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Although a growing body of research links leadership behavior to follower health, comparatively little is known about the health effects of being in the lead. This longitudinal study of 315 team members and 67 leaders examined the crossover of emotional exhaustion and work engagement from followers to leaders. Leader emotional self-efficacy was tested as a moderator in the crossover process. Multiple regression analyses revealed that followers' work engagement was positively related to leaders' work engagement eight months later, controlling for followers' tenure with the leader, leader gender, autonomy, workload, and work engagement at Time 1. Leaders' emotional self-efficacy did not moderate the crossover of work engagement. Followers' emotional exhaustion was not directly related to leaders' emotional exhaustion over time. We did find a significant interaction effect for follower emotional exhaustion and leader emotional self-efficacy. This study is the first to show that crossover of emotional exhaustion and work engagement can unfold over time from team members to leaders. Main theoretical implications lie in the finding that-in line with job demands-resources theory-followers' psychological states can pose a demand or resource for leaders, and influence their well-being. For practitioners, our results offer valuable insights regarding the design of organizational health interventions as well as leadership development measures. (PsycINFO Database Record, ((c) 2016 APA, all rights reserved).)

Research has shown that self-efficacy is often one of the most important personal resources in the work context. However, because this research has focused on cognitive and task-oriented self-efficacy, little is known about social and emotional dimensions of self-efficacy at work. The main aim of the present study was to investigate social and emotional self-efficacy dimensions at work and to compare them to a cognitive and task-oriented dimension. Scales to measure social and emotional self-efficacy at work were developed and validated and found to be well differentiated from the cognitive task-oriented occupational self-efficacy scale. Confirmatory factor analyses of data from 226 Swedish and 591 German employees resulted in four separate but correlated self-efficacy dimensions: (1) occupational; (2) social; (3) self-oriented emotional; and (4) other-oriented emotional. Social self-efficacy explained additional variance in team climate and emotional self-efficacy in emotional irritation and emotional exhaustion, over and above effects of occupational self-efficacy. Men reported higher occupational self-efficacy, whereas social and emotional self-efficacy revealed no clear gender differences. The scales have strong psychometric properties in both Swedish and German language versions. The positive association between social self-efficacy and team climate, and the negative relationships between self-oriented emotional self-efficacy and emotional irritation and emotional exhaustion may provide promising tools for practical applications in work settings such as team-building, staff development, recruitment or other training programs aiming for work place health promotion. The next step will be to study how social and emotional self-efficacy relate to leadership, well-being and health over time., (© 2016 Scandinavian Psychological Associations and John Wiley & Sons Ltd.)

Objective: The mechanism underlying cerebral infarction in the borderzone between the territories of deep and superficial perforating arteries has not yet been clarified. This study was performed to investigate the prevalence, volume, site, and etiology of this type of subcortical infarction in a large unselected group of stroke patients., Methods and Patients: We analyzed a continuous series of 383 patients with recent cerebral infarction observed in our Stroke Unit. Patients underwent a complete clinical and instrumental workup. The subgroup of subjects with internal borderzone infarct alone were compared with the subgroups of patients with other types of cerebral infarcts by uni- and multivariate statistical tests., Results: There were 90 internal borderzone infarcts of 725 ischemic lesions (12%of the total), with a median volume of 0.32 ml (95% confidence interval 0.24-0.44; range: 0.012- 20.2 ml). Internal borderzone infarcts alone occurred in only 13 of 383 (3.4%) patients. A comparison between patients with 'pure' internal borderzone infarction and patients with other types of cerebral infarcts by multiple logistic regression analysis demonstrated a significant independent causal role of carotid stenosis or occlusion., Conclusion: Our study suggests that 'pure' internal borderzone infarctions are quite rare findings in patients with ischemic stroke, and that the hemodynamic impairment due to atherosclerotic occlusion or stenosis of the carotid system could be the cause in the large majority of cases.

We studied 383 consecutive patients with stroke and ischemic lesions on CT scan for the presence of symptomatic cerebral infarction (SCI) and asymptomatic cerebral infarction (ACI). We evaluated risk factors as well as volume, site and number of the lesions. ACIs occurred in 34% of the cases (130/383); 88% of ACIs were lacunes and internal borderzone infarctions, with a volume of less than 2 ml. Larger infarctions were asymptomatic in 27 patients (20.8%); 114 (68.7%) out of 166 patients with two or more SCIs (68.7%) had one or more ACIs. Infarctions in the lateral middle cerebral artery (MCA) territory were SCIs, in the medial MCA territory ACIs. Independent risk factors for ACI were age above 70 years and smoking; cardioembolism prevailed in SCI, small vessel disease in ACI; high levels of disability prevailed in SCIs.

