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Aim: To assess whether periodontitis is associated with cognitive decline and its progression as well as with certain blood-based markers of Alzheimer's disease., Materials and Methods: Data from a 2-year follow-up prospective cohort study (n = 101) was analysed. Participants with a previous history of hypertension and aged ≥60 years were included in the analysis. All of them received a full-mouth periodontal examination and cognitive function assessments (Addenbrooke's Cognitive Examination (ACE) and Mini-Mental State Examination [MMSE]). Plasma levels of amyloid beta (Aβ) 1-40 , Aβ 1-42 , phosphorylated and total Tau (p-Tau and t-Tau) were determined at baseline, 12 and 24 months., Results: Periodontitis was associated with poor cognitive performance (MMSE: β = -1.5 [0.6]) and progression of cognitive impairment (hazard ratio [HR] = 1.8; 95% confidence interval: 1.0-3.1). Subjects with periodontitis showed greater baseline levels of p-Tau (1.6 [0.7] vs. 1.2 [0.2] pg/mL, p < .001) and Aβ 1-40 (242.1 [77.3] vs. 208.2 [73.8] pg/mL, p = .036) compared with those without periodontitis. Concentrations of the latter protein also increased over time only in the periodontitis group (p = .005)., Conclusions: Periodontitis is associated with cognitive decline and its progression in elderly patients with a previous history of hypertension. Overexpression of p-Tau and Aβ 1-40 may play a role in this association., (© 2023 The Authors. Journal of Clinical Periodontology published by John Wiley & Sons Ltd.)

Alzheimer's disease (AD) is the most common degenerative disorder in the elderly in developed countries. Currently, growing evidence is pointing at endothelial dysfunction as a key player in the cognitive decline course of AD. As a main component of the blood-brain barrier (BBB), the dysfunction of endothelial cells driven by vascular risk factors associated with AD allows the passage of toxic substances to the cerebral parenchyma, producing chronic hypoperfusion that eventually causes an inflammatory and neurotoxic response. In this process, the levels of several biomarkers are disrupted, such as an increase in adhesion molecules that allow the passage of leukocytes to the cerebral parenchyma, increasing the permeability of the BBB; moreover, other vascular players, including endothelin-1, also mediate artery inflammation. As a consequence of the disruption of the BBB, a progressive neuroinflammatory response is produced that, added to the astrogliosis, eventually triggers neuronal degeneration (possibly responsible for cognitive deterioration). Recently, new molecules have been proposed as early biomarkers for endothelial dysfunction that can constitute new therapeutic targets as well as early diagnostic and prognostic markers for AD.

Alzheimer's disease (AD) is considered the most prevalent neurodegenerative disease and the leading cause of dementia worldwide. Sphingolipids, such as ceramide or sphingosine 1-phosphate, are bioactive molecules implicated in structural and signaling functions. Metabolic dysfunction in the highly conserved pathways to produce sphingolipids may lead to or be a consequence of an underlying disease. Recent studies on transcriptomics and sphingolipidomics have observed alterations in sphingolipid metabolism of both enzymes and metabolites involved in their synthesis in several neurodegenerative diseases, including AD. In this review, we highlight the most relevant findings related to ceramide and neurodegeneration, with a special focus on AD.

