Gliomas cerebrales de bajo grado en el adulto / Low grade gliomas un adults

Objetivo. Bajo esta denominación se incluyen a los astrocitomas fibrilares y protoplasmáticos, a los oligodendrogliomas, y a los oligoastrocitomas o tumores mixtos, que corresponden a los grados II de la nueva clasificación de la OMS . Los astrocitomas de bajo grado representan el 15% de los gliomas hemisféricos cerebrales en el adulto. Los oligodendrogliomas tienen una incidencia del 4% (2,4). Presentamos la experiencia de nuestro grupo de trabajo con este tipo de tumores entre enero de 1972 y diciembre de 2006.Material y método. Se analizaron las historias clínicas de 25 pacientes adultos que presentaron esta variedad de tumor, de los cuales 15 eran mujeres y 10 varones, que representan el 15,6% de los gliomas cerebrales en este grupo etario. Resultados: Quince eran astrocitomas fibrilares, ocho oligodendrogliomas y dos oligoastrocitomas. El principal estudio de imagen fue la resonancia nuclear magnética con espectroscopia. El tratamiento dependió de la ubicación y del volumen tumoral, siendo la cirugía y la radioterapia las modalidades terapéuticas mas empleadas. El tumor recidivó en 16 enfermos, con una media de 37 ± 21 meses después del diagnóstico, cuyas histopatologías mostraron ser: astrocitomas anaplásicos en 7 y glioblastomas multiformes en 9. Han fallecido 16 enfermos, 14 por el tumor cerebral, uno por cáncer de lengua y otro por embolia pulmonar producida a los 10 días de la cirugía, con una mediana de sobrevida de 44 meses (10 días a 120 meses). De los 9 pacientes que viven, 7 tienen oligodendrogliomas, 2 astrocitomas, y uno tiene un oligoastrocitoma; 7 requieren medicación antiepilética, ninguno tiene secuelas neurológicas, con una mediana de sobrevida de 36 meses (6 a 120 meses); dos han tenido recidiva, correspondientes a un oligodendroglioma y a un oligoastrocitoma, a los 22 y 60 meses respectivamente del diagnóstico, en los dos casos el tumor pasó de ser un grado II a grado III...

Objective. Gliomas reviewed in this article are grade II tumors according to the World Health Organization (WHO), that include: fibrillary and protoplasmic astrocytomas, oligodendrogliomas and oligoastrocytomas or mix tumors (1,2,3).Low grade astrocytomas constitute 15% of brain tumors in adults, while low grade oligodendrogliomas represent 4% (2,4). We present our experience with this type of tumor operated on between January 1972 and December 2006.Material and Method. The clinical reports of 25 patients with this type of tumor were analyzed, 15 women and 10 men, which represent 15,6% of hemispheric brain gliomas in adults in our series.Results. Fifteen were fibrillary astrocytomas, 8 oligodendrogliomasand 2 oligoastrocytomas. Treatment depended on tumor localization and size. Surgery and radiotherapy were thetherapeutic modalities most frequently used. Tumor recurrence was observed in 16 patients, with a media of 37+/- 21 months after diagnosis: 7 anaplastic astrocytomas and 9 glioblastomasmultiforme. In this series, 16 patients died with a median of 44 months (10 days to 120 months) after diagnosis. Cause of death were: tumor itself, in 14 cases, tongue cancer in 1, and pulmonaryembolism after surgery in another. From the 9 surviving patients, 6 have oligodendrogliomas, 2 astrocytomas and 1 an oligoastrocytoma. Seven patients need antiepileptic drug and none of them presents neurological sequels. The survival mediana was 36 months (6 to 120 months). Two of them had tworecurrences between 22 and 60 months after diagnosis, one oligodendroglioma and the other an oligoastrocytoma; in both cases tumors grade II became tumors grade III. Conclusion. The relative incidence of 15,6% in adult gliomas of our series is similar to the international experience. Age, younger as 40 years, seizures, as clinical presentation, extension of surgical resection, low Ki 67 index in astrocytomas, and...

The effects on auditory neurocognitive evoked responses and contingent negative variation activity of frontal cortex lesions or ablations in man: three new case studies.

