bluuebunny/crossref_metadata_2025_split huggingface dataset:
Intracranial hypertension after resection of cerebral arteriovenous malformations. Predisposing factors and management strategy.
Authors: Awad I A , Magdinec M , Schubert A 
Published: June 2011

Surgical excision of cerebral arteriovenous malformations (AVMs) may be complicated by postoperative breakthrough edema and hemorrhage and by intracranial hypertension. Embolization, staged resection, and meticulous surgical technique have decreased but not completely eliminated this complication. In this study we prospectively assess the prevalence of intracranial hypertension after excision of cerebral AVMs, examine factors predisposing to this complication, and document the outcome of aggressive monitoring and treatment of elevated intracranial pressure (ICP).
During a 4-year period at a single institution, 32 consecutive patients with cerebral AVMs underwent surgical excision after staged embolization. All patients underwent postoperative monitoring of ICP and a uniform management protocol of intracranial hypertension.
Intractable intracranial hypertension was encountered after resection of 9 of 32 cerebral AVMs, including 3 of 20 (15%) AVMs 6 cm or less in maximum diameter and 6 of 12 (50%) AVMs greater than 6 cm in maximum diameter. This complication occurred in 5 of 10 (50%) lesions located in distal or border-zone locations, in 4 of 9 (44%) AVMs arising directly off proximal cerebral arteries, and in none of 13 AVMs in other locations. Preoperative single-photon emission-computed tomography perfusion scans were performed in 17 patients and demonstrated parenchymal hypoperfusion beyond the AVM nidus in 5 of 10 AVMs 6 cm or less in maximum diameter, none of which manifested postoperative intractable ICP. Hypoperfusion was observed on single-photon emission-computed tomography in 7 of 7 AVMs greater than 6 cm that were studied by this modality, and intractable ICP was observed postoperatively in 5 of these cases despite preoperative staged embolization in every case. Patients with symptomatic intractable ICP were treated with intravenous short-acting barbiturates under a strict critical care protocol. There was no instance of uncontrollable intracranial hypertension or break-through edema while on barbiturate therapy. There was no permanent morbidity related to this treatment and no mortality or new disability morbidity in this series.
We conclude that intractable intracranial hypertension remains a common complication after resection of a subgroup of cerebral AVMs despite preoperative embolization, modern neuroanesthesia and critical care management, and microsurgical technique. A proactive management protocol aimed at ICP control is safe and effective in the management of this complication.
Tirilazad treatment does not decrease early brain injury after transient focal ischemia in cats.
Authors: Takeshima R , Kirsch J R , Koehler R C , Traystman R J 
Published: June 2011

We tested the hypothesis that administration of the antioxidant tirilazad mesylate improves electrophysiological recovery and decreases infarct volume after transient focal cerebral ischemia in cats.
Halothane-anesthetized cats underwent 90 minutes of left middle cerebral artery and bilateral common carotid artery occlusion followed by 180 minutes of reperfusion. Cats were assigned to receive tirilazad (1.5 mg/kg plus 0.2 mg/kg per hour IV infusion) either at the beginning (n = 9) or conclusion (n = 9) of ischemia. Control cats received an equal volume of diluent (citrate buffer, pH 3.0; n = 7) at the beginning and conclusion of ischemia in a blinded fashion. Infarct volume was measured by 2,3,5-triphenyltetrazolium chloride staining.
Blood flow to the left temporoparietal cortex decreased to less than 10 mL/min per 100 g with ischemia but was minimally affected on the right side. Blood flow distribution during ischemia or reperfusion was not different in the tirilazad-treated groups. No group demonstrated postischemic hyperemia or delayed hypoperfusion. Somatosensory evoked potential recorded over the left cortex was ablated during ischemia and recovered to less than 15% of baseline amplitude at 180 minutes of reperfusion in all groups. There were no differences among groups in infarct volume of left hemisphere (pretreatment, 25 +/- 6% [mean +/- SE]; posttreatment, 33 +/- 5%; control, 28 +/- 8% of hemisphere) or caudate nucleus (pretreatment, 46 +/- 7%; posttreatment, 41 +/- 10%; control, 55 +/- 13% of hemisphere).
In an experimental model of focal ischemia involving severe reductions of blood flow followed by reperfusion in cats, administration of tirilazad at the onset of either ischemia or reperfusion does not ameliorate infarct volume assessed during early reperfusion. Our study does not address potential efficacy of tirilazad in the setting of a different dosing strategy or duration of reperfusion.
Increase in extracranial atherosclerotic carotid lesions in patients with brain ischemia in Japan. An angiographic study.
Authors: Nagao T , Sadoshima S , Ibayashi S , Takeya Y , Fujishima M 
Published: June 2011

