The study of pain in awake animals raises ethical, philosophical, and technical problems. We review the ethical standards for studying pain in animals and emphasize that there are scientific as well as moral reasons for keeping to them. Philosophically, there is the problem that pain cannot be monitored directly in animals but can only be estimated by examining their responses to nociceptive stimuli; however, such responses do not necessarily mean that there is a concomitant sensation. The types of nociceptive stimuli (electrical, thermal, mechanical, or chemical) that have been used in different pain models are reviewed with the conclusion that none is ideal, although chemical stimuli probably most closely mimic acute clinical pain. The monitored reactions are almost always motor responses ranging from spinal reflexes to complex behaviors. Most have the weakness that they may be associated with, or modulated by, other physiological functions. The main tests are critically reviewed in terms of their sensitivity, specificity, and predictiveness. Weaknesses are highlighted, including 1) that in most tests responses are monitored around a nociceptive threshold, whereas clinical pain is almost always more severe; 2) differences in the fashion whereby responses are evoked from healthy and inflamed tissues; and 3) problems in assessing threshold responses to stimuli, which continue to increase in intensity. It is concluded that although the neural basis of the most used tests is poorly understood, their use will be more profitable if pain is considered within, rather than apart from, the body's homeostatic mechanisms.

Animal Models of Nociception

The aim of this paper is to review briefly our understanding of the phenomenon of spasticity based in current evidence.

Spasticity: Clinical perceptions, neurological realities and meaningful measurement

The lower limb flexion reflex in humans.

1. General methodology 2. Monosynaptic Ia excitation and post-activation depression 3. Muscle spindles and fusimotor drive: microneurography and other techniques 4. Recurrent inhibition 5. Reciprocal Ia inhibition 6. Ib pathways 7. Group Ii pathways 8. Presynaptic inhibition of Ia terminals 9. Cutaneomuscular, withdrawal and flexor reflex afferent responses 10. Propriospinal relay for descending motor commands 11. Involvement of spinal pathways in different motor tasks 12. The pathophysiology of spasticity and parkinsonian rigidity.

The Circuitry of the Human Spinal Cord : Its Role in Motor Control and Movement Disorders

Measurable sources of muscle tension include viscoelastic tone, physiological contracture (neither of which involve motor unit action potentials), voluntary contraction, and muscle spasm (which we define as involuntary muscle contraction). The latter two depend on motor unit action potentials to generate the tension. Total muscle tension is most accurately measured as stiffness. Thixotropy of muscle is an ubiquitous and functionally important phenomenon that is not commonly recognized. A clinical pain condition associated with increased muscle tension is tension-type headache, which is largely muscular in origin; it is often caused by myofascial trigger points, but not by a pain-spasm-pain cycle, which is a physiologically and clinically untenable concept. Clinical conditions associated with painful muscle spasm include spasmodic torticollis, trismus, unnecessary muscle tension, nocturnal leg cramps, and stiff-man syndrome.

M. R. Dimitrijević

Papers

Studies of spasticity in man. 3. Analysis of revlex activity evoked by noxious cutaneous stimulation.