RECENT study has revealed a cephalically directed brain stem system whose stimulation desynchronizes the electrical activity of the cerebral cortex in a manner simulating that observed in awakening from sleep or in the EEG arousal reaction (8). This system was found to be distributed in the reticular formation of the medulla, the tegmentum of the pons and midbrain and the sub-and hypothalamus. The means by which its activating influence became exerted upon the cortex was speculated upon and, because of the generalized distribution of the cortical effects, it seemed likely that the diffuse thalamic projection system was concerned. Some evidence favoring this possibility was obtained but the problem was left for further investigation.Following preliminary determination of the organization of the diffuse thalamic projection system (12), the present study has explored this matter further: (i) by determining the thalamic regions whose electrical activity is desynchronized by stimulation of the reticular formation of the lower brain stem, (ii) by determining the distribution of thalarnic sites from which evoked potentials are recorded upon single shock stimuli to the reticular activating system, (iii) by exploring the thalamic areas whose direct excitation desynchronizes the electrocorticogram, (iv) by ascertaining the distribution of cortical potentials evoked by single shock stimulation of the reticular activating system, and (v) by determining the effect of diencephalic lesions on ascending conduction of the reticular influence. The results indicate that the ventromedial part of the thalamus is most critically involved in transmission of the reticular activating influence, with the rest of the thalamus (including the diffuse thalamic projection system) playing a subsidiary role. Evidence, moreover, is provided that a proportion of the influence of the reticular activating system upon the cortex may be exerted by an extra-thalamic route, paralleling that of the secondary response system described by Morison et al, (1, 10, 11). METHODSCats immobilized with B-erythroidine were used, with a Palmer respirator providing artificial respiration. Exposures were made under local procaine. S m d doses of chloralo---
SYNOPSIS Abnormalities of the cervical epithelium are set out in two main groups: bland lesions which are regarded as unrelated to malignancy, and malign lesions which are considered as potential precursors of invasive carcinoma. The histological features of each condition and the cytological pattern of the corresponding cervical smear are described and correlated.Cone biopsy is advocated as the only satisfactory form of cervical biopsy for both the diagnosis and evaluation of lesions such as dysplasia and carcinoma in situ. It is emphasized that further study is necessary to determine their natural history and prognosis in relation to invasive carcinoma.It is now widely accepted that certain abnormalities of structure and arrangement in the cells of cervical squamous epithelium may be the precursor of invasive carcinoma. These changes within the epithelium are termed mild or severe dysplasia according to their severity, and in their extreme form are described as carcinoma in situ.Usually these abnormalities produce no signs or symptoms, and are not detectable at ordinary clinical examination. Cytology, however, by the study of cells scraped or exfoliated from the cervix, provides a routine screening method. The discovery of cells in the cytological smear suggestive of severe dysplasia or carcinoma in situ is an indication for cervical cone biopsy. It is not only in the interests of the patient that these lesions should be detected in this way, but it also provides material for further study of their relationship to invasive carcinoma, a subject on which there is as yet little precise information. If such a study is to be valid, then there must be uniformity in the terminology and histological criteria used in assessing the lesions. This paper attempts to describe and classify abnormalities of the cervical epithelium in a manner suited to this purpose. Many of the views expressed have crystallized from the study the authors were asked to make of histological material in the survey of carcinoma in situ being carried out by the Royal College of Obstetricians and Gynaecologists (Govan, Haines, Langley, Taylor, and Woodcock, 1966 The paper deals particularly with dysplasia and carcinoma in situ, but includes other changes which, although unrelated in their natural history, have histological patterns sometimes confused with these conditions. Clinically invasive carcinoma is not discussed. The detection of abnormalities in the cervical smear is often the first step in the diagnostic sequence of the more serious lesions; for this reason an attempt is also made at a broad correlation between the histological appearances in the biopsy specimen and the cytological pattern of the corresponding smear. It is of great practical importance in discussing any abnormality of the cervical epithelium to decide whether or not it is related to carcinoma. The changes are therefore described in two main groups: first, bland lesions which are regarded as having no proclivities for malignant change, and secondly malign lesions which are ...
Recent research indicates prolonged disorders of consciousness (PDOC) result from structural and functional impairments to key cortical and subcortical networks, including the default mode network (DMN) and the anterior forebrain mesocircuit (AFM). However, the specific mechanisms which underpin such impairments remain unknown. It is known that disruptions in the striatal-pallidal pathway can result in the over inhibition of the thalamus and lack of excitation to the cortex that characterizes PDOC. Here, we used spectral dynamic causal modelling and parametric empirical Bayes on rs-fMRI data to assess whether DMN changes in PDOC are caused by disruptions in the AFM. PDOC patients displayed overall reduced coupling within the AFM, and specifically, decreased self-inhibition of the striatum, paired with reduced coupling from striatum to thalamus. This led to loss of inhibition from AFM to DMN, mostly driven by posterior areas including the precuneus and inferior parietal cortex. In turn, the DMN showed disruptions in self-inhibition of the precuneus and medial prefrontal cortex. Our results provide support for the anterior mesocircuit model at the subcortical level but highlight an inhibitory role for the AFM over the DMN, which is disrupted in PDOC.
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