bluuebunny/crossref_metadata_2025_split huggingface dataset:
Superior oblique myokymia
Authors: Rosenberg Michael L. , Glaser Joel S. 
Published: January 2005

AbstractSuperior oblique myokymia is an unusual eye movement phenomenon generally considered to be a uniocular rotary microtremor easily treated with carbamazepine. Eleven new cases are presented, one with a unique combination of motility problems, emphasizing that the disorder may have varying clinical manifestations. Long‐term follow‐up of the patients revealed a natural history of recurrent spontaneous remissions and relapses. Treatment with carbamazepine was of short‐term benefit in most patients but failed to affect the long‐term course of the disease. No patient developed other evidence of neurological disease. The condition seems to be a benign, permanent condition limited in its manifestations to the superior oblique muscle.
Lithium interferes with reserpine‐induced dopamine depletion
Authors: Reches Avinoam , Hassan Mohamed N. , Jackson Vernice , Fahn Stanley 
Published: January 2005

AbstractLong‐term lithium treatment attenuated the hypokinetic effect of reserpine in a patient with tardive dyskinesia. In rats, prophylactic lithium administration inhibits reserpine‐induced dopamine depletion in the brain. These data indicate that lithium may limit the therapeutic efficacy of reserpine in tardive dyskinesia.
Delayed onset of post–rabies vaccination encephalitis
Authors: Gamboa E. T. , Cowen D. , Eggers A. , Cogan P. , Ganti R. , Brust J. C. M. 
Published: January 2005

AbstractA 31‐year‐old veterinarian developed seizures, left hemiparesis, loss of memory, and behavioral disorders 5 months after intensive antirabies vaccination, the longest incubation period yet recorded. Computed tomographic scan revealed a right frontal contrastenhanced mass that extended to the left frontal lobe through the corpus callosum. Brain biopsy showed foci of primary demyelination largely confined to the white matter. The lesions were characteristic of the demyelinating encephalomyelitis that follows treatment with certain vaccines against rabies. The hemiplegia improved, but seizures, memory impairment, and abnormal behavior persisted.
Saccadic intrusions in internuclear ophthalmoplegia
Authors: Herishanu Yuval O. , Sharpe James A. 
Published: January 2005

AbstractSaccadic intrusions disrupted forward fixation in four patients with bilateral internuclear ophthalmoplegia (INO). Three had multiple sclerosis and one had brainstem infarction. Sporadic bursts of monocular abducting saccades were recorded in either eye. Each saccade was followed by a slower return to midposition. The presence of the INO prevented conjugate saccades of the fellow eye. The adducting phases were faster than convergence eye movements or the glissadic smooth eye movements that sometimes follow saccades. Dynamic overshoot of the abducting saccadic phase may contribute to the relatively rapid adducting phase. The saccadic intrusions of INO are recognized clinically as monocular horizontal oscillation; low‐amplitude intrusions are evident only during funduscopy. This distinctive dyskinesia is considered a sign of involvement extrinsic to the medial longitudinal fasciculi in patients with INO.
Brainstem glioma: Clinical manifestations of meningeal gliomatosis
Authors: Packer Roger J. , Allen Jeffrey , Nielsen Surl , Petito Carol , Deck Michael , Jereb Berta 
Published: January 2005

AbstractBrainstem gliomas of children are variably malignant tumors that rarely have been reported to produce subarachnoid dissemination. Nevertheless, during a two‐year period, 5 of 15 such patients treated by us developed symptoms of leptomeningeal metastases. The diagnosis of an anaplastic astrocytoma with meningeal gliomatosis was confirmed postmortem in all 5. In 3 children, meningeal symptoms preceded other signs of posterior fossa recurrence. Symptoms of meningeal gliomatosis included local or radiating back pain (5 patients), segmental weakness (3), paresthesia (2), and incontinence (2). Myelography, performed in 4 patients, was the most useful diagnostic technique, disclosing multiple intradural filling defects or a high degree of block in 3 patients. Although the cerebrospinal fluid was abnormal in all 4 examined patients, in only 1 were malignant cells detected. Prolonged survival, which appears to predispose to dissemination of adult malignant gliomas, was not an apparent factor in our patients.
Congenic autoimmune murine models of central nervous system diseas in connective tissue disorders
Authors: Alexander Elaine L , Murphy Edwin D. , Roths John B. , E Garrett E. 
Published: January 2005

