bluuebunny/crossref_metadata_2025 huggingface dataset:
Prognosis of young adults with ischemic stroke. A long-term follow-up study assessing recurrent vascular events and functional outcome in the Iowa Registry of Stroke in Young Adults.
Authors: Kappelle L J , Adams H P , Heffner M L , Torner J C , Gomez F , Biller J
Published: June 2011

Information about the long-term prognosis of young adults with ischemic stroke is limited. Therefore, we performed a follow-up assessment of 296 patients with ischemic stroke who are enrolled in the Iowa Registry of Stroke in Young Adults. We studied young adults (age, 15 to 45 years) who were referred to a tertiary medical center for management of ischemic stroke between July 1, 1977, and January 1, 1992.

Follow-up assessments were performed by means of questionnaires, examinations, telephone interviews, review of medical records, and reports from personal physicians. Data about risk factors, coincident medical diseases, etiology of stroke, treatment, recurrent stroke, other vascular events, and deaths were collected. Outcomes were rated with the Glasgow Outcome Scale, Barthel Index, National Institutes of Health stroke scale, and the Mini-Mental State Examination. Quality of life was assessed with the SF-36 Health Status questionnaire.

Follow-up information about the status of 10 patients was limited except that they were alive. Twenty-one patients (7%) died as the result of their initial stroke, and another 40 patients (14%) died during a mean follow-up of 6.0 years. None of the patients aged 25 years or younger at the time of stroke died during follow-up. Mortality was significantly higher among patients who had a stroke secondary to large-vessel stroke and it was significantly lower in patients with stroke of unknown etiology than in patients with stroke of other causes (relative risk [RR], 1.7; 95% confidence limits [CL], 1.0 to 2.7; and RR, 0.1; CL, 0 to 0.6; respectively). Recurrent strokes occurred in 23 patients (9%) and were fatal in 9. Another 37 patients were treated by a cardiologist during follow-up; 3 had had a myocardial infarct. Fourteen additional patients needed major vascular surgery. Outcomes with the Glasgow Outcome Scale and Barthel Index were generally favorable. Still, only 49% of patients were still alive, were not disabled, had not suffered from recurrent vascular events, or had not undergone major vascular surgery. Only 42% of survivors had returned to work. A majority of survivors reported emotional, social, or physical residuals that lessened the quality of life.

The risks of recurrent vascular events in young adults who have had ischemic stroke are considerable. In addition, a majority of survivors will have residual emotional, social, or physical impairments that hamper employment or lower the quality of life. Further research on the quality of life for young adults who survive stroke is needed.
Cerebral hemodynamics in hypertensive patients compared with normotensive volunteers. A transcranial Doppler study.
Authors: Sugimori H , Ibayashi S , Irie K , Ooboshi H , Nagao T , Fujii K , Sadoshima S , Fujishima M
Published: June 2011

The present study was designed to examine cerebral hemodynamics in early and chronic stages of hypertension using transcranial Doppler sonography.

Our study population consisted of 16 chronic hypertensive patients with chronic and small deep brain infarction, 10 young early-stage hypertensive subjects, and 16 young normotensive healthy volunteers. Using three-dimensional mapping techniques, we identified the M1 portion of the middle cerebral arteries and measured mean blood flow velocity, and we calculated the Gosling pulsatility index (PI), Fourier PI of the first harmonic (Fourier PI1), and cerebrovascular resistance.

Mean blood flow velocity in the young hypertensive group was statistically higher (71.7 +/- 11.7 cm/s [mean +/- SD]) than among chronic hypertensive subjects (56.9 +/- 21.4 cm/s, P < .01) and normotensive subjects (63.2 +/- 11.8 cm/s, P < .05). Gosling PI presented a mirror image of mean blood flow velocity in both hypertensive and normotensive subjects. Chronic hypertensive subjects showed significantly higher Fourier PI1 (0.32 +/- 0.05) and cerebrovascular resistance (2.08 +/- 0.82 mm Hg/cm per second) than normotensive subjects (0.25 +/- 0.03 and 1.31 +/- 0.23 mm Hg/cm per second [P < .005], respectively) or early-stage hypertensive subjects (0.25 +/- 0.04 and 1.44 +/- 0.26 mm Hg/cm per second [P < .02], respectively).

Early-stage hypertensive subjects demonstrated higher velocity, normal Fourier PI1, and near normal vascular resistance, whereas chronic hypertensive subjects showed near normal velocity, higher Fourier PI, and greater vascular resistance. Results may indicate different degrees of cerebral arteriopathy and arteriolopathy between early and late stages of hypertension.
Reduction of central nervous system reperfusion injury in rabbits using doxycycline treatment.
Authors: Clark W M , Calcagno F A , Gabler W L , Smith J R , Coull B M
Published: June 2011

Activated leukocytes appear to potentiate central nervous system reperfusion injury, and agents that block leukocyte adhesion have shown neuroprotective efficacy in experimental models. Doxycycline, a tetracycline antibiotic, inhibits leukocyte function in vitro, presumably through divalent cation binding. We used a model of focal central nervous system reperfusion injury to determine the efficacy of doxycycline treatment in preserving neurological function.

Rabbits randomly received 10 mg/kg i.v. doxycycline 30 minutes before ischemia (pretreatment group) or 45 minutes after ischemia (posttreatment group) or received phosphate-buffered saline vehicle (control group) followed by 10 mg/kg q 8 hours times two. The average length of reversible spinal cord ischemia required to produce paraplegia (P50) at 18 hours was calculated for each group.

