ATTENTION has recently been focused upon the occurrence of abnormalities in the electro-encephalogram (e.e.g.) of apparently normal subjects, and upon the high incidence of these abnormalities in subjects with behaviour disturbances and in other members of their families. Davis (1941) analysed the variations in the e.e.g. of groups of normal subjects and the abnormalities in wave form and frequency which she found in epileptic and psychotic patients. Similarly Lindsley and Cutts (1940) measured the number of waves in different frequency bands in small groups of normal adults and children, and in groups of children considered to be " constitutionally inferior " or presenting definite behaviour problems. Previously Jasper, Solomon, and Bradley (1938) had studied the abnormalities seen in the e.e.g. of behaviour problem children, while Hoagland, Cameron, and Rubin (1937), and Davis and Davis (1939) showed that a relatively high proportion of psychotic, especially schizophrenic, patients had abnormal e.e.g.'s. In a statistical evaluation of the e.e.g. in epilepsy made by Golla, Graham, and Walter (1937), abnormalities were found in the e.e.g.'s of 60 per cent. of a mixed group of epileptics. It has since then been generally accepted as the common experience of most workers that a proportion of undoubted epileptics have a normal e.e.g. between fits. Jasper and Kershman (1941) have recently reported abnormalities in the e.e.g.'s of over 95 per cent. of a large group of epileptic subjects, and in surveying the electro-encephalographic phenomena found in epilepsy they have excluded epileptic subjects with " normal" records as being atypical. Lennox, Gibbs and Gibbs (1940) found that with their methods of interpreting records about 3 per cent. of patients with overt seizures had normal e.e.g.'s. This discrepancy in the percentage abnormality rate of epileptics may possibly be due to a difference in the norm adopted, but as there are not comparable figures for control groups of normals in all the communications this point is obscure. Lowenbach (1939), Strauss, Rahm, and Barrera (1939), and Lennox, Gibbs, and Gibbs (1939 and 1940) have 257 coright.
{"title":"THE SIGNIFICANCE OF AN ABNORMAL ELECTROENCEPHALOGRAM.","authors":"D Williams","doi":"10.1136/jnnp.4.3-4.257","DOIUrl":"https://doi.org/10.1136/jnnp.4.3-4.257","url":null,"abstract":"ATTENTION has recently been focused upon the occurrence of abnormalities in the electro-encephalogram (e.e.g.) of apparently normal subjects, and upon the high incidence of these abnormalities in subjects with behaviour disturbances and in other members of their families. Davis (1941) analysed the variations in the e.e.g. of groups of normal subjects and the abnormalities in wave form and frequency which she found in epileptic and psychotic patients. Similarly Lindsley and Cutts (1940) measured the number of waves in different frequency bands in small groups of normal adults and children, and in groups of children considered to be \" constitutionally inferior \" or presenting definite behaviour problems. Previously Jasper, Solomon, and Bradley (1938) had studied the abnormalities seen in the e.e.g. of behaviour problem children, while Hoagland, Cameron, and Rubin (1937), and Davis and Davis (1939) showed that a relatively high proportion of psychotic, especially schizophrenic, patients had abnormal e.e.g.'s. In a statistical evaluation of the e.e.g. in epilepsy made by Golla, Graham, and Walter (1937), abnormalities were found in the e.e.g.'s of 60 per cent. of a mixed group of epileptics. It has since then been generally accepted as the common experience of most workers that a proportion of undoubted epileptics have a normal e.e.g. between fits. Jasper and Kershman (1941) have recently reported abnormalities in the e.e.g.'s of over 95 per cent. of a large group of epileptic subjects, and in surveying the electro-encephalographic phenomena found in epilepsy they have excluded epileptic subjects with \" normal\" records as being atypical. Lennox, Gibbs and Gibbs (1940) found that with their methods of interpreting records about 3 per cent. of patients with overt seizures had normal e.e.g.'s. This discrepancy in the percentage abnormality rate of epileptics may possibly be due to a difference in the norm adopted, but as there are not comparable figures for control groups of normals in all the communications this point is obscure. Lowenbach (1939), Strauss, Rahm, and Barrera (1939), and Lennox, Gibbs, and Gibbs (1939 and 1940) have 257 coright.","PeriodicalId":54783,"journal":{"name":"Journal of Neurology and Psychiatry","volume":"4 3-4","pages":"257-68"},"PeriodicalIF":0.0,"publicationDate":"1941-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1136/jnnp.4.3-4.257","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40109726","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
From the Biochemical Department, National Hospital, Queen Square, London PREVIOUS work (Cumings, 1940) on the effect of prostigmin (mgm. i) in patients suffering from myasthenia gravis showed that although potassium was liberated from affected muscles and circulated in the blood, the urine did not show any increased amount of potassium. It was assumed that prostigmin did not in any way cause this retention of potassium in that it had no effect on the kidney, and upon this assumption certain deductions were made. The present paper describes an attempt to show that this assumption was correct.
