bluuebunny/crossref_metadata_2025_split huggingface dataset:
Catecholaminergic neurons in the parabrachial nucleus of normal individuals and patients with idiopathic parkinson's disease
Authors: Goto Satoshi , Hirano Asao 
Published: January 2005

AbstractThe parabrachial nucleus is believed to play a role in autonomic regulation. We have used the Fontana‐Masson ammoniacal silver nitrate method and a tyrosine hydroxylase–immunostaining technique to demonstrate the presence of neuromelanin‐containing catecholaminergic neurons in the parabrachial nucleus of normal individuals. In addition, we also show that there is a significant reduction of these catecholaminergic neurons and presence of Lewy bodies in the parabrachial nucleus of patients with idiopathic Parkinson's disease. These findings may be related to the several autonomic disturbances that may occur in idiopathic Parkinson's disease.
Comparison of bitemporal and unitemporal epilepsy defined by depth electroencephalography
Authors: Hirsch Lawrence J. , Spencer Susan S. , Williamson Peter D. , Spencer Dennis D. , Mattson Richard H. 
Published: January 2005

AbstractOf 166 consecutive patients studied with depth electroencephalography (EEG), 87 had seizures arising from one temporal lobe and 23 had seizures arising independently from each temporal lobe. We retrospectively reviewed and compared those patients with unitemporal and those with bitemporal seizures. There were no statistically significant differences between the two groups in terms of age at onset of seizures, duration of epilepsy, localization of scalp EEG abnormalities, surgical results, or pathological findings. The bitemporal group, however, had significantly fewer patients with a history of febrile seizures (p $$ 0.025). Two patients with bitemporal seizures were later found to have extratemporal lesions, and one an extrahippocampal temporal lesion, on magnetic resonance scans; one patient's extratemporal lesion was resected and all habitual seizures stopped. These findings suggest that a single pathophysiological process accounts for unitemporal and some bitemporal epilepsy, but that independent onset of seizures from each temporal lobe detected by depth EEG may also indicate extratemporal foci.
Temporal lobectomy in patients with bitemporal epilepsy defined by depth electroencephalography
Authors: Hirsch Lawrence J. , Spencer Susan S. , Spencer Dennis D. , Williamson Peter D. , Mattson Richard H. 
Published: January 2005

AbstractPatient selection for temporal lobectomy was reviewed for 23 patients with seizures that arose independently from each temporal lobe as detected by depth electroencephalography (EEG). Although neuropsychological testing, interictal EEG findings, imaging studies, and subclinical seizures were also considered, all patients offered temporal lobectomy had (1) at least 50% of the clinical seizures originating from the lobe to be resected, (2) adequate contralateral memory on testing with amobarbital, and (3) no clear evidence of an extratemporal focus. Eleven patients underwent temporal lobectomy. Pathological findings were considered positive in all nine specimens reviewed. Nine patients had no seizures, one had greater than 75% reduction in seizure frequency, and 1 had 50 to 75% reduction. Pathological features and clinical outcome were similar in the 6 patients with fewer than 80% and the 5 patients with at least 80% of seizures originating from the resected lobe. Thus, having fewer than 80% of seizures originate from one temporal lobe should not be an absolute contraindication for temporal lobectomy.
Postictal language assessment and lateralization of complex partial seizures
Authors: Privitera Michael D. , Morris George L. , Gilliam Frank 
Published: January 2005

AbstractWe performed a prospective study of ictal and postictal language function after 105 temporal lobe complex partial seizures in 26 patients. Seizure localization was verified by a greater than 90% reduction in seizure frequency after temporal lobectomy. At the time of the seizure, the patient was asked to read a test phrase aloud until it was read correctly and clearly. In all 62 seizures originating from the left temporal lobe, the patient took more than 68 seconds to read the test phrase correctly (mean, 321.9 seconds); in 42 of 43 seizures from the right temporal lobe, the patient read the test phrase in less than 54 seconds (mean, 19.7 seconds). Postictal paraphasias occurred in 46 of 62 seizures from the left temporal lobe (11 of 14 patients). In this study, quantifying the time delay in reading a test phrase lateralized seizure onset in all 26 patients tested, proving significantly more accurate than any other single noninvasive presurgical test.
Focal neuronal migration disorders and intractable partial epilepsy: Results of surgical treatment
Authors: Palmini André , Andermann Frederick , Olivier André , Tampieri Donatella , Robitaille Yvon 
Published: January 2005