The following points should be considered in dealing with dementia occurring in patients with lacunar infarctions. Lacune is a pathological term and its definition rests on its size (from 2 to 15 mm in diameter). However, terms such as lacunar syndromes and lacunar infarctions are currently used in clinical parlance and recent papers. Patients with lacunar infarctions differ from patients with large infarctions, being more often hypertensive, showing a characteristic but not specific clinical syndrome, and disclosing a significantly lower recurrence rate for new episodes and a significantly higher survival rate. Patients with lacunar infarctions develop a state of dementia 5 times as often as the general population and 25 times as often as in the age group of our patients (65-69 years). Leukoaraiosis, significantly related to arterial hypertension, to lacunar infarction, to an extra risk of future stroke, may be considered an increased risk of cerebral vascular lesions possibly leading to dementia. The relationship between vascular lesions and dementia includes: the strategic location of the lesion (thalamus, corticothalamic areas, bilateral lesions); the whole cerebral hypoperfusion apart from the infarcted area, as shown by PET and SPET; remote effects of cerebral infarctions (diaschisis phenomenon); the so-called incomplete infarction; cerebral atrophy and, particularly, the enlargement of cerebral ventricles, significantly higher in patients with lacunes and dementia as compared with patients with lacunes without dementia.(ABSTRACT TRUNCATED AT 250 WORDS)

By means of transthoracic contrast echocardiography, the prevalence of a patent foramen ovale (PFO) was studied, in a continuous series of 48 patients aged less than 50 years with a recent episode of acute cerebral ischemia. A PFO was found in 11 subjects (23%). In the subgroup of younger patients (aged less than 30 years), the prevalence was much higher than in those aged 30 or more (58% against 11%, p = 0.0022). In the 19 patients with clear evidence of extracardiac causal factors of cerebral ischemia, there was no PFO; of the remaining 29 subjects, a PFO was present in 11 (38%) (p = 0.0015). In conclusion, the possible presence of a PFO must be carefully investigated in subjects with cerebral ischemia aged less than 30, as well as in subjects aged between 30 and 50 in whom there is no acceptable explanation for their cerebral ischemic episode.

Previous experimental studies have shown that the simultaneous administration of gamma-aminobutyric acid (GABA) and phosphatidylserine (PS) can exert an anticonvulsant activity in different seizure models; moreover, a preliminary trial showed some effect of the association GABA-PS in patients with absence seizures. The aim of this study was to investigate the antiepileptic properties of GABA-PS in the model of human photosensitivity. Nine patients with epilepsy associated with an EEG pattern of photoconvulsive response at intermittent photic stimulation entered a 3-day study. The photosensitivity range (PSR) was determined at hourly intervals both in basal conditions and after the administration of a single oral dose of GABA (3000 mg) and PS (600 or 1200 mg). The administration of GABA-PS was not associated with any systematic changes of PSR, nor with any significant differences of time course profiles on each daily session. No correlation was found between PSR percent deviations from baseline and GABA serum levels. These results indicate that a single acute administration of GABA-PS has no effect in the human photosensitivity model, and suggest that the efficacy of GABA-PS in human epilepsy, as shown by a preliminary investigation, may possibly require chronic administration.

Data on efficacy and safety of vigabatrin over very protracted treatment periods are still limited. This study reports the follow up of 23 responder epileptic patients who continued vigabatrin treatment after completion of the first year, to an overall long-term exposure ranging 21-84 months (median 60; mean 58.0 +/- 24.0 sd). The seizure frequency during the follow up was compared with that at the end of the first year on vigabatrin. The rates of patients who gained a further improvement and those who deteriorated were almost identical, ranging 33-45% and 33-46% respectively at individual time points. At the trial endpoint, nine patients (39%) were improved, five (22%) were unchanged and nine (39%) showed some deterioration. All patients still had a 14-100% decrease of seizure frequency as compared with pretreatment baseline. Two patients discontinued vigabatrin for occasional reasons. No patient experienced new adverse events during the follow up after the first year on vigabatrin. No significant effects were noted on any of the routine hematologic or metabolic screening assessments. Although reduction of concomitant treatment was rarely possible, the overall number of associated antiepileptic drugs dropped from 42 at entry to 40 at the trial endpoint. These findings indicate that vigabatrin retains its efficacy and safety in responder patients for periods up to 7 years.