{"title":"THE EFFECT OF PROSTIGMIN ON THE URINARY EXCRETION OF POTASSIUM IN THE NORMAL SUBJECT.","authors":"J N Cumings","doi":"10.1136/jnnp.4.3-4.235","DOIUrl":"https://doi.org/10.1136/jnnp.4.3-4.235","url":null,"abstract":"From the Biochemical Department, National Hospital, Queen Square, London PREVIOUS work (Cumings, 1940) on the effect of prostigmin (mgm. i) in patients suffering from myasthenia gravis showed that although potassium was liberated from affected muscles and circulated in the blood, the urine did not show any increased amount of potassium. It was assumed that prostigmin did not in any way cause this retention of potassium in that it had no effect on the kidney, and upon this assumption certain deductions were made. The present paper describes an attempt to show that this assumption was correct.","PeriodicalId":54783,"journal":{"name":"Journal of Neurology and Psychiatry","volume":"4 3-4","pages":"235-6"},"PeriodicalIF":0.0,"publicationDate":"1941-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1136/jnnp.4.3-4.235","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40109724","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"TRAUMATIC SUBDURAL EFFUSIONS.","authors":"A A McConnell","doi":"10.1136/jnnp.4.3-4.237","DOIUrl":"https://doi.org/10.1136/jnnp.4.3-4.237","url":null,"abstract":"","PeriodicalId":54783,"journal":{"name":"Journal of Neurology and Psychiatry","volume":"4 3-4","pages":"237-56"},"PeriodicalIF":0.0,"publicationDate":"1941-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1136/jnnp.4.3-4.237","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40109725","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
IT has been shown in a previous paper (Cumings, 1939b) that the potassium content of muscle was abnormal in two diseases, except for conditions in which fat or fibrous tissue replacement of muscle occurs. Some further muscles from a variety of diseases have since been examined and the results have not given rise to any change of opinion. It has also been shown (Cumings, 1939b, 1940) that muscles from myasthenia gravis contain an excess of potassium, which was liberated after prostigmin injection, with a resulting increase of the serum potassium level. There was, however, no increased urinary excretion of potassium, the potassium returning to the muscles as the muscles became weaker. The amount of potassium present in excess in the serum did not account for all the potassium which was estimated to have been liberated from the muscles. Two more patients with myasthenia have been investigated to confirm the previous results and to determine whether the red cells also showed an increase in their potassium content, and the results are recorded. Some experimental results are also recorded in which rabbits were injected with substances extracted from gelsemium roots in an endeavour to produce muscular disorders in any way comparable to myasthenia.