For the control group (n = 13), the P50 was 22.8 +/- 2.2 minutes; for the pretreatment group (n = 14), 35.5 +/- 2.4 minutes (P < .01; t = 3.8); and for the posttreatment group (n = 13), 31.4 +/- 4.2 minutes (not significant; t = 1.6). Doxycycline also attenuated postischemic decreases in vivo leukocyte counts and inhibited in vitro leukocyte adhesion. Therapeutic doxycycline levels at 24 hours were confirmed in the plasma and spinal cord.

This significant protective effect suggests that doxycycline, a safe and readily available agent, may play a role in reducing clinical central nervous system reperfusion injury.
Small primary intracerebral hemorrhage. Clinical presentation of 28 cases.
Authors: Kim J S , Lee J H , Lee M C
Published: June 2011

Although there have been sporadic reports of patients with small intracerebral hemorrhages presenting with discrete clinical features, the clinical and distributional characteristics of these hemorrhages have not been adequately investigated.

We studied 28 patients who had primary intracerebral hemorrhage of a longest diameter < or = 1.5 cm as seen in computed tomographic scan and/or magnetic resonance imaging. Small primary intracerebral hemorrhages were found in the basal ganglia in 8 patients (2 with intraventricular hemorrhage), the posterior limb of the internal capsule in 8, the area of the fourth ventricle of the cerebellum in 7 (5 with intraventricular hemorrhage), the pontine tegmentum in 4, and the thalamomesencephalic area in 1. All patients except 3 were hypertensive, suggesting that most of the hemorrhages may have occurred because of rupture of small end arteries secondary to long-standing hypertension. Depending on their location, the hemorrhages clinically manifested as pure motor stroke in 7, pure sensory stroke in 6, vertigo/ataxia in 7, sensorimotor stroke in 4, and ataxic hemiparesis in 2 patients. One patient with thalamomesencephalic hemorrhage showed vertical gaze disturbance, and 1 with basal ganglionic hemorrhage presented with symptoms of acute hydrocephalus secondary to a relatively large amount of intraventricular hemorrhage. The prognosis of small intracerebral hemorrhage was generally excellent except for when patients were very old or when there was a significant amount of intraventricular bleeding.

Small primary intracerebral hemorrhage has its predilection sites: basal ganglia, posterior limb of the internal capsule, area of the fourth ventricle of the cerebellum, and pontine tegmentum. Most of the hemorrhages are probably caused by rupturing of the small end arteries in the setting of chronic hypertension. They produce discrete clinical syndromes often mimicking classic lacunar syndrome, of which pure sensory stroke is relatively common.
Perimesencephalic subarachnoid hemorrhage. Additional perspectives from four cases.
Authors: Schievink W I , Wijdicks E F , Piepgras D G , Nichols D A , Ebersold M J
Published: June 2011

Nonaneurysmal perimesencephalic hemorrhage, a distinct form of subarachnoid hemorrhage, is a recently described variant of intracranial hemorrhage. We describe two patients who presented with unusual features of this type of subarachnoid hemorrhage and also two patients who had a perimesencephalic pattern of hemorrhage due to a ruptured posterior circulation aneurysm.

The first patient, a 41-year-old woman with perimesencephalic hemorrhage, underwent an exploratory craniotomy because angiography had suggested an anomaly of the basilar tip. No source of hemorrhage could be identified at the time of surgery. The second patient was a 3-year-old boy who presented with opisthotonos and who was found to have a perimesencephalic hemorrhage. Angiography revealed no source for the hemorrhage. The third patient, a 54-year-old man, had a perimesencephalic pattern of subarachnoid hemorrhage from a vertebrobasilar junction aneurysm associated with a fenestration that was missed on the initial angiographic study. The fourth patient, a 43-year-old man, suffered a perimesencephalic pattern of subarachnoid hemorrhage from a small posterior cerebral artery aneurysm, which had not been recognized on two angiograms.

These patients elaborate on the clinical spectrum of subarachnoid hemorrhage with a perimesencephalic pattern. First, a negative exploratory craniotomy suggests that the source of nonaneurysmal perimesencephalic hemorrhage may not be arterial. Second, nonaneurysmal perimesencephalic hemorrhage may also occur in children. Finally, the index of suspicion for a posterior circulation aneurysm should remain high in patients who present with a perimesencephalic pattern of subarachnoid hemorrhage, and these aneurysms may rise from unusual locations.
Iron-related damage in acute ischemic stroke.
Authors: Dávalos A , Fernandez-Real J M , Ricart W , Soler S , Molins A , Planas E , Genís D
Published: June 2011

Although iron-mediated mechanisms are important in experimental brain injury after carotid occlusion, their clinical role in acute ischemic stroke has not been determined. We evaluated the influence of iron stores, measured as serum ferritin, on the outcome of acute cerebral infarct.

Admission and fasting glycemia, glycosylated hemoglobin, serum cortisol, serum ferritin, and 24-hour urinary free cortisol levels were measured on the first day of hospitalization in 67 patients admitted with an acute ischemic stroke of less than 24 hours' duration. Patients were classified into two groups according to their Canadian Stroke Scale (CSS) score on day 30: good outcome group (alive and CSS score > 7 points) and poor outcome group (dead or CSS score < or = 7 points).