AbstractTwenty‐six patients with focal or lateralized neuronal migration disorders and intractable partial epilepsy were treated surgically. Twenty‐four had reliable follow‐up ranging from 1 to 15 years (mean, 5.0). Pathologically, they fell into two categories: focal cortical dysplasia (12 patients) and forme fruste of tuberous sclerosis (8 patients). In the remaining 4 patients, the material was inadequate for histological analysis. Outcome regarding seizure control was assessed according to a classification most sensitive to variations in frequency of major attacks. Ten (42°) of the 24 patients achieved good or excellent outcome, 6(25°) had a worthwhile decrease in seizure frequency, and 8 (33°) had only discrete improvement. The variable most strongly correlated with surgical outcome was the amount of lesion removed. Seventy‐seven percent of patients in whom a complete excision or excision of 50° or more of the lesion was accomplished achieved excellent or good surgical outcome. Conversely, no patient with less than 50° of the lesion removed attained the same result. There was no correlation between other clinical, radiological, or electrographic variables and outcome regarding seizure control. Specifically there was no significant correlation between the amount of excision of the epileptogenic area as judged by scalp electroencephalography and electrocorticography studies, and surgical outcome. In patients with neuronal migration disorders and intractable partial epilepsy, removal of the structural abnormality takes precedence over removal of epileptogenic tissue as the main surgical strategy to achieve seizure control.
Excitotoxicity in the embryonic chick spinal cord
Authors: Stewart Gregory R. , Olney John W. , Pathikonda Maya , Snider William D. 
Published: January 2005

AbstractRecent evidence implicates excitatory amino acids (EAAs), acting as excitotoxic agents, in the pathogenesis of neurological disorders involving the spinal cord. In this study, we used the chick embryo spinal cord as an vitro model for studying the sensitivity of spinal neurons to the excitotoxic effects of EAA agonists. Compounds tested include the prototypic receptor‐specific agonists, N‐methyl‐D‐aspartate (NMDA), quisqualic acid (Quis), and Kainic acid (KA), and the plant‐derived excitotoxic food poisons, β‐N‐oxalylamino‐L‐alanine, β‐N‐menthylamino‐L‐alanine, and domoic acid. Each agonist induced concentration‐dependent acute degeneration of neurons distributed throughout the spinal cord. These cytopathological changes consisted of acute edematous degeneration of dendrosomal structures in the dorsal horn and intermediate zone, and dark cell changes with intracytoplasmic vacuolization of motor neurons; this damage is identical to that induced by excitotoxin agonists in other regions of the central nervous system. The NMDA receptor‐specific antagonist MK‐801 completely blocked toxicity of NMDA, and the nonNMDA antagonist CNQX preferentially blocked the toxicity of Quis‐ and KA‐type agonists in the spinal cord. Our findings suggest that (1) the majority of spinal neurons have all three subtypes of EAA receptors, making them acutely vulnerable to excitotoxin exposure; and (2) EAA antagonists are effective in preventing excitotoxin‐induced damage of the spinal cord.
Putamen volume reduction on magnetic resonance imaging exceeds caudate changes in mild Huntington's disease
Authors: Harris Gordon J. , Pearlson Godfrey D. , Peyser Carol E. , Aylward Elizabeth H. , Roberts Joy , Barta Patrick E. , Chase Gary A. , Folstein Susan E. 
Published: January 2005

AbstractThe characteristic pathological features of Huntington's disease (HD) are neostriatal atrophy and neuronal loss. Although neuroradiological studies often show caudate atrophy in patients with moderate HD, frequently no caudate atrophy is found early in the illness. There have been no quantitative reports to date on in vivo putamen volume measures in mild HD, although the structure is known to be neuropathologically involved in the illness. We measured volumes of caudate nucleus and putamen and bicaudate ratios (BCR) from magnetic resonance images, blind to diagnosis, in 15 patients with mild HD and 19 age‐ and sex‐matched control subjects using a computerized image analysis system. The region showing greatest atrophy was the putamen, which was reduced 50.1% in mean volume in HD patients compared with control subjects (p<0.000001). In contrast, caudate volume was reduced 27.7% (p = 0.004). BCR was increased 28.5% in HD patients (p = 0.0002). Discriminant function analysis was 94% effective in identifying the diagnostic group based on putamen volume alone, whereas caudate measures had considerable overlap. Correction of putamen volume for head size led to 100% separation by group. Putamen measures and BCR correlated with neurological examination scores but caudate volume did not. Volumetric measurement of putamen is a more sensitive indicator of brain abnormalities in mild HD than measures of caudate atrophy.
Nerve growth factor prevents experimental cisplatin neuropathy
Authors: Apfel Stuart C. , Arezzo Joseph C. , Lipson Leeanne , Kessler John A. 
Published: January 2005