The effect of electric shock convulsions (ESC) on the function of brain cortex GABAA receptors has been studied in the rabbit. Three single electroconvulsive shocks (ECS) were given at intervals of 48 hours and the brain cortex was sampled 36 hours after the last shock. The dose-response curve was determined for GABA-stimulated 36Cl-accumulation into brain cortex microsacs. The parameters of the curve (maximal accumulation rate, Ka and Hill coefficient, n) were constant when determined in two different series of experiences. Animals handled in the same way as the animals from the electric shock group but which did not receive the ECSs (sham ECS group) showed similar maximal accumulation rate and Ka. However, the average n coefficient was significantly higher in the electric shock group. Naive animals, taken from their cages just before the sacrifice, showed dose-response curves which varied from one experimental series to another. This last result (confirming previous observations) shows modifications and inconsistencies in the evaluation of GABAA receptor function in stressed handling-naive animals.

The i.p. injection in rats of GABA (740 mg/Kg) after sonication with an equal amount of phosphatidylserine (PS) has an antiepileptic effect. The injection of plain GABA has no such an effect. Blood, brain and synaptosomal accumulation of exogenous labeled GABA under the two circumstances are evaluated. In the case of GABA/PS injection there is a higher passage of the exogenous labeled neurotransmitter into the blood and brain nerve endings (synaptosomes). A higher synaptosomal accumulation of the exogenous labeled neurotransmitter is found even when GABA and PS are injected separately. Since these accumulation increases occur at a time when there is the antiepileptic effect, they seem relevant to it. Our interpretation of the chain of the events resulting in the antiepileptic action is that the phospholipid facilitates from the beginning the first passage of the exogenous neurotransmitter form the peritoneum to the blood. Then a higher passage to the brain tissue and eventually to the GABA-ergic nerve endings ensues. The brisker accumulation of the exogenous neurotransmitter in the nerve endings could be at the basis of a more efficient GABA-ergic inhibitory control in the brain.

Although vigabatrin is a promising new antiepileptic drug, its safety has been challenged by the report of dose-dependent central nervous system myelin vacuolation in some preclinical animal studies. Since it has been shown that vacuolation is associated with specific magnetic resonance imaging (MRI) findings in rats and dogs, MRI of the brain was performed in 11 patients with complex partial seizures who had been receiving vigabatrin for 64-78 months (mean 74.0 +/- 5.0 sd) as additional treatment for epilepsy, with a cumulative exposure ranging 4200 to 9360 g. In no case did MRI show white matter changes similar to the pathological findings of microvacuolation observed in animals. These results would appear to confirm that current doses of vigabatrin do not cause myelin vacuolation in humans, even for treatment periods of longer than 5 years.

The accumulation of labeled GABA into brain and brain nerve endings was studied in the adult rat after i.p. injection of large doses of neurotransmitter (740 mg/Kg). In the first 5-30 minutes after the injection the exogenous neurotransmitter reaches a stable plasma level of around 5 mM. The accumulation of radioactive GABA into the brain presents a latency of a few minutes from the time of the injection. Thereafter, the accumulation of the neurotransmitter is almost linear with time. Once in the brain tissue labeled GABA is in part broken down. The exogenous neurotransmitter is taken up in GABA-ergic nerve endings with a steep increase between 20 and 30 minutes after the injection. From a quantitative point of view, the data show that the brain accumulation of labeled GABA at 30 minutes post injection is minimal in the respect of the steady state average concentration of the endogenous neurotransmitter (0.014%). However, the amount of radioactive GABA which accumulates in the nerve endings, at the same post injection time, is around 7% of the endogenous neurotransmitter in that compartment. The data thus show a selective enrichment of exogenous systemic GABA in a physiologically important compartment of the brain.

We studied immunocytochemically with 2 amyloid beta protein (ABP) antisera brains from 5 non-demented elderly subjects with evidence of diffuse periventricular white matter hypodensity on computed tomography. In periventricular white matter of all brains we found ABP reactive deposits arranged around small vessels walls. Furthermore ABP reactive deposits, identical to those currently called diffuse plaques, were detected in neocortex in amount proportional to that of white matter deposits. We suggest that ABP microangiopathy and parenchymal deposition is responsible of white matter rarefaction in a subset of cases with a diffuse hypodensity on CT scan which has been called leukoaraiosis.

