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1.
Neuroimage ; 43(3): 540-53, 2008 Nov 15.
Article in English | MEDLINE | ID: mdl-18718872

ABSTRACT

The coordination of movement between the upper limbs is a function highly distributed across the animal kingdom. How the central nervous system generates such bilateral, synchronous movements, and how this differs from the generation of unilateral movements, remain uncertain. Electrophysiologic and functional imaging studies support that the activity of many brain regions during bimanual and unimanual movement is quite similar. Thus, the same brain regions (and indeed the same neurons) respond similarly during unimanual and bimanual movements as measured by electrophysiological responses. How then are different motor behaviors generated? To address this question, we studied unimanual and bimanual movements using fMRI and constructed networks of activation using Structural Equation Modeling (SEM). Our results suggest that (1) the dominant hemisphere appears to initiate activity responsible for bimanual movement; (2) activation during bimanual movement does not reflect the sum of right and left unimanual activation; (3) production of unimanual movement involves a network that is distinct from, and not a mirror of, the network for contralateral unimanual movement; and (4) using SEM, it is possible to obtain robust group networks representative of a population and to identify individual networks which can be used to detect subtle differences both between subjects as well as within a single subject over time. In summary, these results highlight a differential role for the dominant and non-dominant hemispheres during bimanual movements, further elaborating the concept of handedness and dominance. This knowledge increases our understanding of cortical motor physiology in health and after neurological damage.


Subject(s)
Brain/physiology , Functional Laterality/physiology , Movement/physiology , Nerve Net/physiology , Psychomotor Performance/physiology , Brain Mapping , Electromyography , Humans , Image Interpretation, Computer-Assisted , Magnetic Resonance Imaging
2.
J Laryngol Otol ; 119(10): 806-9, 2005 Oct.
Article in English | MEDLINE | ID: mdl-16259658

ABSTRACT

OBJECTIVE: To determine the access to and the use of the Internet by acoustic neuroma patients as a medical information source, and the influence of the Internet on decision-making, as well as the patients' views on the quality of particular sites. MATERIALS AND METHODS: A retrospective 27-item questionnaire was sent to 138 consecutive acoustic neuroma patients diagnosed between 1997 and 2002. The study included patients treated by conservative, radiotherapeutic and surgical modalities. MAIN OUTCOME MEASURES: Patient demographics, the extent of Internet use as well as quality and quantity of available information. RESULTS: There were 86.95 per cent questionnaires available for analysis. Twenty-four per cent accessed the Internet to obtain information about acoustic neuromas. Ninety-seven per cent of patients said that the information provided in the clinic matched with the information obtained from the websites, 49 per cent said that the information obtained from the Internet did not influence decision making regarding acceptance of treatment of their tumour. Some patients said the Internet information was depressing, devastating, and they would never look up the Internet again for medical information. CONCLUSION: A significant proportion of our patients accessed the Internet for information. Caution should be exercised when advising patients regarding websites as the information on the Internet is often not controlled or checked for accuracy. Acoustic neuroma specialists and ENT surgeons in general should familiarize themselves with related websites so that patients can then be directed to high-quality sites.


Subject(s)
Decision Making , Information Services/statistics & numerical data , Internet/statistics & numerical data , Neuroma, Acoustic/therapy , Attitude to Health , England , Female , Humans , Information Services/standards , Internet/standards , Male , Middle Aged , Patient Education as Topic/methods , Patient Education as Topic/standards , Retrospective Studies , Surveys and Questionnaires
3.
Ann N Y Acad Sci ; 914: 13-21, 2000 Sep.
Article in English | MEDLINE | ID: mdl-11085304

ABSTRACT

Pharmacological studies have shown that blockade of the dopamine D1 receptor attenuates locomotor behaviors and prevents sensitization to psychostimulants. However, due to possible cross-reactivities of the D1 receptor antagonists, the exact role of the D1 receptor in response to psychostimulants is still not definitive. To address this issue, we used D1 receptor mutant mice and tested locomotor responses of the mutant mice and wild-type control mice after cocaine and amphetamine treatments. We found that the D1 receptor mutant mice exhibit significantly reduced locomotor responses to repeated cocaine administration compared to wild-type mice. Moreover, D1 receptor mutant mice were less sensitive than the wild-type mice to acute amphetamine administration over a dose range, although they exhibited apparently similar behavioral responses to those of the wild-type mice after repeated amphetamine administration at the 5 mg/kg dose. These studies suggest that the D1 receptor plays an essential role in mediating cocaine-induced locomotor responses in mice. In addition, the D1 receptor also participates in behavioral responses induced by amphetamine administration. Further molecular studies are in progress to address the intracellular signaling mechanisms in response to D1 receptor activation by psychostimulants.


Subject(s)
Behavior, Addictive/physiopathology , Receptors, Dopamine D1/physiology , Amphetamine/administration & dosage , Animals , Behavior, Addictive/chemically induced , Behavior, Addictive/genetics , Behavior, Animal , Cocaine/administration & dosage , Dopamine Uptake Inhibitors/administration & dosage , Dose-Response Relationship, Drug , Drug Administration Schedule , Mice , Mice, Transgenic , Motor Activity/drug effects , Motor Activity/physiology , Receptors, Dopamine D1/genetics
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