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PubMed2005

Initial ischemic event: perfusion-weighted MR imaging and apparent diffusion coefficient for stroke evolution.

PURPOSE: To prospectively determine if the degree of acute perfusion or diffusion abnormalities measured prior to treatment onset help predict the evolution of brain infarction on magnetic resonance (MR) images. MATERIALS AND METHODS: Local ethics committee approval and informed consent were obtained. On parametric maps obtained in 64 patients (mean age, 64 years +/- 13 [standard deviation]; 37 men and 27 women) with acute middle cerebral artery infarction, lesion volumetry was performed to determine time to peak, mean transit time, cerebral blood volume, and apparent diffusion coefficient obtained within 3 hours of symptom onset. The infarct lesions were assessed on T2-weighted MR images obtained at follow-up on day 8. Cerebrovascular changes were determined on MR angiograms. Inferential and correlation statistics were used. RESULTS: A perfusion delay of more than 6 seconds relative to the nonaffected hemisphere on time-to-peak maps helped to predict the lesion volume on T2-weighted images (r = 0.686, P < .001). In contrast, neither the volume nor the degree of the diffusion abnormality helped to predict the infarct volume (r < 0.46). This was because in one subgroup of patients there was an increase and in one subgroup there was a decrease in infarct volume on the T2-weighted images (P < .001). There was a greater prevalence (P < .02) of cerebral artery abnormalities in the patients with larger infarcts. Clinically, the neurologic impairment was more severe (P < .01) and the mean arterial pressure higher (P < .04) in these patients. CONCLUSION: The results suggest that in acute stroke the severity of the initial ischemic event as determined on time-to-peak maps indicates hemodynamic compromise in addition to internal carotid artery or middle cerebral artery occlusion, because of abnormalities in other cerebral arteries.

Adult↗
PubMedDate not supplied

N-terminal pro-brain natriuretic peptide levels are elevated in patients with acute ischemic stroke.

Brain natriuretic peptide (BNP) is a counterregulatory hormone released by the ventricles of the heart. Its main actions are natriuresis and vasodilation. The authors studied N-terminal pro-brain natriuretic peptide (NT-proBNP) levels soon after an acute ischemic stroke. They compared plasma NT-proBNP concentrations in 30 patients with an acute ischemic stroke with those of 30 controls. The 2 groups were adjusted for age and gender, and there were no significant differences in vascular risk factors and left ventricular systolic and diastolic function. Venous samples were collected within the first 11.8 +/-1.2 hours after the onset of symptoms and again on day 6. Brain computed tomography/magnetic resonance imaging (CT/MRI) was performed on the same days (day 0 and day 6) in order to assess the site (carotid or vertebrobasilar), cause (atherothrombotic, cardioembolic, or lacunar), and size (large, medium, or small) of the brain infarct. NT-proBNP levels were elevated in patients with acute stroke (129.9 +/-9.9 fmol/mL) compared with the controls (90.8 +/-6.3 fmol/mL, p <0.05). These levels remained elevated at day 6 (113.5 +/-13.0 fmol/mL). NT-proBNP at admission was significantly higher in cardioembolic compared with atherothrombotic infarctions. There was no correlation between circulating NT-proBNP and stroke topography, infarct size, or severity as assessed by the National Institutes of Health Stroke Scale (NIHSS) at any of the 2 time points (admission and day 6). NT-proBNP levels were raised in patients with acute ischemic stroke; this effect persisted until day 6. The authors suggest that neurohumoral activation occurs in patients with acute ischemic stroke, either reflecting a counterbalancing vasodilating response to the cerebral ischemia or direct myocardial dysfunction.

Aged↗
PubMed2000

Henoch-Schönlein purpura and stroke: antiphosphatidylethanolamine antibody in CSF and serum.

