bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abnormal breathing patterns during sleep in diabetes
Authors: Mondini Susanna , Guilleminault Christian 
Published: January 2005

AbstractNineteen diabetic patients, 12 type I (insulin‐dependent) and 7 type II (late‐onset, non‐insulin‐dependent), underwent nocturnal polygraphic monitoring after a daytime medical evaluation that included tests of vagal responses and, in 6 patients, pulmonary function and hypercapnic and hypercapnic and hypoxic responses. Five lean type I patients had abnormal sleep‐related breathing patterns with central or obstructive sleep apnea and brief breathing irregularities during states 3 to 4 non‐rapid‐eye‐movement sleep, compared with only 1 overweight type II diabetic with moderate obstructive sleep apnea. There was no correlation between daytime ventilatory study findings and abnormal breathing patterns during sleep, but there was a clear relationship between neuropathy and sleep‐related breathing abnormalities in type I insulin‐dependent diabetics.
Amnesia in monkeys after lesions of the mediodorsal nucleus of the thalamus
Authors: Zola‐Morgan Stuart , Squire Larry R. 
Published: January 2005

AbstractRecent successes in developing an animal model of human amnesia in the monkey have made it feasible to try to identify with certainty the specific structures in the diencephalon and medial temporal region that cause amnesia when damaged. Monkeys with small lesion restricted largely to the posterior portion of the mediodorsal nucleus of the thalamus were given a test of memory sensitive to human amnesia and a second test that is analogous to the skill‐based tasks performed normally by manesic patients. The monkeys exhibited a marked impairment on the first test and performed normally on the second. The results show that circumscribed lesions of the mediodorsal nucleus can cause substantial amnesia.
Information processing speed in Friedreich's ataxia
Authors: Hart Robert P. , Kwentus Joseph A. , Leshner Robert T. , Frazier Robert 
Published: January 2005

AbstractThree patients with Friedreich's ataxia and six controls matched by age and vocabulary and information scores on the Wechsler Adult Intelligence Scale‐Revised were administered a measure of short‐term memory scanning. Patients with Friedreich's ataxia demonstrated a deficit in information processing speed in the relative absence of impairment in attention, memory, language, judgement, reasoning, and other cognitive functions. The short term memory scanning procedure may be useful in documenting cognitive slowing and in distinguishing this impairment from the motor abnormality often associated with a subcortical brain disorder.
Cardiovascular regulation and lesions of the central nervous system
Authors: Talman William T. 
Published: January 2005

AbstractThe central nervous system has an important role in the second‐to‐second regulation of cardiac activity and vasomotor tone. Central lesions that lead to a disturbance in autonomic activity tend to cause electrocardiographic and pathological evidence of myocardial damage, cardiac arrhythmias, and disturbances of arterial blood pressure regulation. To a great extent such cardiovascular disturbances result from alterations in sympathetic activity. Similar alterations in sympathetic activity can occur under conditions of emotional stress and precipitate cardiac arrhythmias that can themselves lead to the syndrome of sudden death. Experimental and clinical evidence suggests that central neural mechanisms may be involved in this important human syndrome, but no central lesion has yet been identified to account for it. Recent experimental evidence, derived from hypertension research, suggests that chemical disturbances in the central nervous system, without accompanying structural lesions, may be found to explain cardiovascular disturbances such as sudden death and hypertension.
Reversible diabetic nerve dysfunction: Structural correlates to electrophysiological abnormalities
Authors: Sima Anders A. F. , Brismar Tom 
Published: January 2005

AbstractStructural alterations of the nodal and paranodal areas were examined in the posterior tibial nerve in insulin‐depleted and insulin‐treated diabetic BB rats. The early metabolic phase of the distal symmetrical polyneuropathy was characterized by paranodal axonal swellings and nodal bulgings of the axon. These alterations correlate with intraaxonal sodium accumulation and decreased sodium equilibrium potentials which account for the early nerve conduction defect. Both the structural and electrophysiological abnormalities were completely normalized after vigorous insulin therapy. In the chronic diabetic polyneuropathy the paranodal area showed loss of paranodal axoglial junctions and paranodal myelin retraction. These changes may be partially responsible for the impaired electrical activity at the node as exemplified by irreversibly impaired sodium permeability and nerve conduction.
Pharmacokinetics of trihexyphenidyl after short‐term and long‐term administration to dystonic patients
Authors: Burke Robert E. , Fahn Stanley 
Published: January 2005

