Helen Goodell

STUDIES ON PAIN. A NEW METHOD FOR MEASURING PAIN THRESHOLD: OBSERVATIONS ON SPATIAL SUMMATION OF PAIN

The purpose of these studies has been to present a new method for measuring pain thresholds, together with experimental observations on the physiology of pain and on the effect of various chemical agents upon pain thresholds. Methods for estimating the intensity of the stimulus required to evoke a painful sensation in the skin may be classified under the headings: mechanical, chemical, electrical, and thermal. Conclusion 1. A quantitative method for measuring pain thresholds in the skin by thermal radiation has been described. The method has the general advantage of measuring a physical quantity which is directly proportional to the changes occurring in the skin. The method has the further advantages of precision, simplicity of technique, rapidity of measurement, and the fact that the stimulus is innocuous upon repeated application except at high intensities. Further, any part of the skin surface may be studied and the size of the stimulated area varied at will. 2. Pain thresholds measured in this way did not vary consistently with time of day, with the general effectiveness, or the emotional state of the 3 subjects. 3. Individual threshold measurements for 3 subjects were 0.229, 0.231, and 0.233 gm. cal./ sec./cm.2 and all measurements were found to be within + 12 per cent of their respective average values. The standard deviation for a single measurement was calculated to be + 2 per cent. 4. Intense pain in any part of the body raised the pain threshold in the skin in other parts as much as 35 per cent. 5. The senses of pain and heat, which were always stimulated together, were shown to be separate sensations through the action of acetylsalicylic acid. This drug lowered the heat threshold and raised the pain threshold. 6. The peripheral structures responsible tor pain sense were distinguished from those of temperature and touch by demonstrating that occluding the blood for 25 minutes did not directly affect the pain threshold in the ischemic hand, whereas other sensations could hardly be elicited. 7. Pain sense was found to have no spatial summation in the sense that the pain threshold for many end organs was no lower than that for a few. This was observed to be the case for minimal stimuli and for supraminimal stimuli after morphine administration. 8. The intensity of radiation which produced blistering in 3 seconds was observed to be twice that necessary for the bare perception of pain. PMID: 16694782 [PubMed] PMCID: PMC435000

Experimental evidence on the nature of cutaneous hyperalgesia.

Hyperalgesia may be defined as a state of increased intensity of pain sensation induced by either noxious or ordinarily non-noxious stimulation of peripheral tissue. Hyperalgesia occurs in both superficial and deep tissues, in areas with pain thresholds that are normal, lowered or raised (1, 2). As seen at the bedside there are apparently several varieties of hyperalgesia, and few clinical phenomena are more difficult to understand and to evaluate. The literature on the subject includes work of a distinguished roster of investigators (3-8). As a result of these studies two classes of hyperalgesia have been loosely formulated, namely, that occurring at the site of injury, and that associated with the injury but occurring in undamaged tissue. Failure to outline clearly the characteristics of these two varieties of hyperalgesia has resulted in a controversy as regards the alterations responsible for the hyperalgesia occurring in undamaged tissue. One group holds that this hyperalgesia is attributable to changes in the periphery, whereas the other maintains that changes in the central nervous system are responsible. Due to the lack of quantitative methods of measuring perception, progress has been slow in clarifying an understanding of the underlying mechanisms. This communication is concerned primarily with that cutaneous hyperalgesia occurring in undamaged tissues adjacent to and at some distance from the site of an injury or a site of noxious stimulation.

Mental symptoms in Parkinson's disease during chronic treatment with levodopa.

Mental symptoms increased in frequency among 100 patients with parkinsonism treated with levodopa. Dementia was found in about one-third of patients throughout the 6-year treatment period. Thirteen patients became demented during the study, and dementia worsened severely in seven others. Agitated confusion became increasingly frequent and was observed in 60 percent of patients taking levodopa for 6 years. Withdrawal from levodopa decreased agitation, but not dementia. Ten patients received L-tryptophan along with levodopa, but no change in mentation was observed. In view of previous studies of mentation in Parkinsons disease and reports of widespread neuronal changes in the brain of autopsied patients with parkinsonism, our results suggest that the high incidence of dementia in patients with Parkinsons disease who take levodopa reflects prolongation of the course of the illness rather than a direct effect of the medication.