Thirty-three patients (49%) had good outcome and 34 (51%) poor outcome. Fasting glycemia (P = .001), serum cortisol (P < .001), and urinary free cortisol (P = .001) but not admission glycemia and glycosylated hemoglobin had higher levels in patients with poor outcome. Serum ferritin values were greater in the poor outcome group (218 +/- 156 micrograms/L versus 133 +/- 125 micrograms/L; P = .004), and a correlation between ferritin values and degree of worsening or improvement of the CSS score on day 30 was found (P = .002). Serum cortisol (odds ratio [OR], 6.7; 95% confidence interval [CI], 1.7 to 26), fasting glycemia (OR, 5.4; 95% CI, 1.2 to 24), and serum ferritin (OR, 4.6; 95% CI, 1.1 to 19) were independently related to poor outcome in a logistic regression analysis.

High serum ferritin levels within the first 24 hours of hospitalization for an acute ischemic stroke are related to a poor prognosis, independent of the stress response. More research is needed to determine the origin of increased serum ferritin levels and the therapeutic implications.
Relations of intimal-medial thickness among sites within the carotid artery as evaluated by B-mode ultrasound. ARIC Investigators. Atherosclerosis Risk in Communities.
Authors: Howard G , Burke G L , Evans G W , Crouse J R , Riley W , Arnett D , de Lacy R , Heiss G
Published: June 2011

B-mode ultrasound is a widely used technique for the clinical and epidemiological assessment of carotid atherosclerosis. This article describes the relation between arterial intimal-medial thickness (IMT) at different sites within the extracranial carotid artery.

IMT was measured by B-mode real-time ultrasound as an index of atherosclerotic involvement in the extracranial carotid arteries as part of the population-based Atherosclerosis Risk in Communities (ARIC) study. The relation between IMT at different sites was described by correlation coefficients and percentile regression techniques based on between 4034 and 9386 pairs of measurements (variation in sample size depending on the paired sites).

Increased IMT at one site was associated with increased IMT at other sites. The correlation between right and left IMT at the same anatomic location in the carotid artery ranged from .34 to .49; the correlation at different anatomic locations in the carotid artery on the same side ranged from .25 to .43. The distribution of IMT, described by the percentiles of IMT at the inference site as a function of IMT at the index site, showed constricted percentiles of IMT at the inference site for small IMT at the index site and an increase in the spread of percentiles with increasing IMT.

Although increased carotid IMT at one site is positively associated with thickened walls at other carotid sites, the ability to accurately predict wall thickness at a site given the wall thickness at other sites is modest. The general association between sites supports the systemic nature of atherosclerosis, while the lack of tight agreement between sites supports the focal nature of the atherosclerotic process.
The importance of family history in cerebrovascular disease.
Authors: Graffagnino C , Gasecki A P , Doig G S , Hachinski V C
Published: June 2011

The role of genetics in cerebrovascular disease remains controversial. The purpose of this study was to assess the influence of family history on atherothrombotic infarction or transient ischemic attack.

Ninety patients with stroke or transient ischemic attack and 90 age- and sex-matched community control subjects were studied prospectively. Medical and family histories were obtained from all subjects, and a complete physical examination was performed.

Eighty-five patients and 86 control subjects knew their family history for ischemic heart disease and stroke. A positive history for ischemic heart disease was present in 62 (73%) of the patients and 46 (53%) of the control subjects (P = .019), and a positive family history for stroke was present in 38 (47%) of the patients and 21 (24%) of the control subjects (P = .014).

Although a positive vascular family history was not an independent risk factor in a multivariate analysis, it was an excellent marker of the presence of other established vascular risk factors. Personal histories of ischemic heart disease, hypertension, and hyperlipidemia were found to be significant independent risk factors for stroke.
Cost of acute stroke care in Toronto, Canada.
Authors: Smurawska L T , Alexandrov A V , Bladin C F , Norris J W
Published: June 2011

Stroke cost consumes a large proportion of the gross domestic product in all developed countries, and while health care costs are rising, the ability to contain them is diminishing.

We calculated the cost of acute stroke care for all first admissions to a teaching hospital in Toronto, Canada, in 1991 through 1992 for 285 consecutive patients.

The average cost per patient was $27,500 Canadian, and strokes in men cost less than in women ($23,000 versus $32,000 Canadian), for a total cost of $8 million Canadian over 2 years. More women died than men (34% versus 17%, P < .02), mainly from systemic complications of stroke, but because women stayed hospitalized longer, they cost more in the long term. The major factor determining cost was social support, and more men than women went home or to rehabilitation units (P < .02). Family support was greater for men (82%) than women (39%, P < .0002).

Significant cost reductions are more likely to be achieved by altering discharge policies and improving social conditions for early return to the home than by reducing laboratory or medical personnel costs.
Spinal cord infarcts during long-term inhibition of nitric oxide synthase in rats.
Authors: Blot S , Arnal J F , Xu Y , Gray F , Michel J B
Published: June 2011

Chronic hypertension is a major predisposing factor for stroke in humans. It has recently been shown that long-term inhibition of nitric oxide synthase activity causes a gradual time-dependent increase in arterial blood pressure in rats. We used this new animal model of chronic hypertension to study the occurrence and spatial features of infarcts in the central nervous system.

Rats were treated with a nitric oxide synthase inhibitor, NG-nitro-L-arginine methyl ester, dissolved in the drinking water at 50 mg/kg per day for 11 weeks. The brains and spinal cords of hypertensive rats with and without motion disturbances were processed for standard microscopic examination.