The efficacy of Cyproheptadine, a serotonin antagonist, in preventing the cerebral ischemic damage was tested on experimental model of transient global cerebral ischemia in Mongolian Gerbil. The semi-quantitative histological evaluation of the severity of ischemic damage showed a protective effect of Cyproheptadine, mainly in the anterior cortical areas.

We immunocytochemically analyzed pieces of olfactory mucosa removed by biopsy in 8 patients with probable Alzheimer's disease (AD) and 6 age-matched controls, with tau and ubiquitin antisera. There were tau-reactive and, partially, ubiquitin-reactive dystrophic neurites in the lamina propria of olfactory mucosa in all AD cases. The tau-reactive neurites contained abnormal straight filaments, 15 to 18 nm in diameter, morphologically identical to those found in AD cerebral brain tissue obtained at autopsy. Tau and ubiquitin immunoreactivity were absent in controls. If these neuritic alterations are confirmed in a larger number of cases, analysis of olfactory mucosa may increase the current reliability of clinical diagnosis of AD.

Pancreatic cysts and pseudocysts had to be treated by surgery until 15 years ago. Nowadays they can be aspirated (or drained) either endoscopically or by ultrasonic and computed tomographic guided punctures. The aim of this study was to see if these non-surgical treatments were efficient enough among the actual treatments. From 1984 to 1988, 33 patients were admitted in one single institution with a pancreatic cyst or pseudocyst, 22 of which were a consequence on an acute pancreatitis and 11 complicated a chronic pancreatitis. Ten cysts were connected with the Wirsung channel while 11 others were not, but the ERCP failed to give any accurate information on this point in 12 cases. As a first treatment, we abstained of any invasive procedure in 9 cases, 18 were treated by percutaneous aspiration guided by ultrasound and 6 patients underwent surgery. The mean follow-up was 30 months. All the patients who had no treatment remained symptom free; their cysts improved in 5 cases and disappeared in 4 cases. Among the cysts treated by percutaneous aspiration, 4 had to be operated, 5 disappeared, 3 improved and 6 recurred; the percutaneous aspiration obtained a lasting symptoms' relief for these patients, whatever the connection the cyst had with the Wirsung channel. This study suggests that percutaneous aspiration or drainage guided by ultrasound may be a treatment of the highest quality for acute and chronic pancreatitis cystic formations. However, it seems to act upon the symptoms rather than upon the cystic formations themselves.

The effects of intraperitoneal injection of 2-amino-5-phosphono-valeric acid (APV) on EEG-monitored penicillin-induced epileptic activity in rats were evaluated. A significant decrease in the frequency of spikes occurred with low APV dosages (10 and 20 mg/kg), while an almost complete disappearance of spike activity was observed at higher APV doses (40 and 160 mg/kg). Our data suggest that excitatory amino acids play a relevant role in penicillin-induced epileptic activity in rats.

The permeation of labeled Cl- ions across single plasma membranes from Deiters' neurons has been studied in the presence of various concentrations of phosphatidylserine (PS) on their extracellular side. PS reduces significantly basal Cl- permeation only at 10(-5) M on the membrane exterior. No effect was found at other concentrations. GABA activable 36Cl- permeation is heavily reduced and almost abolished at 10(-11) - 10(-5) M phosphatidylserine. This exogenous phosphatidylserine effect is difficult to interpret in relation to the function of the endogenous phospholipid. However, it may be involved in the epileptogenic effect in vivo of exogenous phosphatidylserine administration to rats.

In about 30% of the cases suffering from MID an unequivocal diagnosis can be made only on the basis of histopathological evidence. The imperfect diagnosis has a relevant impact on the methodology to be followed in therapeutic trial. The following points have to be considered in a therapeutic trial: (1) distribution of the patients expected to come to the observation, (2) the expected effectiveness of the treatment, (3) the likelihood of obtaining statistical significant results and (4) the required size of the study. The diagnostic inaccuracy gives rise to a decrease in the chance of yielding a statistically significant result and on the other hand produces an increase in the required number of subjects to be submitted to the trial.