AbstractAlthough trihexyphenidyl has been used effectively for many years in the treatment of Parkinson's disease, little is known about its pharmacokinetics. Using a sensitive radioreceptor assay for anticholinergic drugs, we assayed trihexyphenidyl in human serum and studied its pharmacokinetics following short‐term and long‐term administration to patients with dystonia. Previously untreated patients had a biphasic semilogarithmic plot of serum concentration–time consisting of an initial rapid distribution phase and a later slower elimination phase. Patients on long‐term treatment showed only the slower elimination phase. Elimination followed first‐order kinetics and was rapid, with a half‐life of 3.7 ± 0.4 (SEM) hours. There was no relationship between half‐life and peak serum level, age, duration of therapy, or etiology or severity of dystonia. Although acute anticholinergic side effects paralleled the rise and fall of serum anticholinergic levels, the response of dystonia did not.
Volume depletion and natriuresis in patients with a ruptured intracranial aneurysm
Authors: Wijdicks E. F. M. , Vermeulen M. , ten Haaf J. A. , Hijidra A. , Bakker W. H. , van Gijn J. 
Published: January 2005

AbstractWe studied the sodium balance and changes in plasma volume by an isotope dilution technique in the first week after an aneurysmal subarachnoid hemorrhage in 21 patients. In 11 of the patients, the plasma volume decreased by more than 10%. This was accompanied by a negative sodium balance and hyponatremia in 6 patients, a negative sodium balance without hyponatremia in 4 patients, and a positive sodium balance in 1 patient. Together with a decrease in plasma volume, blood urea nitrogen content increased and body weight decreased. Three patients developed hyponatremia without a decrease in plasma volume. Serum vasopressin was measured in 14 of the 21 patients. The values were elevated on admission and declined in the first week, regardless of the presence of hyponatremia. These findings indicate that natriuresis and hyponatremia in aneurysmal subarachnoid hemorrhage reflect salt wasting and not inappropriate secretion of antidiuretic hormone and that these changes should be corrected by fluid replacement rather than by fluid restriction.
Treatment of central nervous system sarcoidosis with radiotherapy
Authors: Bejar Jose M. , Kerby Gerald R. , Ziegler Dewey K. , Festoff Barry W. 
Published: January 2005

AbstractThis report documents the twelve‐year follow‐up of a patient with neurosarcoidosis with multiple progressive central nervous system manifestations. Increased somnolence and seizure activity were associated with proliferation of nodular enhancing brain lesions, as seen on serial computed tomographic (CT) scans. Initially he responded to corticosteroid treatment, but gradually this response became unsatisfactory. After whole‐brain irradiation with a total dose of 3,000 rads, his clinical symptoms improved with disappearance of the enhancing brain lesions seen on CT scan.
Galactosialidosis: Low β‐galactosidase activity in serum after long‐term clotting
Authors: Sakuraba Hitoshi , Iimori Yuichi , Suzuki Yoshiyuki , Kint Jos A. , Akagi Masao 
Published: January 2005

AbstractSerum β‐galactosidase activity was found to be markedly increased in clotting blood from normal subjects, but patients with galactosialidosis showed only a slight increase of this enzyme activity. Consequently, the β‐galactosidase activity was low in serum after long‐term clotting in patients with this disease. The mechanism of the enzyme activation is unknown. The use of anticoagulants completely inhibited the activation.
Brachial plexus neuropathy in the population of Rochester, Minnesota, 1970–1981
Authors: Beghi Ettore , Kurland Leonard T. , Mulder Donald W. , Nicolosi Alfredo 
Published: January 2005

AbstractBrachial plexus neuropathy (BPN) is a clinical entity of unknown cause characterized by the acute or subacute onset of pain and weakness, with occasional atrophy of the arm muscles. Information on the incidence of the disease in a delineated population is lacking, as the data available on BPN have come essentially from case reports or selected series. Using the Mayo Clinic records–linkage system as the source of data, 579 clinical records were reviewed of Rochester, Minnesota, residents in which a diagnosis suggestive of BPN was reported for the period 1970 through 1981. Eleven cases fulfilled all criteria, providing an overall annual incidence rate of 1.64 cases per 100,000 population. An infectious disease and/or tetanus toxoid immunization preceded the onset of BPN in 4 cases. The upper brachial plexus was involved in 6 cases, the lower brachial plexus in 2, and the whole plexus in 3; in 1 case there was bilateral BPN. The neuropathy ran a mild to moderate course in 10 cases, and complete recovery was recorded in 6, with slight residua in the others. The occurrence of antecedent events and the features of the disease are supportive of the concept of an immune‐mediated process.
Complex partial seizures of frontal lobe origin
Authors: Williamson Peter D. , Spencer Dennis D. , Spencer Susan S. , Novelly Robert A. , Mattson Richard H. 
Published: January 2005