Seventy-nine percent of the hypertensive rats showed motion dysfunctions, especially front leg paralysis, and/or died suddenly when their systolic blood pressure reached approximately 215 mm Hg after approximately 7 weeks of treatment. All of the hypertensive rats with stroke had spinal cord infarcts (90% at the cervical or cervicothoracic level) either alone or combined with brain lesions (30%). These structural alterations ranged from focal areas of pale, spongy tissue to large necrotic sites with vascular alterations, including thickened or fibrinoid degenerated vessel wall, macrophage invasion, and reactive astrocytes.

Infarcts occurred in the central nervous system with a high incidence in the spinal cord of hypertensive rats in which nitric oxide synthase was chronically blocked. This location of the hypertensive neuropathologic sequelae contrasts with the model of stroke-prone spontaneously hypertensive rats. The results suggest that nitric oxide is a key factor in spinal cord arteriolar vasomotion and structure in rats.
Brain nitric oxide synthase activity in normal, hypertensive, and stroke-prone rats.
Authors: Clavier N , Tobin J R , Kirsch J R , Izuta M , Traystman R J
Published: June 2011

Nitric oxide-mediated cerebral vasodilation is altered in spontaneously hypertensive stroke-prone rats. Stroke predisposition in this strain could be related to a genetic defect of brain nitric oxide synthase, the enzyme responsible for nitric oxide production. We tested the hypothesis that brain nitric oxide synthase activity is altered in spontaneously hypertensive stroke-prone rats compared with spontaneously hypertensive or Wistar-Kyoto rats.

A colony of spontaneously hypertensive stroke-prone rats was bred, in which the rate of neurological events under salt load was assessed. In a separate cohort of animals brain nitric oxide synthase activity was measured in spontaneously hypertensive stroke-prone rats (n = 6) and in spontaneously hypertensive (n = 6) and genetically related Wistar-Kyoto rats (n = 6). Calcium dependency of nitric oxide synthase was also assessed in cortical brain samples from the three rat strains to determine if altered calcium-dependent activation of nitric oxide synthase was present.

Brain nitric oxide synthase activity was highest in the cerebellum (eg, spontaneously hypertensive stroke-prone rats: cerebral cortex, 10.6 +/- 0.9; cerebellum, 50.1 +/- 12.0; brain stem, 14.7 +/- 10.3 pmol/mg protein per minute); however, there was no difference among the three rat strains in any region (eg, cerebral cortex: spontaneously hypertensive stroke-prone, 10.6 +/- 0.9; spontaneously hypertensive, 10.8 +/- 0.5; Wistar-Kyoto, 10.9 +/- 0.7 pmol/mg protein per minute) or at any calcium concentration tested.

A genetic defect of brain nitric oxide synthase is unlikely to be the cause of stroke predisposition in spontaneously hypertensive stroke-prone rats.
Changes of circadian blood pressure patterns after hemodynamic and thromboembolic brain infarction.
Authors: Sander D , Klingelhöfer J
Published: June 2011

We investigated the changes of circadian blood pressure patterns after thromboembolic and hemodynamic brain infarction and evaluated the relation between circadian blood pressure variation, infarct location, and activation of the autonomic nervous system after thromboembolic stroke.

Repeated 24-hour blood pressure measurements were performed in 45 patients with proven first-ever brain infarctions of different origins. Evaluation of serum norepinephrine concentration, prolongation of the QT interval, and degree of cardiac arrhythmias were used to determine the extent of sympathetic activation after thromboembolic stroke.

Whereas circadian blood pressure variation was significantly increased after hemodynamic infarction compared with a control group (diastolic, -25.2 +/- 4.5% versus -13.8 +/- 6.5%; p < .005), a clearly reduced variation was observed after thromboembolic infarction (diastolic, -5.2 +/- 6.9%). Blood pressure variation was positively related to serum norepinephrine concentration (r = .79; P < .01) after thromboembolic infarction. Patients with involvement of the insular cortex showed a nocturnal rise of blood pressure significantly more frequently (66.7% versus 11.8%; P < .005) and had higher norepinephrine levels (66.7 +/- 110 pg/mL versus 290 +/- 178 pg/mL; P < .01) than patients without insular cortex infarction, indicating increased sympathetic activity. This was associated with a significantly more frequent occurrence of QT prolongation and cardiac arrhythmias.

The observed differences in circadian blood pressure patterns may (1) help to distinguish the pathophysiological basis of the stroke, (2) help to explain worsening in some cases of hemodynamic stroke, (3) confirm the importance of the insular cortex for sympathetic activation, and (4) identify subgroups of patients with increased risk of myocardial infarction and arrhythmia.
Trends in incidence, case-fatality rate, and severity of stroke in northern Sweden, 1985-1991.
Authors: Stegmayr B , Asplund K , Wester P O
Published: June 2011

BACKGROUND AND PURPOSE--Incidence, case-fatality rate at 28 days, and severity of acute stroke were recorded for 7 years in a large population-based stroke register to understand the reasons for the decline in stroke mortality in northern Sweden.

Within the framework of the World Health Organization MONICA Project, acute stroke was monitored in people aged 35 to 74 years in northern Sweden from 1985 through 1991 (target population in 1985, 238,948).

