bluuebunny/crossref_metadata_2025_split huggingface dataset:
Spinal Epidural Lipomatosis: A Complication of Glucocorticoid Therapy
Authors: Russell N. A. , Belanger G. , Benoit B. G. , Latter D. N. , Finestone D. L. , Armstrong G. W. 
Published: July 2016

ABSTRACT:A 21-year-old woman receiving prolonged high dosage glucocorticoids developed spinal cord compression due to excessive accumulation of epidural fat. Computerized tomographic scanning confirmed the diagnosis and revealed a peculiar pattern of spinal cord displacement which we believe to be unique to compression by fat. Laminectomy did not afford relief, possibly because of prolonged neural compression or because of compression at a higher spinal level. Although an unusual complication of Cushing’s syndrome, epidural lipomatosis should be considered when such a patient develops symptoms of spinal cord or cauda equina compression.
Inflammatory Myelopathy Presenting as a Cystic Intramedullary Spinal Cord Lesion
Authors: Tranmer B.I. , Gray T.A. , Horsey W.J. , Gonsalves C.G. 
Published: July 2016

ABSTRACT:A case of subacute progressive spinal tetraparesis had myelographic evidence of cervical spinal cord swelling and a delayed metrizamide computed tomographic myelogram (MCTM) suggested cavitation within the swollen spinal cord. Surgical exploration of the cervical cord revealed inflammatory changes only. No syrinx or intramedullary tumour was found. The accumulation of metrizamide within the spinal cord, as demonstrated by MCTM, did not’respresent a syrinx or a cystic tumour, but more likely an area of inflammation. Because inflammatory myelopathy may simulate an intramedullary tumor or syrinx, careful analysis of all clinical and radiological information is necessary to help make a correct diagnosis.
Visual Loss Secondary to a Giant Aneurysm in a Patient with Tuberous Sclerosis
Authors: Guttman Mark , Tanen S. Mark , Lambert Colin D. 
Published: July 2016

ABSTRACTWe report a fifty three year old man who presented with progressive visual loss. Investigation disclosed a giant aneurysm with optic nerve compression, which was successfully treated surgically. The patient had typical skin lesions of tuberous sclerosis, but did not suffer from a seizure disorder or mental retardation. In the past he had had an enucleation for glaucoma secondary to a retinal phakoma.Cerebral aneurysms are discussed in relation to the tuberous sclerosis disease process. After review of the literature, we propose that the aneurysms are secondary to dysplastic change in the vessel walls, this is in keeping with the abnormal tissue proliferations in this disease.
Is Parkinson’s Disease Acquired or Inherited?
Authors: Duvoisin Roger C. 
Published: July 2016

ABSTRACTA considerable proportion of patients with Parkinson’s disease report having affected relatives. However, anamnestic data obtained from probands on the occurrence of secondary cases among their relatives are of limited value. In considering the possible role of heredity in Parkinson’s disease it is necessary to carefully distinguish between the disease and other disorders such as essential tremor and olivopontocerebellar atrophy which may manifest parkinsonian features. Controlled family studies have shown only a very slight excess of secondary cases among index siblings as compared to spouse siblings. The concordance rate for Parkinson’s disease among identical twins is extraordinarily low and does not significantly exceed that among fraternal twins or that expected from the prevalence rate among siblings found in the controlled family studies. The available evidence indicates that heredity plays no significant role in the etiology of Parkinson’s disease. Consequently the disease must be considered to be acquired.
The Morphological Basis of Dementia in Parkinson’s Disease
Authors: Ball M.J. 
Published: July 2016

ABSTRACTThe literature pertinent to the pathological anatomy subserving dementia in Parkinsonian patients is reviewed. Mechanisms discussed include cerebral cortical atrophy; hydrocephalus; Lewy body inclusions; neocortical lesions of the Alzheimer type; depletion of cholinergic, dopaminergic or noradrenergic transmitter systems; ‘subcortical’ dementia; and neuronal depopulation of the basal forebrain.New autopsy data are presented to confirm that, contrary to published reports, most patients with parkinsonism who exhibit dementia do not have concomitant Alzheimer’s disease, and that some different pathogenetic mechanism must be sought to account for this increasingly common cause of cognitive decline in the sufferers of Parkinson’s disease.
Limitations of Long Term Use of Antiparkinson Drugs
Authors: Yahr Melvin D. 
Published: July 2016

