bluuebunny/crossref_metadata_2025 huggingface dataset:
Diffusion nuclear magnetic resonance imaging in experimental stroke. Correlation with cerebral metabolites.
Authors: Back T , Hoehn-Berlage M , Kohno K , Hossmann K A
Published: June 2011

Diffusion-weighted nuclear magnetic resonance imaging has been shown to detect early ischemia-related alterations in experimental stroke. This raises the question of whether the observed increase in signal intensity is correlated with changes in cerebral metabolism. After middle cerebral artery occlusion, nuclear magnetic resonance diffusion images were recorded and compared with the regional concentration of cerebral metabolites and with histology of identical planes.

Seven anesthetized Fischer rats were subjected to permanent occlusion of the middle cerebral artery. T1, T2, and diffusion images (b factors ranging from 0 to 1500 s/mm2) were measured in three to five planes after 7 hours. Thereafter, brains were frozen in situ for histology and quantitative bioluminescence imaging of ATP, glucose, lactate, and for fluorescence imaging of tissue pH.

Seven hours after middle cerebral artery occlusion, the apparent diffusion coefficient was reduced from 615 +/- 97 x 10(-6).mm2.s-1 (contralateral brain) to 359 +/- 42 x 10(-6).mm2.s-1 (ischemic brain; mean +/- SD, P < .01). A precise topical coincidence was demonstrated between changes in nuclear magnetic resonance diffusion images, pattern of histological damage, ATP-depleted areas, and local tissue acidosis, the lesion area amounting to between 24.1% and 27.6% of the hemisphere at the level of the caudate-putamen. The area of elevated brain lactate clearly exceeded the acidic core of the infarct and included the slightly alkaline border zone.

The data demonstrate that after 7-hour middle cerebral artery occlusion, the reduction of the apparent diffusion coefficient in nuclear magnetic resonance diffusion images reflects precisely the region of histological injury, breakdown of energy metabolism, and tissue acidosis.
Motor recovery after early brain damage. A case of brain plasticity.
Authors: Sabatini U , Toni D , Pantano P , Brughitta G , Padovani A , Bozzao L , Lenzi G L
Published: June 2011

Motor recovery is remarkable when the brain is damaged early in life. We describe a case of early damage to the right hemisphere with remarkable reorganization and plastic functional changes, studied by computed neuroimaging.

A 31-year-old man had a left-sided hemiplegia at the age of 12, followed by good motor recovery despite a large right cortical-subcortical lesion. Single-photon emission computed tomography with motor activation study showed cerebral blood flow increase in the left premotor and sensorimotor cortices irrespective of the hand he was moving, without flow changes in the right hemisphere.

A remarkable reorganization and plastic brain functional changes occurred in a patient after early diffuse damage of the right hemisphere. The study points to a potential role of ipsilateral cortical efferent pathways in subserving hand movements after early cerebral damage.
Malignant brain stem hyperthermia caused by brain stem hemorrhage.
Authors: Kitanaka C , Inoh Y , Toyoda T , Sasaki T , Eguchi T
Published: June 2011

We report two cases of brain stem hemorrhage characterized by severe hyperthermia, rhabdomyolysis, acute renal failure, and a rapidly fatal course.

A 55-year-old man and a 65-year-old man were admitted with coma-producing brain stem hemorrhage accompanied by hyperthermia. Both underwent ventricular drainage.

Within 1 day of onset, both patients developed hyperthermia of over 41 degrees C, increased serum creatine phosphokinase (CPK) level indicating rhabdomyolysis, and acute renal failure. One patient died on the second day and the other on the third day after onset despite supportive treatment.

These cases of brain stem hemorrhage with fulminant hyperthermia should be distinguished from those with simple hyperthermia. They may represent a kind of malignant hyperthermia, in which case dantrolene sodium might be beneficial. Monitoring serum CPK levels would be of help in making the diagnosis early in the course.
Asymptomatic carotid lesions and silent cerebral infarction.
Authors: Hougaku H , Matsumoto M , Handa N , Maeda H , Itoh T , Tsukamoto Y , Kamada T
Published: June 2011

Few studies have investigated the relationships between asymptomatic carotid lesions and silent infarcts confirmed on magnetic resonance imaging.