AbstractComplex partial seizures of medial or orbital frontal origin were documented in 10 of 90 patients with intractable epilepsy who were studied with depth electrodes. The clinical features that, in part, served to distinguish these seizures from complex partial seizures originating elsewhere included brief, frequent attacks, complex motor automatisms with kicking and thrashing, sexual automatisms, vocalization, and frequent development of complex partial status epilepticus. The constellation of clinical characteristics was often bizarre, leading to the erroneous diagnosis of hysteria. Stereotyped attack patterns helped establish the diagnosis of epilepsy. Interictal and ictal scalp electroencephalograms were often not helpful and were sometimes misleading.
Autoimmune response of patients with paraneoplastic cerebellar degeneration to a Purkinje cell cytoplasmic protein antigen
Authors: Jaeckle Kurt A. , Graus Francesc , Houghton Alan , Cardon‐Cardo Carlos , Nielsen Surl L , Posner Jerome B. 
Published: January 2005

AbstractSera from 6 of 12 patients with paraneoplastic cerebellar degeneration (PCD) contained anti–Purkinje cell antibodies, as determined by indirect immunofluorescence on frozen sections of normal human cerebellum. Samples of cerebrospinal fluid from 2 of the patients with serum antibodies were tested, and both specimens contained anti–Purkinje cell antibody. The anti‐Purkinje cell antibodies were polyclonal, fixed complement, and were present in all patients at serum dilutions of 1:1,000 or greater. Antibody activity could not be suppressed by preabsorption of sera with human or animal brain and tissue powders or with fresh crude human cerebellar extracts. No anti–Purkinje cell antibodies were detected in control sera from 167 neurologically normal cancer patients, 32 normal volunteers, 10 patients with other causes of cerebellar degeneration, or 8 patients with other paraneoplastic neurological diseases. Preliminary evidence suggests that the Purkinje antigen is a protein that is often concentrated in the periphery of the cytoplasm in disc‐shaped structures. Patients with antibodies often developed signs of PCD near the time of detection of the tumor and had relentless progression of neurological disease. Patients without antibodies frequently had cancer for months to years before PCD developed, and often had spontaneous stabilization of neurological disease with time. Four patients without and 3 patients with antibodies underwent plasmapheresis without response.
Recovery of herpesviruses from cerebrospinal fluid of immunodeficient homosexual men
Authors: Dix Richard D. , Bredesen Dale E. , Erlich Kim S. , Mills John 
Published: January 2005

AbstractOver a one‐year period the cerebrospinal fluid (CSF) obtained from a series of homosexual men immunocompromised with either Hodgkin's disease or acquired immune deficiency syndrome (AIDS) was cultured to assess the frequency with which infectious viruses could be recovered. Of 58 patients examined, 4 (6.9%) had CSF cultures that showed a cytopathology consistent with a virus infection. All isolates proved to be herpesviruses. Cytomegalovirus (CMV) and varicella‐zoster virus were isolated from CSF obtained from 2 patients with neurological features consistent with a subacute encephalitis common among AIDS patients. CMV was also recovered from the CSF of an AIDS patient who developed an ascending myelitis of herpesvirus origin. Finally, a CSF sample obtained from an immunodeficient homosexual man who showed no detectable neurological abnormalities consistently yielded herpes simplex virus type 1 in culture. These results suggest that seeding of the CSF with infectious virus is an uncommon event in this patient population. However, our experience should not dissuade attempts to culture viruses from CSF in similar cases. Successful isolations may prove beneficial in the diagnosis of an accompanying neurological illness and facilitate treatment with antiviral therapy when indicated.
Reversible go–no go deficits in a case of frontal lobe tumor
Authors: Leimkuhler M. E. , Mesulam M.‐M. 
Published: January 2005

