Clinical Evidence Of Stroke Research Articles

Epilepsy in Stroke as De Novo Independent Nosology Unit – Physiology, Pathogenesis, Histology, Clinical Picture, Diagnosis, and Treatment – A Systematic Review

INTRODUCTION: Early seizures are considered complications of stroke, and late seizures are a type of structural epilepsy. If they are separated as a new independent nosology unit, the problem in the diagnostic – treatment approach will be solved. PHYSIOLOGY: Cerebral blood flow is regulated by local factors such as carbon dioxide and oxygen content. Brain activity is also an important factor in the regulation of the volume speed of the blood – with locally increased neuronal activity, the local blood flow increases. Neurons in the CNS are subject to a variety of effects mediated by membrane receptors of two types – ionotropic and metabotropic. PATHOGENESIS: Early seizures are due to transient biochemical dysfunctions, while late seizures are due to gliosis changes affecting neuronal excitability. HISTOLOGY: The highlighted histopathological aspects confirm and support the results of clinical and radiological studies with dead nervous tissue, replaced by numerous newly formed capillaries, and surrounded by lipid-laden macrophages. CLINICAL PICTURE: This is represented by a complex combination of excitatory epileptic manifestations and residual focal symptoms depending on the localization of the lesion. LABORATORY DIAGNOSTICS: A very typical group of patients with post-stroke seizures have a high risk of recurrence when some of the studied biomarkers for this are available in the blood. In summary, the additional expanded package of studies of stroke patients should include screening diagnostics for the risk of epileptic seizures, namely: IL-6, IL-1β, TNF, Mg2+, Ca2+, CD40L, and Hsc70. IMAGING: Transient periodic MRI abnormalities have been demonstrated, possibly as a result of cerebral edema induced by seizure activity. Routine MRI in stroke patients is recommended. TREATMENT: It is possible that rt-PA may increase the risk of early seizures after stroke. Levetiracetam (LEV) as a neuroprotective agent in stroke has been proposed as the drug of first choice, based on safety and efficacy profiles. The usual practice is to treat recurrent early-onset seizures with short-term (3–6 months) treatment with antiepileptic drugs. CONCLUSIONS: Separation of stroke-epilepsy as a new independent nosology entity will solve the diagnostic-treatment problems in this area by changing the minimum package for laboratory tests, as well as routine MRI in patients with clinical evidence of stroke. LEV is the first-line agent for the treatment of these patients, in combination with correction of registered laboratory parameters.

Imaging analysis of ischemic strokes due to blunt cerebrovascular injury.

The timing of stroke onset among patients with blunt cerebrovascular injury (BCVI) is not well understood. All blunt trauma patients at our institution undergo a screening computed tomographic angiography (CTA) of the neck. Most patients with CTA evidence of BCVI are treated with aspirin, and all patients with clinical evidence of stroke are treated with aspirin and undergo magnetic resonance imaging (MRI) of the brain. We conducted a retrospective review to determine the incidence of stroke upon admission and following admission. All neck CTAs and head MRIs obtained in blunt trauma patients were reviewed from August 2017 to August 2019. All CTAs that were interpreted as showing BCVI were individually reviewed to confirm the diagnosis of BCVI. Stroke was defined as brain MRI evidence of new ischemic lesions, and each MRI was reviewed to identify the brain territory affected. We extracted the time to aspirin administration and the timing of stroke onset from patients' electronic health records. Of the 6,849 blunt trauma patients, 479 (7.0%) had BCVIs. Twenty-four patients (5.0%) with BCVI had a stroke on admission. Twelve (2.6%) of the remaining 455 patients subsequently had a stroke during their hospitalization. The incidence of stroke among patients with BCVI was 7.5%; 2.6% were potentially preventable. Only 5 of the 12 patients received aspirin before the onset of stroke symptoms. All 36 patients with BCVI and stroke had thromboembolic lesions in the territory supplied by an injured vessel. With universal screening, CTA evidence of BCVI is common among blunt trauma patients. Although acute stroke is also relatively common in this population, two thirds of strokes are already evident on admission. One third of BCVI-related strokes occur after admission and often relatively early, necessitating rapid commencement of preventative treatment. Further studies are required to demonstrate the value of antithrombotic administration in preventing stroke in BCVI patients. Prognostic and Epidemiologic; Level IV.