Purpose: Recent evidence suggests that PET imaging with amyloid-β (Aβ) tracers can be used to assess myelin integrity in cerebral white matter (WM). Alzheimer's disease (AD) is characterized by myelin changes that are believed to occur early in the disease course. Nevertheless, the extent to which demyelination, as measured with Aβ PET, contributes to AD progression remains unexplored., Methods: Participants with concurrent 18 F-florbetapir (FBP) PET, MRI, and cerebrospinal fluid (CSF) examinations were included (241 cognitively normal, 347 Aβ-positive cognitively impaired, and 207 Aβ-negative cognitively impaired subjects). A subset of these participants had also available diffusion tensor imaging (DTI) images (n = 195). We investigated cross-sectional associations of FBP retention in the white matter (WM) with MRI-based markers of WM degeneration, AD clinical progression, and fluid biomarkers. In longitudinal analyses, we used linear mixed models to assess whether FBP retention in normal-appearing WM (NAWM) predicted progression of WM hyperintensity (WMH) burden and clinical decline., Results: In AD-continuum individuals, FBP retention in NAWM was (1) higher compared with WMH regions, (2) associated with DTI-based measures of WM integrity, and (3) associated with longitudinal progression of WMH burden. FBP uptake in WM decreased across the AD continuum and with increasingly abnormal CSF biomarkers of AD. Furthermore, FBP retention in the WM was associated with large-calibre axon degeneration as reflected by abnormal plasma neurofilament light chain levels. Low FBP uptake in NAWM predicted clinical decline in preclinical and prodromal AD, independent of demographics, global cortical Aβ, and WMH burden. Most of these associations were also observed in Aβ-negative cognitively impaired individuals., Conclusion: These results support the hypothesis that FBP retention in the WM is myelin-related. Demyelination levels progressed across the AD continuum and were associated with clinical progression at early stages, suggesting that this pathologic process might be a relevant degenerative feature in the disease course., (© 2021. The Author(s).)

Patients suffering from periodontitis are at a higher risk of developing cognitive dysfunction. However, the mediation effect of an inflammatory diet and serum vitamin D levels in this link is unclear. In total, 2062 participants aged 60 years or older with complete periodontal diagnosis and cognitive tests from the National Health and Nutrition Examination Survey (NHANES) 2011-2012 and 2013-2014 were enrolled. The Consortium to Establish a Registry for Alzheimer's disease (CERAD) word learning subtest (WLT) and CERAD delayed recall test (DRT), the animal fluency test (AFT) and the digit symbol substitution test (DSST) was used. Dietary inflammatory index (DII) was computed via nutrition datasets. Mediation analysis tested the effects of DII and vitamin D levels in the association of mean probing depth (PD) and attachment loss (AL) in all four cognitive tests. Periodontitis patients obtained worse cognitive test scores than periodontally healthy individuals. DII was negatively associated with CERAD-WLT, CERAD-DRT, AFT and DSST, and was estimated to mediate between 9.2% and 36.4% of the total association between periodontitis with cognitive dysfunction ( p < 0.05). Vitamin D showed a weak association between CERAD-DRT, AFT and DSST and was estimated to between 8.1% and 73.2% of the association between periodontitis and cognitive dysfunction ( p < 0.05). The association between periodontitis and impaired cognitive function seems to be mediated both by a proinflammatory dietary load and vitamin D deficiency. Future studies should further explore these mediators in the periodontitis-cognitive decline link.

The association between white matter hyperintensities (WMH) and amyloid accumulation over time in cognitively normal, amyloid-negative elderly people remains largely unexplored. In order to study whether baseline WMH were associated with longitudinal subthreshold amyloid accumulation, 159 cognitively normal participants from the Alzheimer's Disease Neuroimaging Initiative who were amyloid-negative at baseline were examined. All the participants underwent a T1 and a Fluid-Attenuated Inversion Recovery MRI scan at baseline. Amyloid PET imaging was performed at baseline and follow-up visits in 2-year intervals for up to 8 years. Partial volume correction was applied for quantifying cortical Standardised Uptake Value Ratios (SUVR). The associations between global and regional WMH burden and amyloid accumulation were assessed using linear mixed models adjusted by demographic characteristics and baseline SUVR. Partial volume correction increased the measured annual rate of change (+2.4%) compared to that obtained from non-corrected data (+0.5%). There were no significant correlations between baseline WMHs and baseline subthreshold cortical amyloid uptake. In a longitudinal analysis, increased baseline cortical SUVR and increased baseline burden of global (p ​= ​0.006), frontal (p ​= ​0.006), and parietal WMH (p ​= ​0.003) were associated with faster amyloid accumulation. WMH-related amyloid accumulation occurred in parietal, frontal, and, to a lesser extent, cingulate cortices. These results remained unchanged after a sensitivity analysis excluding participants with the highest cortical SUVRs. This is the first study to identify a specific spatial distribution of WMH which is associated with future amyloid accumulation in cognitively normal elderly subjects without PET-detectable amyloid pathology. These findings may have important implications in prevention trials for the early identification of amyloid accumulation., Competing Interests: Declaration of competing interest AM, DR, JS, JMA, JC, JP, AR, and PA report no relevant conflicts of interest., (Copyright © 2020. Published by Elsevier Inc.)

