3. German Retrospect

1888 ◽  
Vol 34 (146) ◽  
pp. 289-296
Author(s):  
W. W. Ireland

Dr. G. Rabbas (“Zeitschrift für Psychiatrie” xli. Band, 3 Heft), following out the observations of Dr. Rieger, has, in a course of careful experiments, tested the capacity of the insane for reading in progressive dementia. He found that in general paralysis the power of reading was diminished, and in the end totally destroyed, and that this incapacity commenced at an early period of the disease. The words were given wrong or altered in a senseless manner, with a faint connection with the text read, whereas in functional insanity as well as senile dementia the power of reading was long retained even in cases where the mental fatuity seemed greater than in given cases of general paralysis. When maniacs could be induced to read they read on quickly without any regard to stops or beginnings of sentences, but they generally read correctly, without alteration of the words. This early loss of reading power in general paralysis, like the alteration in writing, is of great use for a differential diagnosis.

2010 ◽  
Vol 5 (2) ◽  
pp. 21 ◽  
Author(s):  
Uta Heinemann ◽  
Joanna Gawinecka ◽  
Christian Schmidt ◽  
Inga Zerr ◽  
◽  
...  

There is a broad range of diseases underlying dementia, of which Alzheimer’s disease is the most frequent in senile and pre-senile dementia. While senile dementia is predominantly caused by neurodegenerative or vascular disorders, in early-onset dementia other conditions are more relevant. Autoimmune, metabolic and genetic reasons should be evaluated, as well as toxic causes. A list of mutations associated with dementia is provided in this article. A higher proportion of potentially reversible conditions in pre-senile dementia highlights the value of detailed evaluation. Lumbar puncture is important in the diagnostic process to detect inflammatory changes, but dementia markers such as Aβ1–42 are also helpful in differential diagnosis. The value of cerebrospinal fluid markers for differential diagnosis is discussed in this article.


1968 ◽  
Vol 07 (01) ◽  
pp. 28-36 ◽  
Author(s):  
Władysław Jasiński ◽  
Janina Malinowska ◽  
Henryk Mackiewicz ◽  
Henryk Siwicki ◽  
Krystyna Lukawska

SummaryThe purpose of this investigation was to study the accumulation of 87mSr in the proximal parts of the femoral bones of patients treated previously by external irradiation due to cancer of the uterine cervix. It was assumed that this method may be used in the future for the early diagnosis of postirradiation changes of bone (osteoradionecrosis).The incidence of postirradiation changes of the femoral neck among 5735 patients treated between 1950 and 1961 at the Department of Gynaecology of the Institute, was 0.8%. In the early period of postirradiation changes the patients complain only of pain and limitation of physical activities. If radiological and gynaecological findings were negative, the differential diagnosis between early recurrence and early osteoradionecrosis became impossible.49 selected patients were scanned after intravenous injection of 10—115 μCi of 87mSr per kg of body weight (0.5 up to 6.0 mCi). Illustrative cases of normal pelvic bones as well as postirradiation changes are presented and discussed. The authors conclude that the findings justify further systematic studies on the morphology of accumulation of 87mSr in the bones.