A 15-year-old girl with features of Henoch-Schönlein purpura and brain infarct had a transient IgA antiphosphatidylethanolamine antibody (aPE) in her serum and CSF that disappeared 5 months after presentation. Serum aPE is known to be associated with thrombotic events. The authors found no aPE in the CSF of two control individuals or in the serum of two patients with active Henoch-Schönlein purpura without neurologic involvement. The patient may represent a variant of antiphospholipid antibody syndrome.

Adolescent↗
PubMed1995

Neuropathologic findings after organ transplantation. An autopsy study.

Since 1972 organ transplantations of kidney, bone marrow, liver, heart and lung have been performed at the University Hospital of Essen, Germany. Out of 2535 transplantations until September 1993, autopsies were performed in 157 patients In 25 patients (15.9%) neuropathologic findings (n = 26) were found. In 97 autopsies after bone marrow transplantation, 9 patients (9.3%) exhibited a severe neuropathologic alteration. In six patients (6/9; 66.6%), necrotisizing toxoplasmose encephalitis was found. Other cases showed a septic-metastatic mycotic encephalitis with crypto-coccus neoformans and candida albicans (n = 2) and leucemia infiltrates (n = 1). Massive cerebral hemorrhage was the most frequent neuropathologic finding after liver (4/8) and kidney transplantation (3/6). In addition liver-transplanted patients exhibited septic-metastatic encephalitis (3/8) and embolic brain infarct (1/8) as well as cerebral metastases (2/6) and primary malignant cerebral lymphoma in kidney transplantation (1/6). CNS findings in five autopsies after heart-lung-transplantation were diverse. They comprised intracerebral hemorrhage, intravasal lymphoma and septic-metastatic encephalitis, respectively. In summary, neuropathologic autopsy findings after organ transplantation are diverse and preferentially comprise infections, cerebral hemorrhages, and malignant lymphomas. After bone marrow transplantation, the most frequent neuropathologic autopsy finding was toxoplasmose encephalitis and massive cerebral hemorrhages after liver and kidney transplantations.

Adolescent↗
PubMed2004

Neuroprotective and neurotrophic actions of the mood stabilizer lithium: can it be used to treat neurodegenerative diseases?

The mood stabilizing drug lithium has emerged as a robust neuroprotective agent in preventing apoptosis of neurons. Long-term treatment with lithium effectively protects primary cultures of rat brain neurons from glutamate-induced, NMDA receptor-mediated excitotoxicity. This neuroprotection is accompanied by an inhibition of NMDA-receptor-mediated calcium influx, upregulation of anti-apoptotic Bcl-2, downregulation of pro-apoptotic p53 and Bax, and activation of cell survival factors. Lithium treatment antagonizes glutamate-induced activation of c-Jun-N-terminal kinase (JNK), p38 kinase, and AP-1 binding, which has a major role in cytotoxicity, and suppresses glutamate-induced loss of phosphorylated cAMP responsive element binding protein (CREB). Lithium also induces the expression of brain-derived neurotrophic factor (BDNF) and subsequent activation TrkB, the receptor for BDNF, in cortical neurons. The activation of BDNF/TrkB signaling is essential for the neuroprotective effects of this drug. In addition, lithium stimulates the proliferation of neuroblasts in primary cultures of CNS neurons. Lithium also shows neuroprotective effects in rodent models of diseases. In a rat model of stroke, post-insult treatment with lithium or valproate, another mood stabilizer, at therapeutic doses markedly reduces brain infarction and neurological deficits. This neuroprotection is associated with suppression of caspase-3 activation and induction of chaperone proteins such as heat shock protein 70. In a rat model of Huntington's disease (HD) in which an excitotoxin is unilaterally infused into the striatum, both long- and short-term pretreatment with lithium reduces DNA damage, caspase-3 activation, and loss of striatal neurons. This neuroprotection is associated with upregulation of Bcl-2. Lithium also induces cell proliferation near the injury site with a concomitant loss of proliferating cells in the subventricular zone. Some of these proliferating cells display neuronal or astroglial phenotypes. These results corroborate our findings obtained in primary neuronal cultures. The neuroprotective and neurotrophic actions of lithium have profound clinical implications. In addition to its present use in bipolar patients, lithium could be used to treat acute brain injuries such as stroke and chronic progressive neurodegenerative diseases.