Introduction: Cultural manifestations are frequently used as a source of descriptors in the field of the health sciences. The story of Odysseus (Ulysses) is one of the oldest and most influential works of world literature and has given rise to many subsequent creations, with strong roots in popular culture., Aims: To consider the use of the story of Odysseus in the medical literature, to describe the terms in which it is used, and to discuss its relevance., Development: From a review performed in PubMed, 112 medical publications with references to the myth of Odysseus were found, out of a total of 343 results. Five different conditions named directly after Ulysses were found (three Ulysses syndromes, the Ulysses contract and the Ulysses conflict), together with two others that have been given the names of other characters who are part of the same cycle (Elpenor syndrome and Penelope syndrome), which we analyse in a critical manner referring to the original material from which they have been taken., Conclusions: The story of Odysseus constitutes one of the most frequent sources of inspiration in medicine, both for the creation of descriptors and for the use of similes, metaphors or other rhetorical figures, particularly in the area of neuroscience.

Aim: To investigate whether periodontitis is associated with amyloid beta (Aβ) peptides and whether systemic inflammation could act as a potential mediator of this link., Materials and Methods: A case-control study was designed including 75 patients with periodontitis (cases) and 75 age-balanced and gender-matched participants without periodontitis (controls). Full-mouth periodontal evaluation was performed in all participants. Demographic, clinical and behaviour data were also recorded. Fasting blood samples were collected, and serum levels of interleukin 6 (IL-6), high-sensitivity C-reactive protein (hs-CRP), Aβ 1-40 and Aβ 1-42 were determined., Results: Cases showed higher levels of IL-6 (8.7 ± 3.2 vs. 4.8 ± 0.5 pg/ml), hs-CRP (3.3 ± 1.2 vs. 0.9 ± 0.7 mg/L), Aβ 1-40 (37.3 ± 6.0 vs. 30.3 ± 1.8 pg/ml) and Aβ 1-42 (54.5 ± 10.6 vs. 36.5 ± 10.0 pg/ml) when compared to controls (all p < .001). Diagnosis of periodontitis was statistically significantly associated with circulating Aβ 1-40 ( β coefficient adjusted  = 6.9, 95% CI: 5.4-8.3; p < .001) and Aβ 1-42 ( β coefficient adjusted  = 17.8, 95% CI: 14.4-21.3; p < .001). Mediation analysis confirmed hs-CRP and IL-6 as mediators of this association., Conclusions: Periodontitis is associated with increased peripheral levels of Aβ. This finding could be explained by enhanced systemic inflammation that can be seen in patients with periodontitis., (© 2020 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)

It is unclear whether episodic memory is an appropriate descriptor of the cognitive continuum in mild cognitive impairment (MCI). Here, we investigated the ability of episodic memory to track cognitive changes in patients with MCI with biomarker evidence of Alzheimer's disease (AD). We examined 387 MCI amyloid-positive subjects, cognitively staged as "early" or "late" on the basis of episodic memory impairment. Cross-sectional and longitudinal comparisons between these 2 groups were performed for each amyloid, tau, and neurodegeneration (AT(N)) profile. Cross-sectional analyses indicate that "early" MCI represents a transitional phase between normal cognition and "late" MCI in the AD biomarker pathway. After adjusting by confounders and levels of A, T, and (N), "late" MCI progressed significantly faster than "early" MCI only in profiles with both abnormal amyloid and tau markers (A+T+(N)- p < 0.05, A+T+(N)+ p < 0.001). Episodic memory staging is useful for describing symptoms in prodromal AD and complements the AT(N) profiles. Our findings might have implications for the Numeric Clinical staging scheme of the National Institute on Aging and Alzheimer's Association research framework., (Copyright © 2019 Elsevier Inc. All rights reserved.)