61 of 1,590 (3.8%) patients with cerebrovascular disease showed suprabulbar palsy of the pure form (42 patients; 2 had autopsy) and striate form (19 patients; 3 had autopsy). 25 patients with the pallidopyramidal syndrome were included since the clinical picture bordered on the striate form. The pure variety was characterized by dysarthria, dysphagia and automatic voluntary dissociation of facial movements. Half of the patients also had hemiparesis, primitive reflexes and short-step gait. In the striate form, the main signs were dysarthria, dysphagia, automatic voluntary dissociation, rigidity and hypokinesia. Brisk tendon reflexes, primitive reflexes, short-step gait and mental deterioration were also present in half of the patients. The pure variety was caused by multiple infarcts and/or lacunae (85.7%), while the striate form had vascular lesions by computed tomography in only 36.8% of the cases. Histological findings, showing lipohyalinosis of the arterial wall leading to stenosis and occlusion of the lumen and tissue rarefaction and disintegration, support the assumption that microinfarctions, sometimes found only by histopathological examination, are the leading pathogenetic factor in this form. Hypertension, cardiopathy, smoking habit, dyslipemia and diabetes are the most frequent risk factors in both forms.

CSF endorphins levels have been measured in neuropsychiatric patients, in relation to controls. The results we obtained don't allow us to suggest any specific pathophysiological role to endorphins; their levels seemed to be modified in relation to a generic stress-response.

The efficacy and safety of oral vigabatrin (VGB) as add-on therapy in the long-term treatment of poorly controlled epilepsy were evaluated in 19 patients with complex partial seizures, either with or without secondary generalization. The study was run with a single-blind, placebo-controlled, crossover design, and included 2 months of placebo and 13-15 months of treatment with VGB, at doses ranging from 1 to 4 g/day. Of the 14 patients who completed the trial, 2 were seizure free, in 5 seizure frequency dropped by more than 75% and in another 5 by more than 50% with respect to baseline. The decrease in seizure frequency in the group as a whole was significant at all observation points of the trial. Three patients were not entered into the long-term phase due to lack of improvement (an increase in seizure frequency was observed in one of them), and 2 were excluded later because improvement disappeared leading to unauthorized changes in comedication. Side effects were mild and never caused discontinuation of treatment. In conclusion, VGB showed a remarkable efficacy and safety in the long-term treatment of complex partial seizures.

The term lacuna or lacunar cavity defines the pathological lesion while the clinical pictures due to lacuna or lacunes are referred to as 'lacunar syndromes'. The lacunar syndromes include: (1) the typical lacunar syndromes or lacunar syndromes proper--pure motor hemiplegia, pure sensory stroke, ataxic hemiparesis including dysarthria and clumsy hand, sensorimotor stroke and abnormal movement syndromes, (2) reversible ischemic attacks (TIA and/or PTIA or RIND), (3) other clinical syndromes which may be due to lacunar lesions such as suprabulbar palsy; lacunar dementia, or subacute arteriosclerotic encephalopathy (or Binswanger's disease). The different clinical pictures are reviewed, some mechanisms underlying the lacunar lesion are briefly discussed and the old label 'small vessel diseases' in cases with lacunes is reconsidered.

Late-onset focal epileptic seizures occurred in 8 patients with ischemic cerebro-vascular disease (ICVD) and were associated with TIAs in 6 of them. History, physical, laboratory, ancillary examinations and follow-up revealed no other disease which might be responsible for the seizures. Moreover, time of onset and appropriate signs of ICVD suggested that transient cerebral ischemia was the most likely cause of seizures.

The effect of the combined administration of gamma-aminobutyric acid (GABA) and phosphatidylserine was evaluated in a pilot study of 42 patients with drug-resistant epilepsy. The group included patients with complex partial seizures, simple partial seizures and absence seizures. Patients with complex partial seizures and simple partial seizures showed no significant improvement; on the other hand, there was a remarkable decrease in absence seizures, linearly related to the dose of GABA and phosphatidylserine. Side effects occurred in 9 patients and were usually mild.

