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At least 901 records · Page 50Linked to original sources
PubMed2003

Cortical reorganisation and chronic pain: implications for rehabilitation.

Recent neuroscientific evidence has revealed that the adult brain is capable of substantial plastic change in such areas as the primary somatosensory cortex that were formerly thought to be modifiable only during early experience. These findings have implications for our understanding of chronic pain. Functional reorganisation in both the somatosensory and the motor system was observed in neuropathic and musculoskeletal pain. In patients with chronic low back pain and fibromyalgia the amount of reorganisational change increases with chronicity; in phantom limb pain and other neuropathic pain syndromes cortical reorganisation is correlated with the amount of pain. These central alterations may be viewed as pain memories that influence the processing of both painful and nonpainful input to the somatosensory system as well as its effects on the motor system. Cortical plasticity related to chronic pain can be modified by behavioural interventions that provide feedback to the brain areas that were altered by somatosensory pain memories or by pharmacological agents that prevent or reverse maladaptive memory formation.

Back Pain↗
PubMedDate not supplied

Alzheimer disease and its management: a review.

Alzheimer disease is a progressive degenerative disorder of the brain characterized by a slow, progressive decline in cognitive function and behavior. As the disease advances, persons with Alzheimer disease have tough time with daily usage of things like using the phone, cooking, handling money, or driving the car. The disease is more common in elder population. It is estimated that Alzheimer disease affects 15 million people worldwide and approximately 4 million Americans. The clinical features of Alzheimer disease overlaps with common signs of aging, and other types of dementia, hence the diagnosis remains difficult. The neuropathologic hallmarks of the disorder are amyloid-rich senile plaques, neurofibrillary tangles, and neuronal degeneration. Drugs approved for treating Alzheimer disease include acetylcholinesterase inhibitors and N-methyl-D-aspartate (NMDA) receptor antagonist. Caregivers not getting adequate information about Alzheimer disease may believe that nothing can be done to manage its symptoms. Understanding the extent of Alzheimer disease related knowledge can assist disease management that result in improved disease management and reduced care costs. This article attempts to focus on some of the important recent developments in understanding and management of Alzheimer disease.

Alzheimer Disease↗
PubMed2005

Is there a double standard when it comes to dementia care?

Dementia, a diagnostic syndrome that includes Alzheimer's disease (AD) and vascular dementia, affects more than 4 million Europeans. Its prevalence will increase as the population ages, even though half of cases remain undiagnosed. Dementia has a marked impact on the general health economy. The direct costs of caring for persons with AD alone exceed the cost of heart disease, cancer and stroke combined, primarily because of the need for expensive care in the later stages of the disease. Yet research spending for AD remains disproportionately small. Effective planning for the public health issues posed by AD mandates reduction of either the dependency or the prevalence of the disease. Some drug treatments have alleviated the symptoms of AD and improved the quality of life for patients and their families. However, many countries have introduced inappropriately stringent regulations for the use of medical therapy. These and related issues were addressed during the recent Facing Dementia Forum, in which 175 experts in dementia care discussed results of an extensive international survey. The experts identified three main barriers to effective care: (i) dementia is not considered a health care priority; (ii) there is a mistaken belief that nothing can be done about dementia; and (iii) early dementia is difficult to recognise. These observations provided a basis for the Agenda for Change, a series of strategies to overcome these barriers. The specific findings of the survey, as well as the Agenda for Change, will be reviewed in subsequent articles in this supplement.

Alzheimer Disease↗
PubMed1986

Locomotion and stereotyped behaviours induced by 1-amino-3,5-dimethyladamantane (D 145) and apomorphine in the rat: a comparison.

The locomotion and stereotyped behaviours induced by the two dopamine agonists, 1-amino-3,5-dimethyladamantane (D 145) and apomorphine in rats have been investigated using a holeboard apparatus. Unlike apomorphine, D 145 did not induce compulsive gnawing, but it did induce locomotion dose-dependently. However, the pattern of locomotion was different from that induced by apomorphine and the locomotion itself was potently antagonized by haloperidol but not by sulpiride; this is the opposite to apomorphine-induced locomotion. This indicates that locomotion induced by dopamine agonists is not a unitary phenomenon but that different 'types' of locomotion, with different pharmacological properties, can be induced. Low doses of D 145, given before apomorphine, reduced apomorphine-induced gnawing and enhanced apomorphine-induced locomotion. The long lasting 'priming' effect known to occur after repetitive injections of apomorphine was not mimicked by D 145. Apomorphine and D 145 are considered to be two specific DA agonists; their behavioural-pharmacological profiles, however, are quite different.

Amantadine↗
PubMed2003

Pharmacological modulation of perceptual learning and associated cortical reorganization.

The pharmacological basis of perceptual learning and associated cortical reorganizations remains elusive. We induced perceptual learning by Hebbian coactivation of the skin of the tip of the right index finger in humans. Under placebo, tactile two-point discrimination was improved on the coactivated but not on the left index finger. This augmentation was blocked by an N-methyl-D-aspartate-receptor blocker, but doubled by amphetamine. No drug effects were found on the left index finger. The individual amount of cortical reorganization as assessed by mapping of somatosensory evoked potentials was linearly correlated with the pharmacological modulation of discrimination thresholds, implying that perceptual learning and associated cortical changes are controlled by basic mechanisms known to mediate and modulate synaptic plasticity.

Adult↗
PubMed1975

Effect of five dopaminergic drugs on plasma growth hormone levels in acromegalic subjects.

The effect of 5 dopaminergic drugs, 2-Br-alpha-ergocryptine (CB 154), L-dopa, 1-(2-pyrimidyl)-4-piperonylpiperazine (Piribedil), amantadine and 1,3-dimethyl-5-amino-adamantan (d 145), on human growth hormone levels (hGH) was studied in 38 acromegalic subjects. Acute administration of CB 154 (2.5 mg p.o.) in 34 patients was followed by a significant and sustained fall in plasma hGH levels; in 19 cases (55.6%) the observed fall was clearly below the +/- 2SD of the mean GH changes present in the same subjects after placebo. In patients previously shown to be responsive to CB 154, Significant GH falls were also present following the single administration of L-dopa (500 mg p.o.) (9 patients) and Piribedil (100 mg p.o.) (5 patients), although CB 154 exhibited a more frequent, striking (reduction of up to 1-2 ng/ml) and long-lasting (4 h more) effect. In contrast, amantadine (200 mg p.o.) or D 145 (20 or 50 mg p.o.) did not induce significant changes in hGH levels (7 patients). These results broaden and corroborate previous findings on the hGH-lowering effect of dopaminergic stimulation in acromegaly. The possible reason(s) for the difference in hGH response with different dopaminergic compounds is discussed.

Acromegaly↗