Magnetic resonance imaging (MRI) volumetric measures have become a standard tool for the detection of incipient Alzheimer's Disease (AD) dementia in mild cognitive impairment (MCI). Focused on providing an earlier and more accurate diagnosis, sophisticated MRI machine learning algorithms have been developed over the recent years, most of them learning their non-disease patterns from MCI that remained stable over 2-3 years. In this work, we analyzed whether these stable MCI over short-term periods are actually appropriate training examples of non-disease patterns. To this aim, we compared the diagnosis of MCI patients at 2 and 5 years of follow-up and investigated its impact on the predictive performance of baseline volumetric MRI measures primarily involved in AD, i.e., hippocampal and entorhinal cortex volumes. Predictive power was evaluated in terms of the area under the ROC curve (AUC), sensitivity, and specificity in a trial sample of 248 MCI patients followed-up over 5 years. We further compared the sensitivity in those MCI that converted before 2 years and those that converted after 2 years. Our results indicate that 23% of the stable MCI at 2 years progressed in the next three years and that MRI volumetric measures are good predictors of conversion to AD dementia even at the mid-term, showing a better specificity and AUC as follow-up time increases. The combination of hippocampus and entorhinal cortex yielded an AUC that was significantly higher for the 5-year follow-up (AUC = 73% at 2 years vs. AUC = 84% at 5 years), as well as for specificity (56% vs. 71%). Sensitivity showed a non-significant slight decrease (81% vs. 78%). Remarkably, the performance of this model was comparable to machine learning models at the same follow-up times. MRI correctly identified most of the patients that converted after 2 years (with sensitivity >60%), and these patients showed a similar degree of abnormalities to those that converted before 2 years. This implies that most of the MCI patients that remained stable over short periods and subsequently progressed to AD dementia had evident atrophies at baseline. Therefore, machine learning models that use these patients to learn non-disease patterns are including an important fraction of patients with evident pathological changes related to the disease, something that might result in reduced performance and lack of biological interpretability., (Copyright © 2019 The Authors. Published by Elsevier Inc. All rights reserved.)

Introduction: Periodontal disease and dementia are very prevalent, especially in elderly populations. Multiple studies have shown a link between these diseases; however, the conditions are highly heterogeneous and so is the diagnostic methodology, which may hinder interpretation and comparison of the results. The aim of this article is to provide a critical review of the literature linking these 2 processes., Development: We retrieved 22 studies, most of which were retrospective, and analysed various methodological variables including study population, diagnosis of periodontitis, definition of dementia, adjusted variables, and results. The different aetiopathogenic mechanisms that may affect the progression and interaction of these 2 conditions were also analysed., Conclusions: Although available evidence indicates a positive association between periodontitis and dementia, both the strength of that association and the presence of a causal relationship have yet to be determined., (Copyright © 2016 Sociedad Española de Neurología. Publicado por Elsevier España, S.L.U. All rights reserved.)

Background: In the last decade, several observational studies have suggested that there exists an association between periodontal disease (PD) and Alzheimer's disease (AD). The aim of this systematic review was to investigate whether or not this link exists., Summary: The Preferred Reporting Items for Systematic Reviews and Meta-Analysis guideline for systematic review was used and registered at PROSPERO (CRD42016035377). The search strategy included using electronic databases and by hand searching articles published up to January 2016. MEDLINE via PubMed, EMBASE and Web of Science were searched by 2 independent reviewers. Observational studies including patients meeting criteria for both AD and PD were eligible to be included in the analysis. Quality assessment of selected studies was performed by the Newcastle-Ottawa Scale. From a total of 550 titles and abstracts, 5 studies were included (2 cross-sectional, 2 case-control and one cohort study) in the review. A fixed effects meta-analysis showed that the presence of PD is associated with the presence of AD (OR 1.69, 95% CI 1.21-2.35). When only severe forms of PD were evaluated, a significant association was also observed (OR 2.98, 95% CI 1.58-5.62). Key Messages: In the present review, a significant association was observed between PD and AD. Further studies should be carried out in order to investigate the direction of the association and factors that may confound it., (© 2017 S. Karger AG, Basel.)