A consecutive series of 117 subjects (average age, 62 +/- 9.4 years) who were free from neurological deficit but had at least one established risk factor for stroke were investigated by B-mode carotid ultrasonography and magnetic resonance imaging of the brain. Carotid lesions were evaluated by plaque score, maximum percent stenosis, and the existence of ulcerated lesions. The relations between the carotid lesions and the incidence, size, or localization of the brain lesions were investigated.

The incidence of silent infarcts was 42% in all subjects and significantly increased with advancing age (P < .05). Most lesions were smaller than 1 cm in diameter and were usually localized in the subcortical white matter or the basal ganglia. The percentage of subjects with infarcts increased significantly as the plaque score increased (P < .05) or when subjects had high-grade stenosis (P < .05) or ulcerated lesions (P < .01). These relationships were also noted in each decade of age. A higher incidence of larger lesions (> 1 cm) was found in the brain hemisphere ipsilateral to the carotid lesion, particularly in subjects with high-grade stenosis or ulcerated lesions (P < .01). Multivariate analysis indicated significant correlations with silent infarcts for age, hypertension, and plaque score.

Both the severity and characteristics of asymptomatic carotid lesions estimated by B-mode ultrasonography were closely related to the appearance of silent infarcts. These results demonstrate that noninvasive assessment of carotid lesions can be useful in predicting the existence of silent cerebral infarction even in patients free from neurological deficits.
Cerebral blood flow and effects of cerebrospinal fluid on calcium transport in patients with cerebral infarction.
Authors: Akopov S E , Grigorian G S , Gabrielian E S
Published: June 2011

In this study we investigated whether cerebrospinal fluid in patients with brain infarction possesses an activity that contributes to the evolution of brain ischemia. As a test, the effect of cerebrospinal fluid on Ca2+ influx into the intracellular space was chosen because this process is a mechanism for vasospasm, platelet aggregation as thrombi, and neuron damage.

Effects of cerebrospinal fluid taken from 48 patients with cerebral hemispheric infarction on the concentration of cytosolic free Ca2+ in platelets were studied using the fluorescent probe quin-2. Hemispheric cerebral blood flow was measured using 133Xe intravenous injection.

Cerebrospinal fluid in 19 of 48 patients with cerebral hemispheric infarction increased the level of cytosolic free Ca2+ in platelets. The course of the disease in the patients who showed a positive effect of cerebrospinal fluid on Ca2+, when compared with that of patients who showed a negative effect, was characterized by a more severe clinical manifestation and mortality. The decrease in hemispheric cerebral blood flow was more marked in both ischemic and contralateral hemispheres in patients with positive effects of cerebrospinal fluid on the level of Ca2+.

These data suggest that the ability of cerebrospinal fluid to evoke Ca2+ influx into the intracellular space in patients with brain infarction is a factor that aggravates ischemic brain damage.
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.
Cerebral infarction immediately after ingestion of hydrogen peroxide solution.
Authors: Sherman S J , Boyer L V , Sibley W A
Published: June 2011

We report the clinical and neuroimaging findings of a patient who sustained multiple cerebral infarcts after the ingestion of concentrated hydrogen peroxide solution sold as a "health food" product.

An 84-year-old man sustained focal neurological deficits immediately after ingesting 30 mL of 35% hydrogen peroxide solution. Physical examination disclosed a left hemiparesis, frontal release signs, and cerebellar dysfunctions. Magnetic resonance imaging revealed multiple cerebral and cerebellar infarctions in the anterior, middle, and posterior vascular territories.