AbstractCisplatin is a widely used antitumor agent, the dose‐limiting toxicity of which is predominantly large‐fiber sensory neuropathy. Prevention of such a neuropathy would extend the usefulness of this agent, allowing higher doses and longer periods of treatment. We report here that we have successfully established cisplatin neuropathy in mice measured by using behavioral, biochemical, and electrophysiological techniques, and that subcutaneous administration of human recombinant nerve growth factor (NGF) prevents or delays the neuropathy. Cisplatin administration reduced sensory ganglion levels of the peptide transmitter, calcitonin gene–related peptide, slowed nerve conduction in the tail and impaired proprioception as measured by the ability to balance on a rotating dowel. NGF coadministration appeared to prevent all these abnormalities. Treatment of the human toxic neuropathy with its well‐established time of onset, simple clinical course, and the accessibility of nerve to NGF administered systemically may provide the best clinical setting for the first human trials of NGF.
Proton magnetic resonance spectroscopic imaging for metabolic characterization of demyelinating plaques
Authors: Arnold Douglas L. , Matthews Paul M. , Francis Gordon S. , O'Connor John , Antel Jack P. 
Published: January 2005

AbstractWe used proton magnetic resonance (MR) spectroscopic imaging to determine the serial changes in MR signals from choline, creatine, lactate, and N‐acetylaspartate in and around a large demyelinating lesion followed over a period of 8 months. Elevated lactate and choline signals were observed at the first examination 3 days after the onset of symptoms. Reduced N‐acetylaspartate signals were observed a few days afterward. The abnormals metabolite signals varied in different regions of the lesions and extended beyound the borders of abnormal signal intensity seen on conventional MR imaging (MRI). On the last examination at 8 months when the lesion appeared much smaller on MRI, choline signals from the center of the lesions were still high, but were falling. Choline signals outside the lesions on MRI had returned to normal as had lactate signals everywhere. Importantly, there was no recovery of N‐acetylasparatate signals in or adjaccent to the lesion on MRI. This serial study demonstrates the potential of MR spectroscopic imaging for characterizing the chemical pathological evolution of demyelinating lesions in ways that conventional MRI cannot. We propose that abnormal signals from choline can indicate recent regional demyelination, while persistent abnormal signals from N‐acetylaspartate can provide an index of irreversible damage in the nervous system.
In vivo imaging of glucose consumption and lactate concentration in human gliomas
Authors: Herholz K. , Heindel W. , Luyten P. R. , denHollander J. A. , Pietrzyk U. , Voges J. , Kugel H. , Friedmann G. , Heiss W.‐D. 
Published: January 2005

AbstractTwenty patients with histologically confirmed gliomas were studied with positron emission tomography (PET) and proton magnetic resonance spectroscopy (1H‐MRS). PET with 18F‐2‐fluoro‐2‐deoxy‐D‐glucose (FDG) provided tomograms of the metabolic rate of glucose. MRS images were obtained by combining volume‐selective excitation with phase‐encoded acquisition. With 32 × 32 gradient phase‐encoding steps, an in‐plane resolution of 7 × 7 mm was achieved. From this set of spectra, lactate maps were created and compared with PET maps of glucose metabolism. Maximum glucose metabolic rates within tumors (relative to metabolic rates of glucose in contralateral regions of the brain) were correlated significantly with maximum lactate concentrations (relative to N‐acetyl aspartate peaks in the contralateral part of the brain). In 8 tumors, no lactate was detected, and in 7 of these the maximum glucose metabolic rate was below the median value. The tumor with the highest lactate concentration also had the highest glucose metabolic rate. The topographic relation between glucose metabolic rate and lactate concentration could be analyzed in 9 patients by three‐dimensional alignment of the PET and MRS images. In that analysis, maximum lactate concentrations were often not found in the same location as maximum glucose metabolism, but lactate tended to accumulate in tumor cysts, necrotic areas, and the vicinity of the lateral ventricles. The combination of FDG PET and 1H‐MRS imaging demonstrates details of the spatial relation between the two poles of nonoxidative glycolysis, glucose uptake and lactate deposition. Both methods can be used as diagnostic tools to study an abnormality of energy metabolism that may be an indicator of dedifferentiation and malignancy.
Detection of JC virus DNA in peripheral lymphocytes from patients with and without progressive multifocal leukoencephalopathy
Authors: Tornatore Carlo , Berger Joseph R. , Houff Sidney A. , Curfman Blanche , Meyers Karen , Winfield David , Major Eugene O. 
Published: January 2005