AbstractCongenic mice of the MRL/Mp strain spontaneously develop an autoimmune connective tissue disease that shares immunological and histopathological features with systemic lupus erythematosus, rheumatoid arthrithritis, and Sjögren's syndrome. The autoimmune disorder in these mice is accelerated markedly by the recessive gene lpr. By 6 month of age, MRL/Mp‐lpr/lpr mice developed prominent mononuclear cell infiltrates restricted to the choriod plexus and meninges, whereas congeneric MRL/Mp‐+/+ mice (which lack the lpr gene) showed delayed but widespread inflammatory infiltrates involving cerebral vessels and meninges, with sparing of the choroid plexus. These distinctive patterns of cerebral inflammation, which are comparable in many respects to those seen in human connective tissue disease, provide some of the first animal models of relevant central nervous system histopathological processes associated with underlying connective tissue disease.
Alzheimer's disease: Choline acetyltransferase activity in brain tissue from clinical and pathological subgroups
Authors: Bird T. D. , Stranahan S. , Sumi S. M. , Raskind M. 
Published: January 2005

AbstractCholine acetyltransferase activity was measured postmortem in five brain regions to determine if such activity provided biochemical support for clinical and pathological subgrouping of Alzheimer's disease. Sixteen patients with Alzheimer's disease were divided into groups based on age at onset, severity of neuropathological changes, history of myoclonus, family history of dementia, cerebellar amyloid plaques, and congophilic angiopathy. Thirty‐two age‐matched normal control subjects and 17 neurological control patients with Huntington's disease were also studied. Patients with early‐ onset and late‐onset Alzheimer's disease did not differ in the clinical duration of their disease. Choline acetyltransferase activity was significantly lower in patients with early‐onset Alzheimer's disease than in age‐matched control subjects in frontal cortex, temporal cortex, hippocampus, and cerebellum. In contrast, choline acetyltransferase activity in patients with late‐onset Alzheimer's disease was significantly lower than in age‐matched control subjects only in hippocampus. There was a tendency for choline acetyltransferase activity to be lower in cortex from patients with early‐onset Alzheimer's disease compared with cortex from the late‐onset group, and this difference was significant in temporal cortex. Choline acetyltransferase activity was also measured in the substantia innominata from 9 patients with Alzheimer's disease and 5 age‐matched control subjects. Subjects with early‐onset Alzheimer's disease had significantly lower choline acetyltransferase activity in substantia innominata than did control subjects. Patients with Alzheimer's disease and a history of myoclonus had significantly lower choline acetyltransferase activity than did affected patients without myoclonus. Multivariate regression analysis showed myoclonus to be the single best predictor of low brain choline acetyltransferase activity. These results provide further evidence for clinical, pathological, and biochemical heterogeneity in Alzheimer's disease.
Recent advances in understanding brain capillary function
Authors: Goldstein Gary W. , Betz A. Lorris 
Published: January 2005

AbstractThe endothelial cells in brain capillaries form a blood‐brain barrier which limits and controls the movements of solutes between blood and brain. These cells contain continuous tight junctions and exhibit a low rate of pinocytosis, resulting in formation of a permeability barrier to macromolecules and many polar compounds. However, brain capillary endothelial cells also contain specialized transport systems that facilitate blood‐to‐brain transfer of some solutes and actively pump other solutes from brain to blood. Several investigators have developed methods to isolate microvessels from brain or to grow brain capillary endothelial cells in tissue culture. This review summarizes progress made with these model systems and discusses their usefulness in increasing our knowledge of brain capillary function.
Brain microvessel endothelial cells in tissue culture: A model for study of blood‐brain barrier permeability
Authors: Bowman Phillip D. , Ennis Steven R. , Rarey Kyle E. , Lorris Betz A. , Goldstein Gary W. 
Published: January 2005