ABSTRACTEffective control of parkinsonian symptoms can be achieved in a substantial number of patients by the judicious use of dopaminergic agents. To a considerable extent these drugs produce optimal therapeutic effects during the first 3–5 years of their use. Subsequently, efficacy diminishes with reemergence of parkinsonian symptoms as well as a number of untoward responses. The nature, frequency and mechanisms underlying the limitations of long term use of presently available anti-parkinson agents are discussed in this presentation.
Should Levodopa Therapy for Parkinsonism be Started Early or Late? Evidence Against Early Treatment
Authors: Fahn Stanley , Bressman Susan B. 
Published: July 2016

ABSTRACTWe define the meaning of early and late treatments and present arguments opposed to early treatment with levodopa. These are based on the development of complications with long-term Sinemet which include clinical fluctuations, loss of efficacy, and painful dystonic cramps. By delaying the onset of levodopa therapy until the symptoms require this most potent of antiparkinsonian agents, we can delay the onset of these disabling problems. Also, using as low a dosage as possible should reduce the risk of any long-term complication related to accumulative dose.We also present the serial evaluations of 26 patients followed for as long as 7.5 years before levodopa therapy was initiated. Three scoring scales on these patients are compared. Arguments are presented which suggest that the Columbia University and the ADL scales are superior to the UCLA scale, and more closely approximate the curve of the progressive clinical disability of the disease as assessed by global evaluation. We conclude that the ultimate answer to any clinical debate must come from well-designed, controlled studies to assess the differences between two treatment modalities.
Should Dopamine Agonists Be Given Early or Late? A Review of Nine Years Experience with Bromocriptine
Authors: Lieberman Abraham N. , Gopinathan Govindan , Hassouri Hassan , Neophytides Andreas , Goldstein Menek 
Published: July 2016

ABSTRACTExperience with bromocriptine in 106 patients treated over nine years was reviewed. Most of the patients were already being treated with levodopa (combined with a peripheral decarbosylase inhibitor). These patients, after having initially achieved a good response to levodopa, were no longer responding satisfactorily. Most of the patients were also experiencing diurnal oscillations in performance: “wearing off” and “on-off” phenomena. In these patients previous attempts at changing the dose (increasing or decreasing) or changing the scheduling of levodopa had been unsuccessful. Bromocriptine was added to levodopa beginning at a dose of 5mg/day, and each week was increased by another 5mg/day. At a dose of bromocriptine of at least 25 mg/day, there was a decrease in disability in the majority of patients with a decrease in the severity of the diurnal oscillations in performance (especially “wearing off” phenomena). In most patients, the addition of bromocriptine resulted in an approximately 10% reduction in the dose of levodopa. The majority of patients sustained their improvement at least one year. In some patients improvement was sustained for up to five years. The therapeutic efficacy of bromocriptine was limited in many patients by the occurrence of adverse effects including mental changes, dyskinesias, orthostatic hypotension, and nausea. These adverse effects could often be minimized by reducing the dose of bromocriptine or levodopa. All adverse effects were reversible upon stopping the drug. We have found bromocriptine to be a valuable adjunct in the treatment of these patients.
Pineal Region Tumors
Authors: Boyd Michael C. , Steinbok Paul 
Published: July 2016

ABSTRACT:The management of pineal region tumors has changed considerably since the introduction of microsurgery and CT scanning. Analysis of our own series of 36 patients, comparing those treated in the pre-CT scan and microsurgery era with those treated afterwards, shows the important role these two techniques play. Current controversies in treatment and our own approach to management of pineal region tumors are discussed.
The Changing Picture of Pseudotumor Cerebri in Children
Authors: Couch R. , Camfíeld P.R. , Tibbies J.A.R. 
Published: July 2016

ABSTRACT:Among 38 children with pseudotumor cerebri only 3 cases were due to ear disease or its complications. The commonest cause was a refeeding syndrome either due to nutritional deprivation or as an early finding in the treatment of cystic fibrosis. It is uncommon to find the cause of pseudotumor in older children but in those under 6 years the cause was found in 85%. Because of the adverse effects of steroids we use this treatment in the more resistant cases.
delta-Opioid Modulation of Striatal Dopaminergic Activity in Mice
Authors: Dua Ashok K. , Pinsky Carl 
Published: July 2016