Atherosclerotic lesions in the cerebral arteries are distributed heterogeneously among different races. Intracranial carotid lesions are reported to be more common than extracranial carotid lesions among Japanese people, which is in sharp contrast to the pattern of cerebral atherosclerosis in whites. However, several Japanese clinicians have the impression, which has yet to be clinically proven, that extracranial carotid diseases are recently increasing in number.
One hundred twenty-one patients who developed ischemic stroke and underwent angiography were examined in the study. Seventy were admitted to our clinic from 1963 to 1965 (early group); the remaining 51 patients were seen from 1989 to 1993 (recent group). Angiographic findings and vascular risk factors were compared between the two groups.
Severe atherosclerotic lesions of the extracranial internal carotid arteries increased significantly during the ensuing 24 years between the end of the first period until the beginning of the second period (from 1965 to 1989), whereas lesions in the intracranial carotid system were similar between the two groups. Severe atherosclerosis in the extracranial internal carotid artery was more frequent in patients with diabetes mellitus, which proved to be the only risk factor that showed a temporal increase.
The proportion of severe atherosclerosis in Japanese patients with brain ischemia has been increasing in the extracranial internal carotid artery, while that in the intracranial carotid system remains unchanged. Such a temporal change may be the result, at least in part, of an increase in the prevalence of diabetes mellitus.
Patent foramen ovale and brain infarct. Echocardiographic predictors, recurrence, and prevention.
Authors: Hanna J P , Sun J P , Furlan A J , Stewart W J , Sila C A , Tan M 
Published: June 2011

Paradoxical embolism through a patent foramen ovale is a recognized cause of stroke, but clinical predictors, recurrence rate, and prevention of brain infarcts in patients with patent foramen ovale have not been determined. We reviewed transesophageal echocardiographic records to ascertain echocardiographic predictors and optimal prophylaxis for patent foramen ovale-related infarcts.
A patent foramen ovale was identified in 74 patients during 615 transesophageal echocardiograms by color Doppler or saline contrast during a 60-month period. On the basis of final clinical situation, the patients were divided into the following groups: group 1, infarct with patent foramen ovale a likely cause (n = 16); group 2, infarct with patent foramen ovale an unlikely cause (n = 23); and group 3, no infarct (n = 35). Transesophageal echocardiograms were reviewed to assess patent foramen ovale characteristics and associated cardio-embolic sources without knowledge of clinical details or group assignment. Follow-up after a patent foramen ovale-related infarct was obtained by telephone or written correspondence in 15 of 16 group 1 patients.
Atrial septal aneurysms were more common in group 1 (38%) compared with group 2 (10%) and group 3 (8%) (P = .02). Contrast right-to-left shunting occurred in 88% of group 1 (P = .06) and 86% of group 2 (P = .07) compared with 60% of group 3. Prevention of recurrence in subjects with presumed patent foramen ovale-related brain infarcts varied. Aspirin was usually chosen after initial brain ischemia. Warfarin and patent foramen ovale closure were usually reserved for subjects with symptoms of brain ischemia while taking aspirin or those who required warfarin or cardiac surgery for other indications. No recurrent infarcts occurred in 15 patients during a mean follow-up period of 28 months.
Atrial septal aneurysm and right-to-left shunt may be predictive of a patent foramen ovale that predisposes a patient to stroke. Aspirin may provide sufficient infarct prophylaxis after initial ischemia. Warfarin and surgical correction should likely be reserved for those in whom aspirin is not effective or those who require warfarin or cardiac surgery for other reasons until prospective studies are available.
Cardiovascular autonomic reflexes in brain infarction.
Authors: Korpelainen J T , Sotaniemi K A , Suominen K , Tolonen U , Myllylä V V 
Published: June 2011