AbstractEndothelial cells were prepared from bovine brain microvessels and grown in tissue culture. They contained factor VIII/von Willebrand antigen, the most specific marker available for determination of the endothelial origin of cells in culture. The cultured cells formed complex tight junctions and contained few pinocytotic vessels. These properties are responsible for formation of the blood‐brain barrier in vivo. When monolayers of the endothelial cells were exposed briefly to a calcium‐free solution or treated with 1.6 M arabinose, distinctive morphological changes occurred in the intercellular contacts. In either case, a normal structure was reestablished following return to control medium. To assess the effect of these treatments on transcellular permeability, we measured the movement of sucrose labeled with carbon 14 across a monolayer of endothelial cells cultured on a collagen‐coated nylon mesh. Removal of external calcium increased the rate of sucrose movement by 120%; the arabinose treatment increased transcellular flux by 40%.
{18F}fluorodeoxyglucose positron emission tomography in refractory complex partial seizures
Authors: Theodore William H. , Newmark Michael E. , Sato Susumu , Brooks Rodney , Patronas Nicholas , de la Paz Robert , Dichiro Giovanni , Kessler Robert M. , Margolin Richard , Manning Ronald G. , Channing Michael , Porter Roger J. 
Published: January 2005

AbstractPositron emission tomography with simultaneous electroencephalographic monitoring was performed with {18F}fluorodeoxyglucose in 20 patients with complex partial seizures who had normal computed tomographic scans. Seven patients had only unilateral epileptiform discharges on the electroencephalogram, 3 had predominantly unilateral discharges, and 10 had nonlocalized epileptiform abnormalities. Positron emission tomography showed a hypometabolic lesion in 16 of the 20 patients. Pathological changes in the hypometabolic region were found in postoperative specimens in 4 of 5 patients studied. Positron emission tomography was unaffected by the seizure frequency, state of alertness, or number of spike discharges during the scan. There was a tendency for patients to have higher overall metabolic rates when taking less medication. Seizures occurring during {18F}fluorodeoxyglucose uptake in 3 patients produced a hypermetabolic area at the interictal hypometabolic focus. Positron emission tomography sometimes showed more widespread hypometabolism than suspected on the basis of the scalp‐recorded electroencephalogram. The frontal lobe showed a greater degree of hypometabolism than the temporal lobe in 3 patients. Focal lesions may be identified by positron emission tomography even if the electroencephalographic abnormality is not well localized.
Cerebellar degeneration caused by high‐dose cytosine arabinoside: A clinicopathological study
Authors: Winkelman Marc D. , Hines John D. 
Published: January 2005

AbstractTwenty‐four patients with leukemia or lymphoma refractory to conventional chemotherapy were given a course of systemic, high‐dose cytosine arabinoside (3 gm/m2 every 12 hours for twelve doses). Four patients developed cerebellar degeneration during treatment. Ataxia of gait and limb movements, dysarthria, and nystagmus appeared five to seven days after the first dose, worsened over the next two to three days, and then remained stable for two to six days. Incomplete improvement occurred over the following one to two weeks. Postmortem examination disclosed loss of Purkinje cells in the depths of cortical sulci with relative preservation of those at the crests of folia and those in the most posterior inferior portions of the cerebellum. Other patients developed a mild, reversible cerebellar syndrome over the same time course as that of the irreversible disorder. Manifestations ranged from nystagmus alone to dysarthria and unsteadiness of gait without limb ataxia. We conclude that cytosine arabinoside at this dosage causes a cerebellar degeneration with characteristic clinical and pathological features. Among the present patients with refractory hematological malignancies, such degeneration occurred with an incidence of 16.7%, more than twice that reported in previous series.
Herpes zoster ophthalmicus and delayed contralateral hemiparesis caused by cerebral angiitis: Diagnosis and management approaches
Authors: Hilt Dana C. , Buchholz David , Krumholz Allan , Weiss Howard , Wolinsky Jerry S. 
Published: January 2005

