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S Finger

Publications and source records attributed to S Finger.

At least 37 records · Page 2Linked to original sources
PubMed1997

David Hartley's psychobiological associationism and the legacy of Aristotle.

The idea that there are certain "laws" of learning (similarity, contrast, contiguity) can be traced to Aristotle. He maintained that external stimuli cause small movements in the vessels to the dominant heart, the vestiges of which can be linked to one another. Aristotle's laws of learning were incorporated into the writings of Hobbes, Locke, and Berkeley, men who said nothing about the physiological correlates of mental associations. This left the door open for David Hartley to combine mental associationism with the Newtonian idea that sensations can cause minute particle vibrations in the nerves. Hartley's amalgam of psychology, philosophy, and neurology was first presented in 1746, as a "trial balloon" at the end a little-known monograph on a treatment for kidney stones. It was repeated three years later in his better-known Observations on Man. In many ways, modern psychobiological connectionism can be traced back to Hartley's Conjectures of 1746, in which Aristotle's original thoughts were modified with then current ideas about functions of the mind and the nervous system.

Greece↗
PubMed1996

Gilles de la Tourette and the discovery of Tourette syndrome. Includes a translation of his 1884 article.

In 1885, Gilles de la Tourette described 9 patients who suffered from a disorder characterized by involuntary movements, echolalia, echopraxia, coprolalia, and strange, uncontrollable sounds. In his article, Gilles de la Tourette presented some earlier descriptions of this disorder. To appreciate what first led Gilles de la Tourette to Tourette syndrome, however, it is necessary to turn to an article that he published a year earlier. In his 1884 article, Gilles de la Tourette cited several movement disorders that he thought were similar to each other, yet different from true chorea. After describing these disorders, namely, "jumping" of Maine, latah of Malaysia, and miryachit of Siberia, he briefly mentioned a boy in Charcot's ward in Paris, France, who seemed to exhibit the same condition. In an addendum, he then said that other cases were now surfacing in Paris and that he would write an additional article describing these individuals. To achieve a more thorough understanding of the events that led Gilles de la Tourette to his 1885 description of the disorder that now bears his name, we herein present an English-language translation of his 1884 article along with a commentary.

Eponyms↗
PubMed1996

Gustave Dax and the early history of cerebral dominance.

In 1863, 2 years before Paul Broca published his heralded paper on the special role of the left hemisphere in speech, Gustave Dax sent a paper to the Académie de Médecine in Paris, France. His lengthy submission included an insightful memoir presumably written by his father Marc in 1836 and supportive material that he had collected himself. The present article examines the events leading to Gustave's 1863 submission to the Académie. It also presents an English translation of the negative response that this paper received and a translation of the short article that Gustave published in 1865. These materials help to show how cerebral dominance was first discovered, how it was made public, and how the first advocates of the concept were judged by their contemporaries.

Dominance, Cerebral↗
PubMed1996

Gustave Dax and his fight for recognition: an overlooked chapter in the early history of cerebral dominance.

The year 1865 was revolutionary in neuroscience. In this year, three papers were published on the topic of cerebral dominance for speech. These papers were authored by Paul Broca, Marc Dax, and Gustave Dax, and they contributed to a priority debate that cannot be easily resolved. Gustave Dax claimed that his long dead father had written a memoir and presented it orally in Montpellier in 1836, thus making him the first person to write about cerebral dominance. He also claimed that he was the second person to write on the subject, the first to support his father's claims, and the first to try to localize the center for speech in just one part the left hemisphere, the middle (temporal) lobe. Paul Broca, however, was now getting much of the credit for these discoveries. To set the record straight, Gustave published several letters. This paper presents translations of Gustave's letters of 1866, 1875, and 1877, as well as the historical note written by Raymond Caizergues in 1879, and recreates the events that triggered the younger Dax's anger.

France↗
PubMed1996

Gram stain detection of infection during revision arthroplasty.

We reviewed 194 revision arthroplasties of the hip and knee performed over a ten-year period. The results of intraoperative Gram staining were available in 169 (87%). Thirty-two were found to be infected (11 hips and 21 knees) and 137 had no evidence of infection. Intraoperative Gram staining was negative in all 169 cases. The method therefore had a sensitivity of 0% for detecting infection. We conclude that the absence of organisms on intraoperative Gram staining during revision arthroplasty does not confirm the absence of infection.

Gentian Violet↗
PubMed1994

Holeboard performance of rats after hippocampal lesions and treatment with nimodipine.

Rats were taught to select eight holes in a 4 x 4 holeboard for food reinforcements. Upon reaching criterion, they were given subtotal lesions of the anterior hippocampus or sham operations. They then received either the calcium channel blocker, nimodipine, or vehicle alone. Retention testing revealed a significant main effect of lesion and evidence for nimodipine reducing this effect. These data are consistent with previous findings from this laboratory in which it was demonstrated that nimodipine can enhance performance on higher cognitive tasks after hippocampal damage.