ABSTRACT:Mu- and delta-opioid subtype receptor antagonists were tested in the mouse for their effects on vertical climbing activity, an index of striatal dopaminergic activity. The selective delta-opioid antagonist ICI 154 129 (1/1) by itself enhanced vertical climbing activity in a dose-related manner, whereas the mu-opioid antagonist naloxone by itself was inactive on climbing behavior. Naloxone increased the climbing-stimulant effect of I/I. Unstimulated vertical climbing activity was reduced, and all opioid-antagonist enhancement of climbing behavior was antagonized, by the competitive dopamine antagonist haloperidol in dose-related fashion. The observed motor-enhancement effect of a selective delta-opioid receptor antagonist is the first demonstration of physiologically-significant tonic activity on a central opioid receptor. Our observations suggest that 1/1 may be useful clinically in striatal dopamine-deficient disease conditions such as parkinsonism.
Kenneth Edwin Livingston M.D., D.A.B.N., F.A.C.S., F.R.C.S. (C) (1914 – 1984)
Authors: Morley T. P. 
Published: July 2016

Kenneth Livingston was born in 1914 in Pendleton, Oregon. He attended Stanford University and obtained his BA in 1936. His medical student days were spent at Harvard where he graduated MD in 1939.His neurosurgical education began in 1942 at Strong Memorial Hospital, Rochester, N.Y.; then, after two years at the U.S. Naval Hospital in Oakland, California, he was appointed to the Attending Staff at the Lahey Clinic in Boston from 1946-1948. He returned to Oregon as Assistant Clinical Professor of Neurosurgery at the University of Oregon Medical School in 1948.
Pitfalls of Incomplete Myelography with Thoracic Spinal Lesions
Authors: Cohen Hart C.M. , Tucker William S. 
Published: July 2016

ABSTRACT:This paper describes four patients with thoracic spinal lesions in whom the initial clinical presentation was highlighted by complaints in the lower back and lower extremities, in the absence of thoracic spinal or radicular symptoms. Initial myelography, confined to the lumbar region, failed to reveal a cause for the patients’ symptoms. Subsequently, diagnostic consideration of a thoracic spinal lesion prompted repeat myelography of the thoracic region which demonstrated a relevant lesion in each case. It is important to visualize the thoracic cord when myelography is performed for the investigation of pain or neurological symptoms in the lower back or lower extremities.
Pupillary Abnormalities in Congenital Neurosyphilis
Authors: Sundaram M.B.M. 
Published: July 2016

ABSTRACT:Pupils in congenital neurosyphilis differ from the classic Argyll-Robertson pupil in acquired cases, and often tend to be large and unreactive. Constriction to pilocarpine in the reported patient would suggest that peripheral parasympathetic damage is responsible for such pupillary findings. Congenital neurosyphilis should be included among the causes of “tonic” pupil.
Hemorrhagic Changes in Experimental Spinal Cord Injury Models
Authors: Khan Moe , Griebel Robert , Rozdilsky Bodan , Politis Michael 
Published: July 2016

ABSTRACT:Early hemorrhagic changes in the spinal cord were compared in three experimental spinal cord injury models in the rat in order to determine the nature and consistency of spinal cord hemorrhage following specific and quantitated forces of injury. The spinal cords were injured by weight-dropping, aneurysm clip and extradural balloon compression techniques. Hemorrhagic changes were assessed quantitatively by the image analyser at 1 and 3 hours after injury. Tissue damage was assessed by determining the percentage of total cross sectional area containing hemorrhage. The extent of hemorrhage at site of injury in the clip and balloon preparations was equal, but several times lower in the weight-drop induced injury. Within each experimental group no appreciable differences were observed at the site of injury between the 1 and 3 hours preparations. The variability of damage within experimental groups was most in the weight-dropping and balloon and least in the clip preparations. Differences were also indicated with respect to the distribution of hemorrhage in grey versus white matter. These findings may be of significance when functional recovery is considered in various experimental acute spinal cord injury models.
Aqueduct Gliosis Caused by Keratin and Cholesterol In a Case of Craniopharyngioma
Authors: Horoupian Dikran S. , Wisniewski Henryk M. , Gamble Robert , Liebeskind Arie L. 
Published: July 2016