Animals↗
PubMed2005

Cerebral ischemia and brain histamine.

Cerebral ischemia induces excess release of glutamate and an increase in the intracellular Ca(2+) concentration in neurons, which provokes enzymatic process leading to irreversible neuronal injury. Histamine plays a role as a neurotransmitter in the mammalian brain, and histamine release from nerve endings is enhanced in ischemia by facilitation of histaminergic activity. Dissimilar to ischemia-induced release of glutamate, histamine release is gradual and long lasting. The enhancement may contribute to neuroprotection against ischemic damage, because suppression of histaminergic activity aggravates the histologic outcome caused by ischemia. Preischemic administration of histamine (i.c.v.) suppresses ischemic release of glutamate and ameliorates neuronal damage, whereas blockade of central histamine H(2) receptors aggravates ischemic injury. These suggest that histamine provides beneficial effects against ischemic damage through histamine H(2) receptors, when administered before induction of ischemia. Postischemic loading with histidine, a precursor of histamine, alleviates both brain infarction and delayed neuronal death. Since the alleviation is abolished by blockade of central histamine H(2) receptors, facilitation of central histamine H(2) action caused by histidine may prevent reperfusion injury after ischemic events. Because the ischemia-induced increase in the glutamate level rapidly resumes after reperfusion of cerebral blood flow, beneficial effects caused by postischemic loading with histidine may be due to other mechanisms besides suppression of excitatory neurotransmitter release. Anti-inflammatory action by histamine H(2) receptor stimulation is a likely mechanism responsible for the improvement.

Animals↗
PubMed1999

Risk factors for stroke in different levels of cerebral arterial disease.

BACKGROUND AND PURPOSE: Despite recent studies on risk factors of stroke, it is still unclear whether certain risk factors differently affect different levels of cerebral arteries in stroke patients. We attempted to study risk factors and lifestyle factors in patients with cerebrovascular diseases affecting different levels of the cerebral arteries. METHODS: We studied 343 Korean patients (222 men and 121 women) with acute stroke. Strokes were subdivided into large vessel infarction (LVI, n = 156), small vessel infarction (SVI, n = 105), intracerebral hemorrhage (ICH, n = 82) according to modified TOAST criteria. Patients with cardiogenic embolic infarction, undetermined causes, and miscellaneous causes were excluded. Among the patients with LVI and SVI, 104 and 49 underwent angiographic studies, respectively, who were designated as having definite LVI and definite SVI. Definite LVI was further subdivided into proximal LVI when the internal carotid artery (n = 25), vertebral artery (n = 13) or basilar artery (n = 14) were primarily involved, and distal LVI when the middle cerebral artery (n = 35), anterior cerebral artery (n = 7) or posterior cerebral artery (n = 10) were involved. Using a structured interview, we assessed the risk factors and lifestyles: hypertension, diabetes mellitus (DM), cigarette smoking (CS), alcohol consumption, physical activity and exercise, and the amount of consumption of salt, vegetables, fat, fish and fruits. Serum cholesterol, body mass index and total body fat were also measured. RESULTS: Multivariate analysis showed that in men, DM was a discriminant factor favoring brain infarction (BI) over ICH, definite LVI or ICH and proximal LVI over ICH. Decreased fruit intake differentiated distal LVI from definite SVI, and distal LVI from ICH. In women, DM and abdominal obesity differentiated BI from ICH, while DM favored definite LVI over ICH, proximal LVI over ICH and definite SVI over ICH. Multivariate analysis including sex as a separate variate showed that DM was a factor favoring BI over ICH, definite LVI over ICH, proximal LVI over ICH, distal LVI over ICH and definite SVI over ICH. CS was a factor favoring BI over ICH, while heavy CS was a factor discriminating distal LVI from definite SVI. Male sex was a factor favoring definite LVI over ICH and proximal LVI over ICH. A lesser amount of fruit consumption favored definite SVI over distal LVI. CONCLUSION: Our results demonstrate that DM in all sexes and central obesity in women are factors discriminating BI from ICH. However, these factors as well as others were not found to discriminate the sizes of the vessels involved in the patients with ischemic stroke, except that being male may be a factor favoring proximal large vessel disease over ICH. Genetic factors or other not yet identified risk factors may be responsible for the differences in the subtypes of ischemic stroke among different ethnic populations.