Introduction: Intracerebral hemorrhage (HIC) represents 10-30% of all stroke. Epidemiological studies have shown factors associated with its high mortality, but those which might lead to lower morbidity are little known., Objective: To find the factors which may influence the functional state of a series of patients with intracerebral hemorrhage., Patients and Methods: We made a prospective study of 203 patients with intracerebral hemorrhage. We recorded vascular risk factors, arterial blood pressure, laboratory and neuroimaging parameters obtained on admission. The functional condition when discharged from hospital was evaluated on the Rankin Scale, in three categories: independent (Rankin 0-1), partially dependent (Rankin 2-3) and totally dependent patients (Rankin 4-5)., Results: There was a 23.2% death rate. Of the 156 patients who survived, at the time of hospital discharge 35.8% had a score of 0-1, 50.6% a score of 2-3 and 13.4% a score of 4-5 on the Rankin Scale. Age (p < 0.005), hyperglycaemia (p < 0.05) and size of hemorrhage (p < 0.05) were associated with increased morbidity., Conclusions: The functional condition on hospital discharge was better in younger patients with lower levels of glycemia on admission and smaller hematomas on CT.

Introduction: Acute cerebrovascular disease is a serious neurological problem. Mortality is between 6% and 30%. Most studies are in agreement that advanced age, type of ictus, size of lesion and clinical deterioration are factors determining mortality. However, its relationship to vascular risk factors is not completely clear., Objective: To analyze the repercussion of different vascular risk factors on mortality during the acute phase of ictus., Patients and Methods: We studied all patients with ictus admitted to the Servicio de Neurología of the Hospital Xeral de Galicia de Santiago de Compostela over a period of 3 years (n = 915). We recorded vascular risk factors and analyzed the causes of mortality whilst in hospital., Results: Hospital mortality due to ictus was 16.8%. Mortality was 14.5% in cerebral infarct, 23.2% in intracerebral haemorrhage and 19.4% in subarachnoid haemorrhage. A total of 20.8% of the patients died of neurological causes, 24.7% of vascular causes, 26% due to infection and of uncertain causes in the remaining 28.6%. There was a neurological cause of death in 46.1% of the patients with subarachnoid haemorrhage, 25.5% with intracerebral haemorrhage and 14.8% with cerebral infarcts. Vascular risk factors associated with greater mortality were age (p < 0.001) and a history of cardiopathy (p < 0.05)., Conclusions: Vascular risk factors which indicated worse prognosis were: age, type of ictus and a history of cardiopathy.

Introduction: Hyperglycemia increases morbimortality in cerebral infarcts. In animal models, this relationship is only seen during the initial moments of cerebral ischaemia. The time needed in humans for cerebral damage to occur due to hyperglycemia is not known., Material and Methods: We included 194 patients admitted within 24 hours of the start of their first clinical episode of cerebral hemisphere infarction. The glucemia was determined on admission and after 24, 48 and 72 hours. The neurological defect was evaluated on the Canadian scale on the seventh day. The volume of the infarct was determined on a second CT scan done between the fourth and seventh days after the episode., Results: There was a positive association between the volume of the infarct and the glycemias on admission and after 24 hours, but this was not seen in later determinations. The difference in scoring, on the Canadian scale, on the seventh day, between patients with glycemias above or below 120 mg/dl decreased from the time of admission up to the time samples were taken 72 hours later. However, statistical significance persisted during the whole period studied. Nevertheless, in a logistic regression model, the glycemia on admission was the only determination associated with the Canadian scale on the seventh day (OR = 1.02; IC 95% = 1.01-1.02)., Conclusions: There is a clear association between hyperglycemia and the worst stage of the infarct, and this is most intense in the first hours after onset of the clinical features.

