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Silent cerebral infarcts occur in patients with chronic nonvalvular atrial fibrillation and asymptomatic or symptomatic carotid stenosis. There is not a well-defined prevalence of asymptomatic lesions in patients with transient ischemic attack or completed strokes. We attempted to determine the occurrence rate of silent brain infarction in a hospital population, including a comparison of the risk factors with those of symptomatic infarction and an evaluation of the relevance of infarction size and location.

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.

Reliable, simple and safe criteria are needed for the early prediction of short-term outcome in patients with acute ischemic stroke. The aim of our study was to evaluate, in terms of their individual and combined power, the prognostic value of a few widely available clinical and instrumental variables obtained during the acute phase. The study involved 351 consecutive patients who were examined within 48 hours of their first ischemic stroke. Eight variables were chosen: age, initial level of consciousness, limb paresis, arterial blood pressure, glycemia, the results of electrocardiography and electroencephalography, and the infarct size revealed by computed tomography. Mortality and disability were evaluated on Day 30, when the variables that significantly correlated with disability were the severity of limb paresis, electroencephalographic abnormalities, infarct size and (less significantly) the level of consciousness and hyperglycemia. There was no statistical correlation with blood pressure. Logistic analysis confirmed only infarct size, the severity of limb paresis and electroencephalographic abnormalities as independent variables. The variables that significantly correlated with early death were the severity of limb paresis, infarct size, electrocardiographic abnormalities, the level of consciousness, electroencephalographic abnormalities and hyperglycemia. More intriguingly, logistic analysis confirmed only the electroencephalographic and electrocardiographic abnormalities as independent variables. The predictive prognostic value of limb paresis, infarct size, the level of consciousness and hyperglycemia is well known, but we would like to stress the fact that only a few independent variables are predictive of early death (electroencephalographic and electrocardiographic abnormalities) and poor recovery (infarct size, the severity of limb paresis, electroencephalographic abnormalities). The prognostic value of electroencephalography may express the potential involvement of dynamic non-structural phenomena, such as penumbra ischemica and diaschisis.

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)

We report open-label clinical observations of additional lamotrigine (LTG) in 16 adult patients with refractory epilepsy, aimed to assess the long-term efficacy and safety of LTG in clinical use. LTG was added to the current antiepileptic drug (AED) regimen at a daily dosage of 200-400 mg depending on the concomitant treatment. Ten patients completed one year's treatment and were followed up to an overall exposure ranging 15-38 months. Six patients (38% of the initial group) had a reduction of seizure frequency greater than 50% of pre-treatment baseline after one year; the further follow-up indicated some efficacy decline, since the percentage of improved patients dropped to 19% after 2 years and 13% after 3 years. The dropouts during the first year were due to seizure breakthrough (two patients), Steven-Johnson-like syndrome (one patient) and reasons unrelated to treatment (three patients); in one patient LTG treatment was stopped due to macrocytic anemia after 23 months. Other reported adverse events were dizziness, mild ataxia, diplopia and localized purpura. No other hematological or biochemical changes were noted. LTG was not associated with any significant changes in plasma concentrations of concomitant AEDs. These findings confirm the moderate efficacy and low toxicity of long-term LTG in severe epilepsy.

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.

A single-blind, placebo-controlled multicenter trial of vigabatrin was carried out in 101 epileptic patients (mostly with partial seizures) refractory to conventional therapy. The study design included four consecutive periods: (i) an observation phase (run-in), (ii) a placebo period, (iii) fixed-dosage add-on vigabatrin (2 g/day) and (iv) dose titration (up to a maximum of 4 g/day) to optimize clinical response. Each period lasted 8 weeks, except for the titration phase, which could be extended to 16 weeks. 90 patients completed the trial. Eleven dropped out, one patient developing absence status and 4 cases showing an increased seizure frequency. In the patients completing the trial, the median number of seizures/month decreased from 16 (inter-quartile range 8–34) during placebo to 5 (2–10) during the last 8 weeks on vigabatrin (p

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.

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.