Animals↗
PubMed1993

Effects of nimodipine on two neurologic measures sensitive to sensorimotor cortex damage.

Seventeen rats with lesions involving the sensorimotor forepaw and hindpaw regions were tested for the ability to run along a narrow bridge without slipping and to hold on to a small-diameter dowel suspended above the ground. Nine of the animals received the calcium channel blocker, nimodipine, once per day for the first 2 weeks after surgery, while the remaining eight rats received vehicle alone. Repeated measurements over the first 3 postoperative weeks showed deficits among the rats with lesions on both tasks. The animals treated with nimodipine, however, showed much better recovery, especially after the initial testing sessions.

Analysis of Variance↗
PubMed1993

Medial frontal cortex lesions: deficits and treatment with nimodipine.

Rats with bilateral lesions of the medial frontal cortex were tested in a T-maze for the ability to learn a position habit and to make four reversals of it. Rats with medial frontal cortical lesions showed deficits in reversal learning. In addition, they were found to be hyperactive in an open field. Treatment with the dihydropyridine calcium channel antagonist, nimodipine, did not reduce these behavioral deficits.

Analysis of Variance↗
PubMed1991

Neurological correlates of unilateral and bilateral "strokes" of the middle cerebral artery in the rat.

Rats with unilateral lesions of the middle cerebral artery (MCA) were tested for the ability to detect (touch) and remove a square of adhesive tape from each forepaw, and for performance on a number of neurological tests (e.g., placing and hopping reflexes, activity). Rats with MCA damage showed deficits in both touching and removing the tape from the paw contralateral to the damage, but not ipsilateral to the damage, while performing within normal limits on the other tests. After scores of the MCA rats dropped into the control group range on the adhesive tape test, they sustained damage to the opposite MCA. This did not reinstate the original deficit, suggesting that the recovery seen after the unilateral lesion was not mediated by the opposite cortex. The second lesion, however, caused a deficit in removing the adhesive tape from the limb opposite the new stroke. Some of the rats that originally had sham operations received bilateral MCA lesions at this time. These animals showed much more severe deficits on the adhesive tape test than the rats with sequential strokes. Rats with bilateral MCA damage (simultaneous or sequential) also slipped on a long narrow plank more often than control animals. Nimodipine did not enhance recovery on any of the behavioral measures.

Animals↗
PubMed1990

Sensorimotor cortical lesion effects and treatment with nimodipine.

Rats with unilateral ablations of the sensorimotor cortex and others with control operations were tested for their ability to touch and remove adhesive tape applied to both forelimbs. Half of each group was administered a calcium channel antagonist (nimodipine) for two weeks following the lesions and the other half received vehicle. The rats with lesions showed a bias to remove the ipsilateral stimulus first and exhibited contralateral deficits relative to control animals. Nimodipine was shown to reduce the contralateral stimulus removal time when the animals began testing two weeks after surgery, but not when testing began 1 day after surgery and overlapped the period of drug administration. Lesion effects also appeared on tests for neurologic impairment and activity, but nimodipine did not reduce these deficits. These findings indicate that nimodipine has the potential to reduce some deficits after sensorimotor cortical lesions, but that the effects of this drug may be task specific.

Animals↗
PubMed1990

Nimodipine enhances new learning after hippocampal damage.

Rats were trained to lever press and then were given either bilateral lesions of the hippocampus or control operations. Half of the rats in each group received oral nimodipine, a calcium entry blocker, while the remaining rats received vehicle, over a 14-day period that began the evening of surgery. The rats were studied on a DRL 20-s schedule of reinforcement (differential reinforcement of low rates of responding) that required them to withhold a response for at least 20 s after their last lever press in order to earn a reward. Rats with lesions that did not receive the drug performed poorly on the DRL 20-s schedule. In contrast, rats sustaining the same hippocampal lesions but given the drug showed scores that were virtually equivalent to those of the sham-operated control animals. Similar trends were observed when the rats were then tested on a DRL 40-s schedule of reinforcement. These findings suggest that nimodipine may attenuate the effects of acute, focal brain lesions on new learning of even difficult behavioral and cognitive tasks.

Animals↗
PubMed1989

Nimodipine enhances growth and vascularization of neural grafts.

The potential of the calcium channel antagonist, nimodipine, to enhance vascularization and growth of neural grafts has been investigated. Four groups of rats received unilateral 6-OHDA lesions of the nigrostriatal pathway followed 16-23 days later by intrastriatal grafts of embryonic ventral mesencephalon. The grafts were derived from (i) Embryonic Day 14 embryos (group E14), (ii) Day 17 embryos (group E17), and (iii) Day 20 embryos (group E20), all implanted within 90 min of preparation, or (iv) Day 14 embryos with a 6-h delay prior to implantation (group E14/6H). Half the rats in each group received intragastric intubation with nimodipine daily for 14 days after transplantation surgery, whereas the other half received control intubations. The rats were killed by perfusion with formalin containing Indian ink 6 weeks after grafting. Nimodipine treatment enhanced the vascularization of the grafts in all four groups and induced a significant increase in the volume of grafts under the three suboptimal transplantation conditions (i.e., groups E17, E20, E14/6H). The results suggest that vascularization of graft tissue is an important determinant of survival and growth of neural transplants prepared by the dissociated cell suspension technique and show that vascular perfusion of grafts can be enhanced by nimodipine.

