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Information for module ANAT3042

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Module code:ANAT3042(Add to my personalised list)
Title:Pain
Credit value:.5
Division:Division of Biosciences
Module organiser:Professor Steve Hunt
Organiser's location:Medawar Building (CDB Department)
Organiser's email:hunt@ucl.ac.uk
Available for students in Year(s):3,
Module prerequisites:None 
Module outline:This module aims to present an integrated approach to pain. Through a series of ten two-hour lectures students will be presented with information about the basic mechanisms of pain and its clinical manifestations. Students will also be introduced to current ideas about therapy and management and to the problems inherent in measurements of pain. A series of seminars based on reading topics will be held at the end of the course. 
Module aims:1. To provide an interdisciplinary view of the neuroscience of pain. 2. To provide a basis for understanding the major clinical problem of chronic pain. 3. To introduce current ideas about pain management. 4. To relate research on pain to broad ideas about the organisation of the nervous system, especially sensory systems. 
Module objectives:BACKGROUND *Until the 1960s, pain was considered an inevitable sensory response to tissue damage. There was little room for the affective dimension of this ubiquitous experience, and nonewhatsoever for the effects of genetic differences, past experience, anxiety, or expectation. In recent years, great advances have been made in our understanding of the mechanisms that underlie pain and in the treatment of people who complain of pain. The roles of factors outside the patient\'s body have also been clarified. Pain is probably the most common symptomatic reason to seek medical consultation. All of us have headaches, burns, cuts, and other pains at some time during childhood and adult life. Individuals who undergo surgery are almost certain to have postoperative pain. Ageing is also associated with an increased likelihood of chronic pain. Health-care expenditures for chronic pain are enormous, rivalled only by the costs of wage replacement and welfare programmes for those who do not work because of pain. Despite improved knowledge of underlying mechanisms and better treatments, many people who have chronic pain receive inadequate care. From Pain: an overview, Loeser JD, Melzack R.( Lancet (1999) 353:1607-9) *In the past two decades, our understanding of how the brain acquires and processes visual, auditory, taste, olfactory and somatosensory information has been revolutionized. However, in no other sensory modality has more rapid and profound progress been made than in our understanding of the mechanisms by which nociceptive information is transmitted and processed in both the normal and pathological state. This rapid progress is due in large part to the multidisciplinary approach simultaneously using systems neurobiology, behavioural analysis, genetics, and cell and molecular techniques that has been taken. Pain is required for survival and maintaining the integrity of the organism, but sustained or chronic pain can result in secondary symptoms such as anxiety and depression and in a marked decrease in the quality of life. Pain pathways terminate in discrete brain areas that monitor the sensory and affective qualities of the stimulus and show remarkable plasticity. Noxious stimulation always results in changes in gene expression within the central nervous system, and different chronic pain states generate unique neurochemical signatures in the brain and spinal cord. New insights into how sensory information is processed as it moves from the sense organ to the cerebral cortex under the influence of a constantly changing molecular architecture will fundamentally change the way that we approach pain control and develop new analgesics. Nociceptive information reaches the brain from the peripheral site of injury through multiple parallel neuronal pathways. Cells in the termination regions within the forebrain and brainstem almost invariably project back, directly or indirectly, in a reciprocal fashion, to the areas of origin of the ascending pathways. At every stage of the pain pathway from sensory nerve to spinal cord, from spinal cord to brain stem and from brain stem to the cerebral cortex information signalling injury is subdivided or shared among these parallel systems. Molecular dissection has begun to reveal distinct functions for these separate pathways and their contribution to the final behavioural outcome. Each neuron in the ascending nociceptive pathway can change its phenotype in the face of a sustained peripheral injury, and there is growing evidence to indicate that the role of particular neuronal subsystems in nociception might only become apparent during the process of injury and repair. From: Stephen P. Hunt and Patrick W. Mantyh, The Molecular Dynamics of Pain Control, Nature Neuroscience Reviews, 2:83-91(2001) 
Key skills provided by module: 
Module timetable:https://cmis.adcom.ucl.ac.uk:4443/timetabling/moduleTimet.do?firstReq=Y&moduleId=ANAT3042 
Module assessment:Unseen three-hour written examination 80.00%.
1 Essay 20.00%.
 
Notes:Runs Term 2, Block D. 
Taking this module as an option?: 
Link to virtual learning environment(registered students only)https://moodle.ucl.ac.uk/course/view.php?id=6647 
Last updated:2014-01-23 15:46:47 by