Transcranial Doppler ultrasound measurements of cerebral hemodynamic parameters in healthy volunteers at 2850 meters altitude

BackgroundTranscranial Doppler ultrasound (TDU) is useful in cerebrovascular patients. TDU findings are operator-dependent; they can also be influenced by anatomical and physiological variables as well as by the altitude at which the study is done. ObjectiveTo report the cerebral hemodynamic parameters measured by TDU in subjects who live in Quito, Ecuador (altitude 2850m). Material and methodsWe recruited 47 volunteers with no history or clinical evidence of stroke, hypertension, metabolic disorders, or hematologic disorders; 2 patients were excluded because they did not have a viable cranial window for TDU study. Thus, we recorded mean cerebral blood flow velocity, peak systolic flow velocity, end-diastolic flow velocity, and pulsatility indices in 45 patients (28 (62.2%) women; mean age, 35.9 years). We recorded patients’ age, sex, and hematocrit. We analysed cerebrovascular hemodynamic parameters by sex and age group. ResultsNo significant differences between hemispheres were observed in mean flow velocities, except in the anterior cerebral arteries with right predominance. Flow velocities were higher in women and in the youngest age group. No significant differences in the pulsatility indices were found between sexes or between age groups. The flow velocities in this series are lower than those reported for other series. ConclusionsThe hemodynamic parameters in this series are lower than in other series and are influenced by the altitude, age, and sex.

Parámetros hemodinámicos cerebrales, determinados mediante Doppler transcraneal, en un grupo de voluntarios sanos a 2.850 metros de altura

BackgroundTranscranial Doppler ultrasound (TDU) is useful in cerebrovascular patients. TDU findings are operator-dependent; they can also be influenced by anatomical and physiological variables as well as by the altitude at which the study is done. ObjectiveTo report the cerebral hemodynamic parameters measured by TDU in subjects who live in Quito, Ecuador (altitude 2850 meters). Material and methodsWe recruited 47 volunteers with no history or clinical evidence of stroke, hypertension, metabolic disorders, or hematologic disorders; 2 patients were excluded because they did not have a viable cranial window for TDU study. Thus, we recorded mean cerebral blood flow velocity, peak systolic flow velocity, end-diastolic flow velocity, and pulsatility indices in 45 patients (28 (62.2%) women; mean age, 35.9 years). We recorded patients’ age, sex, and hematocrit. We analyzed cerebrovascular hemodynamic parameters by sex and age group. ResultsNo significant differences between hemispheres were observed in mean flow velocities, except in the anterior cerebral arteries with right predominance. Flow velocities were higher in women and in the youngest age group. No significant differences in the pulsatility indices were found between sexes or between age groups. The flow velocities in this series are lower than those reported for other series. ConclusionsThe hemodynamic parameters in this series are lower than in other series and are influenced by the altitude, age, and sex.

Longitudinal Evaluation of Neurobehavioral Outcomes After Carotid Revascularization

Carotid revascularization, including carotid endarterectomy (CEA) and carotid angioplasty and stenting (CAS), is performed for stroke risk reduction but may also impact cognitive function. Cognitive outcomes observed after carotid revascularization have been inconsistent, and mechanistic relationships with procedural factors are poorly understood. To further explore associations between carotid revascularization and cognitive outcomes, a prospective longitudinal evaluation was conducted of patients undergoing elective CEA or CAS for hemodynamically significant carotid stenosis. Patients undergoing primary carotid artery revascularization for hemodynamically significant stenosis were evaluated with neurologic and neuropsychological testing at baseline and at 1 and 6 months after revascularization. A subgroup of patients was also studied with baseline and postoperative magnetic resonance imaging (MRI). Outcomes included neurologic or neuropsychological deficits and imaging findings (including quantitative assessment of cerebral blood flow). Sixteen patients underwent carotid revascularization with both preoperative and postoperative neurologic and neuropsychological testing; preoperative and postoperative MRIs were also performed on eight patients. Five of 16 treated carotid lesions (31%) were considered symptomatic, and severity of carotid stenosis was 60-79% for 6 of 16 lesions and 80% or more in all others. A single perioperative neurologic deficit was identified; all other patients (15/16) had no abnormalities detected by neurologic examination. Neuropsychological testing identified new postoperative deficits in 3 patients (19%), among whom 2 had a normal neurologic examination at all time points, whereas 1 had clinical evidence of stroke. Quantitative analysis of mean cerebral blood flow revealed postrevascularization increases for both gray matter (48.6 ± 13.9 mL per 100 g/min vs 75.3 ± 70.8 mL per 100 g/min) and white matter (31.8 ± 10.6 mL per 100 g/min vs 55.2 ± 30.1 mL per 100 g/min)(P = 0.04). New postoperative MRI foci of restricted diffusion were identified in 2 patients, both of whom had no neurologic or neuropsychological deficit. Among patients with postoperative neuropsychological deficits, MRI revealed globally increased cerebral perfusion without new postoperative abnormalities in 2 of 3. The relationship between carotid revascularization and cognitive function is complex, and cognitive deficits may occur in the presence of increased cerebral perfusion without detectable embolization.