AbstractA 50‐year‐old woman had been treated for a psychiatric disorder for three years. Findings during the elementary neurological examination were essentially normal. However, a computed tomographic scan revealed a large meningioma in the falx involving the medial aspects of the frontal lobes bilaterally. Neuropsychological examination demonstrated deficits in complex attentional tasks and also many errors of commission in the go–no go test. Following surgical excision of the tumor, her go–no go performance became normal. This patient shows that damage to the medial frontal lobe can cause deficits in go–no go performance, and that these deficits can be reversible following resolution of the lesion.
Polymorphonuclear neutral protease activity in multiple sclerosis and other diseases
Authors: Guarnieri Biancamaria , Lolli Francesco , Amaducci Luigi 
Published: January 2005

AbstractPolymorphonuclear neutral protease activity (PMN‐NPA) was examined in 87 patients with definite multiple sclerosis (MS) (48 active, 39 inactive), 49 patients with other neurological diseases (OND), 24 patients with immune‐mediated non‐neurological diseases (INND), and 32 normal subjects. PMN‐NPA was found to be significantly increased in active MS compared with inactive MS and compared with each of the control groups. No differences were found between the group of normal subjects and the groups of patients with OND, INND, or inactive MS. Levels of PMN‐NPA were significantly higher in the OND group than in inactive MS group. The differences for INND versus normal controls, neurological controls, and patients with inactive MS were not significant. No significant differences have been detected between active and inactive INND. These results suggest that PMN‐NPA may be useful in the diagnosis and evaluation of MS.
Fragile X syndrome: Associated neurological abnormalities and developmental disabilities
Authors: Wisniewski K. E. , French J. H. , Fernando S. , Brown W. T. , Jenkins E. C. , Friedman E. , Hill A. L. , Miezejeski C. M. 
Published: January 2005

AbstractThe fragile X syndrome is a frequent cause of developmental disabilities. It is associated primarily with nonprogressive X‐linked mental retardation. The neurodevelopmental abnormalities of 25 males and 3 females are described. Mental retardation was mild in 4, moderate in 11, severe in 6, and profound in 2 patients, while 4 patients had only learning disabilities. The presence or absence of a developmental disability could not be determined in the youngest (8 months). Seven patients had had infantile autism and 7 had epilepsy. Generally no major focal neurological abnormalities were observed but most of the patients exhibited minor signs. The severity of developmental disabilities in our patients varied between and within families and between genders. All adult males had macroorchidism. Unusual facial features were present in 13 males but none were seen in the females. Familial occurrences were found in 18 cases (64%); 10 cases (36%) were sporadic. Overall, males were more severely affected than females. Diagnostic tests including computed tomographic scans, electroencephalograms, and evoked potentials did not disclose any specific abnormalities.
A clinicopathological study of 323 patients with oligodendrogliomas
Authors: Ludwig Carol L. , Smith Michael T. , Godfrey Alfred D. , Armbrustmacher V. W. 
Published: January 2005

AbstractAll patients with oligodendrogliomas (554) from the repository of the Armed Forces Institute of Pathology were retrospectively analyzed. The pathological diagnosis was confirmed in 323 patients and each case was graded according to a previously established grading system. The clinical features of these 323 verified cases of oligodendroglioma are presented, analyzed, and compared with findings in previous studies. There is a significant age skew according to tumor grade, with 68% of patients with grade A tumors under 40 years and 83% of patients with grade D tumors over 40 years of age. Headache was the most common symptom, followed by seizure, visual loss, papilledema, paralysis, and dementia. No symptoms showed a statistically significant correlation with tumor grade. However, tumor grading allowed significant prognostic statements to be made. Attention is drawn to several often neglected symptoms of oligodendrogliomas: ataxia, hemorrhage, stroke, and cerebrospinal fluid spread. This is, to our knowledge, the largest clinicopathological study of oligodendrogliomas to date.
Age differences in intercorrelations between regional cerebral metabolic rates for glucose
Authors: Horwitz Barry , Duara Ranjan , Rapoport Stanley I. 
Published: January 2005