{"title":"POTASSIUM AND MUSCULAR DISORDERS.","authors":"J N Cumings","doi":"10.1136/jnnp.4.3-4.226","DOIUrl":"https://doi.org/10.1136/jnnp.4.3-4.226","url":null,"abstract":"IT has been shown in a previous paper (Cumings, 1939b) that the potassium content of muscle was abnormal in two diseases, except for conditions in which fat or fibrous tissue replacement of muscle occurs. Some further muscles from a variety of diseases have since been examined and the results have not given rise to any change of opinion. It has also been shown (Cumings, 1939b, 1940) that muscles from myasthenia gravis contain an excess of potassium, which was liberated after prostigmin injection, with a resulting increase of the serum potassium level. There was, however, no increased urinary excretion of potassium, the potassium returning to the muscles as the muscles became weaker. The amount of potassium present in excess in the serum did not account for all the potassium which was estimated to have been liberated from the muscles. Two more patients with myasthenia have been investigated to confirm the previous results and to determine whether the red cells also showed an increase in their potassium content, and the results are recorded. Some experimental results are also recorded in which rabbits were injected with substances extracted from gelsemium roots in an endeavour to produce muscular disorders in any way comparable to myasthenia.","PeriodicalId":54783,"journal":{"name":"Journal of Neurology and Psychiatry","volume":"4 3-4","pages":"226-34"},"PeriodicalIF":0.0,"publicationDate":"1941-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1136/jnnp.4.3-4.226","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40109723","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
SINCE the original description of Tay-Sach's disease in the eighties of the last century a group of allied nervous disorders has become recognized, the common pathological feature of which is a ubiquitous distention of the nerve cells with granules of a lipoid nature. Apart from a few anomalous forms it is customary to classify these amaurotic family idiocies according to the time of onset of the disease, infantile, late infantile, juvenile, late juvenile and adult types being described. The resemblance between the infantile type and Niemann-Pick's disease had been noted by Knox, et alia, in 1916, but it was not until Pick and Bielschowsky's (1927, 1928) demonstration of the closely similar cerebral pathologies of these two conditions that it became generally realized that disordered lipoid metabolism, not heredodegeneration, was responsible for the granular accumulations in the nerve cells. The consequent inclusion of the amaurotic family idiocies in the category of lipoidoses began a new chapter in the history of these much studied diseases and support for this new theory of pathogenesis has since been received from the occasional finding ofthe characteristic type of neuronal swelling in the predominantly mesodermal disorders of Gaucher (Lindau, 1930) and of Hunter-Hurler (Ashby, et alia, 1937). Nevertheless, in many, perhaps most, cases of amaurotic family idiocy lipoid storage is confined to the nervous system, and it might well seem a perversion of nomenclature to classify these apparently purely nervous diseases as " lipoidoses" were it not that in some otherwise typical examples of the infantile and juvenile forms unsuspected lipoid storage in the visceral organs has been found on microscopical search (Schob, 1930; Pick, 1932; Brouwer, 1936). The case recorded in this paper belongs to this theoretically important intermediate group which is characterized by the predominantly cerebral localization of the lipoid deposition, the reticulo-endothelial system being involved only in a minor degree. It differs, however, from Tay-Sach's disease in several respects, notably in its congenital character and in the histochemical reactions of the intracellular lipoid. 175 coright.
{"title":"A CONGENITAL FORM OF AMAUROTIC FAMILY IDIOCY.","authors":"R M Norman, N Wood","doi":"10.1136/jnnp.4.3-4.175","DOIUrl":"https://doi.org/10.1136/jnnp.4.3-4.175","url":null,"abstract":"SINCE the original description of Tay-Sach's disease in the eighties of the last century a group of allied nervous disorders has become recognized, the common pathological feature of which is a ubiquitous distention of the nerve cells with granules of a lipoid nature. Apart from a few anomalous forms it is customary to classify these amaurotic family idiocies according to the time of onset of the disease, infantile, late infantile, juvenile, late juvenile and adult types being described. The resemblance between the infantile type and Niemann-Pick's disease had been noted by Knox, et alia, in 1916, but it was not until Pick and Bielschowsky's (1927, 1928) demonstration of the closely similar cerebral pathologies of these two conditions that it became generally realized that disordered lipoid metabolism, not heredodegeneration, was responsible for the granular accumulations in the nerve cells. The consequent inclusion of the amaurotic family idiocies in the category of lipoidoses began a new chapter in the history of these much studied diseases and support for this new theory of pathogenesis has since been received