Risk factors for stroke among patients with hypertension: A case–control study

BackgroundIn some African countries, more than half of the adult population are estimated to be hypertensive leading to an escalated burden of stroke in the continent. We conducted the first study to unravel the major risk factors for stroke among hypertensive patients (Nigerian-Africans) using a case–control design while also exploring the relative contributions of carotid intima medial thickness (CIMT) and carotid diameter as risk markers for stroke. MethodsUsing conventional techniques, stroke-related demographic, clinical and laboratory data were obtained from 135 consecutive volunteering hypertensive stroke patients and compared with 117 age and gender-matched hypertensive patients with no clinical evidence of stroke, TIA or coronary artery disease. Common carotid IMT and diameters were measured in all participants. Univariate and multivariate analyses were conducted at p=0.05. Results13.2% of the stroke patients were first diagnosed as hypertensive at presentation with stroke. Among hypertensive patients, the modifiable factors significantly (p<0.00001 to p<0.037) associated with stroke occurrence included higher maximum and minimum blood pressures in the preceding 3months, higher fasting plasma glucose, greater alcohol consumption, lesser physical activity and increased CIMT. Using a multivariate model which predicted 84.6% of stroke occurrence, only fasting total cholesterol of >150mg/dl (p=0.021) and common carotid diameter of ≥5.9mm (p=0.008) independently multiplied the risk of stroke. ConclusionsParticularly in resource-limited settings, aside from BP control, stroke prevention efforts should be targeted towards these identified risk factors for stroke among hypertensive patients. Carotid diameter should be further explored as an intermediate risk marker for stroke.

DIFFERENCE IN LIPID LEVELS;

Objectives: To determine the frequency of dyslipidemias in patients with stroke and to compare the lipid levels in ischemic andhemorrhagic stroke patients. Study design: An observational study. Setting: Medical wards of Civil Hospital Karachi. Period: January 2010 toJune 2011. Methodology: A total of three hundred and fifty- five patients above the age of 18 years with clinical evidence of stroke. CT scanbrain and fasting lipid levels were done in all patients. The lipid levels were compared between the ischemic and hemorrhagic stroke patients.Data was analyzed with SPSS version 16.0. Results: Out of the 355 patients 161 (45.4%) had dyslipidemia. Among the dyslipidemic patients,there was not a statistically significant difference in serum cholesterol, triglycerides, and LDL and HDL levels between ischemic andhemorrhagic stroke. (p- value &gt; 0.05). Conclusions: There is a high frequency of dyslipidemia in stroke patients. While comparing ischemicand hemorrhagic strokes there was not a significant difference between the various lipid fractions.

Cognitive Dysfunction in Children and Adolescents with Sickle Cell Disease without Evidence of Stroke: Preliminary Results.