Our previous research in patients with extensive surgical ablations of the prefrontal cortex contradict the hypothesis of some authors that the generators of several auditory event-related potentials (ERPs) (N100; P200; N200; P300; SW), recordable in humans with depth/scalp electrodes and MEG over the prefrontal dorsolateral cortical areas, are essentially located in medial prefrontal and anterior cingulate-limbic cortices. Using a standard CNV paradigm, 21 EEG electrodes and topographic mapping analysis, the post-warning (S1) auditory N100a b c, P200, P300 (binaural clicks) and CNV activity were recorded in three additional patients after extensive dorsolateral and/or medial prefrontal cortex ablations, verified through CT/MRI examinations. No true post-S1/CNV components were recordable over the ablated frontal areas, only sporadic volume-conducted ERPs probably generated in the temporo-parietal lobes or posterior cingulate gyrus. For one of these patients, after excision of a vast right frontal epileptogenic cortical region (including extensive dorsolateral areas, but sparing the fronto-medial cortex and anterior/middle cingulate gyrus), no post-S1/CNV components were recordable over the ablated regions. These latest observations again indicate that independent neuronal generators of several post-S1 auditory and CNV components are located in the dorsolateral supramodal premotor/prefrontal cortical areas which are directly, ipsilaterally connected to the uni/multimodal temporo-parieto-occipital sensory and associative regions through the long, two-way, fairly superficial, superior arcuate-longitudinal and deeper superior and inferior occipito-frontal bundles. Clear and almost constant differences in the latency of some post-S1 N100 subcomponents (especially the time-lapses between onset and the highest amplitude of the N100 a and c) over various posterior, central and anterior cortical areas sequentially involved, roughly measured in 10 normal subjects along the scalp and with MRI cerebral imaging, may probably be accounted for by the transcortical homohemispheric conduction time, which varies in our scalp recordings from 1 cm/0.74-1.28 ms, mean approximately 1 cm/1.02 ms ( approximately 9.8 ms).

Presenile primary cognitive decline or Alzheimer's dementia: 7-year clinical and neuropsychological follow-up.

Early diagnosis of presenile Alzheimer's disease (AD), which would serve for prognosis and for guiding choices of treatment, is still an important, difficult task for the clinical neurologist. We studied 24 patients, 12 of whom had minor cognitive impairment or questionable dementia (PICD) and 12 who met NINCDS-ADRDA criteria for presenile AD (PAD). Using clinical, neuropsychological, neurophysiological and neuroradiological methods, we followed the patients up to two disease end-points: death or untestable condition. This paper concentrates on the main clinical and neuropsychological findings relative to these two end-points. All PAD patients evolved into clinically evident Alzheimer-type dementia, became untestable within 60 months and died within 72 months. Only 3 of the PICD patients became demented; 2 of them died during the follow-up and 1 died eight months later. The other 9 PICD patients showed only moderate cognitive decline, compatible with normal aging processes. Neurophysiological and neuroradiological findings might be an important tool for arriving at a correct early diagnosis, when they are assessed with clinical neuropsychological data.

Brain electrical activity (quantitative EEG and bit-mapping neurocognitive CNV components), psychometrics and clinical findings in presenile subjects with initial mild cognitive decline or probable Alzheimer-type dementia.

Clinical, neuropsychological and neuropsychophysiological data (Q-EEG, ERPs and CNV/RT activity) were obtained from 24 patients who had more or less severe presenile primary cognitive decline without depression, and compared with similar data from 10 age-matched healthy volunteers (mean age, 59.4 years). All of the patients (15 M and 9 F; mean age 59.6 years) were selected according to the DSM III-R, ICD-10 and NINCDS-ADRDA criteria and underwent CT and MRI scanning, in addition to a standard clinical examination, a battery of psychometric tests, spectral EEG, and bit-mapped CNV complex and RT to S2 analyses. Twelve of the 24 patients presented an initial presenile idiopathic cognitive decline (PICD) but did not wholly fulfil the clinical and neuropsychological criteria for primary dementia or for a diagnosis of probable AD; the remaining 12 patients showed characteristic clinical signs and symptoms of a very probable early stage of presenile Alzheimer-type dementia (PAD). ANOVA, correlational and discriminant analyses of the neuropsychological test scores, and the neurophysiological and RT to S2 data revealed 22 highest-ranked between-group discriminant factors (all with a significance level of p < 0.01). The conclusive discriminant analysis retained 13 of these factors as final canonical functions, and these showed a 97% grouping accuracy (33 of the 34 subjects examined); the same percentage of correct classifications was also achieved using only the 15 best indicators in the group of CNV/RT findings. Using both of these sets of highest-ranked discriminators, all of the normal subjects and all of the PAD patients were correctly classified; only 1 PICD patient was misclassified as normal when the first group of 13 factors was used, and another PICD patient was misclassified as PAD using the second group of 15 factors. Our findings suggest that, providing they are correctly performed and interpreted, these non-invasive techniques may be an important tool for identifying incipient stages of presenile Alzheimer-type dementia.