The annual incidence of stroke decreased by an average of 2.3%/y in men aged 35 to 64 years (P = .074) and increased significantly by 1.1%/y in men aged 65 to 74 years (P = .041). No significant changes in incidence occurred in either age group in women. The 28-day case-fatality rate in first-ever strokes (both sexes together) declined from 21.9% to 15.4% in patients aged 65 to 74 years (P = .02). Among survivors, the proportion with extensive motor deficits (at any time during the first 28 days) declined in patients younger than 65 years as well as in those older than 65 years (P = .007 and P = .019, respectively). In patients aged 35 to 64 years, the proportion with aphasia/dysphasia also decreased significantly (P = .032), but no such trend was seen in those aged 65 to 74 years.

A shift toward higher ages has been noted in the occurrence of first-ever strokes in men, while incidence has remained unchanged in women. During the 7 years of observation, stroke has become a less severe disease.
Dynamic transcranial Doppler assessment of positional vertebrobasilar ischemia.
Authors: Sturzenegger M , Newell D W , Douville C , Byrd S , Schoonover K
Published: June 2011

A hemodynamic as opposed to an embolic origin of vertebrobasilar ischemia may be suspected when symptoms are brief and triggered by changes in the position of the head or neck. It may be difficult, and not without risk, to reproduce the symptoms and to prove the short-lived hemodynamic changes during angiography. If transcranial Doppler sonography (TCD) could detect these changes, it would be useful as a noninvasive screening method to select patients for further diagnostic evaluation.

TCD monitoring of the P1 segments of both posterior cerebral arteries was performed during different head movements in 14 patients referred for evaluation of suspected hemodynamic vertebrobasilar ischemia and in 10 healthy control subjects with a two-channel, 2-MHz, computerized Doppler system. Patients' symptoms were correlated with the Doppler findings.

Four patients with stereotypical symptoms had a severe drop in posterior cerebral artery blood flow velocities (BFVs) to 20% of baseline (mean; SD, 14.3; range, 0% to 48%) and subsequent reactive hyperemia with an increase in BFV to 149% (mean; SD, 20.6; range, 110% to 186%) dependent on head rotation to one side (group 1). Compared with the values found in group 2 patients and in control subjects, these drops were significant (P = .0001 for both). Symptoms together with BFV changes could be reproduced several times. Angiography confirmed severe vertebral artery obstruction during head rotation and the presence of anomalies in the posterior circulation. In 10 patients (group 2), symptoms were not short-lived, stereotyped, or clearly dependent on head movements and could not be reproduced during TCD testing. Their BFVs dropped to 88% (mean; SD, 9.0; range, 64% to 102%) of baseline values during maximal head rotation, to 86% (mean; SD, 10.3; range, 64% to 100%) during flexion, and to 88% (mean; SD, 6.7; range, 75% to 103%) during extension. In the 10 control subjects, BFVs dropped to 86% (mean; SD, 8.8; range, 61% to 98%) of baseline values during rotation, to 90% (mean; SD, 10.3; range, 74% to 107%) during flexion, and to 76% (mean; SD, 17.1; range, 54% to 104%) during extension.

Monitoring posterior cerebral artery BFV during head movements is a simple, noninvasive method to document a hemodynamic etiology of symptoms in patients with suspected positional vertebrobasilar ischemia. The correlation of symptoms to the hemodynamic findings proved a useful screening method to identify those patients with true position-evoked hemodynamic insufficiency in the posterior circulation. These patients should be selected for angiographic evaluation to identify the source and site of arterial compression.
Callosal atrophy in patients with lacunar infarction and extensive leukoaraiosis. An indicator of cognitive impairment.
Authors: Yamauchi H , Fukuyama H , Ogawa M , Ouchi Y , Kimura J
Published: June 2011

It is unclear why only some patients with lacunar infarction and radiological evidence of diffuse white matter abnormalities have dementia. The purpose of this study is to investigate the value of callosal atrophy as an indicator of cognitive impairment.

We used magnetic resonance imaging to evaluate 11 right-handed male patients with lacunar infarction and extensive white matter hypodensities on computed tomography (8 with dementia and 3 without dementia). The midsagittal corpus callosum area on T1-weighted images was compared with the IQ determined by the Wechsler Adult Intelligence Scale. The relation between these parameters and cerebral oxygen metabolism measured with positron emission tomography was also evaluated in the 8 patients with dementia.

All patients showed diffuse high-intensity areas in the bilateral hemispheric white matter on T2-weighted images. Compared with 19 age- and sex-matched right-handed normal control subjects, the patients had a significantly smaller callosal area. The severity of callosal atrophy, which varied from mild to severe, was significantly related to the total IQ. In the 8 demented patients, the total callosal area was significantly correlated with the mean level of oxygen metabolism in the cerebral white matter.

In patients with lacunar infarction and diffuse white matter abnormalities, the presence of callosal atrophy may indicate cognitive impairment. Callosal atrophy may reflect the severity and extent of white matter damage associated with a decrease in oxygen metabolism, which may determine the severity of intellectual decline.
ST segment depression detected by continuous electrocardiography in patients with acute ischemic stroke or transient ischemic attack.
Authors: McDermott M M , Lefevre F , Arron M , Martin G J , Biller J
Published: June 2011

Forty percent of patients with a history of ischemic stroke or transient ischemic attack (TIA) have concomitant coronary artery disease. ST segment depression, detected by continuous electrocardiography, is associated with increased cardiac morbidity and mortality in patients with known coronary artery disease. While electrocardiographic changes have been associated with acute stroke, the etiology and significance of these changes remain unclear. In this pilot study we report the prevalence of ST segment depression and ventricular arrhythmias in patients with acute ischemic stroke or TIA monitored by continuous electrocardiography. Clinical predictors of ST segment depression and ventricular arrhythmia are also identified.