The likely mechanism of pathogenesis involves cerebral oxygen gas embolization. The use of hyperbaric therapy should be considered in treating hydrogen peroxide poisoning.
Cognitive correlates of ventricular enlargement and cerebral white matter lesions on magnetic resonance imaging. The Rotterdam Study.
Authors: Breteler M M , van Amerongen N M , van Swieten J C , Claus J J , Grobbee D E , van Gijn J , Hofman A , van Harskamp F
Published: June 2011

Ventricular enlargement and white matter lesions are frequent findings on cerebral magnetic resonance imaging scans of elderly subjects. In demented subjects they seem related to the severity of the dementia, but in nondemented subjects their clinical significance is less clear. We investigated the relation of size of the lateral ventricles and white matter lesions with cognitive function in a population-based random sample of nondemented elderly persons.

The study population consisted of 90 subjects, aged 65 to 84 years, who were randomly selected from the cohort of the Rotterdam Study, and who were not demented. The presence of white matter lesions and the ventricle-to-brain ratio were assessed on magnetic resonance scans. Participants were tested with a neuropsychological battery that covered a broad range of cognitive functions.

Ventricular enlargement and white matter lesions were both and independently associated with poorer performance on all tests. After adjustment for age and sex, ventricular enlargement was significantly associated with worse scores on tests assessing global cognitive function (Mini-Mental State Examination, P = .02; Groninger Intelligence Test, P = .01), memory (Word List Learning delayed recall, P = .03), and executive control functions (Stroop part II, P = .02; Trial Making Test B, P < .01); for white matter lesions the differences were significant for tests measuring executive control functions and mental speed (Trail Making Test A and B, P = .01 and P < .01, respectively; verbal fluency, P = .01), and memory (Word List Learning delayed recall, P = .04).

This study suggests that white matter lesions are primarily related to impairment of subcorticofrontal functions, whereas enlargement of the lateral ventricles is associated with disturbances of cortical functions as well.
Carotid plaque, aging, and risk factors. A study of 457 subjects.
Authors: Fabris F , Zanocchi M , Bo M , Fonte G , Poli L , Bergoglio I , Ferrario E , Pernigotti L
Published: June 2011

The aim of this study was to assess the prevalence of extracranial carotid artery atherosclerosis and its relation to principal cardiovascular risk factors at different ages in a sample of the general population.

B-mode ultrasonography was used to investigate the carotid district in 457 subjects (231 men and 226 women; mean age, 55.4 +/- 18.7 years; range, 18 to 97 years) in the metropolitan area. The ultrasonographic findings were then related to risk factors.

Carotid plaques were found in 178 subjects (38.9%). The prevalence of atherosclerosis, number of plaques, and severity of stenosis were observed to increase with age. Age (P < .0001), cigarette smoking (P < .0001), male sex (P < .001), total cholesterol (P < .05), and, inversely, the ratio of high-density lipoprotein cholesterol to total cholesterol (P < .05) were found to be independently associated with carotid atherosclerosis. Stratified analysis by sex and age showed effect modifications by age on cigarette smoking, total cholesterol, and the ratio of high-density lipoprotein cholesterol to total cholesterol. After multivariate analysis including interaction terms, cigarette smoking and cholesterol levels were not longer found to be associated with carotid atherosclerosis in elderly subjects. Age (P < .01), total cholesterol (P < .05), and diabetes (P < .05) were positively related to the severity of vascular narrowing.

There is a high prevalence of asymptomatic carotid atherosclerosis in the general population, particularly among the very old. The association between risk factors and carotid atherosclerosis is less pronounced in the elderly than in younger subjects.
Cost-effectiveness of ticlopidine in preventing stroke in high-risk patients.
Authors: Oster G , Huse D M , Lacey M J , Epstein A M
Published: June 2011

Ticlopidine, an antiplatelet agent, when compared with aspirin has been found to reduce the risk of stroke in high-risk patients, ie, those with recent transient ischemic attack, reversible ischemic neurological deficit, amaurosis fugax, or minor stroke. Its cost-effectiveness in such use, however, is unknown.