Adult↗
PubMed2004

A review of standing balance recovery from stroke.

Recently, interest in the mechanisms underlying balance recovery following stroke has grown, because insight into these mechanisms is necessary to develop effective rehabilitation strategies for different types of stroke. Studies dealing with the recovery of standing balance from stroke are, however, limited to rehabilitation inpatients with a unilateral supratentorial brain infarction or haemorrhage. In most of these patients, stance stability improves in both planes as well as the ability to compensate for external and internal body perturbations and to control posture voluntarily. Although there is evidence of true physiological recovery of paretic leg muscle functions in postural control, particularly during the first three months post-stroke, substantial balance recovery also occurs in patients when there are no clear signs of improved support functions or equilibrium reactions exerted through the paretic leg. This type of recovery probably takes much longer than 3 months. Apparently, mechanisms other than the restoration of paretic leg muscle functions may determine the standing balance recovery in patients after severe stroke. No information is available about the role of stepping responses as an alternative to equilibrium reactions for restoring the ability to maintain upright stance after stroke. The finding that brain lesions involving particularly the parieto-temporal junction are associated with poor postural control, suggests that normal sensory integration is critical for balance recovery. Despite a considerable number of intervention studies, no definitive conclusions can be drawn about the best approach to facilitate the natural recovery of standing balance following stroke.

Biofeedback, Psychology↗
PubMedDate not supplied

[An accident after an accident--an unusual death in a hospitalized patient].

The authors present a case of accidental fatal laryngopharyngeal obstruction with bolus of food, in hospital, in a patient who has been treated for twenty days because of injuries sustained in a traffic accident. The injuries were multiple fractures and brain contusions that were not clinically diagnosed, while their symptomatology (somnolence) was attributed to morbous lesions--multifocal brain infarction. Mechanical asphyxiation and death occurred when the patient was fed in hospital by his brother. Unofficially we got an information that whole event was very dramatical, and that medical staff tried to attempt resuscitative measures, but without any written note about that in medical documentation. The terminal phase of his chronic desompensated cardiomyopathia was clinically announced as a cause of death. For forensic pathologists it was relatively easy task to prove mechanical asphyxiation due to laringopharyngeal blockage as a real cause of death on medicolegal autopsy.

Accidents, Traffic↗
PubMed2005

Rapid tolerance to focal cerebral ischemia in rats is induced by preconditioning with electroacupuncture: window of protection and the role of adenosine.

The aim of the present study was to investigate the first protective window of preconditioning with electroacupuncture (EA) against focal cerebral ischemia, and to explore whether adenosine is involved in the rapid tolerance phenomenon. Sixty-four male Sprague-Dawley rats were randomly assigned to eight groups (n=8 in each). Animals in the control group received no treatment, and animals in EA1-EA4 groups received EA at 0.5, 1, 2 and 3 h before induction of focal cerebral ischemia, respectively. Rats in DPCPX group were intraperitoneally injected with 1 mg kg-1 8-cyclopentyl-1,3-dipropylxanthine (DPCPX), 3 h before induction of focal cerebral ischemia. Animals in vehicle group and EA+DPCPX group were pretreated with 1 ml kg-1 dimethyl sulfoxide (DMSO, the solvent of DPCPX) and 1 mg kg-1 DPCPX 30 min before preconditioning with EA, respectively. All rats were anesthetized with 40 mg kg-1 pentobarbital sodium intraperitoneally. Animals that required EA preconditioning, received EA with intensity of 1 mA and frequency of 15 Hz at the Baihui acupoint (GV 20) for 30 min. The focal cerebral ischemia was produced by the right middle cerebral artery occlusion (MCAO) for 120 min. The neurologic deficit scores (NDS) and brain infarct volumes were evaluated at 24 h after reperfusion. All rats survived until 24 h after reperfusion. Preconditioning with EA at 2 h before induction of focal cerebral ischemia improved neurologic outcome (P<0.05 versus control) and reduced the infarct volume (P<0.01 versus control) at 24 h after reperfusion. These beneficial effects were reversed by pretreatment with 1 mg kg-1 DPCPX, whereas this agent itself did not affect the NDS and volume in drug-ischemic controls after ischemia. The results show that preconditioning with single EA session induces rapid tolerance to focal cerebral ischemia. The rapid ischemic tolerance appears at 2 h (but not at 0.5, 1, or 3 h) after preconditioning, and is possibly mediated through an adenosine A1 receptor-related mechanism.