from the occasional finding ofthe characteristic type of neuronal swelling in the predominantly mesodermal disorders of Gaucher (Lindau, 1930) and of Hunter-Hurler (Ashby, et alia, 1937). Nevertheless, in many, perhaps most, cases of amaurotic family idiocy lipoid storage is confined to the nervous system, and it might well seem a perversion of nomenclature to classify these apparently purely nervous diseases as \" lipoidoses\" were it not that in some otherwise typical examples of the infantile and juvenile forms unsuspected lipoid storage in the visceral organs has been found on microscopical search (Schob, 1930; Pick, 1932; Brouwer, 1936). The case recorded in this paper belongs to this theoretically important intermediate group which is characterized by the predominantly cerebral localization of the lipoid deposition, the reticulo-endothelial system being involved only in a minor degree. It differs, however, from Tay-Sach's disease in several respects, notably in its congenital character and in the histochemical reactions of the intracellular lipoid. 175 coright.","PeriodicalId":54783,"journal":{"name":"Journal of Neurology and Psychiatry","volume":"4 3-4","pages":"175-90"},"PeriodicalIF":0.0,"publicationDate":"1941-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1136/jnnp.4.3-4.175","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40109720","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
THE local use of sulphanilamide and sulphapyridine in wounds is proving valuable both by preventing infection and in controlling established infection. These drugs may be expected to have the same bacteriolytic and bacteriostatic effects in cerebral wounds as in wounds of other tissues, for the reaction of the brain to wounding and infection is basically similar. The reaction of other tissues to these drugs has not prevented their use locally in wounds. Healing has been shown to be delayed slightly but not significantly. Acute inflammatory reaction in response to the presence of sulphanilamide or sulphapyridine has been transitory in most tissues even though large amounts of drug have been applied. In cerebral wounds the inevitable local reaction to any foreign material and the potential remote toxic effects on nerve cells, neuroglia, and myelin may make it undesirable to implant sulphonamides. The purpose of these experiments was to determine whether such undesirable local and remote reactions followed the introduction of large amounts of sulphanilamide or sulphapyridine into cerebral wounds, and if they were sufficiently marked to contra-indicate their use. Observations were also made on the time taken for the drugs to disappear from the wounds, the levels of each drug reached in the blood, and the reaction of the tissue to these two drugs.
{"title":"SULPHANILAMIDE AND SULPHAPYRIDINE IN EXPERIMENTAL CEREBRAL WOUNDS.","authors":"E H Botterell, E A Carmichael, W V Cone","doi":"10.1136/jnnp.4.3-4.163","DOIUrl":"https://doi.org/10.1136/jnnp.4.3-4.163","url":null,"abstract":"THE local use of sulphanilamide and sulphapyridine in wounds is proving valuable both by preventing infection and in controlling established infection. These drugs may be expected to have the same bacteriolytic and bacteriostatic effects in cerebral wounds as in wounds of other tissues, for the reaction of the brain to wounding and infection is basically similar. The reaction of other tissues to these drugs has not prevented their use locally in wounds. Healing has been shown to be delayed slightly but not significantly. Acute inflammatory reaction in response to the presence of sulphanilamide or sulphapyridine has been transitory in most tissues even though large amounts of drug have been applied. In cerebral wounds the inevitable local reaction to any foreign material and the potential remote toxic effects on nerve cells, neuroglia, and myelin may make it undesirable to implant sulphonamides. The purpose of these experiments was to determine whether such undesirable local and remote reactions followed the introduction of large amounts of sulphanilamide or sulphapyridine into cerebral wounds, and if they were sufficiently marked to contra-indicate their use. Observations were also made on the time taken for the drugs to disappear from the wounds, the levels of each drug reached in the blood, and the reaction of the tissue to these two drugs.","PeriodicalId":54783,"journal":{"name":"Journal of Neurology and Psychiatry","volume":"4 3-4","pages":"163-74"},"PeriodicalIF":0.0,"publicationDate":"1941-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1136/jnnp.4.3-4.163","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40109719","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