Increased sympathetic activity is associated with cardiovascular complications in stroke, but the role of the parasympathetic nervous system has not been carefully outlined. In the present study our purpose was to assess quantitatively autonomic cardiovascular disturbances in brain infarction by measuring cardiovascular autonomic reflexes.
We studied the autonomic regulation of cardiovascular functions prospectively in 40 patients with brain infarction (acute phase, 1 month, and 6 months) and in 55 healthy control subjects by recording heart rate and blood pressure responses to normal and deep breathing, the Valsalva maneuver, tilting, and isometric work.
In the acute phase, heart rate responses to normal breathing, deep breathing, the Valsalva maneuver, and tilting were significantly (P < .05) impaired in both hemispheric and brain stem infarctions, thus indicating hypofunction of the parasympathetic nervous system. At 1 month heart rate responses to normal breathing (brain stem, P < .05), the Valsalva maneuver (brain stem, P < .01), and tilting (hemispheric, P < .05) were still significantly lower than those of the control subjects, but at 6 months significant suppression of the response was found only in tilting (hemispheric, P < .05).
These findings suggest that in addition to the previously well-established sympathetic hyperfunction, brain infarction also seems to cause parasympathetic hypofunction, brain which may be involved in cardiovascular and other known manifestations of autonomic failure associated with stroke.
Background factors and clinical symptoms of major depression with silent cerebral infarction.
Authors: Fujikawa T , Yamawaki S , Touhouda Y 
Published: June 2011

We previously reported that major depression developing during or after the presenile period is frequently combined with silent cerebral infarction and that these patients have a high risk of stroke. Therefore, we investigated whether the background factors and clinical symptoms of patients with major depression with silent cerebral infarction [SCI(+)] different from those in patients with major depression without silent cerebral infarction [SCI(-)] before medical treatment.
Patients with major depression with onset after 50 years of age were classified based on magnetic resonance imaging findings into the SCI(+) (n = 37) or SCI(-) (n = 20) group. The diagnostic criteria for major depression were those of the American Psychiatry Association (DSM-III-R). Patients with stroke or focal neurological symptoms were excluded. The SCI(+) group was subclassified according to whether the infarction area was perforating, cortical, or mixed artery. Family history of affective disorder, risk factors for stroke, and Zung's Self-rated Depression Scale (SDS) score before medical treatment of the group were compared.
The SCI(+) group had a significantly lower (P < .05) frequency of family history of affective disorder but a significantly higher (P < .01) frequency of hypertension than did the SCI(-) group. The mean SDS score in the SCI(+) group was significantly higher than that in the SCI(-) group (P < .01). The mean SDS score of the mixed artery infarction group was higher than that of the perforating artery infarction group (P < .05).
Patients with major depression with silent cerebral infarction present more marked neurological factors and more severe depressive symptoms than do those without silent cerebral infarction. Because these features were more prominent in the patients with mixed artery infarction with broad obstructions, we consider that the area of brain damage caused by cerebral infarction is positively related to the severity of depressive symptoms.
The influence of stroke unit rehabilitation on functional recovery from stroke.
Authors: Kalra L 
Published: June 2011

Shorter lengths of hospital stay in stroke units could be due to quicker functional recovery or mechanisms of expediting hospital discharge.
Stroke survivors with an intermediate prognosis at 2 weeks after stroke (n = 146) were randomized for management in a stroke rehabilitation unit or in general wards. Barthel scores were monitored at weekly intervals until hospital discharge. The duration and type of physiotherapy and occupational therapy received by patients in either setting were also recorded. The rate of change of Barthel scores, therapy input, and the duration of hospital stay were compared between the two settings.
Neurological deficits and median initial Barthel scores were comparable between patients in the stroke unit (n = 73) and general wards (n = 68). Median discharge Barthel score of patients managed in the stroke unit was significantly higher than that of patients managed in general wards (15 versus 12). Median Barthel scores in the stroke unit group rose rapidly after 2 weeks, reaching a plateau at 6 weeks. The change in median Barthel score in patients in general wards was significantly slower, reaching a plateau at 12 weeks despite similar therapy input. There was a significant delay in discharging stroke patients in general wards (20 weeks) compared with those in the stroke unit (6 weeks).
Functional recovery is significantly greater and more rapid in a stroke rehabilitation unit compared with general wards despite similar therapy input. These units also shorten hospital lengths of stay by expediting appropriate discharges.
Regional cerebral blood flow in familial hypercholesterolemia.
Authors: Rodriguez G , Bertolini S , Nobili F , Arrigo A , Masturzo P , Elicio N , Gambaro M , Rosadini G 
Published: June 2011