The clinical definition of transient ischemic attacks (TIAs), besides the ischemic pathogenesis is based (i) upon 24 h. duration and (ii) complete reversibility. The limit of 24 h. has been chosen arbitrarily and episodes clearing completely after more than 24 h. do exist. In addition TIAs lasting less than 5 min. would have a higher incidence of subsequent completed stroke. Complete reversibility has also been disregarded: ischemic attacks leaving slight neurological deficits or showing an hypodense area at CT scanning have been shown to have the same significance at TIAs. Different clinical definitions and classifications account for very different natural history features reported in the literature. Transient attacks may be conveniently assessed under the label of Reversible Ischemic Attacks (RIA) covering attacks of 24 h. duration (TIA) and attacks of more than 24 h. duration (Protracted Transient Ischemic Attacks. PTIA). Terms such a RIND or PRIND (Reversible Ischemic Neurological Deficit or Prolonged Reversible Ischemic Neurological Deficit) should be disregarded since they are too general terms covering both cases with 24 and more than 24 h. duration. TIAs and PTIAs should be characterized by a complete clinical regression and normal CT, to avoid relevant wrong diagnostic statements (transient attacks in cases of lacunar stroke, hemorrhages, tumours); where clinical regression is partial and/or CT shows low attenuation areas the case should be labelled as one with partial non progressing stroke (PNS) or minor stroke. The question however arises whether TIA, PTIA or PNS significantly differ from each other from the clinical, prognostic and therapeutic standpoint or, on the contrary, any attempt to differentiate them on these grounds should be considered futile as suggested be Caplan (1983).(ABSTRACT TRUNCATED AT 250 WORDS)

The natural history and follow-up (5-7 years) of 76 patients with transient ischemic attacks (TIA), 45 patients with protracted transient ischemic attacks (PTIA), 85 patients with minor strokes (labelled as partial nonprogressing stroke; PNS) has been studied with the purpose of a comparative evaluation, since TIA, PTIA and PNS are often grouped together. Multiple attacks significantly recurred more frequently in patients with TIA and PTIA with respect to those with PNS. Patients with PNS significantly survived the follow-up with respect to patients with TIA and PTIA. At present, the distinction into TIA, PTIA and PNS should be maintained. Vascular surgery in cases with PNS should not be regarded a reasonable therapeutic strategy except in some individual cases.

The clinical diagnosis of dementia includes medical history, neurological examination, psychiatric interview and dementia scale. The identification of conditions producing dementia can only be achieved by adding to the clinical information the data gathered from ancillary investigations. The usual ancillary diagnostic investigations (biochemical tests, cerebrospinal fluid (CSF), EEG, CT, MRI, angiography) can rather easily identify brain disorders due to tumors, vascular malformations, hematomas, infections, toxins and drugs, deficiency diseases, normal-pressure hydrocephalus, metabolic and endocrine derangements. The differential diagnosis between degenerative and vascular dementia needs laboratory tests such as CSF, EEG, Somatosensory Evoked Potentials, CT (which constitutes a major role in a modified ischemic score) and MRI. The three final diagnostic labels are possible, probable and definite vascular dementia, which include clinical features and laboratory investigations concurrently confirming the diagnosis. If ancillary investigations fail to show multiple infarct lesions or if mixed forms are suspected an unequivocal diagnosis can be made only on histopathological evidence.

To assess the relationships between the efficacy and blood levels of progabide (PGB) and its active acidic metabolite (PGA) in epileptics, observations were carried out on 89 adult patients with epilepsy of different types and severity in two groups at Paris and Genoa. The Paris group received progabide in addition to other antiepileptic drugs for 6 to 12 months, whereas the Genoa group received a polytherapy for the first two months then a monotherapy with progabide alone for up to 22 months. Blood levels from monthly or bimonthly samples were significantly higher in both surveys when there was a satisfactory therapeutic response and levels were also higher in those receiving monotherapy suggesting a synergism among antiepileptic drugs. It is concluded that therapeutic drug monitoring of PGB and PGA blood concentrations may be a useful technique in optimizing progabide treatment in epileptic patients.

The natural history represents a basic reference point for evaluating temporal profile of a disease as well as the effect of the employed therapy. The incidence and the risk factors of the subarachnoid hemorrhage due to single aneurysm are presented. In particular the survival rate and mortality are evaluated in conservative treated group versus radical surgery group. The most relevant factors that affect survival are: time and clinical grades of severity. The best chance of alternating overall mortality from subarachnoid hemorrhage due to aneurysm seems to be: surgery within 1-2 days or secondary prevention.