We developed a model of primary stroke prevention in which a hypothetical cohort of 100 high-risk men and women 65 years of age was assumed to receive either ticlopidine (500 mg daily) or aspirin (1300 mg daily). Using published data, we estimated lifetime incidence of stroke, life expectancy (unadjusted and adjusted for changes in quality of life), and lifetime medical care costs associated with each therapy.

Patients who receive ticlopidine would experience two fewer initial strokes per hundred than those treated with aspirin. Life expectancy would be extended by approximately one-half month, and lifetime medical care costs (discounted at 5%) would increase by about $2300. The cost-effectiveness of ticlopidine, compared with aspirin, is estimated to range from $31,200 to $55,500 per quality-adjusted life-year gained as the utility of life after nonfatal stroke is assumed to vary from 0.75 to 0.95.

Ticlopidine therapy to prevent stroke in high-risk patients is cost-effective by current standards of medical practice.
Sensory stimulation promotes normalization of postural control after stroke.
Authors: Magnusson M , Johansson K , Johansson B B
Published: June 2011

In a randomized study of hemiparetic stroke patients with a median age of 75 years, functional recovery was significantly better in those who received additional sensory stimulation (n = 38), including electrostimulation, than in control patients (n = 40) given the same physiotherapy and occupational therapy; group differences for balance, mobility, and activities of daily living were significant. The present study was designed to investigate postural control in patients who survived more than 2 years after stroke onset.

The 48 survivors (mean, 2.7 years; range, 2.0 to 3.8 years), 22 from the treatment group and 26 from the control group, were compared with 23 age-matched healthy subjects. Subjects were perturbed by vibrators applied to calf muscles or with galvanic vestibular stimulation. We evaluated postural control in terms of sway variances or sway velocities and the dynamics of postural control as a feedback system using system identification with a model previously validated for human postural control.

Significantly more patients of the treatment group than of the control group maintained stance during perturbations (P < .01). Among patients capable of maintaining stance during perturbation, the control patients were characterized by significant divergence from normal values in two of the three characteristic parameters of dynamic postural control (ie, swiftness and stiffness; P < .05) compared with the treatment subgroup or age-matched subjects.

The course of sensory stimulation enhanced recovery of postural function, an enhancement still significant 2 years after the lesion and treatment. The differences and near normalization of characteristic parameters of dynamic postural control among treated patients suggest that improved recovery after sensory stimulation may be achieved by patients regaining normal or near normal dynamics of human postural control.
Should cerebral ischemic events in cancer patients be considered a manifestation of hypercoagulability?
Authors: Chaturvedi S , Ansell J , Recht L
Published: June 2011

Previous studies, mainly autopsy-based, suggest that the spectrum of stroke in cancer patients differs from that of the general population. These studies also suggest that cerebrovascular events frequently are a manifestation of hypercoagulability. However, no studies that address this question in the adult oncological population from a clinical perspective are available. We therefore assessed the clinical impact of cerebral ischemic events in cancer patients and attempted to determine whether their occurrence represents a manifestation of Trousseau's syndrome.

A computerized database that records all neurological admissions and consultations at a tertiary medical center was used to retrospectively identify all patients with cerebral ischemic events and cancer.

Thirty-three patients representing 3.5% of all stroke consultations and admissions seen at the University of Massachusetts Medical Center were identified during the period 1988 through 1992. Large-vessel atherosclerosis was the most frequent cause of stroke. Furthermore, although 30% were determined to have hypercoagulability as a cause using clinical criteria, in only one of nine patients in whom tests were done was sufficient evidence present to make a presumptive diagnosis of disseminated intravascular coagulation. Irrespective of therapy, recurrent cerebral ischemic events were noted in only 6% of patients during a follow-up period averaging greater than 9 months, a figure that is similar to that for the risk of repeated events in the noncancer population.