Adenosine↗
PubMedDate not supplied

Assessment of transient ischemic attack with diffusion- and perfusion-weighted imaging.

BACKGROUND: Diagnosing TIA can be difficult, since evidence of brain ischemia is habitually lacking on CT and conventional MR imaging. It has been suggested that patients with acute brain infarction on neuroimaging should be considered stroke cases instead of TIA, regardless of duration of symptoms, implying that optimal diagnostic methods need to be utilized. We therefore postulated that perfusion-weighted MR imaging (PW imaging) would be useful in the diagnosis of TIA. METHODS: Retrospective analysis of 22 patients with reversible neurologic symptoms lasting less than 24 hours, assessed with DW and PW imaging. RESULTS: MR imaging was abnormal in 15 patients (68%): 12 had abnormal DW imaging, four had both DW and PW imaging defects (all with a mismatch) and three had an isolated PW imaging abnormality. There were no differences in symptom duration, stroke etiology or cardiovascular risk factors between patients with abnormal MR imaging and those with unremarkable scan. Patients with mismatch were more likely to need conventional angiography or other cerebrovascular procedures. CONCLUSION: The combined use of DW imaging and PW imaging provided evidence of brain ischemia in most patients with clinical diagnosis of TIA. Prospective studies using follow-up MR imaging are required to determine the outcome of affected tissue, as well as the clinical implications of DW-PW imaging abnormalities.

Aged↗
PubMed2004

Rifampicin attenuates brain damage in focal ischemia.

Rifampicin is an antibacterial agent that is widely used in tuberculosis and leprosy therapy. Interestingly, some experimental studies indicate that rifampicin acts as a hydroxyl radical scavenger and a glucocorticoid receptor activator. In this study, the neuroprotective effect of rifampicin was evaluated after transient and permanent focal cerebral ischemia. Anaesthetized male C57BL/6j mice were submitted to permanent or transient thread occlusion of the middle cerebral artery (MCA). Reperfusion in transient ischemia was initiated 30 min later by thread retraction. Rifampicin or vehicle were applied intraperitoneally before permanent or immediately after 30 min of transient ischemia. Later, 24 h after permanent or transient ischemia, animals were re-anesthetized and decapitated. Brain injury was evaluated by triphenyltetrazolium chloride staining (TTC), terminal transferase biotinylated-dUTP nick end labeling (TUNEL) and cresyl violet staining. A 20-mg/kg sample of rifampicin showed a significant neuroprotection after cerebral ischemia. The number of TUNEL-positive cells in the striatum, where disseminated tissue injury was observed, was also reduced by application of rifampicin as compared with vehicle-treated animals. The present report shows that administration of rifampicin efficiently reduces brain injury after permanent and transient focal cerebral ischemia in mice.

Animals↗
PubMed1996

Registration and display of brain SPECT and MRI using external markers.

