Informed consent in Australia

Recent decisions in Australian courts affirm three important principles relating to consent to therapy. First, patients must be appropriately and adequately informed. Second, the scope and detail of the information supplied should be based on the reasonable patient's need to know rather than on the actions of the reasonable doctor. Third, the doctor must take care to ensure that the information imparted is understood by the patient. This publication reviews the basis of informed consent and traditional beneficent-style consent. The occasions when beneficence is more appropriate are outlined.

Reginald S. A. Lord 1 , 2
1 Department of Surgery, St Vincent's Hospital, University of New South Wales. Sydney. Australila
Correspondence to 2 Professor R. S. A. Lord, Level 17, St Vincent's Hospital. Victoria Street. Darlinghurst. NSW 2010. Australia.
*Presented at the 1st John Plunkett Seminar on Medical Ethics, Sydney. June 1994.

to induce a patient's participation by appeal to their nonrational preferences, this is also a violation of their autonomy

In this paper we argue that the standard focus on problems of informed consent in debates about the ethics of human experimentation is inadequate because it fails to capture a more fundamental way in which such experiments may be wrong. Taking clinical trials as our case in point, we suggest that it is the moral offence of using people as mere means which better characterizes what is wrong with violations of personal autonomy in certain kinds of clinical trials. This account also helps bring out another important way in which the autonomy of the participants in clinical trials my be violated, even in cases where they have given informed consent to their involvement. Where relevant information about the trial is framed in such a way as to induce a patient's participation by appeal to their nonrational preferences, this is also a violation of their autonomy, and one which is distinct from a failure of informed consent. The underlying wrongness of both kinds of violations, we argue, is plausibly captured by the moral offence of using people as mere means.  MEDICAL EXPERIMENTATION, INFORMED CONSENT AND USING PEOPLE DE AN COCKING 1 JUSTIN OAKLEY 1 1 Centre for Human Bioethics Monash University

Sympathectomy induces mast cell hyperplasia

Mast cell hyperplasia is found in different pathologies such as chronic inflammatory processes, fibrotic disorders, wound healing or neoplastic tissue transformation. The functional significance of the accumulation of mast cells in these processes is largely unknown. It is now established that bone marrow-derived mast cell progenitors circulate in peripheral blood and subsequently migrate into the tissue where they undergo final maturation under the influence of local microenvironmental factors. Cytokines are of particular importance for mast cell recruitment, development, and function.
http://www.ncbi.nlm.nih.gov/pubmed/11919420

Long-term superior cervical sympathectomy induces mast cell hyperplasia and increases histamine and serotonin content in the rat dura mater
Copyright © 1999 IBRO. Published by Elsevier Science Ltd.

Immune and Glial Cells Contribute to Pathological Pain States

Alterations in sympathetic fibers rapidly follow peripheral nerve injury. This occurs as sprouting of
sympathetic fibers, creating aberrant communication pathways from the new sympathetic terminals to
sensory neurons (35). Sympathetic sprouting has been documented in the region of peripheral terminal
fields of sensory neurons (262), at the site of nerve trauma (57), and within the dorsal root ganglia
(DRG) containing cell bodies of sensory neurons (248, 343). Each of these sites develops spontaneous
activity and sensitivity for catecholamines and sympathetic activation (8, 53).
The clearest evidence that immune activation participates in sympathetic sprouting comes from studies of
the DRG. DRG cells receive signals that peripheral nerve injury has occurred via retrograde axonal
transport from the trauma site. These retrogradely transported signals trigger sympathetic nerve sprouting
into DRG (205, 308). As a result of nerve damage-induced retrogradely transported signals, glial cells
within the DRG (called satellite cells) proliferate and become activated; macrophages are
recruited to the DRG as well. In turn, the activated satellite glial cells (and, presumably, the
macrophages) release proinflammatory cytokines and a variety of growth factors into the extracellular
fluid of the DRG (206, 246-248, 258, 277, 308, 358). These substances stimulate and direct the growth
of sympathetic fibers, which form basket-like terminals around the satellite cells that, in turn, surround
neuronal cell bodies.
Physiological Reviews, Vol. 82, No. 4, October 2002, pp. 981-1011; 10.1152/physrev.00011.2002.
Copyright ©2002 by the American Physiological Society

Intraneural activated T cells cause focal breakdown of the blood-nerve barrier

These findings demonstrate that activated T cells cause focal breakdown of the BNB, allowing circulating antimyelin antibody to enter the endoneurium with consequent focal demyelination.
Brain. 1995 Aug;118 ( Pt 4):857-68
Intraneural activated T cells cause focal breakdown of the blood-nerve barrier.