Fifty-one brains showing lacunae and 30 with cribriform cavities have been identified out of 191 examined brains. A histologic and immunohistochemical study with the peroxidase-antiperoxidase method for glial fibrillary acidic protein has been carried out in selected cases. The number, site, associated arterial lesions and the microscopic appearance of lacunae and cribriform cavities are reported. Lacunae are small cavities usually, but not always due to softenings; cribriform cavities are dilatations of the perivascular space. Two types of cribriform cavities have been identified, according to the histological appearance of the surrounding tissue: type 1 with normal and type 2 with rarefied and abnormally gliotic surrounding nervous tissue. Sixteen cases showing a cribriform state in the basal ganglia exhibited a pseudobulbar palsy or extrapyramidal rigidity. Pseudobulbar palsy of striate form or parkinsonism may be ascertained in some cases only by histological and immunohistochemical examination.

A clinicopathological study of a patient with a 'locked-in syndrome' due to an acute inflammatory polyradiculoneuropathy is reported.

In a consecutive series of 1018 cases of focal cerebro-vascular disease there were 42 cases of stroke followed by a full recovery after a variable time interval from 4 to 60 days. Some clinical features deserve mention: the vascular district involved was chiefly the carotid area; the onset was gradual in many cases; the impairment of consciousness was unusual; motor impairment was in many cases limited to one limb; the EEG and brain scan showed abnormalities in few cases with subsequent recovery; the angiographie examination showed occlusion of the sylvian artery in one case, severe stenosis of the internal carotid artery in one case, absence of visualisation of the terminal branches of the sylvian artery in 12 cases; the follow-up (mean duration years 4,25,SD +/- 2.09) showed a favourable course since subsequent stroke appeared in a minority of cases. The term "stroke with full recovery" and the problem of the sensitivity of the brain to oxygen deficiency is discussed.

CSF metabolites of dopamine (HVA), norepinephrine (MHPG) and serotonine (5HIAA) in 9 patients affected by Huntington's Chorea before and after therapy with phenotiazine derivatives (Fluphenazine) have been studied. A close relationship seems to exist between therapeutical results and CSF HVA modifications: improvement of choreatic movements is associated with marked increase in CSF HVA values. Biochemical bases of Huntington's Chorea are discussed.

Carbamazepine-induced cardiac conduction disturbance is reported in 2 patients suffering from epilepsy. The cardiac defects disappeared in both patients after carbamazepine was discontinued, and reappeared in 1 patient after treatment was resumed.

MPHG urinary changes were investigated in a group of patients affected by different forms of depressive illness. No significant difference was noticed depending on age, diagnosis, number and duration of episodes. Considering the group as a whole, a significant increase of MHPG urinary levels was noted after the recovery, although the patients received different drugs (Tricyclic + phenothiazine, Trazodone, IMAO). Specifically, the patients treated with IMAO and Trazodone, either recovered or ameliorated, showed a remarkable increase of MHPG urinary levels, whereas a decrease was noticed in the group who was administered tricyclic antidepressants.

A parenteral penicillin model of epilepsy in the rat was investigated with the aim of evaluating its reliability. Behavioral and EEG patterns were strongly variable in a group of 100 rats injected with 1,000,000 IU/kg of penicillin i.p. Gross counts of spikes were Fourier transformed and grouped into two time windows in 24 out of the 100 rats. Analysis of variance applied to compare the two time windows showed a sufficient suitability of the phenomenon for antiepileptic drug testing purposes. Five subsequent injections of penicillin performed in 8 rats showed that a spontaneous decrease of the response takes place, preventing a crossover design in pharmacological analyses. Evans Blue studies demonstrated that there was not a breakdown of the blood-brain barrier; this model can be used for testing anticonvulsants unable to penetrate the blood-brain barrier.

A sensitive analysis of pentaerythritol in plasma has been devised, based on the formation of its tetra-p-methoxybenzoate derivative and high-performance liquid chromatography employing an ultraviolet photometric detector. The method permits analysis of pentaerythritol in the ppm range.

Sprague-Dawley rats with interictal and ictal spike activity induced by intraperitoneally injected isoniazid (INH) were treated, 5 min before or 30 min later, with liposome-entrapped gamma-aminobutyric acid (GABA) (LEG) or GABA or phosphatidylserine. Crossover injections were given in random sequence and INH alone ws also injected in every animal as a control. LEG inhibited either seizures or interictal spikes in both groups. No decrease of epileptogenic activity was seen after GABA or phosphatidylserine treatment alone. It is suggested that LEG could contribute to the reconstitution of the GABA pool decreased by INH.