AbstractPatterns of cerebral metabolic intercorrelations were compared in the resting state in 15 healthy young men (ages 20 to 32 years) and 15 healthy elderly men (ages 64 to 83 years). Controlling for whole‐brain glucose metabolism, partial correlation coefficients were determined between pairs of regional cerebral metabolic rates for glucose determined by positron emission tomography using [18F]fluorodeoxyglucose and obtained in 59 brain regions. Compared with the young men, the elderly men had fewer statistically significant correlations, with the most notable reductions observed between the parietal lobe regions, and between the parietal and frontal lobe regions. These results suggest that cerebral functional interactions are reduced in healthy elderly men.
Spontaneous dissection of the cervical internal carotid artery
Authors: Mokri Bahram , Sundt Thoralf M. , Wayne O. Houser , Piepgras David G. 
Published: January 2005

AbstractWe studied 36 patients (21 women and 15 men) with spontaneous dissection of the internal carotid arteries. The ages of these patients ranged from 21 to 63 years. Focal unilateral headache was the most common symptom. Other common clinical manifestations (in decreasing order of frequency) included focal cerebral ischemic symptoms, oculosympathetic paresis, bruits, light‐headedness, and neck pain. Less common symptoms were syncope, amaurosis fugax, scalp tenderness, swelling in the neck, and dysgeusia. Common angiographic manifestations (in decreasing order of frequency) were elongated, irregular, and frequently tapered narrowing of the lumen; abrupt luminal reconstitution (often at the carotid canal); aneurysms; intimal flaps; slow internal carotid artery–middle cerebral artery flow; tapered occlusion; and distal branch occlusions. The incidence of hypertension in these patients was considerably higher than that in the general population. Angiographic evidence of fibromuscular dysplasia was found in 14% of the patients, but atherosclerotic changes were uncommon. Follow‐up ranged from 14 to 140 months (mean, 58.5 months). Twenty‐three patients with 29 dissected internal carotid arteries were also restudied angiographically. The stenosis of the internal carotid artery either completely resolved or substantially improved in more than 85% of the dissected vessels. About two‐thirds of the dissecting aneurysms either resolved or decreased in size. Clinically more than 85% of the patients had an excellent or complete recovery. Recurrence of the dissection or rupture of a dissecting aneurysm was not noted. Despite their disconcerting appearance on angiography, spontaneous dissections of the internal carotid arteries are often associated with a good prognosis.
Striatal dopamine depletion, dopamine receptor stimulation, and GABA metabolism: Implications for the therapy of Parkinson's disease
Authors: Bennett James P. 
Published: January 2005

AbstractDopamine‐denervated rat striata exhibit increased synaptosomal gamma‐aminobutyric acid (GABA) synthetic capacity (glutamate decarboxylase activity) without an alteration in GABA transport capacity. Stimulating denervated striatal dopamine receptors with apomorphine selectively increases in vivo steadystate striatal GABA turnover. The striatal response in animals to isolated loss of dopamine innervation is an increase in glutamate decarboxylase activity, not the decrease frequently found in the brains of patients with Parkinson's disease. Neurochemical expression of denervated striatal dopamine receptor stimulation may involve increased synaptic activity of striatal GABA neurons. For these reasons, enhancement of basal ganglia GABA function may improve responsiveness to dopamimetic therapies in patients with Parkinson's disease.
Distribution of the molecular forms of acetylcholinesterase in human brain: Alterations in dementia of the Alzheimer type
Authors: Fishman Eric B. , Siek Gordon C. , MacCallum Robert D. , Bird Edward D. , Volicer Ladislav , Marquis Judith K. 
Published: January 2005

AbstractAcetylcholinesterase (AChE), the enzyme that degrades acetylcholine, is a heterogeneous enzyme that can be separated into multiple molecular forms. A tetrameric membrane‐bound form (G4) and a monomeric soluble form (G1) are the two predominant enzyme species in mammalian brain. The distribution of AChE molecular forms was defined by sucrose density gradients of 11 anatomical regions of postmortem brains from 10 patients with dementia of the Alzheimer type (DAT) and 14 nondemented controls of similar ages. The results demonstrate an overall loss of protein and enzyme activity in all areas of the DAT brains studied and a selective loss of the G4 form of AChE in Brodmann areas 9, 10, 11, 21, 22, and 40, and the amygdala. There was no change in the G4/G1 ratio in areas 17 and 20, in the hippocampus, or in the cerebellum. There was a high regional correlation of the G4/G1 ratios with published values for choline acetyltransferase activity but lower correlation with total AChE activity. We propose that there is a predominant loss of the G4 form of AChE in DAT and that this loss is correlated with the degeneration of presynaptic elements.