The connection between migraine and brain haemorrhage is controversial. We present the case of eight nonhypertense patients all aged under 57 with migraine antecedents who suffered brain haemorrhage during an attack. All underwent analytical study, chest X-ray, electrocardiography, computerized tomography scan and brain panangiography. The study was completed in six cases with an immunological analysis and in a further five with brain magnetic resonance. Seven patients habitually took vasoactive drugs to relieve migraine. The results do not show any other cause of brain haemorrhage. It is possible haemorrhage may be related to vascular lesion brought about by ischaemia secondary to vasospasms.

Background and Purpose: The pathophysiology of headache occurring at stroke onset is unknown. Migraine and ischemia share an excessive release of neuroexcitatory amino acids. Inhibitory amino acids also may be implicated in both diseases. We investigated whether fluctuations of these amino acids occur in headache accompanying cerebral infarction., Methods: We studied 100 patients with infarction in the territory of the middle cerebral artery. Neurological impairment was assessed using the Canadian Neurological Scale and Barthel Index. Size of infarction was determined with CT. Twenty-eight patients developed headache. Glutamate, aspartate, and taurine were quantified in blood and cerebrospinal fluid (CSF) within 24 hours of stroke onset with cationic exchange chromatography., Results: Stroke subtypes, size of infarct on CT, and clinical scales were similar in patients with and without headache. Plasma glutamate level was 321.14 +/- 149.53 mumol/L in patients with headache and 233 +/- 107.23 mumol/L in those without headache (P < .005). Glutamate in CSF was higher in patients with headache (4.6 +/- 1.49 mumol/L) than in patients without headache (3.11 +/- 1.18 mumol/L) (P < .001). Aspartate concentrations in plasma and CSF were similar in both groups. Taurine concentrations in plasma were 103.10 +/- 52.82 mumol/L and 177.49 +/- 90.92 mumol/L in headache and nonheadache patients, respectively (P < .001). Taurine levels in CSF were 5.42 +/- 2.42 mumol/L in patients with headache and 9.27 +/- 5.31 mumol/L in those without headache (P < .001). No significant correlation was found between amino acid levels in plasma or CSF and size of infarction., Conclusions: Amino acid neurotransmitters play a role in the pathophysiology of headache that occurs at the onset of stroke. The ischemic penumbral area, more than the infarction itself, may cause a state of cortical hyperexcitability that would be responsible for the cortical release of amino acids and the induction of headache by altering pain perception mechanisms.

The frequency and clinical characteristics of headache were assessed in a prospective study carried out among 100 patients suffering from ischaemic infarct in the area of the middle cerebral artery. Headache was found in 28 out of the 100 patients studied and proved to be significantly more frequent in those infarcts located in the superficial branches (p < 0.001) and in the dominant hemisphere (p < 0.05). We found no relationship between the existence of headache and the type of infarct, its extension or level of neurological affectation. Severe headache preceded stroke in 28.5% of cases, was simultaneous in 57.1% and followed in 14.2%. The average intensity of headache was 2.14 +/- 1.69 headache units. It was bilateral in 46.4% of patients, generalized in 14.2%, unilateral on the side of the infarct in 28.5% and counterlateral in the remaining 10.7%.

Five patients were examined suffering from bilateral paramedian thalamic infarction, caused by occlusion of the posterior paramedian thalamo-subthalamic arteries, when they begin from one single pedicle. All cases began with obnubilation or transitory coma, followed by hypersomnia. Four patients showed vertical gaze paralysis, and the fifth vertical nystagmus. In three cases, nuclear lesion of the III cranial nerve was observed along with alteration of the photomotor reflexes, and there was miosis in one case. All were suffering from weakness in one or another limb or facial paresis and generalised acute hypotonia: only one patient had hemihypostesia. All five had dysarthria, ataxy and dysmetria, one had asterixis and two spasmodic crying. Between 5 and 12 months later, one had akinetic mutism and vertical gaze paralysis as the most noteworthy signs. The neuroradiological images show a bilateral ischemic lesion in the paramedian thalamic region, which extends in some cases to the anterior nucleus and in one case to the pulvinars; the lesion continues through the subthalamic regions and the medial part of the mesencephalic tegmentum, with a clear extension to the medial region of the cerebral peduncles in three cases and to the tectum in one case.