SummaryKeratin and cholesterol particles released by a craniopharyngioma were shown to be the agents involved in the production of a foreign-body granulomatous arachnoiditis and ependymitis. Some of the particles were seen embedded in the reactive subepen-dymal glial tissue along the aqueduct of Sylvius. It was thought they were a major factor leading to the aqueduc-tal stenosis. However, we have also considered that the change in cerebro-spinal fluid hydrodynamics following the ventriculopleural shunt contributed to the occlusion of the aqueduct.
Diphenylhydantoin and Pulmonary Function
Authors: Smith Ronald J. , Man Godfrey C. W. , Paul Man S. F. , McLean Donald R. 
Published: July 2016

SummaryThirty-nine epileptic patients underwent pulmonary function testing. Twenty-one of these patients, ranging in age from 16 to 44 years, had taken diphenylhydantoin (DPH) for 2 to 17 years. Eighteen patients, who had taken other anticonvulsants for similar time periods served as controls. Five patients in the DPH group had lung volume abnormalities, four had abnormal airway function, and five had abnormalities of alveolar gas mixing. One patient in the control group had lung volume abnormalities, two had abnormal airway function, and five had abnormalities of alveolar gas mixing. Statistical analysis revealed no significant differences between the groups, or between either group and predicted values.
Vitamin E Deficiency and Seizures in Animals and Man
Authors: Ogunmekan A.O. 
Published: July 2016

SummaryStudy of 100 children with grand mal convulsive disorders and 100 medically healthy children of matching age showed significantly lower plasma levels of vitamin E in the former (means 632.2 ± 17.3 and 822.5 ± 2\.Zßg/dl respectively; p < 0.001). This finding accords with the ability to prevent seizures in rodents by giving a-tocopherol before exposing them to a convulsion-inducing environment.
Etude Histopathologique et Neurochimique Suite a des Lesions Unilaterales du Locus Coeruleus Chez le Rat et de la Region Postlocus Chez le Chat (Part 2)
Authors: Marchand R. , Chauvel P. , Fantino M. , Poirier L.J. 
Published: July 2016

SummaryUnilateral lesions involving the area immediately caudal to the locus coeruleus in the cat are associated with slight decreases of noradrenaline (NA) in both sides of the spinal cord without any important change of serotonin (5-HT) concentration in the spinal cord and of N A and 5-HT concentrations in the cerebral cortex of both sides. In other cats with similar lesions involving the same area bilaterally (postlocus lesions) NA is markedly decreased and 5-H T slightly decreased in the hypothalamus and spinal cord but the concentrations of NA and 5-HT of the cerebral cortex, striât urn and thalamus are not conspicuously modified by such postlocus lesions.Unilateral lesions in the area of the loci coeruleus and subcoeruleus in the rat are associated with a marked decrease of noradrenaline (NA) in the ipsilateral cerebral cortex without any important change of NA in the contralateral cortex and in the spinal cord of both sides. Under such conditions the concentrations of serotonin (5-HT) are not significantly modified in the cerebral cortex and spinal cord of both sides. NA and 5-HT concentrations of the cerebral cortex of both sides are unmodified by unilateral lesions of the cerebellar nuclei in the rat. In the latter group of animals slight increases of NA and 5-HT in the spinal cord are significant in comparison to the values obtained in the control animals but not from one side of the spinal cord to the other.These results further support the suggestion that the noradrenergic coeruleo-cortical pathway originating in the loci coeruleus and subcoeruleus ascends on the same side and ends in the ipsilateral cerebral cortex. In the light of the results of this investigation and of those reported in a companion paper (Marchand et ai, 1979) NA fibers reaching the hypothalamus and spinal cord most likely arise from neurons located caudally in respect to the locus coeruleus. Moreover NA fibers ending in the hypothalamus do not ascend in the dorsolateral part of the isthmic area and, therefore, have a different course than the N A fibers reaching the cerebral cortex and thalamus.
Cerebellar Form of Progressive Multifocal Leukoencephalopathy (PML)
Authors: Parr Justin , Horoupian Dikran S. , Winkelman A. Charles 
Published: July 2016

SummaryA case of progressive multi-focal leukoencephalopathy (PML) with selective involvement of cerebellum and brain stem is compared with nine other published cases. Recognition of PML presenting with ataxia before cerebral manifestations is stressed especially, since promising results with some antiviral drugs have been claimed.
Computed Tomography of Posterior Fossa in Hereditary Ataxias
Authors: Langelier R. , Bouchard J.P. , Ouchard R.B 
Published: July 2016