Although epidemiologic investigations are trying to clarify the role of plasma lipid concentrations (primarily cholesterol and its subfractions) as risk factors for both ischemic and hemorrhagic stroke, little information is available regarding the effect of sustained hypercholesterolemia on cerebral perfusion.
Regional cerebral blood flow (CBF) was measured by the 133Xe inhalation method in 25 heterozygous patients (four untreated) affected with familial hypercholesterolemia. In 15 patients regional CBF was repeated 20 minutes after intravenous administration of acetazolamide (10 mg/kg body wt) to evaluate cerebrovascular reactivity. Correlations among cerebral perfusion data, present or pretreatment plasma lipid concentrations, and certain other clinical features were assessed by ANOVA.
Both basal regional CBF and cerebrovascular reactivity were normal in the vast majority of patients compared with age- and sex-matched normal control subjects. CBF was significantly dependent on pretreatment low-density lipoprotein cholesterol (LDL-C) concentration (P = .005) and the presence of symptomatic ischemic heart disease (P = .015). CBF was only slightly dependent on age (P = .05) and was not dependent on either lipoprotein(a) or present LDL-C concentration. CBF did not differ between treated and untreated patients, and the perfusional increase induced by acetazolamide was not related to any other variable.
Cerebral perfusion and cerebrovascular reactivity were maintained within the normal range despite long-lasting, severe hypercholesterolemia, even if a somewhat lower CBF was found in those patients with the highest LDL-C pretreatment levels. These results are in accord with the epidemiologic data that implicate hypercholesterolemia as a minor risk factor, if a risk factor at all, for intracranial atherosclerosis and ischemic stroke.
Nitric oxide synthase inhibition reduces caudate injury following transient focal ischemia in cats.
Authors: Nishikawa T , Kirsch J R , Koehler R C , Miyabe M , Traystman R J 
Published: June 2011

We tested the hypothesis that inhibiting nitric oxide production either before or during transient focal ischemia affects early postischemic brain injury.
Halothane-anesthetized cats underwent 1 hour of left middle cerebral artery occlusion plus 3 hours of reperfusion. Pretreatment groups received either intravenous N omega-nitro-L-arginine methyl ester (L-NAME; 10 mg/kg, n = 10) or an equal volume of diluent (10 mL saline, n = 10) over 30 minutes before ischemia. Posttreatment groups received intravenous L-NAME (10 mg/kg) over 30 minutes from 45 minutes of ischemia to 15 minutes of reperfusion (n = 10) or intravenous L-NAME (10 mg/kg) plus L-arginine (200 mg/kg) over the same period followed by continuous L-arginine infusion (200 mg/kg per hour) for the remainder of reperfusion (n = 10).
Microsphere-determined blood flow to ipsilateral caudate nucleus and inferior temporal cortex decreased to the same extent during ischemia and recovered to the same extent during reperfusion in the four groups. Triphenyltetrazolium-determined injury volume of ipsilateral caudate nucleus in cats treated with L-NAME before or during ischemia (42 +/- 7% and 42 +/- 3% of caudate nucleus, respectively; mean +/- SE) was less (P < .05) compared with that in cats pretreated with saline (72 +/- 5%) or cats treated with L-NAME plus L-arginine (68 +/- 5%). Ipsilateral cerebral hemispheric injury volume was similar among the four groups (23 +/- 5%, 13 +/- 3%, 18 +/- 5%, and 29 +/- 5% of hemisphere in groups treated with L-NAME before ischemia and during ischemia, the saline-treated group, and the group treated with L-NAME plus L-arginine, respectively).
Inhibition of nitric oxide synthase decreases caudate injury volume from transient focal cerebral ischemia in cats. The beneficial effect is reversed by L-arginine and is not caused by favorable redistribution of blood flow during ischemia and reperfusion. Because L-NAME was efficacious when administered at reperfusion, nitric oxide generated during reperfusion appears to contribute to caudate injury.
Middle cerebral artery occlusion due to hydatid cysts of myocardial and intraventricular cavity cardiac origin. Two cases.
Authors: Benomar A , Yahyaoui M , Birouk N , Vidailhet M , Chkili T 
Published: June 2011