THE concept of the body schema in its present form originated from the investigations of Head and Holmes (1911-12) into sensory disturbances from cerebral lesions. They showed that appreciation of posture and passive movement requires a " standard against which all subsequent changes of posture are measured before they enter consciousness." For this fundamental standard they introduced the term schema or postural model of the body. They came to postulate a similar schema for the localization of stimuli applied to the body surface. These schemata they supposed to be formed by the past sensory impressions. Claude (1909) assumed that mistakes in localization and estimation of posture can be caused by the disturbance of certain " mnestic centres for the topoand kinesthetic impressions and for the representations of the different parts of the body." Jones (1910) suggested an amnestic disturbance of the association between the sensory perceptions and the " autosomatognostic group of memory feelings " for his cases of allochiria. Pick, who had spoken of " spatial images of the body " (1908), adopted the term schema and stated that these schemata together with the optic image of the body are the essential framework for the consciousness of the body (1915). Earlier theories (Hartmann, Mach, Wernicke, Wundt) of the knowledge one has of one's own body have been summarized by Zingerle (1913). Schilder (1923, 1935) extended the concepts of Head and Holmes and of Pick. His " body schema " (or " body image ") is a complex built up by many somatic factors, among which the postural, kinmsthetic and tactile, as well as the optic and vestibular impressions are the most significant. The body schema contains the representations of the different parts of the body and their spatial relations to each other. The idea of the body schema has proved indispensable for the understanding of a variety of neurological and psychopathological conditions. In this paper it is proposed to deal with the group of body schema disorders that is most widely known as " anosognosia." This term was originally introduced by Babinski (1914) for cases of left hemiplegia who were completely unaware of and even denied the paralysis, no matter how often one had tried to convince 191 coright.
{"title":"IMPERCEPTION FOR THE POSITION OF THE EYELIDS ON ONE SIDE.","authors":"L H Rubinstein","doi":"10.1136/jnnp.4.3-4.191","DOIUrl":"https://doi.org/10.1136/jnnp.4.3-4.191","url":null,"abstract":"THE concept of the body schema in its present form originated from the investigations of Head and Holmes (1911-12) into sensory disturbances from cerebral lesions. They showed that appreciation of posture and passive movement requires a \" standard against which all subsequent changes of posture are measured before they enter consciousness.\" For this fundamental standard they introduced the term schema or postural model of the body. They came to postulate a similar schema for the localization of stimuli applied to the body surface. These schemata they supposed to be formed by the past sensory impressions. Claude (1909) assumed that mistakes in localization and estimation of posture can be caused by the disturbance of certain \" mnestic centres for the topoand kinesthetic impressions and for the representations of the different parts of the body.\" Jones (1910) suggested an amnestic disturbance of the association between the sensory perceptions and the \" autosomatognostic group of memory feelings \" for his cases of allochiria. Pick, who had spoken of \" spatial images of the body \" (1908), adopted the term schema and stated that these schemata together with the optic image of the body are the essential framework for the consciousness of the body (1915). Earlier theories (Hartmann, Mach, Wernicke, Wundt) of the knowledge one has of one's own body have been summarized by Zingerle (1913). Schilder (1923, 1935) extended the concepts of Head and Holmes and of Pick. His \" body schema \" (or \" body image \") is a complex built up by many somatic factors, among which the postural, kinmsthetic and tactile, as well as the optic and vestibular impressions are the most significant. The body schema contains the representations of the different parts of the body and their spatial relations to each other. The idea of the body schema has proved indispensable for the understanding of a variety of neurological and psychopathological conditions. In this paper it is proposed to deal with the group of body schema disorders that is most widely known as \" anosognosia.\" This term was originally introduced by Babinski (1914) for cases of left hemiplegia who were completely unaware of and even denied the paralysis, no matter how often one had tried to convince 191 coright.","PeriodicalId":54783,"journal":{"name":"Journal of Neurology and Psychiatry","volume":"4 3-4","pages":"191-205"},"PeriodicalIF":0.0,"publicationDate":"1941-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1136/jnnp.4.3-4.191","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40109721","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
A Summary of 200 Neurological and Psychiatric Admissions from the Canadian Army Service Forces. W. Baillie. 753. Present Day Trends in Neuropsychiatric Research. A Round Table Discussion. S. B. Wortis. 780. Report of Progress in Developing a Mental Hygiene Component of a City Health District. P. Lemkau, C. Tietze, and M. Cooper. 805. Personality Disorders with Brain Tumors. M. Kanzer. 812. An Evaluation of Manic-Depressive Psychosis in the Light of Follow-Up Studies. P. Hoch and H. L. Rachlin. 83 1. Prolonged Coma in Insulin Therapy. H. Cleckley and C. M. Templeton. 844. The Internal Environment and Behaviour. Introduction and the R6le of Oxygen. R. S. McFarland. 858. The Internal Environment and Behaviour. Internal Secretions. C. P. Richter. 878.