Recognizing the limitations of this retrospective study, it appears nonetheless that conventional stroke origins account for the majority of cerebral ischemic events in the adult cancer population. Although hypercoagulability is present to a greater extent than in the nononcological population, recurrent strokes seem to occur no more frequently than in the nononcological population, and antiplatelet agents seem sufficient therapy for most patients.
Pretreatment of transient focal cerebral ischemia in rats with the calcium antagonist AT877.
Authors: Ohtaki M , Tranmer B
Published: June 2011

The efficacy of pretreatment with the recently developed intracellular calcium antagonist AT877 against transient focal cerebral ischemia was investigated in rats subjected to middle cerebral artery occlusion and reperfusion using the endovascular suture method.

Halothane-induced moderate hypotension (60 mm Hg) was used during 100 minutes of temporary middle cerebral artery occlusion. In the treated animals (n = 10), an intravenous infusion of AT877 (0.03 mg/kg per minute) was initiated 30 minutes before the ischemic event and continued during the ischemic period. The control rats (n = 10) received physiological saline in a similar fashion. Local cerebral blood flow was measured by the hydrogen clearance technique. Neurological examinations were performed daily during the 48-hour observation period, and infarct size was assessed by triphenyltetrazolium chloride staining.

A continuous infusion of AT877 significantly improved local cerebral blood flow during ischemia. The treated animals showed a better neurological outcome after a 24-hour observation period, and a significant reduction in ischemic brain injury resulted in both the neocortex (149 +/- 20 versus 41 +/- 14 mm3, P < .01) and the striatum (80 +/- 5 versus 46 +/- 8 mm3, P < .05). The size of the neocortical infarct was reduced, with increasing mean ischemic cerebral blood flow in the control and treated animals (r = .923, P = .0001).

AT877 pretreatment was effective in preventing brain injury during transient focal cerebral ischemia and improving neurological status. This beneficial effect seems to be mediated, in part, by its primary action of increasing cerebral blood flow.
Interrater agreement in evaluation of stroke patients with the unified neurological stroke scale.
Authors: Treves T A , Karepov V G , Aronovich B D , Gorbulev A Y , Bornstein N M , Korczyn A D
Published: June 2011

We sought to determine interrater agreement in evaluation of stroke patients with the Unified Form for Neurological Stroke Scales (UFNSS).

Fifty inpatients were independently examined by three neurologists. Kendall coefficients of concordance were computed for the different items of the UFNSS. There was a high concordance among the raters. The best agreements were obtained for motor functions and the worst for grading of eye movements.

The UFNSS was shown to be reliable for evaluation of motor functions, verbal communication, orientation, and vigilance in stroke patients.
A comparison of transesophageal echocardiography and transcranial Doppler sonography with contrast medium for detection of patent foramen ovale.
Authors: Jauss M , Kaps M , Keberle M , Haberbosch W , Dorndorf W
Published: June 2011

Patent foramen ovale as a possible stroke risk factor can be diagnosed with transcranial Doppler sonography (TCD) by detecting intravenous contrast medium crossing from the right to the left atrium. The present study evaluates the reliability of this method.

We performed TCD and transesophageal echocardiography simultaneously in 50 patients using galactose microbubbles. We observed bubble signals passing the middle cerebral artery in 7 patients less than 20 seconds after injection; we found positive TCD tests in 14 patients using the Valsalva maneuver. With transesophageal echocardiography patent foramen ovale could be detected in 15 patients (sensitivity, 0.93; specificity, 1; P < .01).

TCD with echo contrast is a reliable screening tool for patent foramen ovale. A standardized procedure including the Valsalva maneuver is essential to prevent false-negative results.
Central retinal artery occlusion from carotid dissection diagnosed by cervical computed tomography.
Authors: Rao T H , Schneider L B , Patel M , Libman R B
Published: June 2011

Carotid dissection may lead to many different types of neurological deficits, both transient and permanent.

We present a patient with an isolated central retinal artery occlusion who was found to have an ipsilateral carotid dissection by neck computed tomographic scan, later confirmed by angiography.

This is the first reported case of carotid dissection causing central retinal artery occlusion without any other neurological deficits. It demonstrates the diagnostic usefulness of computed tomographic imaging in such cases.