Spies JM, Westland KW, Bonner JG, Pollard JD.
Institute of Clinical Neurosciences, University of Sydney, NSW Australia.

Autoregulation of cerebral blood flow in orthostatic hypotension

The most common patterns of cerebral response to OH are autoregulatory failure with a flat flow-pressure relationship or intact autoregulation with an expanded autoregulated range. The least common pattern is autoregulatory failure with a steep flow-pressure relationship. Patients with patterns 1 and 2 have an enhanced capacity to cope with OH, while those with pattern 3 have reduced capacity.
Stroke. 1998 Jan;29(1):104-11. Links
Autoregulation of cerebral blood flow in orthostatic hypotension.

Novak V, Novak P, Spies JM, Low PA.

Autonomic Disorders Center, Department of Neurology, Mayo Clinic and Foundation, Rochester, Minn. 55905, USA.

Autonomic dysfunction is a common complication of peripheral neuropathies. It is often of little clinical importance, but some conditions may cause profound disturbance of autonomic function, including postural hypotension, impotence and impairment of heart rate and bladder and bowel control. Autonomic function can be evaluated by a number of investigations, some of which can be performed in a neurophysiology laboratory. Diseases that primarily affect small nerve fibres or cause acute demyelination of small myelinated fibres are most likely to cause autonomic dysfunction. Management includes treating the underlying cause and symptomatic therapy.
Autonomic neuropathy, I. Clinical features, investigation, pathophysiology, and treatment.

McDougall AJ and McLeod JG

Journal of the neurological sciences 137(2):79-88, 1996 May

sensory, limbic, and autonomic systems

The frontal lobes receive information from sensory, limbic, and autonomic systems and engage in complex cognitive functions.

The basis for prefrontal lobotomy is the apparent loss of anxiety resulting from disconnection of perceptions from normal emotional responses.
Physiology
by Roger Thies, Kirk W. Barron - 1995 - Science - 280 pages

lobotomy is often associated with hyperhidrosis

"lobotomy is often associated with hyperhidrosis. Nerves from the hypothalamus apparently pass through the pons and medulla into the cervical spinal cord, since injury to certain areas of these structures results in anhidrosis of specific regions of the body surface.
Nerves leaving the ventral ramus of the spinals nerve cord pass through the chain of sympathetic ganglia so that from thoracic roots T2 to T4 the head and neck are innervated and from T2 to T8 the upper limbs are supplied.
There is some evidence of some innervation of the face and upper extremities from T1, even though autonomic function is presumed to arise only below the first thoracic root. For example, destruction of stellate ganglia (C8-T1 or T2) produces anhidrosis of the upper body and it's extremities. Despite these generalizations, the supply of nerves to small areas such as a finger may originate from as many as seven spinal segments. It may also be very important to recognize that the anatomy of the sympathetic chain is highly varied and that many nerves may bypass the ganglia entirely, thus accounting for numerous discrepancies in the literature concerning pathways and control.
List and Peet concluded from lesions at various levels that that section of the spinal cord and specific lesions within the cord result in loss of sweating in response to heat, but not to exogenous drugs. On the other hand, destruction of peripheral nerves by interruption of the nerve trunk results in loss of sweating in response to heat and drugs within two week.
Antiperspirants and Deodorants by Karl Laden

Edition: 2, illustrated, revised

Published by CRC Press, 1999, p.31

Neuromodulation Surgery for Psychiatric Disorders

Increasingly, psychiatric changes are believed to not be attributed to a "center" of mood or behavior but, rather, are secondary to an imbalance in communication of multiple neuronal loops. However, the efficacy of DBS is typically attributed to a small generated electrical field that encompasses a very limited amount of cerebral tissue. Perhaps the stimulation generated at a certain target propagates downstream into the rest of the circuitry, gaining an amplified effect.

Currently, 6 targets for neuromodulation surgery have been published: the Cg25, the anterior internal capsule (AIC), the nucleus accumbens (NA), the ventral striatum (VS), the inferior thalamic peduncle (ITP), and the left vagus nerve. Each of these regions can be seen as nodes in the aforementioned circuitry. Putative modulation at these nodes is the basis of the current efforts investigating neuromodulation surgery for refractory psychiatric disease. The highlighted areas of Images 14, 15, 16, 17, 18, 19, 20, 21, 22, and 23 show how neuromodulation at each target may influence the aforementioned circuitry.
Brian H Kopell, MD,
Jerry L Halverson, MD
http://emedicine.medscape.com/article/1343677-overview