AbstractProgressive multifocal leukoencephalopathy (PML) results from lytic infection of oligodendrocytes by JC virus (JCV). Although JCV has been identified in mononuclear cells in bone marrow and hematogenous dissemination of the virus to the central vervous system has been suspected, JCV has never been clearly demonstrated in the peripheral circula‐tion. Using polymerase chain reaction technology, we examined peripheral lymphocytes of 19 patients with brain biopsy–proven PML for the JCV genome. Two non‐PML control groups, consisting of 26 patients seropositive for human immunodeficiency virus type 1 (HIV‐1) and 30 immunocompetent patients with Parkinson's disease, were also examined for the presence of the JCV genome in lymphocytes. Cerebrospinal fluid from 10 patients with PML was exmimined for the presence of the JCV genome as well. The JCV genome was detected in the lymphocytes of 89% (17) of the patients with PML, 38% (10) of the HIV‐1–seropositive patients without PML, and none of the patients with Parkinson's disease. Sequencing of the JCV regulatory region from the lymphocytes of three patients revealed the prototype MAD‐1 strain of JCV in one patient with PML, a MAD‐4 strain in a second patient with PML, and a slightly modified MAD‐4 strain in an HIV‐1–positive patient without PML. Only 3 of 10 patients with PML who had JCV detected in lymphocytes had the JCV genome in their cerebrospinal fluid. These results demonstrate that the JCV genome can be found in circulating lymphocytes from patients with PML and suggest that lymphocytes are an important vector for hematogenous dissemination of JCV to the central nervous system. We also identified the JCV genome in the lymphocytes of a group of HIV‐1–seropositive patients with no clinical evidence of PML, suggesting that they may be at risk for development of PML and can be identified in a presymptomatic state.
Functional reorganization of the brain in recovery from striatocapsular infarction in man
Authors: Weiller Cornelius , Chollet François , Friston Karl J. , Wise Richard J. S. , Frackowiak Richard S. J. 
Published: January 2005

AbstractWe used positron emission tomography (PET) to study organizational changes in the functional anatomy of the brain in 10 patients following recovery from striatocapsular motor strokes. Comparisons of regional cerebral blood flow maps at rest between the patients and 10 normal subjects revealed significantly lower regional cerebral blood flow in the basal ganglia, thalamus, sensorimotor, insular, and dorsolateral prefrontal cortices, in the brainstem, and in the ipsilateral cerebellum in patients, contralateral to the side of the recovered hand. These deficits reflect the distribution of dysfunction caused by the ischemic lesion. Regional cerebral blood flow was significantly increased in the contralateral posterior cingulate and premotor cortices, and in the caudate nucleus ipsilateral to the recovered hand. During the performance of a motor task by the recovered hand, patients activated the contralateral cortical motor areas and ipsilateral cerebellum to the same extent as did normal subjects. However, activation was greater than in normal subjects in both insulae; in the inferior parietal (area 40), prefrontal and anterior cingulate cortices; in the ipsilateral premotor cortex and basal ganglia; and in the contralateral cerebellum. The pattern of cortical activation was also abnormal when the unaffected hand, contralateral to the hemiplegia, performed the task. We showed that bilateral activation of motor pathways and the recruitment of additional sensorimotor areas and of other specific cortical areas are associated with recovery from motor stroke due to striatocapsular infarction. Activation of anterior and posterior cingulate and prefrontal cortices suggests that selective attentional and intentional mechanisms may be important in the recovery process. Our findings suggest that there is considerable scope for functional plasticity in the adult human cerebral cortex.
Idiopathic childhood stroke is associated with human leukocyte antigen (HLA)–B51
Authors: Mintz Mark , Epstein Leon G. , Koenigsberger M. Richard 
Published: January 2005