来自加拿大陆军服务部队的200例神经病学和精神病学入院总结。W.贝利。神经精神病学研究的当今趋势。圆桌讨论。S. B.沃提斯。发展城市卫生区的精神卫生组成部分的进展报告。P. Lemkau, C. Tietze, M. Cooper. 805。脑肿瘤的人格障碍。肯泽先生。从随访研究的角度评价躁狂抑郁精神病。P. Hoch和H. L. Rachlin。胰岛素治疗中的长期昏迷。H.克莱克利和C. M.坦普尔顿。内部环境和行为。氧的介绍和原理。r.s.麦克法兰。858. 内部环境和行为。内部的分泌物。C. P.里希特。
{"title":"EPITOME OF CURRENT JOURNALS","authors":"E. L. Gibbs","doi":"10.1136/jnnp.4.2.147","DOIUrl":"https://doi.org/10.1136/jnnp.4.2.147","url":null,"abstract":"A Summary of 200 Neurological and Psychiatric Admissions from the Canadian Army Service Forces. W. Baillie. 753. Present Day Trends in Neuropsychiatric Research. A Round Table Discussion. S. B. Wortis. 780. Report of Progress in Developing a Mental Hygiene Component of a City Health District. P. Lemkau, C. Tietze, and M. Cooper. 805. Personality Disorders with Brain Tumors. M. Kanzer. 812. An Evaluation of Manic-Depressive Psychosis in the Light of Follow-Up Studies. P. Hoch and H. L. Rachlin. 83 1. Prolonged Coma in Insulin Therapy. H. Cleckley and C. M. Templeton. 844. The Internal Environment and Behaviour. Introduction and the R6le of Oxygen. R. S. McFarland. 858. The Internal Environment and Behaviour. Internal Secretions. C. P. Richter. 878.","PeriodicalId":54783,"journal":{"name":"Journal of Neurology and Psychiatry","volume":"4 1","pages":"147 - 162"},"PeriodicalIF":0.0,"publicationDate":"1941-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1136/jnnp.4.2.147","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"63907599","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
IN a series of papers published ten years ago Berger reported abnormally slow waves in the electro-encephalogram (e.e.g.) of patients with diverse intracranial abnormalities. This work has already been adequately reviewed (Jasper, 1937, Walter, 1938). Since then these abnormally slow changes in electrical potential have been investigated in relation to tumours, abscesses, and other local lesions (Walter, 1936, 1937), high intracranial pressure (Williams, 1939), intoxications (Gibbs, Gibbs and Lennox, 1937) and degenerative diseases (Williams and Gibbs, 1939). Similar slow waves are associated with such general cerebral disturbances as the epilepsies (Gibbs, 1939), the psychoses (Hoagland, Cameron and Rubin, 1937) and abnormal personalities (Lindsley and Cutts, 1940). No such specific characteristics as have been described in relation to the epilepsies have been found in the abnormal slow waves resulting from demonstrable cerebral damage. It appears, on the contrary, that most conditions detrimental to cerebral activity are associated with suppression of the normal frequencies and a concomitant increase in the slower components of the frequency spectrum of the e.e.g. (Gibbs, Williams and Gibbs, 1940). These abnormal conditions range from the genetic abnormality of unstable personalities and epileptics to cerebral destruction by tumours or infection, and include transitory changes in blood constituents or cerebral blood flow. The abnormally slow waves are therefore non-specific, but there appears to be a direct relationship between their number, size, and period and the severity of cerebral change. During an earlier investigation of intracranial abnormalities (Williams, 1939) an attempt was made to correlate electro-encephalographic changes with different pathological states, and during the course of this work it was found that cerebral trauma produced abnormally slow waves, similar to those already mentioned. These changes seemed to be more variable in extent and degree, and to have a less constant relationship to the apparent severity of the lesion, than did similar changes in other abnormal states. Head injuries are notorious