Consecutive patients presenting with acute ischemic stroke or TIA were enrolled within 72 hours of hospital admission and monitored by continuous electrocardiography for 48 hours. The electrocardiographic results were analyzed for periods of ST segment depression and ventricular arrhythmias.

Of 51 patients with ischemic stroke or TIA, 15 (29%) had episodes of ST segment depression (95% confidence interval, 15% to 43%), and 18 (35%) had ventricular arrhythmias (95% confidence interval, 21% to 49%). In logistic regression analysis, increasing age (P < .02) and a left-sided neurological event (P < .01) were significant predictors of ST segment depression. Increasing numbers of atherosclerotic risk factors, a history of cardiac disease, and increasing or decreasing mean arterial pressure were not predictive of ST segment depression.

Patients with acute ischemic stroke or TIA have a 29% prevalence of ST segment depression within the first 5 days after their event. In comparison, the prevalence of ST depression is 2.5% to 8% in asymptomatic adults and 43% to 60% in patients with symptomatic coronary artery disease. The association of ST segment depression with left-sided neurological events suggests that the electrocardiographic changes are in part neurologically mediated. Further study is necessary to better define the brain-heart interaction and to determine whether ST segment depression in patients with ischemic stroke or TIA reflects underlying coronary artery disease.
Focal ischemia causes an extensive induction of immediate early genes that are sensitive to MK-801.
Authors: Collaço-Moraes Y , Aspey B S , de Belleroche J S , Harrison M J
Published: June 2011

There is strong evidence to implicate glutamate in the cerebral damage caused by ischemia. In this study we investigated the role of glutamate receptors in mediating effects of middle cerebral artery occlusion (MCAO) on immediate early gene expression in the rat by quantitation of mRNA levels.

The effect of MCAO on the induction of immediate early genes was studied in five regions, both ipsilateral and contralateral to the occlusion: the "core" ischemic area of the cortex in the central region of the middle cerebral artery territory, the surrounding area, frontal cortex, occipital cortex, and hippocampus. Levels of c-fos, c-jun, zif-268, and krox-20 mRNA were measured by Northern and slot blot analysis.

A large induction of c-fos mRNA was obtained in all four cortical regions ipsilateral to the occlusion, with the greatest effect detected in the core area. Little effect was detected in the ipsilateral hippocampus and in all contralateral regions. Pretreatment with MK-801 (3 mg/kg) largely inhibited the induction of c-fos mRNA, indicating that the induction was mediated through an N-methyl-D-aspartate subtype of glutamate receptor. MCAO also produced a significant induction of c-jun and zif-268 mRNA in ipsilateral cortical regions.

These results indicate that MCAO causes a profound modulation of the expression of multiple genes in an extensive area of cerebral cortex extending beyond the immediate area supplied by the middle cerebral artery. The marked effect of MK-801 indicates the potential importance of glutamate antagonists in restricting the widespread deleterious effects of glutamate.
Bilateral distal upper limb amyotrophy and watershed infarcts from vertebral dissection.
Authors: Pullicino P
Published: June 2011

Vertebral artery disease may give rise to lower motor neuron deficits, but the pathogenesis is unknown. I describe a man with a right vertebral artery dissection who developed bilateral distal upper extremity amyotrophy. He had symmetrical bilateral focal hyperintensites of the anterior cervical spinal cord on magnetic resonance imaging, compatible with watershed infarction.

A 39-year-old man developed sudden vertigo, chest and bilateral arm pain, bilateral arm weakness, and wasting involving muscles innervated by the sixth cervical to the first thoracic spinal cord segments. Magnetic resonance imaging showed an extensive right vertebral artery dissection and a right posterior inferior cerebellar infarct. Magnetic resonance scans showed a small focal hyperintensity in the region of each anterior horn, extending from the mid to lower cervical spinal cord. Minimal recovery of function was present after 3 months.

Unilateral vertebral artery dissection may give rise to disabling bilateral upper extremity amyotrophy. Watershed infarction within the anterior spinal artery territory, involving both anterior horns, appears to be the mechanism of the lower motor neuron injury.
Physiological Outcomes of Aerobic Exercise Training in Hemiparetic Stroke Patients
Authors: Potempa Kathleen , Lopez Martita , Braun Lynne T. , Szidon J. Peter , Fogg Louis , Tincknell Tyler
Published: June 2011

Background and Purpose
In hemiparetic individuals, low endurance to exercise may compound the increased energy cost of movement and contribute to poor rehabilitation outcomes. The purpose of this investigation was to describe how hemiparetic stroke patients responded to intense exercise and aerobic training.

Methods
Forty-two subjects were randomly assigned to an exercise training group or to a control group. Treatments were given three times per week for 10 weeks in similar laboratory settings. Baseline and posttest measurements were made of maximal oxygen consumption, heart rate, workload, exercise time, resting and submaximal blood pressures, and sensorimotor function.

Results
Only experimental subjects showed significant improvement in maximal oxygen consumption, workload, and exercise time. Improvement in sensorimotor function was significantly related to the improvement in aerobic capacity. After treatment, experimental subjects showed significantly lower systolic blood pressure at submaximal workloads during the graded exercise test.