AbstractFour patients with herpes zoster ophthalmicus and delayed contralateral hemiparesis are described, and their findings are compared with those in patients previously reported in the English language literature. The current patients evidenced multifocal ipsilateral cerebral angiitis by angiography and multifocal infarcts in the distribution of the ipsilateral middle cerebral artery by computed tomographic scanning. Cerebrospinal fluid showed mononuclear pleocytosis, positive oligoclonal bands, and an elevated immunoglobulin G index. Two patients were treated with corticosteroids and acyclovir, and 1 with corticosteroids alone, all without apparent response. Necrotizing angiitis ipsilateral to the herpes zoster ophthalmicus was demonstrated postmortem in 1 patient with multifocal cerebral infarction and progressive leukoencephalopathy. Neither herpes varicella zoster immunocytochemical reactivity nor viral inclusions were seen. The leukoencephalopathy associated with herpes varicella zoster either may be caused by cerebral angiitis or, as previously reported, may be a temporally remote manifestation of persistent herpes varicella zoster infection. The cerebral angiitis associated with herpes varicella zoster is histologically similar to granulomatous angiitis, and both may be related to herpes varicella zoster infection of the cerebral vasculature.
Immunoreactive myelin proteolipid protein—like activity in cerebrospinal fluid and serum of neurologically impaired patients
Authors: Trotter John L. , Wegescheide Cindy L. , Garvey William F. 
Published: January 2005

AbstractTwo hundred seventy‐eight samples of cerebrospinal fluid and 273 samples of sera from a variety of neurological patients were examined by radioimmunoassay for myelin proteolipid protein–like reactivity as an index of structural damage to myelin. Groups of patients with active central nervous system damage could be distinguished easily, although there was a small percentage of false positive reactions. The reactivity was most marked in the demyelinative, encephalitic, and stroke categories. A radioimmunoassay for proteolipid protein of proper sensitivity and specificity may prove to be a useful objective clinical measure of the presence and degree of disease activity in multiple sclerosis and other diseases.
External ophthalmoplegia, alpha and spindle coma in imipramine overdose: Case report and review of the literature
Authors: Pulst Stefan‐M. , Lombroso C. T. 
Published: January 2005

AbstractA 13‐year‐old boy with imipramine overdose developed seizures, respiratory arrest, and coma. Abnormalities of oculovestibular reflexes, electroencephalograms, and brainstem auditory evoked potentials were monitored in relation to measurements of drug levels. An alpha‐coma electroencephalographic pattern evolved into one evidencing spindle coma and eventually into a normal pattern. Prolonged brainstem auditory evoked potentials also normalized as coma and oculocephalic reflex abnormalities resolved. In spite of the history that suggested hypoxic damage, the absence of reflex eye movements in a comatose patient and the presence of alphaand spindle‐coma electroencephalographic patterns, even with prolonged brainstem auditory evoked potentials, are not reliable prognostic indicators in tricyclic drug overdose.
Cerebral vasospasm after subarachnoid hemorrhage: An update
Authors: Heros Roberto C. , Zervas Nicholas T. , Varsos Vassilios 
Published: January 2005

AbstractSymptomatic vasospasm, or delayed cerebral ischemia associated with arteriographic evidence of arterial constriction, is currently the most important cause of morbidity after acute subarachnoid hemorrhage. The development of vasospasm is directly correlated with the presence of thick blood clots in the basal subarachnoid cisterns, which can be detected by an early computed tomographic scan. Symptomatic vasospasm usually develops between 4 and 12 days after subarachnoid hemorrhage. The onset is gradual, occurring over hours or days. There is typically a gradual deterioration of the level of consciousness, accompanied by focal neurological deficits that are determined by the arterial territories involved. Hyponatremia frequently occurs and may exacerbate the symptoms. The patients are usually volume depleted, and therefore many authorities now treat them with replenishment and expansion of their intravascular volume with colloid and blood. Volume expansion, together with elevation of the systemic blood pressure and reduction of the intracranial pressure when elevated, constitute the only currently available effective therapy for symptomatic vasospasm. The cause of vasospasm remains obscure. Mechanisms of smooth muscle cell contraction and relaxation and experimental efforts to elucidate the nature of vasospasm are reviewed.
Gerstmann‐Sträussler‐Scheinker disease with coincidental familial onset
Authors: Hudson Arthur J. , Farrell Michael A. , Kalnins Renate , Kaufmann John C. E. 
Published: January 2005