Animals↗
PubMed1989

Comparison of behavioral effects of nucleus basalis magnocellularis lesions and somatosensory cortex ablation in the rat.

Cholinergic neurons in the nucleus basalis region of the forebrain project to various portions of the cerebral cortex, including somatosensory cortex. Degeneration of these neurons and their cortical projections is a major feature of the neuropathology of Alzheimer's disease. Injecting an excitotoxin into the basal forebrain to destroy nucleus basalis neurons provides a potentially useful animal model for studying the role of these neurons in Alzheimer's disease. Previously, we demonstrated that rats with nucleus basalis excitotoxin lesions performed poorly on a tactile discrimination task and on a test of working memory. In an effort to clarify further the role of impaired memory versus other types of impairment (e.g. disrupted somatosensory processing due to cholinergic deafferentation of somatosensory cortex), we compared a group of rats with bilateral nucleus basalis excitotoxin lesions and a group with bilateral somatosensory cortical ablations on a variety of behavioral tasks. Rats with nucleus basalis lesions performed as well as controls on a battery of neurological tests but exhibited increased emotionality unlike rats with somatosensory cortical ablations which performed poorly on the battery but were not hyperemotional. The two lesion groups were impaired significantly and to a comparable degree in performing two-choice tactile discriminations in a T-maze. In contrast, only rats with nucleus basalis lesions showed deficits in working memory as tested in an eight-arm radial maze. Both lesion groups performed comparably to sham controls on a test of reference memory involving a black/white discrimination in a T-maze. The findings suggest that rats with nucleus basalis lesions manifest disturbances in several of the same spheres (emotionality, somatosensory information processing, memory) that are disrupted in Alzheimer's disease and further confirm the utility of the excitotoxin lesion approach for studying the pathophysiology of Alzheimer's disease.

Animals↗
PubMed1988

The 'Kennard effect' before Kennard. The early history of age and brain lesions.

The role of age in recovery of function after brain damage has been of particular interest since the mid-1930s when Kennard described sparing of motor function following brain damage in infant monkeys. In the years since her initial papers, this phenomenon has become known as the "Kennard principle." This article describes a number of observations of the Kennard principle prior to Kennard's first publication. Included are descriptions of both early animal research and neurologic cases.

Aging↗
PubMed1988

Behavioral and neurochemical evaluation of a transgenic mouse model of Lesch-Nyhan syndrome.

Two transgenic strains of mutant mice lacking hypoxanthine-guanidine phosphoribosyltransferase (HPRT) activity were examined behaviorally and neurochemically for phenotypic similarity to the human Lesch-Nyhan syndrome. In this syndrome, male children markedly deficient in the enzyme HPRT develop self-mutilation and severe motoric difficulties, and exhibit a pronounced deficiency of dopamine in the basal ganglia. The HPRT-deficient mice showed no evidence of self-mutilation, no detectable motor impairments on tests selected for sensitivity to basal ganglia dysfunction, and no differences in response to apomorphine. Biochemical analyses revealed significantly lower levels of striatal dopamine in the HPRT-deficient mice than in HPRT normal littermates, but the depletion was only of the order of 19%. The results suggest that mice lacking HPRT activity do not phenotypically resemble children born with the same enzymatic deficiency in part because mutant mouse striatal dopamine levels are not as low as those seen in clinical cases with Lesch-Nyhan disease. In contrast to Lesch-Nyhan children, mice may be able to utilize alternative pathways more effectively to maintain purine and neurotransmitter levels within the ranges required for normal brain development and function.

Animals↗
PubMed1987

Tactile-visual acquisition and reversal learning deficits in rats with prefrontal cortical lesions.

Rats with prefrontal cortex (PFC) lesions or sham operations were tested for acquisition and reversal learning with tactile-visual stimuli. PFC rats performed extremely poorly during acquisition and also differed from control rats in reversal learning. Both higher-order processing and subtle motoric dysfunctions may have combined to account for the marked effects of these cortex lesions.

Animals↗
PubMed1987

Behavioral correlates of vitamin D deficiency.

Rats deprived of vitamin D at weaning were compared to control rats on open field, stabilimeter, radial arm maze and spatial reversal tasks in order to test the hypothesis that vitamin D deficiency alters behavior and learning. The deficient animals engaged in statistically less open field rearing activity and spent more time each day negotiating the radial maze than did the control rats. These findings are consistent with the known influence of vitamin D on the musculoskeletal system. The deprived rats did not differ from the control animals on the learning measures. This would indicate that vitamin D deficiency may not significantly impair cognitive functions in young adult rats.

Animals↗