1943 ◽  
Vol 89 (374) ◽  
pp. 1-20 ◽  
Author(s):  
E. Stengel

Many problems concerning Alzheimer's disease and Pick's disease are still awaiting clarification. In this country Henderson was the first to draw attention to the considerable importance of Alzheimer's disease in clinical psychiatry. Valuable work has been contributed by various writers in recent years (Grunthal, 1936; Critchley, 1929, 1930, 1931, 1938; Schottky, 1932; Thorpe, 1932; Rothschild, 1934; Malamud, Lowenberg and co-workers, 1929; Mayer-Gross, 1938; Kasanin and Crank, 1933; Jervis and Soltz, 1936; McMenemy, a.o., 1939). While Pick's disease has retained its position as a clinical entity based mainly on the characteristic anatomical picture, the position of Alzheimer's disease in the system of psychiatry has become more complicated; for instance atypical cases have been described presenting the anatomical characters of Alzheimer's disease, though not fitting into the original clinical conception of that disease. Lowenberg and his co-workers (1929) are inclined to regard Alzheimer's disease as a syndrome rather than a clinical entity. Many contributors have directed their main interest to the pathological changes. The knowledge of the symptomatology of those conditions is still incomplete. Further intensive study may enable us not only to base the diagnosis and differential diagnosis of Alzheimer's disease and Pick's disease on more solid clinical knowledge than hitherto, but also to recognize the early stages of those diseases before advancing cerebral degeneration effaces their characteristic clinical features. Unfortunately, most of the cases come under the observation of the psychiatrist only in the later stages of their illness, and it seems that the comparatively small proportion of the mental hospital population they represent does not reflect the incidence of those diseases. It is very likely that many patients die from intercurrent illnesses before their mental condition is recognized or sufficiently advanced to make admission to a mental hospital necessary. The differential diagnosis of those conditions offers considerable difficulties which often may prove insuperable. Alzheimer's disease and Pick's disease have to be distinguished not only from each other but from conditions of vascular origin, from senile dementia and various atypical conditions which occur at the same age period during which Alzheimer's disease and Pick's disease usually develop. Only careful collection and analysis of clinical observations and their scrutiny by pathological investigations can increase our still limited knowledge in this important field of psychiatry.


1915 ◽  
Vol 22 (4) ◽  
pp. 492-516 ◽  
Author(s):  
Henry A. Cotton

From the data provided by our investigations we may conclude that in all pathologic processes of the cortex which end in dementia and death, the fatty degeneration of the elements of the cortex plays a not unimportant part. The characteristic change for most of the psychoses is found in a great increase in amount of fatty deposits when compared to normal individuals of the same age. In some processes such as senile dementia and dementia præcox the fatty substance appears to fill completely the cell body, and these cells have apparently lost all their functioning power. It is not common to find the fatty deposits in the processes of the ganglion cells except in dementia præcox, and to a limited extent in senile dementia. In other cases the pathological variety of the fatty deposits in the ganglion cells is seen to be diffused over the whole ganglion cell. We were able especially to observe this in infectious psychoses, in general paralysis, and in epilepsy. The so called central neuritis assumes a peculiar attitude in that it plainly leads swiftly to an acute fatty degeneration of the ganglion cells, in which there exists an inclination of the fatty granules to flow together into large masses. Frequently the fatty degeneration of the ganglion cells appears to be connected with the sclerosis of the cells, especially when it is a matter of slowly progressing alterations of degeneration. The behavior of the glia is not wholly uniform in the various disease processes. In chronic disease processes we often find that the extent of the fatty accumulations in the ganglion cells does not correspond to an equal increase in the glia cells, while the otherwise acutely degenerative alteration in the nuclei of the glia is noticeable. In acute processes we see regularly an equal accumulation of the fat in both species of cell. The conditions of the cells in the vascular wall are wholly similar to those of the glia cells. We must therefore assume that in chronic diseases the fatty substance has been carried out of the glia and the vascular walls while it has been retained longer in the ganglion cells. Among all the disease processes amaurotic idiocy assumes a peculiar position. We have observed that in addition to the fatty materials of the scarlet fat stain, still other fatty materials, lipoid in character, have made their appearance. While the study of the fatty deposit in the cerebral cortex offers some points for a differential diagnosis, yet it is not adopted in all cases, since the distinction in individual disease processes is not always characteristic. From the preceding examination, however, in many cases there result important findings which briefly we summarize as follows: 1. In all degenerative alterations in the cerebral cortex the mass of the lipoid materials in the ganglion cells in comparison with that in healthy individuals of equal age is found to be considerably augmented. In the alteration of the lipoid materials in the ganglion cells two types in general may be distinguished: (a) An augmentation of the lipoid materials in the ganglion cells, in places where normally a small amount of fat is found, (b) An augmentation of the lipoid materials over the entire cell. 2. The first type we find also characteristic in senile dementia. The second type occurs in acute infectious psychoses, general paralysis, and well advanced epilepsy. 3. While the advanced lipoid degeneration of the ganglion cells in senile dementia has already been described in many ways, it has appeared from our investigations that also in the young chronic cases of dementia præcox far-reaching fatty degeneration of the ganglion cells, especially in the second and third cortical strata, likewise occurs. These findings should constitute an important contribution to the pathological anatomy of dementia præcox. 4. The so called central neuritis represents a peculiar disease process according to the appearance of the fatty degeneration, since this fatty degeneration reaches a very advanced degree, and also in so far as it deviates from other disease processes in that here there comes out very distinctly in the picture an inclination of the fatty granules to flow together. 5. Amaurotic idiocy also represents a particular disease process in respect to the lipoid degeneration, since here in addition to otherwise distributed scarlet stain lipoid materials, still other specific lipoid materials make their appearance.