Hemispheric strokes of hydatid origin are very rare. We describe two cases of middle cerebral artery occlusion by a cyst of cardiac origin.
Cerebral angiography demonstrated occlusion of the initial segment of the middle cerebral artery. Myocardial and pericardial cysts were diagnosed by echography and pathological examination. Subsequent development of hydatid cysts within the necrotic area of the infarcted hemisphere suggests cerebral hydatid embolism of cardiac origin.
In endemic areas, embolism of hydatid cysts should be considered in the diagnosis of stroke in young patients.
Does endothelin-1 play a role in the pathogenesis of cerebral vasospasm?
Authors: Cosentino F , Katusić Z S 
Published: June 2011

Endothelin-1 is a very powerful endogenous vasoconstrictor substance produced by endothelial cells. Its long-lasting vasoconstrictor and hypertensive action has been well documented in several species, including humans.
It is generally accepted that endothelin-1 may contribute to the pathogenesis of a number of cardiovascular diseases. In the cerebral vasculature, endothelin-1 has been proposed as a key mediator of cerebral vasospasm following subarachnoid hemorrhage. Availability of endothelin-1 antagonist provided a pharmacologic tool to test the role of endothelin in the development of vasospasm.
This brief review is focused on the controversial results reported by different groups concerning the possible role of endothelin-1 in narrowing of cerebral arteries exposed to autologous blood.
Ultrasonographic evaluation of vertebral artery to detect vertebrobasilar axis occlusion.
Authors: Kimura K , Yasaka M , Moriyasu H , Tsuchiya T , Yamaguchi T 
Published: June 2011

We performed the present study to determine whether the site of occlusion in the vertebrobasilar circulation could be identified by the measurement of blood flow velocity in the bilateral vertebral arteries.
Using color-coded duplex carotid ultrasonography, we measured the time-averaged mean and end-diastolic flow velocities with incident angle correction in 130 bilateral vertebral arteries between the C3 and C6 segments of the spine in 65 stroke patients with or without occlusive diseases in the vertebrobasilar circulation. The site of occlusion was confirmed by cerebral angiography. The subjects included 12 patients with unilateral subclavian artery occlusion (SA group), 11 patients with unilateral occlusion at the origin of the vertebral artery (V1 group), 6 patients with unilateral vertebral artery occlusion before the branching of the posterior inferior cerebellar artery (V2 group), 14 patients with unilateral vertebral artery occlusion after the branching of the posterior inferior cerebellar artery (V3 group), 5 patients with basilar artery occlusion (BA group), 5 patients with unilateral posterior cerebral artery occlusion (PCA group), and 12 patients without any occlusive lesions in the vertebrobasilar circulation (control group).
In the control group the mean and end-diastolic blood flow velocities were 25.5 +/- 6.9 cm/s and 16.2 +/- 4.3 cm/s, respectively, and the side-to-side differences of these velocities were 4.8 +/- 5.2 cm/s and 4.7 +/- 4.1 cm/s, respectively. All patients in the SA group demonstrated retrograde flow on the affected side. In the V1 group no flow signals were detected on the occluded side. In the V2 group the mean velocity (7.2 +/- 3.1 cm/s) was lower than in the control group, and the end-diastolic velocity was zero on the affected side. In the V3 group the mean and end-diastolic velocities (11.5 +/- 3.1 cm/s and 5.9 +/- 2.8 cm/s, respectively) on the occluded side were lower than in the control group. Flow velocities on the unaffected side were higher than those on the affected side in the SA, V1, V2, and V3 groups. However, there were no differences in flow velocity between the control, BA, and PCA groups.
Measurement of vertebral artery blood flow velocity may help in localizing the site of occlusion in the subclavian and vertebral arteries.
Brain SPECT in a case of cortical blindness.
Authors: Drubach D A , Carmona S , Meyerrose G E , Peralta L M , Sostre S 
Published: June 2011

Published reports on patients with cortical blindness describe bilateral brain hemispheric lesions visualized in radiological and functional imaging studies.
We present a case with a unilateral lesion on radiological studies and bilateral abnormalities on single-photon emission-computed tomographic (SPECT) scanning.
SPECT images correlated much more closely than radiological studies with the patient's clinical status. We suggest that SPECT scanning can be a useful indicator of focal brain dysfunction in brain injury in spite of normal radiological studies. We also hypothesize that our patient's clinical and functional imaging findings could be attributed in part to the process of diaschisis.