The current assessment of dementia due to vascular causes in terms of terminology, classification, clinical features and diagnostic criteria, neuropathological lesions, risk factors, and possible treatment is reported. The term vascular dementia (VD) covers all syndromes with dementia of vascular origin. The clinical workout may reach a diagnostic sensitivity ranging from 70 to 85%. Verified ischemic lesions associated with dementia include multiple large and small infarctions, multiple lacunes, and, less frequently, watershed infarctions and other vascular diseases. However, the pathological evidence of infarction does not necessarily mean that cerebral vascular lesions are responsible for a state of dementia. The mixed forms (degenerative and vascular dementia) are difficult to assess both from the diagnostic and neuropathological point of view. The etiology of VD is multifactorial.

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 Italian Longitudinal Study on Aging (ILSA) evaluates the rates of diabetes, cardiovascular and neurological disorders in a random sample of 5632 Italians aged 65-84 years.The ILSA has two components: a first screening phase administered to all participants, that includes a personal interview, physician examination, laboratory and diagnostic tests, and a second phase, consisting of the clinical confirmation of suspected cases by a specialist.Prevalence rates were significantly higher among men for myocardial infarction (10.7% versus 4.8%), cardiac arrhythmia (25.1% versus 20.3%) and peripheral artery disease (8.1% versus 5.2%), and among women for hypertension (67.3% versus 59.4%), heart failure (7.3% versus 5.4%) and dementia (7.2% versus 5.3%). No gender difference was found for stroke, angina, diabetes, Parkinsonism and distal symmetric neuropathy. Unreported diagnoses accounted for 85% of cases of distal symmetric neuropathy, for more than half the cases of cardiac failure, for 40% of cases of angina, and for more than one-third of cases arrhythmia, myocardial infarction, peripheral artery disease, hypertension, Parkinsonism. Data from the phase 1 interview showed substantial overreporting for myocardial infarction, peripheral artery disease, diabetes, and stroke.The authors conclude that self-reported information would lead to inaccurate estimates of prevalence rates suggesting the need for including the clinical ascertainment in any population-based epidemiological study.

Vascular dementia (VAD) is currently considered to be the second most common cause of dementia in Europe and the USA, second to dementia of the Alzheimer's type (DAT). However, in Asia and many developing countries the incidence of VAD exceeds that DAT. The positive clinical diagnostic workup for VAD requires six steps: (1) clear-cut quantitative assessment of cognitive deficits utilizing standard neuropsychological tests to establish and quantify the dementia syndrome and rule out pseudo-dementia OF depression; (2) ascertaining the presence of risk factors for stroke; (3) identifying cerebral vascular lesions by neuroimaging (MRI, Iodine or Xenon contrasted CT, PET and SPECT); (4) exclusion of other causes of dementia; (5) differential diagnosis of possible, probable or definite VAD versus DAT and ascertaining when there are mixtures of the two; and (6) temporal identification of causality between onset and progression of the dementia with identified cerebral vascular lesions. There are eight subtypes of VAD: (1) multi-infarct dementias. These are due to large cerebral emboli, and are usually readily identifiable; (2) strategically placed infarctions causing dementia; (3) multiple subcortical lacunar lesions. Patients with these develop VAD at least five to twenty-five times more frequently than those in age-matched general population samples; (4) Binswanger's disease (arteriosclerotic subcortical leuko-encephalopathy). This form is rare. Neuroimaging confirms the diagnosis during life but the diagnosis can not be made by neuroimaging alone; (5) mixtures of two or more of above VAD subtypes; (6) hemorrhagic lesions causing dementia; (7) subcortical dementias due to cerebral autosomally dominant arteriolopathy with subcortical infarcts and leuko-encephalopathy (CADASIL), or to familial amyloid angiopathies and coagulopathies all of which present with multiple subcortical lacunar lesions similar to Binswanger's disease; (8) mixtures of DAT and VAD. The clinical significance of leukoaraiosis and its suspected relationships to VAD remains to be better established. The presence of ischemic infarctions, single or multiple large or multiple small (lacunar) by neuroimaging are necessary for the diagnosis of VAD, but identifying their presence, by neuroimaging alone, does not permit the diagnosis of dementia which can only be established by neuropsychological assessments. VAD is a clinical entity, identifiable in at least 30–70% of patients after strokes but mechanisms responsible for the cognitive impairments are complex. Some of these mechanisms are incompletely understood but provide subjects for important future research.