Conclusions
We conclude that hemiparetic stroke patients may improve their aerobic capacity and submaximal exercise systolic blood pressure response with training. Sensorimotor improvement is related to the improvement in aerobic capacity.
Progressive Cerebral Occlusive Disease After Radiation Therapy
Authors: Bitzer M. , Topka H.
Published: June 2011

Background
A case of progressive irradiation-induced cerebral vasculopathy with abnormal netlike vessels and transdural anastomoses (moyamoya syndrome) is presented. Radiological findings in an additional 40 cases reported in the literature are analyzed, and their clinical relevance is discussed.

Case Description
A 19-year-old woman presented with recurrent ischemic brain lesions after radiation therapy for treatment of a craniopharyngioma during childhood. Cerebral angiography 6 and 12 years after completion of radiation therapy revealed progressive cerebral arterial occlusive disease involving the internal carotid artery on either side of the circle of Willis, with abnormal netlike vessels and transdural anastomoses (moyamoya syndrome).

Conclusions
Extensive similarities between irradiation-induced cerebral vasculopathy and primary moyamoya syndrome (Nishimoto’s disease) support the notion that both disorders share common pathophysiological mechanisms. The occurrence of moyamoya-like vascular changes may not depend on specific trigger mechanisms but may rather represent a nonspecific response of the developing vascular system to a number of various noxious events.
Race-Ethnicity and Determinants of Intracranial Atherosclerotic Cerebral Infarction
Authors: Sacco Ralph L. , Kargman D. E. , Gu Qiong , Zamanillo M. C.
Published: June 2011

Background and Purpose
The aim of this investigation was to determine the importance of race as a determinant of intracranial atherosclerotic stroke in a community-based stroke sample.

Methods
Residents from northern Manhattan over age 39 years hospitalized for acute ischemic stroke (n=438, black 35%, Hispanic 46%, white 19%) were prospectively evaluated. Index ischemic strokes were classified as atherosclerotic (17%), lacunar (30%), cardioembolic (21%), cryptogenic (31%), and other (1%). Atherosclerotic infarcts were subdivided into extracranial (9%) and intracranial (8%) atherosclerosis.

Results
The proportion of extracranial atherosclerotic stroke was similar among the three race-ethnic groups, while intracranial atherosclerosis was more frequent in blacks and Hispanics. The unadjusted odds ratio for nonwhites (blacks and Hispanics combined) was 0.8 (confidence interval [CI], 0.4 to 1.8) for extracranial and 7.8 (CI, 1.04 to 57.7) for intracranial atherosclerosis. Patients with intracranial disease were significantly younger and had an increased frequency of hypercholesterolemia and insulin-dependent diabetes compared with those with nonatherosclerotic disease. The odds ratio for the association of nonwhite race-ethnicity and intracranial atherosclerosis was reduced to 5.2 (CI, 0.7 to 40) after controlling for age and to 4.4 (CI, 0.6 to 35) after controlling for age, education, insulin-dependent diabetes, and hypercholesterolemia.

Conclusions
The greater prevalence of diabetes and hypercholesterolemia among blacks and Hispanics from northern Manhattan accounted for much of the increased frequency of intracranial atherosclerotic stroke. Further control of these risk factors could reduce the frequency of this stroke subtype and minimize the disparities among different race-ethnic groups.
Carotid Intima-Media Thickness and Plaque in Borderline Hypertension
Authors: Lemne Carola , Jogestrand Tomas , de Faire Ulf
Published: June 2011

Background and Purpose
In this study, we investigated intima-media thickness and plaque occurrence in the carotid arteries of men with borderline hypertension compared with that in normotensive control subjects and investigated the relations of these variables to atherosclerotic risk factors.

Methods
Using B-mode ultrasonography, we compared carotid artery intima-media thickness and plaque occurrence in men with borderline hypertension (diastolic blood pressure of 85 to 94 mm Hg, n=73) with that in age-matched normotensive control subjects (diastolic blood pressure of 80 mm Hg, n=72). We evaluated the relationships of intima-media thickness and plaque occurrence to atherosclerotic risk factors such as age, smoking, lipoprotein levels, and fasting insulin levels.

Results
The borderline hypertensive group exhibited a slight increase in overall intima-media thickness (0.73 versus 0.69 mm,
P
=.07), which was most evident in the right carotid artery (0.72 versus 0.67 mm,
P
<.05). There were more borderline hypertensive subjects with plaque (26% versus 16%, NS), again more evident on the right side (18% versus 6%,
P
<.05). Age and high-density lipoprotein cholesterol were consistently related to intima-media thickness (
t
=1.94 to 3.24 and
t
=−2.25 to −2.69, respectively,
P
<.05), whereas age was the only significant determinant for plaque/nonplaque (F=6.4,
P
<.05). In addition, there was a significant difference in intima-media thickness between the right and left carotids, irrespective of group (F=4.43,
P
<.05).

Conclusions
Our results indicate that vascular structural changes occur even in borderline hypertension, although this seems more related to general atherosclerotic risk factors than to blood pressure alone. Additionally, a possible difference in the development of atherosclerotic lesions of the left and right carotid arteries is suggested, emphasizing the importance of measuring and reporting values from both sides when studying carotid intima-media thickness and plaque occurrence.
Platelet Activation in the Cerebral Circulation in Different Subtypes of Ischemic Stroke and Binswanger’s Disease
Authors: Iwamoto Toshihiko , Kubo Hideki , Takasaki Masaru
Published: June 2011

Background and Purpose
The sites of platelet activation in ischemic stroke are still unclear because previous reports have not identified them and various factors accompanied by stroke can activate platelets. We therefore examined the sites of platelet activation in patients with various types of ischemic stroke.

