected, well-diagnosed cohort of consecutive stroke survivors was followed prospectively. METHODS: Consecutive admissions to a regional stroke center who met World Health Organization and National Institute of Neurological Disorders and Stroke criteria for stroke were eligible. Subarachnoid hemorrhage and brain stem strokes were excluded. Patients underwent CT, single-photon emission CT, and standardized neurological and cognitive examinations at entry. At 3 months and 1 year after stroke, depressive symptoms were assessed with the Montgomery Asberg Depression Rating Scale (MADRS) and the Zung Self-Rating Depression Scale (SDS). Functional outcome was measured with the Functional Independence Measure, and handicap was assessed by the Oxford Handicap Scale. RESULTS: We assessed 436 patients at entry (mean +/- SD age, 74.9 +/- 11.6 years). There were 150 patients available for assessment at 3 months and 136 at 1 year. Marked depressive symptoms were noted in 22% (SDS) to 27% (MADRS) at 3 months and 21% (SDS) to 22% (MADRS) at 1 year. Patents with marked depressive symptoms had more neurological impairment (P<.008), were more likely to be female (P<.05), and were more likely to have previous histories of depression (P<.03). There was no relationship between depressive symptoms and age, lesion volume, or side of lesion. Depressive symptoms were correlated with functional outcome (r = -.31, P<.0001) and handicap (r = .41, P<.0001) at 3 months and 1 year (r= -.28, P<.001; r = .35, P<.0001). CONCLUSIONS: Depressive symptoms and functional outcome are correlated. In view of the prevalence of depressive symptoms in this population, diagnosis and treatment of depression are important in optimizing recovery.     

Stroke patterns of internal carotid artery dissection in 40 patients

BACKGROUND and PURPOSE: Internal carotid artery dissection (ICAD) is a frequent cause of ischemic stroke in young patients. Whether cerebral ischemia is of embolic or hemodynamic origin remains to be determined. Heparin is often administered in ICAD; however, a drug trial can hardly be conducted because of the low recurrence rate after the acute stage. Therefore, the best therapeutic approach should be determined on the basis of the presumed mechanism of cerebral ischemia. One way to approach the mechanism of stroke in ICAD is to determine stroke patterns. We postulated that most cortical and large subcortical infarcts (>/=15 mm) are of embolic origin and that small subcortical infarcts (<15 mm) and junctional infarcts are not. The aim of our study was to determine the stroke patterns in 40 consecutive patients with ICAD. METHODS: The patients (26 women and 14 men; mean age, 42.8 years) had a total of 65 ICADs. Seventeen patients were free of any vascular risk factor. CT scans, MRI scans, and angiographic features were analyzed by observers who were blinded to the clinical findings. RESULTS: We found 34 cortical infarcts, 25 large subcortical infarcts, 1 small subcortical infarct, and 5 junctional infarcts. CONCLUSIONS: Most infarcts related to ICAD are cortical infarcts or large subcortical infarcts; small subcortical infarcts and junctional infarcts are infrequent. Therefore, these findings suggest that most infarcts occurring in carotid artery dissection (CAD) are probably embolic rather than hemodynamic in origin. According to this presumed mechanism, anticoagulation seems a logical treatment at the early stage of CAD.     

Repeated application of carvone-induced bacteria to enhance biodegradation of polychlorinated biphenyls in soil

OBJECTIVE: To determine the correlation between metabolite concentrations and clinical outcome during the acute or subacute phase of ischemic stroke by using single-voxel localized proton magnetic resonance spectroscopy (1H-MRS). SETTING: A university hospital neurologic department. PATIENTS AND METHODS: Combined single-voxel 1H-MRS and magnetic resonance imaging were performed on 26 patients with a recent ischemic stroke (on 8 patients during the first 24 hours after the stroke and on 18 during the first week). For all patients, the signals from N-acetylaspartate, choline-containing compounds, and creatine-phosphocreatine were compared with those on the contralateral side as peak area ratios. The data for 1H-MRS were related to scores on the Scandinavian Stroke Scale and the Barthel Index at a 6-month clinical follow-up. RESULTS: The signals from N-acetylaspartate, choline-containing compounds, and creatine-phosphocreatine were significantly reduced in all infarcted areas (P<.001, P<.001, and P=.003, respectively, Wilcoxon signed rank test). A lactate signal was present in 19 patients. The statistical analysis showed a significant positive correlation between N-acetylaspartate signals and Scandinavian Stroke Scale scores and between reduction of N-acetylaspartate signals and Barthel Index scores (Spearman rank correlation test). Patients in whom lactate was present had Scandinavian Stroke Scale scores significantly lower than patients in the group without lactate (Mann-Whitney U test). CONCLUSION: Single-voxel 1H-MRS performed during the acute or subacute phase of ischemic stroke may provide prognostic information.     

Imaging of delta- and mu-opioid receptors in temporal lobe epilepsy by positron emission tomography

The authors report the postoperative magnetic resonance (MR) imaging findings in 36 patients with advanced Parkinson's disease who underwent unilateral microelectrode-guided posteroventral pallidotomy. The lesions were placed within 1 mm of the ventral border of the globus pallidus internus (GPi) to include pallidothalamic outflow pathways. Sequential MR studies were obtained within 1 to 3 days postoperatively and at 6-month follow-up examination. Thirty-four (94%) of the 36 patients enjoyed sustained moderate or marked improvement of their parkinsonian symptoms 6 months postoperatively. Transient side effects occurred in five patients (14%), but there were no persistent complications. The pallidal radiofrequency lesions were prolate spheroid shaped and were composed of three concentric zones in the early postoperative studies. The mean volume of the middle zone, corresponding to the area of hemorrhagic coagulation necrosis, was 44.4 +/- 17.6 mm3; the mean lesion volume as defined by the outer zone, corresponding to perilesional edema, was 262.2 +/- 111.6 mm3. Additional edema spreading to the internal capsule was noted in 32 of 34 cases and to the optic tract in 11 of 34 cases. In two patients small ischemic infarctions involving the corona radiata were found, and in one a venous infarction was detected. Ischemic infarction resulted in mild transient Broca's aphasia in one patient, but there was no detectable neurological deficit in the other two. The mean volume of late-phase (6 months) lesions was 22 +/- 28.8 mm3. In three patients no lesion was identified despite sustained clinical improvement. The lesion was located in the posteroventral GPi in all cases except in one patient in whom it was confined to the GP externus (GPe). This 49-year-old woman did not experience sustained benefit. The authors found no consistent correlations between lesion size and location and clinical outcome as measured by a global outcome score, the Unified Parkinson's Disease Rating Scale motor, activities of daily living, and bradykinesia "off" scores or rating of dyskinesias. Lesioning of pallidal and subpallidal pathways may contribute to the sustained clinical benefit in this series. Magnetic resonance imaging analysis showed that intraoperative microelectrode recording facilitated accurate placement of the lesion in this critical area.