(1995). The history of vascular dementia. Journal of the History of the Neurosciences: Vol. 4, No. 2, pp. 121-126.

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.

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.

Neurotransmitter postsynaptic receptors, as integral membrane proteins, are located within the phospholipid bilayer of the acceptive membrane. Therefore it appears reasonable that the phospholipid environment of the plasma membrane influences and modulates the functional activity of these receptors. In addition, the phospholipid composition of the two leaflets of the bilayer may introduce a further element able to influence the function of these receptors.

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.

The purpose of this study was to assess the number of patients with lacunar lesions who develop dementia and to evaluate in patients with and without dementia the relevance of risk factors for cerebrovascular disease, the occurrence of leukoaraiosis, the volume and location of vascular lesions, the size of ventricular and subarachnoid spaces, and stroke recurrence. One hundred eight patients in whom computed tomograms revealed lacunar lesions that could account for their clinical neurological pictures were followed up for an average of 4 years after their first lacunar stroke. Twenty-five patients (23.1%) developed dementia. The prognosis regarding occurrence of dementia during the follow-up period, evaluated by the Kaplan-Meier method, was significantly worse in subjects with the greatest evidence of cerebral atrophy (p less than 0.009) and in subjects who underwent new focal cerebrovascular episodes (p less than 0.000001). No differences were seen in the frequency of vascular risk factors or the site or volume of lesions between the demented and nondemented groups. Patients with lacunar infarcts suffer from dementia 4-12 times more frequently than the normal population. Cerebral atrophy and recurrent stroke, as well as other as-yet unclarified factors, are involved in producing dementia.

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 immunocytochemically analyzed pieces of olfactory mucosa removed by biopsy in 8 patients with probable Alzheimer9s 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.

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 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.

The association between some hypothetical risk factors (previous TIA, hypertension, ECG ischemic abnormalities, diabetes, cigarette smoking, atrial fibrillation, hypercholesterolemia, hypertriglyceridemia, high hematocrit) and lacunar syndromes has been evaluated by a matched sample case-control study involving 108 consecutive, incident cases with lacunar syndrome and 216 hospital control subjects, matched for sex and age. A significant increase of Relative Risk (RR) has been shown for: 1. Previous history of TIA; 2. Hypertension; 3. Smoking; 4. Diabetes. No relevance was shown for: 1. Atrial fibrillation; 2. Hypercholesterolemia; 3. Hypertriglyceridemia; 4. High hematocrit. The analysis of the triplets of subjects (1 case + 2 controls) without hypertension showed a significant RR increase for: 1. Previous history of TIA; 2. Ischemic cardiac abnormalities; 3. Atrial fibrillation. Such findings support the hypothesis that, in a minority of cases with lacunar syndrome, the pathogenetic mechanism could be different from occlusion of penetrating arteries in hypertensive patients.

Two groups of 30 multiple sclerosis (MS) patients were randomly treated with corticotrophin (ACTH) and “bolus” 6-methylprednisolone (B/6-MP) to compare the effectiveness of the two treatments. Both ACTH and B/6- MP showed a similar effect, improving acute neurological deficits of MS patients without modifying the long term course of the disease. B/6-MP, showing prompt effectiveness and lack of side effects, may be regarded as a useful alternative to conventional treatment of MS.

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.

Le risposte corticali evocate da stimoli somatici, sia periferici che centrali, aumentano di ampiezza durante il sonno profondo. Tale amplificazione e dovuta, almeno in parte, ad una facilitata trasmissione degli impulsi ascendenti a livello del nucleo ventro-postero-laterale del talamo.