1929 ◽  
Vol 75 (308) ◽  
pp. 107-113
Author(s):  
John P. Steel

In this hospital we have a routine differential diagnosis which is applied in all cases of suspected epilepsy and which is as follows: (a)High blood-pressure.(b)Trauma of vessels and angiospasm.(c)Nephritis, subacute and chronic.(d)Diabetes.(e)Tabes dorsalis, tabo-paresis, neuro-syphilis and general paralysis.(f)Hysteria.(g)Epilepsy.


1920 ◽  
Vol 66 (274) ◽  
pp. 305-306
Author(s):  
Sydney J. Cole

This prolific writer here surveys the diverse opinions of authors respecting the significance of injury in the ætiology of general paralysis, since the first description of the disease by Bayle in 1822, and gives eighty-four references. He considers that injury can act neither as a determining nor as a predisposing cause, and that it is very doubtful whether it can act even as an occasioning cause. Injury can, of course, accelerate or aggravate a pre-existing general paralysis, but it is not certain that it can give rise to the disease, even in a syphilitic subject. On this point, scientifically, an attitude of the greatest reserve is necessary, but for medico-legal purposes it is often right that an injured person should have the benefit of the doubt. The writer sets forth the differential diagnosis between traumatic dementia (strictly so-called) and post-traumatic general paralysis. His account of the medico-legal aspects of the question is mainly of French interest.


1990 ◽  
Vol 73 (4) ◽  
pp. 623-627 ◽  
Author(s):  
Adam P. Brown ◽  
Judy C. Lane ◽  
Shigeo Murayama ◽  
Dennis G. Vollmer

✓ Whipple's disease is infrequently considered in the differential diagnosis of patients presenting with progressive neurological deterioration. This is in part a result of the relative rarity of this entity and in part due to the more frequent initial presentation of the disease with gastrointestinal, musculoskeletal, or cardiovascular symptoms. A case is described in which the neurological symptoms of progressive dementia and weakness were seen in the relative absence of non-neurological symptomatology. The diagnosis of Whipple's disease was made from a brain biopsy. The neuropathology of Whipple's disease of the central nervous system is described and the importance of considering it as a treatable entity in the differential diagnosis of progressive neurological deterioration, despite the absence of systemic symptomatology, is stressed.


2018 ◽  
Vol 2018 ◽  
pp. 1-4
Author(s):  
Parmvir Parmar ◽  
Curtis L. Cooper ◽  
Daniel Kobewka

Rapidly progressive dementia is a curious and elusive clinical description of a pattern of cognitive deficits that progresses faster than typical dementia syndromes. The differential diagnosis and clinical workup for rapidly progressive dementia are quite extensive and involve searching for infectious, inflammatory, autoimmune, neoplastic, metabolic, and neurodegenerative causes. We present the case of a previously highly functional 76-year-old individual who presented with a 6-month history of rapidly progressive dementia. His most prominent symptoms were cognitive impairment, aphasia, visual hallucinations, and ataxia. Following an extensive battery of tests in hospital, the differential diagnosis remained probable CJD versus autoimmune encephalitis. He clinically deteriorated and progressed to akinetic mutism and myoclonus. He passed away 8 weeks after his initial presentation to hospital, and an autopsy confirmed a diagnosis of sporadic CJD. We use this illustrative case as a framework to discuss the clinical and diagnostic considerations in the workup for rapidly progressive dementia. We also discuss CJD and autoimmune encephalitis, the two main diagnostic possibilities in our patient, in more detail.


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