SummaryNine cases of Friedreich's ataxia and seven cases of autosomal recessive spastic ataxia of Charlevoix-Saguenay (ARSACS) were submitted to neuroradiological procedures to determine the extent of atrophie processes in the central nervous system. All cases had a computerized cerebral tomography and five were studied with pneumencephalo-graphy. The results show a correlation between the two tests and the comparison between Friedreich's ataxia and ARS ACS.In Friedreich's ataxia, the radiological signs are variable and discrete in most of the cases. In A RSA CS there are constant signs of cerebellar atrophy almost limited to the superior parts of the vermis and anterior lobes.
Glucose Tolerance and Erythrocyte Insulin Receptors in Friedreich's Ataxia
Authors: Draper P. , Shapcott D. , Larose A. , Stankova J. , Levesque F. , Lemieux B. 
Published: July 2016

SummaryDetailed in vivo and in vitro studies of glucose and insulin metabolism in Friedreich's ataxia patients and unaffected family members have further defined the extent of the abnormalities in carbohydrate metabolism. The high incidence of glucose intolerance and a hyper-insulinemic response to a glucose challenge in a high percentage of Friedreich's ataxia patients has been confirmed. An increased incidence of glucose intolerance among hétérozygotes is suggested, while the siblings show a more normal distribution of diabetes and a nearly normal insulin response to the glucose tolerance test. Human growth hormone patterns are normal for all groups.Preliminary studies of insulin binding to erythrocytes suggest a difference in the binding characteristics among diabetic Friedreich's ataxia patients, while the binding in the non-diabetic Friedreich's ataxia group is similar to that of non-diabetic controls. Results from a small group of non-diabetic siblings suggest a normal insulin binding, while a tendency toward increased binding at low insulin concentrations among diabetic family members is noted.
Pyruvate Dehydrogenase, Lipoamide Dehydrogenase and Citrate Synthase Activity in Fibroblasts from Patients with Friedreich's and Charlevoix-Saguenay Ataxia
Authors: Melancon S. B. , Potier M. , Dallaire L. , Rollin P. , Fontaine G. , Grenier B. 
Published: July 2016

SummaryThe activity of lipoamide dehydrogenase and two closely related enzymes was studied simultaneously in early, mid, and late passage fibroblast cultures. Friedreich's ataxia fibroblasts tended to lose pyruvate dehydrogenase and citrate synthase activities, while lipoamide dehydrogenase activity remained constant with aging of the cells. Mean pyruvate dehydrogenase activity was lower over-all in fibroblasts from ataxies. Mean citrate synthase activity was higher in ataxie fibroblasts. Present tissue culture media do not represent the best conditions in which to reproduce cofactor binding defects such as those found in other genetic diseases with structural enzyme mutations.
The Development of Behaviour Therapy in Australia: Reply to Russo, Tarrier and Sakano
Authors: Lovibond Syd H. 
Published: July 2016

It was with considerable interest that I read the comments on my paper (Lovibond, 1993) offered by our three international colleagues. It is at once apparent from the commentaries that the issues in clinical psychology to which I drew attention are in no way unique to Australia. Quite clearly, however, in Japan behaviour therapy (or CBT) has not yet reached that stage of development where the problems I posed become relevant. For this reason I shall concentrate mainly on the comments of Professors Russo and Tarrier. Each of the commentators, but particularly Dr. Russo, found points of agreement with my statement of the issues, but none expressed support for the program of action I suggested. Surprisingly however, none had alternative solutions to offer.I believe the most important issue I raised was the threat to the primacy of the scientist-professional model in the education/training/practice of clinical psychologists. Professor Russo clearly shares my concerns here, but Professor Tarrier makes no mention of the scientist-professional model or the need to maintain links with the basic discipline of psychology. From the general tenor of his remarks, I gather that Professor Tarrier does not regard the fate of the scientist-professional model as a major issue, and indeed he seems quite satisfied with the status of clinical psychology in the UK. Interestingly however, the report of the Manpower Planning Advisory Group, which Professor Tarrier quotes at another point, suggests that in the UK “clinical psychologists' roles are seen as ambiguous by others, confused with the roles of other disciplines and further confused by the variety of ways in which psychology services are delivered and practised. The research also found poor promotion of clinical psychologists' contributions to services and an inappropriately low profile in view of the impact that clinical psychologists could be having on the effectiveness of services” (MPAG, 1990, p. 8).