Accurate anatomical localisation of abnormalities observed in brain perfusion single-photon emission computed tomography (SPECT) is difficult, but can be improved by correlating data from SPECT and other tomographic imaging modalities. For this purpose we have developed software to register, analyse and display 99mTc-hexamethylpropyleneamine oxime SPECT and 1.0 T MRI of the brain. For registration of SPECT and MRI data external skin markers containing 99mTc (220 kBq) in 50 microliters of coconut butter were used. The software is coded in the C programming language, and the X Window system and the OSF/Motif standards are used for graphics and definition of the user interface. The registration algorithm follows a noniterative least-squares method using singular value decomposition of a 3 x 3 covariance matrix. After registration, the image slices of both data sets are shown at identical tomographic levels. The registration error in phantom studies was on average 4 mm. In the two-dimensional display mode the orthogonal cross-sections of the data sets are displayed side by side. In the three-dimensional mode MRI data are displayed as a surface-shaded 3 D reconstruction and SPECT data as cut planes. The usefulness of this method is demonstrated in patients with cerebral infarcts, brain tumour, herpes simplex encephalitis and epilepsy.

Brain↗
PubMed2002

Molecular mechanisms of cerebral ischemia-induced neuronal death.

The mode of neuronal death caused by cerebral ischemia and reperfusion appears on the continuum between the poles of catastrophic necrosis and apoptosis: ischemic neurons exhibit many biochemical hallmarks of apoptosis but remain cytologically necrotic. The position on this continuum may be modulated by the severity of the ischemic insult. The ischemia-induced neuronal death is an active process (energy dependent) and is the result of activation of cascades of detrimental biochemical events that include perturbion of calcium homeostasis leading to increased excitotoxicity, malfunction of endoplasmic reticulum and mitochondria, elevation of oxidative stress causing DNA damage, alteration in proapoptotic gene expression, and activation of the effector cysteine proteases (caspases) and endonucleases leading to the final degradation of the genome. In spite of strong evidence showing that brain infarction can be reduced by inhibiting any one of the above biochemical events, such as targeting excitotoxicity, up-regulation of an antiapoptotic gene, or inhibition of a down-stream effector caspase, it is becoming clear that targeting a single gene or factor is not sufficient for stroke therapeutics. An effective neuroprotective therapy is likely to be a cocktail aimed at all of the above detrimental events evoked by cerebral ischemia and the success of such therapeutic intervention relies upon the complete elucidation of pathways and mechanisms of the cerebral ischemia-induced active neuronal death.

Animals↗
PubMed1996

Combination tissue plasminogen activator and ticlopidine therapy in a rabbit model of acute thromboembolic stroke.

The successful application of thrombolytic therapy to acute myocardial infarction has prompted a reinvestigation of thrombolytic therapy for acute stroke. However, an examination of safety and efficacy of thrombolytic therapy in acute thromboembolic stroke has precluded the entry of patients taking either antiplatelet or anticoagulant therapy. It was therefore of interest, in an established rabbit model of thromboembolic stroke, to examine the use of tissue plasminogen activator therapy in combination with ticlopidine treatment. Following ticlopidine administration (10 mg kg-1, i.v., daily for 5 days), rabbits (n = 7) were embolized by injecting a tin-laden clot into the internal carotid artery with clot placement confirmed by x-ray. Three hours later, t-PA was initiated as a square-wave pulse (6.3 mg kg-1 total dose, given as a 20% bolus, with the remainder administered over 2 h as a continuous infusion). The protocol was continued for a total of 7 h following embolization. Complete clot lysis was demonstrated in 6 of 7 animals. Brain infarct size (triphenyltetrazolium chloride staining) was 36.0 +/- 12.9% hemisphere (mean +/- SEM). Both clot lysis rate and infarct size were very similar to that previously seen following administration of t-PA alone (58% and 31.6 +/- 6.4% hemisphere, respectively) but in marked contrast to previous results seen with intravenous aspirin (no clot lysis). These results suggest that antiplatelet agents used clinically for stroke prophylaxis (aspirin or ticlopidine) may influence the success rate of thrombolysis following initiation of thrombolytic therapy for acute thromboembolic stroke.