Abstract 4623 INTRODUCTIONSickle cell disease (SCD) is the most frequent cause of stroke in children. It is possible that cognitive dysfunction occurs in the absence of identifiable stroke due to silent cerebrovascular disorders. OBJECTIVETo evaluate SCD compromises cognitive functions of patients with no radiological nor clinical evidence of stroke. METHODSThirty eutrophic children with SCD, with normal neurological examination and imaging (brain CT) and without past cerebrovascular disease were submitted to neuropsychological assessment between 2002 and 2008. The neuropsychological battery included the following tests: WISC-III, BTN (battery of neuropsychological tests, assessing laterality), Rey complex figure (visual perception and memory), and behavioral screening for ADHD, learning disorders and antisocial behavior. RESULTS66.7% of patients were male. The average age of patients was 9.6 years (6 - 15 years). The mean total IQ was 78.8 (50 - 105) and the executive IQ was 77.9 (47 - 108), both at the borderline limit. The verbal IQ mean was 84.9 (55 - 113), on lower average. Verbal comprehension verbal was on average 87.4 (58 - 115). The results of visual memory was at the lower limit of normal (mean percentile 16 to 18). There was no correlation between the rates of behavior disorders (inattention, hyperactivity, learning difficulties and conduct disturbance) and IQ results. There was no statistically significant difference between the results of males and females or between age groups. 40% of the sample had not developed manual preference. CONCLUSIONThe subjects of this sample showed significant cognitive impairment in the absence of clinical or radiological evidence of cerebrovascular disease. The study has limitations as the sample size, the imaging technique used and neuropsychological battery comprehensiveness, but the results are quite suggestive of a relationship between SCD and cognitive impairment. The research group is developing a study with a larger sample (100 patients) to clarify the correlations between these findings. This will be important to outline earlier neuroprotective measures, which will provide improvements in neurodevelopment, learning, quality of life and social inclusion. Disclosures:No relevant conflicts of interest to declare.

Frequency of thromboembolic events associated with endovascular aneurysm treatment: retrospective case series

There is little evidence addressing whether procedures requiring adjunctive devices lead to an increased frequency of thromboembolic complications. The authors report their experience with 155 aneurysms treated with and without adjunctive devices. The authors retrospectively reviewed their last 155 aneurysm coil placement procedures. The patients' records were reviewed for the following phenomena: 1) evidence of procedure-related thrombus formation; 2) clinical evidence of stroke; and 3) the presence of acute ischemia in the treated vascular territory on diffusion-weighted (DW) imaging. Of the 155 aneurysms treated in 132 patients, 66 were treated with coils only, 45 had stent-assisted coil placement, 33 underwent balloon remodeling, and in 11 stents were placed after balloon remodeling. Small DW imaging abnormalities were present in the treated vascular territory in 24% of cases (37 lesions). Specifically, 21 (32%) of 66 lesions in the coil-treated group, 6 (13%) of 45 in the stent-assisted coil treatment group, 8 (24%) of 33 in the balloon remodeling group, and 2 (18%) of 11 in the balloon and stent group showed DW imaging positivity. Furthermore, 25 (68%) of the 37 cases that were positive on DW imaging occurred in patients presenting with subarachnoid hemorrhage (SAH). Clinically evident stroke or transient ischemic attack was present in 10 (27%) of 37 cases, with 70% occurring in patients presenting with SAH. Use of adjunctive devices in treating aneurysms does not appear to increase the frequency of embolic or ischemic events. The presence of DW imaging abnormalities and clinically evident stroke was actually less frequent when adjunctive devices were used and in electively treated cases. This was probably related to perioperative antiplatelet medical management.

Cerebral Oxygen Saturation in Sickle Cell Patients Treated with Hydroxyurea:.