Cognitive potentials: ipsilateral corticocortical interconnections in prefrontal human cortex ablations.

The research deals with the possible role of the essentially monosynaptic bidirectional corticocortical connections between occipito-temporo-parietal association cortical areas and frontal areas in the genesis of some contingent negative variation (CNV) components, especially on the supramodal dorsolateral prefrontal regions. With standard and topographic mapping methods of analysis, the multicomponent CNV complex formation was examined in 7 patients with extensive frontal cortex ablations exactly identified through CT/MRI examinations, and in 10 normal subjects. On the scalp over the ablated frontocortical areas, no consistent post-warning auditory N100 a-b-c, P200, P300, early and late CNV components were recordable. The hypothesis is proposed that the bidirectional ipsilateral long-distance pathways which interconnect uni-polymodal occipito-temporo-parietal cortical areas to prefrontal ones, in particular the arcuate-superior longitudinal and superior/inferior occipito-frontal fasciculi, play an important role in the genesis of several CNV complex components, especially the multicomponent post-S1 auditory N100. The posteroanterior sequential latency differences of these neurocognitive components, roughly measured along the scalp or on MRI imagings, is probably accounted for by the transcortical ipsilateral conduction time of about 1 cm/ms (10 m/s).

Changes in bit-mapped contingent negative variation (CNV) activity due to initial normal involutional processes of the human brain.

Bit-color mapped multicomponent CNV complexes and RTs to S2 evoked with a simple warned CNV/RT paradigm were recorded and measured in 20 selected right-handed very healthy volunteers (10 young adults and 10 presenile subjects, mean age 28.3 and 59.6, respectively). EEG and CNV components (post S1, N1, P2, P3; early CNV; N1200; late CNV; CNV resolution) were recorded from Fz, C3, Cz, C4, P3, Pz, and P4 referenced to linked mastoid electrodes. EOG, RT and stimuli were also recorded. The presenile group differed significantly from the younger group in the auditory post-S1 N1 and early (O-wave) and late (P-wave) CNV complex components. A progressive amplitude reduction limited to frontal leads between O-wave and P-wave, the lowest point being reached in the P-wave, was characteristic in the presenile group. Moreover, presenile subjects showed relatively flat CNV waveshapes of low amplitude and, on the whole, performed a little less well than young ones. This finding suggests that the statistically significant changes in auditory post-S1 N1 and CNV activity recorded in our presenile subjects, without any appreciable deficits in behavioral or mental performance, could be alerting signs of early brain involutional processes related to minimal and subclinical decline in orienting, attentiveness and response preparation capabilities. If such is the case, and it could be confirmed in a larger sample of very healthy subjects, these age-related changes in the presenium might prove to be of considerable practical importance for clinical research.

Effect of physiological and pathological aging processes on topographic bit-mapped cognitive evoked potentials in presenile subjects.

Bit-mapped multicomponent CNV complex and reaction time (RT) were recorded and measured in 24 presenile patients with initial symptoms of very mild to moderately severe primary mental deterioration without depression, and in 10 age-matched controls. All patients underwent CT and MRI examinations, EEG spectral analysis and a battery of psychometric test. Significant group differences were obtained for measures of some post-S1 ERP and CNV components, particularly of the post-S1 N1b, P300 and early and late pre-S2 CNV. P300 with increased latency, no significant CNV activity, very prolonged RTs, EEG slowing down and diffuse brain atrophy were observed in the majority of patients with probable presenile Alzheimer's dementia. These results suggest that CNV/RT and EEG activity changes similar to those observed in our patients may constitute a valuable clue for the study of brain dysfunction in the early stage of presenile idiopathic cognitive impairment.

Topographic CNV activity mapping, presenile mild primary cognitive decline and Alzheimer-type dementia.

The CNV complex evoked with a standard paradigm (S1-2 sec-S2-motor response) and reaction time (RT) to the imperative signal (S2) were recorded and measured in 12 patients with initial presenile idiopathic cognitive decline (PICD), 12 with presenile Alzheimer-type dementia (PAD) and 10 healthy age-matched controls. Significant group differences were obtained for measures of some CNV components, particularly of the late pre-S2 CNV. No significant CNV activity, very prolonged RTs and sometimes characteristic post-imperative negative variations (PINV) were observed in the majority of patients with PAD. These results suggest that similar CNV complex and RT changes to those observed in our patients may constitute a valuable clue in the study of pathophysiological brain functioning in the early stages of presenile idiopathic mental deterioration.