{"title":"THE ELECTRO-ENCEPHALOGRAM IN ACUTE HEAD INJURIES.","authors":"D Williams","doi":"10.1136/jnnp.4.2.107","DOIUrl":"https://doi.org/10.1136/jnnp.4.2.107","url":null,"abstract":"IN a series of papers published ten years ago Berger reported abnormally slow waves in the electro-encephalogram (e.e.g.) of patients with diverse intracranial abnormalities. This work has already been adequately reviewed (Jasper, 1937, Walter, 1938). Since then these abnormally slow changes in electrical potential have been investigated in relation to tumours, abscesses, and other local lesions (Walter, 1936, 1937), high intracranial pressure (Williams, 1939), intoxications (Gibbs, Gibbs and Lennox, 1937) and degenerative diseases (Williams and Gibbs, 1939). Similar slow waves are associated with such general cerebral disturbances as the epilepsies (Gibbs, 1939), the psychoses (Hoagland, Cameron and Rubin, 1937) and abnormal personalities (Lindsley and Cutts, 1940). No such specific characteristics as have been described in relation to the epilepsies have been found in the abnormal slow waves resulting from demonstrable cerebral damage. It appears, on the contrary, that most conditions detrimental to cerebral activity are associated with suppression of the normal frequencies and a concomitant increase in the slower components of the frequency spectrum of the e.e.g. (Gibbs, Williams and Gibbs, 1940). These abnormal conditions range from the genetic abnormality of unstable personalities and epileptics to cerebral destruction by tumours or infection, and include transitory changes in blood constituents or cerebral blood flow. The abnormally slow waves are therefore non-specific, but there appears to be a direct relationship between their number, size, and period and the severity of cerebral change. During an earlier investigation of intracranial abnormalities (Williams, 1939) an attempt was made to correlate electro-encephalographic changes with different pathological states, and during the course of this work it was found that cerebral trauma produced abnormally slow waves, similar to those already mentioned. These changes seemed to be more variable in extent and degree, and to have a less constant relationship to the apparent severity of the lesion, than did similar changes in other abnormal states. Head injuries are notorious","PeriodicalId":54783,"journal":{"name":"Journal of Neurology and Psychiatry","volume":"4 2","pages":"107-30"},"PeriodicalIF":0.0,"publicationDate":"1941-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1136/jnnp.4.2.107","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40109717","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
THE electro-encephalographic changes following a recent head injury have been described (Williams, 1941). The observations were made upon 74 cases of head injury selected from a total of 600 because the injury had occurred less than 20 days previously. From these observations it was concluded that the electro-encephalogram (e.e.g.) accurately reflects the abnormal cerebral state caused by a recent head injury, that the progressive changes are a direct indica-tion of improvement or deterioration in this state, and that in the milder degrees of cerebral dysfunction it may demonstrate residual damage after all clinical signs have subsided. presence
{"title":"THE ELECTRO-ENCEPHALOGRAM IN CHRONIC POST-TRAUMATIC STATES.","authors":"D Williams","doi":"10.1136/jnnp.4.2.131","DOIUrl":"https://doi.org/10.1136/jnnp.4.2.131","url":null,"abstract":"THE electro-encephalographic changes following a recent head injury have been described (Williams, 1941). The observations were made upon 74 cases of head injury selected from a total of 600 because the injury had occurred less than 20 days previously. From these observations it was concluded that the electro-encephalogram (e.e.g.) accurately reflects the abnormal cerebral state caused by a recent head injury, that the progressive changes are a direct indica-tion of improvement or deterioration in this state, and that in the milder degrees of cerebral dysfunction it may demonstrate residual damage after all clinical signs have subsided. presence","PeriodicalId":54783,"journal":{"name":"Journal of Neurology and Psychiatry","volume":"4 2","pages":"131-46"},"PeriodicalIF":0.0,"publicationDate":"1941-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1136/jnnp.4.2.131","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40109718","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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