Recently we reported the use of a non-invasive near-infrared optical spectroscopy technique to measure cerebral oxygenation (cerebral oximetry, rSO2%) in agroup of 27 adult patients with sickle cell disease (Eur J Clin Invest, 34:143,2004). The sickle cell patients' rSO2 values were significantly lower (mean 47.7%) than those in normal subjects (mean 61.3%) even though none of the patients had clinical evidence of stroke or cerebral ischemia. We included patients with all Hb phenotypes, and regardless of hydroxyurea (HU) treatment. Transfusions improved cerebral oxygen saturation but the post-transfusion values still did not reach normal levels. Our findings were corroborated independently by Raj et al. who studied 25 children with sickle cell disease (J Pediat Hematol Oncol 26:279,2004). In order to determine if long-term HU treatment affects rSO2, we analyzed cerebral oximetry results in a subset of 31 patients with sickle cell anemia (Hb SS). Eleven of them were on long-term (more than 6 months) HU treatment at stable doses (1000–1500 mg/day). The table shows that the mean rSO2, Hb, Hct, and MCV in HU-treated patients were significantly higher than those in sickle cell anemia (SCA) patients not on HU. The rSO2 in HU-treated patients was 12.5% higher than in SS patients not on this drug. By comparison, we previously reported a 24% increment in rSO2 following transfusions.A group of 8 patients who were on long-term HU treatment were given also single 1000 mg oral doses of HU and their rSO2 was measured for 12 hours without noticeable change in cerebral oxygenation. Nor did rSO2 change after oxygen inhalation (3L/min). The cause of the low rSO2 in sickle cell patients is unknown and still under investigation. It is probably not related exclusively to the anemia, since, as previously reported, anemic subjects without sickle cell disease appear to have normal rSO2. These preliminary results indicate that chronic HU treatment is associated with higher rSO2 values in SCA. If validated in a larger number of patients, our findings suggest that cerebral oximetry could be a useful, non-invasive method for assessing a new in vivo effect of HU and red cell transfusion in sickle cell disease: increased blood oxygen saturation in the cerebral vasculature.HYDROXYUREA AND CEREBRAL OXYGEN SATURATION IN PATIENTS WITH SICKLE CELL DISEASENO HYDROXYUREA (N=20)HYDROXYUREA (N=11)P value*Mean rSO2 (%)41 ± 6.646 ± 7.60.025Mean Hb (g/dl)8.4 ± 1.49.68 ± 1.20.029Mean Hct (%)24± 3.428± 4.40.027Mean MCV (fl)89± 8102± 70.028rSO2 = cerebral oxygen saturation. *= t-test. Plus/minus figures represent SD

Prevalence of Renal Artery Stenosis in Autopsy Patients With Stroke

Atherosclerotic renal artery stenosis commonly exists as one manifestation of more generalized atherosclerosis. It is a progressive but potentially curable disorder. Thus, information on renal artery involvement in atherosclerotic diseases could be important. We investigated the prevalence of renal artery stenosis in autopsied patients with stroke over 40 years of age. From 2167 consecutive autopsy patients who died between 1980 and 1997, we studied 346 cases of mean age of 69+/-11 years with clinical evidence of stroke. Atherosclerotic renal artery stenosis (>/=75% luminal area narrowing) was found in 36 patients (10.4%). Patients with renal artery stenosis were older and had worse renal function. Renal artery stenosis was found in 14.7%, 28.6%, and 23.9% of patients with hypertension, renal insufficiency, and aortic aneurysm, respectively. Extracranial carotid artery stenosis (>50% luminal area narrowing) was found in 101 patients (29.2%). Of the 346 stroke patients, 256 had a history of brain infarction. In patients with brain infarction, renal artery stenosis was found in 31 (12.1%) and carotid stenosis was found in 81 (33.6%). Patients with carotid artery stenosis were more likely to have renal artery stenosis than patients without carotid artery stenosis (24.4% versus 5.9%, P<0.0001). Multiple logistic regression analysis identified renal insufficiency, hypertension, female gender, and presence of carotid artery stenosis as independent predictors of renal artery stenosis in patients with brain infarction. These data reveal that atherosclerotic renal artery stenosis is common in patients with stroke, especially in those with brain infarction.

Quantitative MRI of the brain in children with sickle cell disease reveals abnormalities unseen by conventional MRI