NEURAL MECHANISMS INVOLVED IN ITCH, “ITCHY SKIN,” AND TICKLE SENSATIONS

Available evidence suggests that the sensation of itching is closely related to that of pain (1). Titchener (2) observed that when the skin was explored with a fine hair, well-defined points were found which gave rise to itching when the intensity of stimulation was low, and to pain on stronger stimulation. Bishop (3) found that itching resulted from repetitive low intensity electrical stimulation of pain spots in the skin. Lewis, Grant and Marvin (4) pointed out that noxious stimuli, if their intensity be decreased, can be made to produce itching instead of pain. Forster (5) and Bickford (6) reported that in patients who had

STUDIES ON PAIN. MEASUREMENT OF THE EFFECT OF MORPHINE, CODEINE, AND OTHER OPIATES ON THE PAIN THRESHOLD AND AN ANALYSIS OF THEIR RELATION TO THE PAIN EXPERIENCE

Though valuable observations have been made of the action of analgesic agents, these have been based in the main on animal experimentation and No adequate method for assaying their effects on the pain threshold in man has been available. However, since the prime purpose of an analgesic drug concerns its action in man, it is desirable to measure accurately its effect on mans pain threshold. For such measurement a suitable method has now been developed (12). Also, it is important to define precisely other analgesic effects. It has thus been possible to evaluate the therapeutic effectiveness of the opiates, and to make inferences concerning the nature of the pain experience in man. METHOD Quantitative measurements of the pain threshold were made by exposing 3.5 cm.2 of skin surface for 3 seconds to thermal radiation. The intensity of radiation which barely evoked pain was denoted as the pain threshold. In this way the normal pain threshold level was established to + 2 per cent by making observations at 5-minute intervals until a constant threshold was obtained. This usually required four observations. After the control measurements an analgesic agent was administered and observations of the pain threshold were made at 10-minute intervals until the threshold had returned to the control level, that is, until all pain threshold-raising action had ceased. The height of the pain threshold-raising effect was expressed in per cent elevation above the control level. The protocols were distributed so that the threshold of each subject was measured by a colleague who in turn was unfamiliar with the change in his own threshold. Occasionally, observers not participants in the experiment made threshold readings. Thus, three independent protocols were made, no individual knowing how much his own threshold had been altered. Occasionally sterile salt was introduced into one of the syringes so that it was known to all that one of the subjects had not received an analgesic drug, although which one had been so treated was not revealed until the end of the experiment. All agents were administered intramus-cularly. With each pain threshold reading the subject made a concise statement of his psychological state. In the 10-minute interims between readings the subjects sat comfortably and engaged in reading, writing, or conversation. Sleep was not permitted for reasons to be discussed later, and if drowsiness became difficult to manage the subjects walked about the laboratory. During long experiments food was taken, …

THE PARTICIPATION OF THE NERVOUS SYSTEM IN THE INFLAMMATORY REACTION

The history of medicine several times has recorded alternations between principal concern with the specific localmized manifatations of disease and a greater emphasis on the patient as a whole. When the latter concern is dominant, interest naturally turns to the possibility of neural influences on pathological reaotions and disease. In ancient times, Galen taught that any part of the body may influence any other part through neurd connections. In the 18th century, Cdlen, Pinel, and Baglivi held the view that disorders of the nervous system underlay most disease processes. This emphasis gave rise to the school of “systematic correlative neuropathologists” which dominated French concepts of disease in the first half of the 19th century. In the latter half of the 19th century, growing emphasis on localized cellular alterations overshadowed the earlier interest in generalized reactions. A traditional em1phasSis on the nervous system and on the influence of the total environment in disease has continued to the present in the Soviet Union,’,* and is implicit in the recent “psychosomatic” formulations of Western medicine. Despite widespread contemporary acceptance of a loosely formulated relationship between the nervous system and at least some categories of non-neural disease processes, except for neuroendocrine relationships, relatively few studies have focused specifically on mechanisms by which the nervous system might influence pathological reactlions and the initiabion and murse of disease. In this paper, we will attempt a brief survey of this topic, with an emdphasis on studies conducted in the laboratory of the late Harold G. Wolff at the New York Hospital-Cornell University Medical College.

LSD-LIKE DELIRIUM FOLLOWING INGESTION OF A SMALL AMOUNT OF ITS BROM ANALOG (BOL-148)

Excerpt In 1943 Hoffmann1detected in himself strange mental effects from a compound that he and Stoll2had prepared in 1938 and reported in 1943 as an oxytocic agent similar to ergonovine. This obse...