AbstractWe report four children with idiopathic stroke syndromes who were assayed for human leukocyte antigen (HLA) class I markers and found to have HLA‐B51 in common. This finding suggests that may be a genetic predisposition for “idiopathic” childhood stroke, and host factors, possibly in concert with environmental factors or viruses, may play a major role in the mechanism of unexplained occlusion of the cerebral vasculature in children.
Alzheimer's disease and hereditary cerebral hemorrhage with amyloidosis–dutch type share a decrease in cerebrospinal fluid levels of amyloid β‐protein precursor
Authors: van Nostrand William E. , Wagner Steven L. , Haan Joost , Bakker Egbert , Roos Raymund A. C. 
Published: January 2005

AbstractThe amyloid β‐protein is a 39‐42 amino acid peptide that is deposited in senile plaques and in cerebral vessel walls in individuals with Alzheimer's disease, Down's syndrome, hereditary cerebral hemorrhage with amyloidosis–Dutch type (HCHW A‐D), and, to a much lesser extent, normal aging. It is derived from abnormal proteolytic processing of its parent protein, the amyloid β ‐protein precursor. Here we show that individuals with the HCHWA‐D mutation and clinically manifesting the disease have markedly decreased cerebrospinal fluid levels of soluble amyloid β‐protein precursor (0.7 ± 0.4 μg/ml) compared with age‐matched normal subjects (3.0 ± 0.2 μg/ml) as determined by quantitative immunoblotting and enzyme‐linked immunosorbent assays. Similarly, age‐matched patients diagnosed with probable Alzheimer's disease also have decreased cerebrospinal fluid levels of soluble amyloid β‐protein precursor (1.0 ± 0.3 μg/ml). These parallel findings suggest a common biochemical marker for these two diseases and further establish the pathogenic relatedness of HCHWA‐D and Alzheimer's disease.
Spectrum of human immunodeficiency virus–associated neocortical damage
Authors: Masliah Eliezer , Achim Cristian L. , Ge Nianfeng , DeTeresa Richard , Terry Robert D. , Wiley Clayton A. 
Published: January 2005

AbstractA spectrum of neurocognitive defects, termed human immunodeficiency virus type 1 (HIV‐1)–associated cognitive/motor complex, has been described in patients with acquired immunodeficiency syndrome (AIDS). AIDS dementia complex (ADC) is a severe form of this disease seen in 20 to 30% of terminally ill patients. The etiology of this complex is distinct from commonly observed opportunistic infections seen in brains of patients with AIDS and has been attributed to HIV infection within the brain. At autopsy, the brains of patients with ADC contain numerous HIV‐infected macrophages/microglia with prominent subcortical damage, together termed HIV encephalitis. We retrospectively analyzed all 107 brains from a three‐year period (1988–1990) of AIDS autopsies using immunocytochemistry to detect HIV. Rather than breaking into distinct groups of HIV encephalitis versus non‐HIV encephalitis, the specimens revealed a spectrum of severity of HIV infection. Although only 16% of the brains showed the histological hallmarks of HIV encephalitis, more than 50% of the autopsies showed moderate to severe HIV infection. In a subset of 23 AIDS autopsies during which short postmortem times and absence of significant opportunistic infection permitted quantitative analysis of dendritic and synaptic complexities, we identified a strong correlation between neocortical dendritic and presynaptic damage and abundance of HIV envelope protein in the neocortical gray and deep white matter. This correlation suggests that the presence of HIV‐1 in the neocortex may be responsible by direct or indirect mechanisms for dendritic and synaptic damage.
Facilitation of responses to motor cortex stimulation: Effects of isometric voluntary contraction
Authors: De Noordhout A. Maertens , Pepin J. L. , Gerard P. , Delwaide P. J. 
Published: January 2005

AbstractIn 7 normal subjects we compared the facilitatory effect of isometric contraction of the tibialis anterior on the size of electromyographic responses evoked in this muscle by electric stimuli applied over the cervical column and by electric and magnetic percutaneous stimulation of the motor cortex. No significant difference was found between the degrees of facilitation of the responses to any of the stimuli. Using collision techniques, we also showed that the pyramidal fibers activated by spinal and cortical stimuli are the same. Facilitation induced by isometric contraction (20% maximum) was of similar or greater magnitude than that found with constant vibration of the tendon of the target muscle. In cases where vibration and contraction had equal facilitatory effects, there was no further facilitation of the responses when both conditions were applied together. These findings indicate that the facilitatory effect of isometric contraction of the target muscle essentially originates at a spinal level rather than in the motor cortex.