Conventional MRI (cMRI) has shown that brain abnormalities without clinical stroke can manifest in patients with sickle cell disease (SCD). We used quantitative MRI (qMRI) and psychometric testing to determine whether brain abnormalities can also be present in patients with SCD who appear normal on cMRI. Patients 4 years of age and older with no clinical evidence of stroke were stratified by cMRI as normal (n = 17) or abnormal (n = 13). Spin-lattice relaxation time (T1) of gray and white matter structures was measured by the precise and accurate inversion recovery (PAIR) qMRI method. Patient cognitive ability was assessed with a standard psychometric instrument (WISC-III or WISC-R). In all 30 patients with SCD, qMRI T1 was lower than in 24 age- and race-matched controls, in cortical gray matter (P < .0006) and caudate (P < .0009), as well as in the ratio of gray-to-white matter T1 (P < .008). In the 17 patients who were shown to be normal by cMRI, qMRI T1 was still lower than in controls, in both cortical gray matter (P < .02) and caudate (P < .004). Histograms of voxel T1 show that the proportion of voxels with T1 values intermediate between gray and white matter (ie, consistent with encephalomalacia) was 9% higher than controls in patients shown to be normal by cMRI (P < .05) and 15% higher than controls in patients shown to be abnormal by cMRI (P < .0005). The full scale intelligence quotient (FSIQ) of all patients with SCD was 75, compared to the FSIQ of 88 in a historical control group of patient siblings (P < .001). The FSIQ of patients shown to be normal by cMRI was 79, significantly lower than the FSIQ of patient siblings (P < .04). The FSIQ of 71 in patients shown to be abnormal by cMRI was significantly lower than both the patient siblings (P < .005) and the patients shown to be normal by cMRI (P < .04). Patients shown to be abnormal by cMRI scored lower than patients shown to be normal by cMRI, specifically on the subtests of vocabulary (P = .003) and information (P = .03). Cognitive impairment is thus significant, even in patients with SCD who were shown to be normal by cMRI, suggesting that cMRI may be insensitive to subtle neurologic damage that can be detected by qMRI. Because cognitive impairment can occur in children normal by cMRI, our findings imply that prophylactic therapy may be needed earlier in the course of SCD to mitigate neurologic damage.

Haemodynamic classification of symptomatic obstructive carotid artery disease.

63 subjects with symptomatic obstructive carotid artery disease were investigated with transcranial Doppler ultrasonography. Their blood velocities at rest (V) in the middle and posterior cerebral artery (MCA and PCA) and in the extracranial internal carotid artery were measured and the pulsatility index (PI) and Uhem index (VMCA.PIMCA/VPCA.PIPCA) calculated. The vasomotor responses in both MCAs were also tested. The subjects were divided into groups based on the findings on physical examination and cerebral computed tomography. In the patient group with lacunar/territorial infarction we found in the stroke hemisphere: VMCA > VPCA, PIMCA = PIPCA and normal values for the Uhem index and total vasomotor reactivity. In the patient group with watershed infarction this hemisphere was characterized by: VMCA < VPCA, PIMCA < PIPCA and subnormal scores for the Uhem index and total vasomotor reactivity. Displaying features from both stroke groups, we obtained in the hemisphere of interest in patients with transient ischaemic attacks: VMCA = VPCA, PIMCA < PIPCA and normal values for the Uhem index and total vasomotor reactivity. Five patients with clinical evidence of stroke but with negative cerebral computed tomography findings had scores similar to those of the watershed group of patients. For the stroke patients, individual measurements of V, PI and total vasomotor reactivity failed to clearly identify to which stroke group a subject might belong. However, such an identification was achieved in all subjects when using the Uhem index. The Uhem index data in patients with transient ischaemic attacks suggest two subgroups with different pathogenesis underlying, the ischaemic events.

Vascular pathology in three cases of progressive cognitive deterioration

The clinical condition known as vascular dementia remains poorly defined. Few studies have attempted a correlative link between the clinical syndrome and the structural abnormalities of the brain. Classically the clinical progression of the vascular dementing process is thought to be a multi-step process punctated by repeated episodes of ischemia, that are clinically expressed as strokes. In most instances it has been assumed that the substrate of vascular dementias consists of atherothrombotic infarcts. The objective of this report is to illustrate 3 cases of progressive (rather than stepwise) cognitive deterioration without clinical evidence of stroke, evolving over a period of several years, in which there were prominent vascular lesions. A complete autopsy and detailed neuropathologic examination demonstrated cerebral vascular lesions involving small arterial vessels (< 200 μm in diameter). The lesions consisted of moderate-to-severe arteriolosclerosis in two cases, and mild-to-moderate arteriolosclerosis in a case of Alzheimer's disease with severe cerebral amyloid angiopathy. Parenchymal lesions consisted of small cortical and subcortical infarcts, most of them smaller than 0.1 cm in average diameter, and subcortical leukoencephalopathy severe in two cases and mild-to-moderate in the third case. Severe atherosclerosis not accompanied by large infarcts was also present in one case. Arterial changes affecting small, distal branches causing sometimes small parenchymal lesions in association with diffuse cerebral white matter disease, appear to be the anatomical substrate that accompanies progressive cognitive impairment in some patients who are frequently diagnosed with Alzheimer's disease because in their clinical records there is neither history of strokes nor stepwise progression of symptoms.