AbstractA family with Gerstmann‐Sträussler‐Scheinker disease had coincidental clinical onset in three members of two generations, a phenomenon suggesting a common source of a transmissible agent. A regular dietary supplement in this family was home‐bred rabbit. The clinical picture, although generally similar to that in previous accounts, included the unusual findings of visual loss (one patient) and sensory loss (one patient), and dementia was not apparent until late in the illness in two patients. Pathological examination of a cerebellar cortical biopsy specimen from one patient and postmortem tissue from two patients revealed multicentric amyloid plaques located in cerebral and cerebellar cortex, basal ganglia, and white matter with degeneration of corticospinal, dorsal spinocerebellar, dentatorubral, and geniculocalcarine tracts and dorsal columns. Spongiform change was focal and confined to the superficial cerebral cortical layers.
Coma and thyrotoxicosis
Authors: Newcomer John , Haire William , Hartman Charles R. 
Published: January 2005

AbstractA patient with Graves' disease was in coma with evidence of corticospinal tract disease. Treatment with standard pharmacological measures and plasmapheresis resulted in the reduction of total thyroxine from 28.8 μg/ dl to 10.0 μg/dl and of triiodothyronine from 332 ng/dl to 150 ng/dl. These laboratory findings were associated with clinical stabilization, improvement of mental status, and resolution of the findings of corticospinal tract disease. These data support previous contentions relating reversible corticospinal tract disease to thyrotoxicosis.
Collateral reinnervation of sweat glands
Authors: Kennedy William R. , Sakuta Manabu 
Published: January 2005

AbstractThe collateral reinnervation of mouse sweat glands has been studied by a method that allows serial evaluation of the course of reinnervation in intact animals. The method is based on the finding that the activation of secretion from newly denervated sweat glands by pilocarpine or nerve stimulation is completely absent seven days after nerve section but returns with reinnervation. These characteristics allowed serial detection of footpad sweat glands newly reinnervated by collateral sprouting of the remaining intact saphenous nerve after section of the sciatic nerve. The number of saphenous innervated glands increased five‐to sevenfold and the total saphenous sweat territory was greatly expanded across the volar surface of the hind paw. There was less enlargement when the sciatic nerve was allowed to regenerate and participate in reinnervation of sweat glands. None of the reinnervated glands were dually innervated by saphenous and sciatic nerves, as is the case in normal glands. When the saphenous nerve was sectioned after saphenous collateral sprouting was complete and after sciatic regeneration had innervated an apparent maximal number of glands, the sciatic nerve reacted by advancing farther into the formerly enlarged saphenous territory and re‐reinnervated many of the glands. Collateral sprouting by sudomotor axons is more abundant and more widely dispersed than reported for larger nerve fibers to skeletal muscle and to low‐threshold mechanoreceptors, It more closely resembles sprouting of nociceptive axons.
Comparison of cognitive ability, personality profile, and school success in epileptic children with pure right versus left temporal lobe eeg foci
Authors: Camfield Peter R. , Gates Robert , Ronen Gabriel , Camfield Carol , Ferguson Anne , Macdonald G. Wayne 
Published: January 2005

AbstractBy reviewing electroencephalographic reports compiled over five years and checking clinical details, we identified and studied 27 children with apparently pure left or pure right temporal lobe epilepsy. The children underwent neurological examination and neuropsychological testing (Halstead‐Reitan Battery, Wechsler Intelligence Scale for Children [WISC] and Wide Range Achievement Test), and parents completed the Personality Inventory for Children (PIC). Of 15 boys and 12 girls with a mean age of 12.7 years, 14 had right and 13 left temporal lobe epilepsy. Seizure control was excellent in 17. Five (2 with left, 3 with right temporal lobe epilepsy) had received professional emotional help, 6 (3 with left, 3 with right focus) received special help at school, and 5 (3 with left, 2 with right focus) had failed a grade in school. No significant left–right differences were seen in WISC full scale, verbal, or performance IQ scores, neuropsychological test battery findings, or clinical scale scores on the PIC. Most of the children with unilateral temporal lobe epilepsy had no measurable cognitive or emotional difficulties. Cognitive, personality, and school problems were equally distributed between left and right temporal lobe epilepsy groups. When the two groups were combined, however, 10 patients (5 with left, 5 with right focus) were identified by the PIC as maladjusted, and as a group showed significantly lower neuropsychological test functioning than did the normally adjusted children.