Animals↗
PubMed2004

Repetitive transcranial magnetic stimulation as treatment of poststroke depression: a preliminary study.

BACKGROUND: Depression has a significant impact on poststroke recovery and mortality. There are a proportion of patients with poststroke depression (PSD) who do not respond to antidepressants. Repetitive Transcranial Magnetic Stimulation (rTMS) might be a safe and effective alternative in these refractory cases. METHODS: We conducted a randomized, parallel, double-blind study of active versus sham left prefrontal rTMS in patients with refractory PSD. After discontinuing antidepressants, patients were randomly assigned to receive 10 sessions of active (10 Hz, 110% of the motor threshold, 20 trains of 5 seconds duration) or sham left prefrontal rTMS. Efficacy measures included HAM-D scores, response and remission rates. Patients completed a neuropsychological battery at baseline and after completing the protocol. RESULTS: When compared with sham stimulation, 10 sessions of active rTMS of the left dorsolateral prefrontal cortex were associated with a significant reduction of depressive symptoms. This reduction was not influenced by patient's age, type or location of stroke, volume of left frontal leukoaraiosis or by the distance of the stimulating coil to the prefrontal cortex. However, there was a significant positive correlation between the percentage of reduction of Ham-D scores and frontal gray and white matter volumes. There were no significant changes in cognitive functioning between the active and the sham stimulation groups. In addition, there were few and mild adverse effects that were equally distributed among groups. CONCLUSIONS: Taken together, these preliminary findings suggest that rTMS may be an effective and safe treatment alternative for patients with refractory depression and stroke.

Aged↗
PubMed2006

Interleukin-12 in acute ischemic stroke patients.

Cytokines are important mediators of stroke-induced immunological/inflammatory reaction which contributes to brain infarct progression as well as to the disease severity and outcome. The aim of the study was to evaluate the levels of the proinflammatory and immunomodulatory cytokine interleukin-12 (IL-12) in serum of acute ischemic stroke patients, and to investigate the relation between these levels and demographic, laboratory, neuroimaging, and clinical data. The study comprised 23 first-ever ischemic stroke patients and 15 age- and sex-matched controls. Blood sampling for the determination of IL-12 and such peripheral markers of inflammation as erythrocyte sedimentation rate (ESR) and leukocyte count, together with cranial CT were performed within 24 h of stroke, while neurological and functional deficits were estimated, respectively, with the Scandinavian Stroke Scale (SSS) and Barthel Index (BI) within the same period and two weeks later. Stroke patients displayed significantly higher serum IL-12 levels in comparison with controls. The serum IL-12 levels in stroke patients correlated significantly with the ESR values, the volume of early brain CT hypodense areas, and with the SSS and BI scores calculated within both studied times. The results indirectly suggest that IL-12 may play a role in the pathophysiology of ischemic stroke.

Aged↗
PubMed1981

[Transient loss of consciousness in ischaemic cerebral events. A study of 557 ischaemic strokes and transient ischaemic attacks (author's transl)].

A study was done of 31 episodes of transient loss of consciousness occurring at the onset of 557 cerebral ischaemic events selected on the basis of a well known mode of onset, excluding prolonged comas. The following conclusions can be drawn: Transient loss of consciousness is uncommon in ischaemic strokes (6.5 p. cent), occurring twice as often in cardiac emboli (13.2 p. cent) as in a atherothrombotic brain infarction (6.2 p. cent), and more often in carotid (8.4 p. cent) than in vertebro-basilar (5.7 p. cent) territory. The incidence is however similar in both territories (4.6 p. cent and 4.8 p. cent) when epilepsy is excluded. Epilepsy accounts for nearly half (3.8 p. 100) of all losses of consciousness in hemispheric strokes, but was encountered neither in lacunar strokes nor in transient ischaemic attacks (T.I.A.). Transient loss of consciousness is uncommon in basilar TIAs, and extremely rare in lacunar strokes (1.5 p. 100) and in carotid TIAs (0 p. 100). Presumed mechanisms and practical implications are discussed.

Aged↗