8 cases of dementia associated with cortical Lewy bodies are dealt with, that were diagnosed in 1993 in examinations for dementia, using the Nottingham's clinical criteria. They make up 15.4% of primary degenerative dementias diagnosed in this examination. All developed a predominantly cortical dementia with variable bradiphrenia and a parkinsonian syndrome which was predominantly of the rigid-bradikinetic type. The dementia established itself rapidly -between 1 and 3 weeks- in 3 cases (37.5%). 50% of patients (4 cases) showed marked psychiatric symptoms. In 2 cases stiffness was predominantly axial and another had supranuclear paralysis of vertical gaze. 3 patients had no tremor, and 2 of the 5 remaining patients showed postural tremor. CT and axial MR images of the encephalon were similar to those observed in dementia of the Alzheimer type. The coronal MR carried out on 3 patients revealed less atrophy of the hypocampus than is normally observed in patients with dementia of the Alzheimer type who are at the same stage of development.

The estimation of the size of the structures of the temporal lobe using magnetic resonance (MR) can be of assistance when diagnosing early degenerative dementia. We have carried out a survey on 17 patients with Alzheimer type dementia (ATD). They were classified in clinical stages according to the Reisberg global deterioration scale. As diagnostic criteria for ATD we used those developed by DSM-III-R and NINCDS-ADRDA. We carried out axial sequences of 10 mm thickness in protonic density and in T2, and crown sequences of 5mm in T1 perpendicular to the axis of the hypofield. We selected the crown incisions at the level of the interpeduncular cistern. We determined the areas of the temporal lobe, hypocampus and ventricular and two linear measurements (the interhypocampus distance and the maximum transverse diameter between internal layers of the craneum). The images were processed by means of a computer programme. The average area of both hypofields in patients at stages 3-5 on the Reisberg scale was 378.6 +/- 86.1 mm2 and in stages 6-7 was of 364.7 +/- 62.2 mm2. The average area of both temporal lobes in patients at stages 3-5 was of 2,177.03 +/- 411.4 mm2 and in stages 6-7, was of 1,945.0 +/- 303.3 mm2. The shrinkage in size of the temporal lobe and the hypocampus in patients with Alzheimer's disease was not found to be related with the degree of dementia.

The introduction of etiological, diagnostic and therapeutical factors have modified the knowledge on the evolutive behaviour of spontaneous intracerebral hemorrhages (ICH). Mortality and morbidity associated to spontaneous ICH were assessed using as independent variables clinical and neuroimage factors obtained upon admission of the patients. We studied 228 patients with spontaneous ICH selected from a data bank of 277 patients with non-traumatic ICH. During the first 24 hours, we assessed several clinical factors (arterial hypertension, Glasgows Neurological Scale and Barthels Scale) and TC images (size, location, extension of bleeding to ventricles, edema and atrophy). Thirty-one per cent of the patients died during the first 2 months. The multiple linear regression study showed that mortality was related to variables of the Glasgows Neurological Scale upon admission, extension to ventricles, size of ICH and perilesional edema, whereas the morbidity was only related to the size of the hemorrhage. Severity of the clinical affection, extension of the bleeding to ventricles, size of the hemorrhage and presence of perilesional edema, but not arterial hypertension, were the main factors affecting mortality at two months of spontaneous ICH.

We present the principal differential characteristics of neuralgia of symptomatic and idiopathic trigeminus. Out of 39 consecutive patients with neuralgia of trigeminus evaluated clinically and with neuroimage study, we find recognizable pathology in 10 (3 arterio-venous malformations, 1 dolichoestasia of basilar artery, 3 tumors, 3 multiple sclerosis). Symptomatic neuralgia occurs in patients with lower average age and is accompanied by atypical symptoms or abnormal neurological signs and is no different from idiopathy as a response to pain from medical treatment. Painful affectation of the trigeminus requires the realization of complementary explorations aiming to dismiss associated neurological pathology.