Methods
The ratio of the plasma concentration of β-thromboglobulin (BTG) in the internal jugular vein to that in the antecubital vein (BTG-B) was calculated as an indicator of platelet activation in the cerebral circulation. Plasma BTG concentration was determined in 75 control subjects and in 186 patients with various subtypes of ischemic stroke including lacunar, atherothrombotic, and cardioembolic strokes, transient ischemic attacks, and Binswanger’s disease. The BTG ratio was evaluated with regard to subtype of stroke, time of blood sampling, size of infarct, presence of vascular lesions, and the effect of ticlopidine administration.

Results
The mean BTG ratio was increased even in the chronic phase of most subtypes of stroke with the exception of cardioembolic stroke, which exhibited a persistent elevation of BTG-B concentrations. Patients with Binswanger’s disease showed a significant (
P
<.01) and frequent elevation of BTG ratio. High BTG ratios occurred in cases with vascular lesions observed on cerebral angiography. There was no correlation between the BTG ratio and infarct size. Use of ticlopidine was partially associated with a lower BTG ratio.

Conclusions
Platelets were activated in the cerebral circulation of patients with stroke even in the chronic phase, which suggests the development of underlying vascular lesions and of thrombogenesis with or without infarction. Platelets were activated mainly within the heart in cases of cardioembolic stroke. An enhanced release reaction secondary to platelet activation was often seen in patients with Binswanger’s disease, which indicates that its pathophysiology differs from that of other subtypes of stroke.
Estimation of Cerebrovascular Reactivity in Migraine Without Aura
Authors: Silvestrini Mauro , Cupini Letizia M. , Troisi Elio , Matteis Maria , Bernardi Giorgio
Published: June 2011

Background and Purpose
The nature and role of vascular abnormalities in migraine are controversial. In this study we evaluated cerebrovascular reactivity to hypercapnia in patients suffering from migraine without aura with unilateral headache.

Methods
Using bilateral transcranial Doppler ultrasound, we studied the changes of flow velocity after hypercapnia in the anterior, middle, and posterior cerebral arteries of 16 migraine patients and 16 healthy control subjects. All patients were studied during an attack-free interval and during a migraine attack. Cerebrovascular reactivity was evaluated with the breath-holding index, obtained by dividing the percent increase in mean flow velocity occurring during breath-holding by the time (seconds) in which the subjects held their breath after a normal inspiration.

Results
The response to breath-holding was similar for all arteries considered in both control subjects and patients during the attack-free interval. During the migraine attack, the breath-holding index in patients was significantly lower than the migraine-free interval in all arteries (
P
<.001). No side-to-side difference in cerebrovascular reactivity was detected in migraine patients either outside or during attacks.

Conclusions
These results suggest that a failure of cerebrovascular regulation occurs during attacks of migraine without aura.
Assessment of Cerebral Vasomotor Reactivity by Transcranial Doppler Ultrasound and Breath-Holding
Authors: Müller M. , Voges M. , Piepgras U. , Schimrigk K.
Published: June 2011

Background and Purpose
Evaluating cerebrovascular vasomotor reactivity seems to be of prognostic relevance for patients with occlusive internal carotid artery disease. To evaluate its clinical usefulness, the recently introduced breath-holding maneuver as a carbon dioxide–dependent vasodilatory stimulus was compared with the acetazolamide challenge by means of transcranial Doppler ultrasound and stable xenon-enhanced computed tomography.

Methods
In a total of 134 middle cerebral arteries of 74 patients (mean±SD age, 62±9 years) with unilateral or bilateral occlusive carotid artery disease, vasomotor reactivity was estimated by the increase of middle cerebral artery mean blood velocity by transcranial Doppler ultrasound, comparing the breath-holding maneuver and 1 g IV acetazolamide as vasodilatory stimuli. The carotid artery findings were classified as normal, stenosis of 50% to <70%, 70% to <90%, 90% to 99%, and occlusion. Eighteen of the 74 patients additionally underwent stable xenon-enhanced computed tomography to calculate the increase of mean cortical regional cerebral blood flow in the middle cerebral artery territory after acetazolamide stimulation.

Results
The percentage of mean regional cerebral blood flow changes (n=36 hemispheres) correlated best with the absolute mean blood velocity changes while breath-holding (
P
=.007,
r
=.4332). The absolute mean regional cerebral blood flow changes correlated best with the percentage of mean blood velocity changes after acetazolamide stimulation (
P
=.004,
r
=.4580). On all 134 middle cerebral arteries, both vasodilatory stimuli correlated highly significantly (
P
<.0001) when comparing increases in absolute (
r
=.5448) or relative (
r
=.3516) mean blood velocity. Both stimulation techniques similarly indicated significantly reduced vasomotor reactivity with increasing degree of internal carotid artery lesions (
P
≤.01). However, the acetazolamide challenge differentiated more accurately between the various groups of internal carotid artery findings.

Conclusions
The assessment of vasomotor reactivity by transcranial Doppler ultrasound correlates with cerebral blood flow changes even when different vasodilatory stimuli are used. In cooperative patients the breath-holding maneuver as vasodilatory stimulus seems clinically useful for a first estimation of cerebral vasomotor reactivity.