Clinical correlates of Alzheimer's disease with and without silent radiographic abnormalities.

To determine whether patients with Alzheimer's disease (AD) who do not have historical or clinical evidence of stroke but who do have computed tomographic or magnetic resonance imaging evidence of noncortical lesions smaller than 2 cm or periventricular "caps" differ from other patients with AD. The computed tomographic or magnetic resonance imaging scans of 158 patients meeting criteria of the National Institute of Neurological Disorders and Stroke-Alzheimer's Disease and Related Disorders Association for probable AD were reviewed by one neuroradiologist. Two measures of disease severity--the Modified Mini-Mental State examination and the Blessed Dementia Rating Scale (Part I)--were subjected to two-way analysis of variance with scan type (computed tomography or magnetic resonance imaging) and lesion number as between-group factors and age and disease duration as covariates. No relationship was seen between lesion number or periventricular caps and disease severity. In this cross-sectional analysis using these clinical measures, patients with AD who have well-defined radiographic abnormalities cannot be differentiated from patients with AD who do not have them.

Validity of clinical diagnosis in age-associated dementia

With neuropathological diagnosis as the point of reference, the validity of clinical diagnosis was studied in 50 patients who had met DSM-III-R criteria for dementia. Clinical diagnosis of ATD (dementia of Alzheimer type) was made in 14 cases, of VD (vascular dementia) in 14 cases, of others in 5 cases and of undefined in 16 cases. At necropsy, 16 cases fulfilled the histological criteria for ATD, while 15 cases were VD, 3 cases were mixed dementia and 14 cases were other CNS disorders. In 2 other cases, the neuropathological picture was considered to be nondiagnostic. The accuracy of clinical diagnosis of VD was higher than that of ATD. Clinical diagnostic sensitivity was 81.8% for ATD and 91.7% for VD; corresponding specificity was 78.3% and 86.4%. With our clinical criteria, slowly evolving VD with no clinical evidence of stroke would not be identified as VD. On the other hand, AD patients who happened to have a stroke would be diagnosed as VD. These results suggest that further investigations as to VD (its clinical course, findings of computed tomographic scan and magnetic resonance imaging) are needed for more appropriate clinical criteria.

Perioperative management of 63 patients with pheochromocytoma

During a 10-year period, 60 patients with confirmed diagnoses of pheochromocytoma underwent a total of 63 surgical procedure. To control extreme blood pressure elevations, 6 patients received phenoxybenzamine preoperatively and 28 patients received prazosin. The remaining 29 patients received neither drug. Intravenous sodium nitroprusside and nitroglycerin, alone or in combination, were used in all but 10 patients to control intraoperative hypertensive episodes. One patient died after surgery due to pre-existing intracranial malignant tumor. All other patients were discharged from the hospital with no clinical evidence of stroke or myocardial infarction. We conclude that pheochromocytoma patients can undergo successful surgery without preoperative profound and long-lasting alpha adrenergic blockade.

Stroke in pediatric acquired immunodeficiency syndrome

In a 4 1/2-year period, 4 of 68 children in a longitudinal study of neurological complications of human immunodeficiency virus (HIV) infection had clinical and/or neuroradiological evidence of stroke, yielding a clinical incidence of stroke in this population of 1.3% per year. During this period, 32 subjects died, and permission for autopsy was granted in 18 of the patients, including 3 of 4 who had clinical evidence of stroke. The prevalence of cerebrovascular pathological features in our consecutive autopsy series was higher than the clinical incidence. At autopsy cerebrovascular disease was documented in 6 (24%) of 25 children with HIV infection, including all 3 children who had clinical evidence of stroke. Four patients had intracerebral hemorrhages, 6 patients had nonhemorrhagic infarcts, and 3 had both. Hemorrhage was catastrophic in 1 child and clinically silent in 3 children, all of whom had immune thrombocytopenia. One child had an arteriopathy that affected meningocerebral arteries. In another child, the arteries of the circle of Willis were aneurysmally dilated. Two children had coexisting cardiomyopathy and subacute necrotizing encephalomyelopathy with vascular proliferation. These results suggest that stroke should be considered when children with HIV infection develop focal neurological signs.