This study is based upon 25 selected comatose subjects investigated from the clinical, EEG, and anatomical standpoint. 1. 1. For practical purpose the different degrees of coma were subdivided using as parameters signs and symptoms commonly found in comatose patients, as follows: 1. (a) impairment of consciousness (C 1): 2 cases; 2. (b) moderate coma (C 2): 14 cases; 3. (c) deep coma (C 3): 9 cases. 1. 2. The type of EEG activity found was grouped under the following three headings: 1. (a) generalized EEG changes: 15 cases; 2. (b) unilateral EEG changes: 7 cases; 3. (c) focal EEG changes: 3 cases. 1. 3. The site of cerebral lesion was reconstructed on the basis of macro and microscopic sections. Electroclinical results show that a generalized slow organized activity is not necessarily the bioelectric expression of the majority of comatose patients. No definite relationships are found between degree of coma and type of electroencephalographic changes. Moreover the possibility of eliciting a bioelectric response to stimuli does not appear to be related to the depth of coma. Some interpretational problems posed by the EEG findings are discussed.

The effect of a suspension of GABA and phosphatidylserine (PS), phosphatidylcholine, or phosphatidylethanolamine was studied on penicillin-induced epileptic activity in rats. GABA-PS significantly reduced the number of spikes, in comparison with either the other phospholipid compounds or normal saline. No effect was observed after GABA or PS administration alone. We suggest that the different effects probably depend on extracellular and intracellular factors.

The evaluation of headache in patients with transient ischemic attacks (TIA) has various sources of difficulty, the definition of TIA being the most relevant. The classical definition needs to be supplemented with a normal CT scan if a misleading diagnostic statement is to be avoided. The clinical features of 90 patients suffering from TIA and who had contrast-enhanced CT scans are reported. (1) Headache occurred in 30% of the patients. (2) Headache prevailed in patients with vertebrobasilar TIA compared with carotid TIA ( p < 0.05). (3) Headache prevailed as a preceding (24 h) and/or concomitant sign compared with other neurological symptoms (77.8% of the patients). (4) Headache was ipsilateral, in the anterior half of the head in the carotid TIA and in the posterior half of the head in the vertebrobasilar TIA. In about 50% of the patients generalized non-localized headache occurred. Headache usually preceded the neurological symptoms in cases of arterial occlusion (20 carotid, 3 vertebral artery), usually appearing during or after the attack in cases without arterial occlusion. (5) Only 2 cases out of 20 with positive CT scan had headache. These two patients suffered from a rather large hypodense lesion. The other 18 patients showed lacunar lesions. Different hypotheses concerning the physiopathology of the headache associated with TIA are discussed.

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.

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.

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.

The clinical features of 102 cases with transient attacks due to cerebral ischemia were evaluated, and 94 out of 102 cases were followed for an average of 6 years. 1) the clinical study makes comparisons between two groups of patients grouped under the somewhat new definition of Reversible Ischemic Attacks (RIA): classical Transient Ischemic Attacks (TIA) and Stroke with Full Recovery (SFR), in which a complete recovery took place over a longer period, on the average 3 weeks. 2) SFR constitutes the 34.31% of the total cases with transient ischemic episodes. In the carotid district the onset was more frequently gradual in SFR than in TIA and aphasia more frequent in TIA than in SFR. Multiple attacks prevailed in TIA over the SFR group. the definition of transient attack due to ischemia is discussed. 3) Completed strokes occurred in 11 cases (11.7%) with RIA. Hypertension and cardiac disease were significantly frequent in cases with subsequent stroke. The conclusion was reached that TIA is a symptom, not a pathological state, and TIA should be considered an important symptom but not a specific harbinger of completed stroke.

A sonicated liposome suspension of gamma-aminobutyric acid (GABA) and phosphatidylserine (liposome-entrapped GABA), intraperitoneally administered in rats, inhibited EEG epileptic activity induced by penicillin, whereas GABA did not. A significant increase (20.4%) in brain radioactivity accumulation occurred at 5 min after i.p. administration of [14C]GABA associated with phosphatidylserine in comparison with the administration of [14C]GABA; such an increase persisted after 20 min. However, the accumulation of radioactivity into brain synaptosomes demonstrated a 24.1% increase at 5 min and subsequently showed a 43.3% increase at 20 min after injection of liposome-entrapped GABA. The above findings suggest that phosphatidylserine stimulates exogenous GABA uptake into brain GABAergic nerve terminals.

The two most frequently encountered types of dementia are the senile dementia of the Alzheimer type (SDAT), which accounts for approximately 50% of all patients with dementia, and the so-called multi-infarct dementia (MID), comprising about 15–20% of the total.