[Sudor anglicus, or the "English sweate". One of the most enigmatic epidemics in history].
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English sweating disease also known as Sudor Anglicus is one of the least familiar epidemics of the Middle Ages, striking England 5 times during the 15th and 16th centuries before fading. This article will discuss the knowledge available to us about this fascinating epidemic, its characteristics and causes.
An inflight, clinically-oriented investigation of SMS was begun on STS-4 and revealed the following: compared to motion sickness on Earth, autonomic signs are significantly different in space motion sickness (SMS) vs. motion sickness (MS) in that sweating is not present, pallor or flushing may be present, and vomiting is episodic, sudden, and brief. Nausea may be present but is more often absent. Onset ranges from minutes to hours, plateaus, and rapidly resolves in 8-72 h with 36 h as average. Postflight reactions have been mild unless deliberately provoked in the early period of re-exposure to gravity. Postflight there is a period of resistance to all forms of motion sickness. There is some evidence for individual reduction in sensitivity on repeated flights. Etiology could not be proven objectively; however, the sensitivity to angular motion, often pronounced in pitch, and theoretical considerations make an intravestibular conflict the most likely cause. Electro-oculogram (EOG), audio-evoked potentials, measurement of fluid shifts, and other studies are inconsistent with a transient vestibular hydrops or increased intracranial pressure as a cause.
Diazepam has been used empirically for the relief of vertigo and, in addition, there are animal studies to suggest that this drug suppresses the vestibular system. One might anticipate therefore that diazepam would be an effective antimotion sickness drug. To study this, motion sickness was generated in four groups of normal subjects by having the subject make controlled head movements while rotating at constant velocity. Every subject was subjected (using a double-blind technique) to four different drug states, namely no drug, placebo, dimenhydrinate, and diazepam. Each group of subjects received the drug state at a different time interval (i.e. 30, 60, 90, and 120 min) prior to the motion sickness exposure. Motion sickness endpoints were measured subjectively using a nausea scale and objectively using a sweat sensor. The results showed significant antimotion sickness properties for both dimenhydrinate and diazepam as compared to the placebo. For the time intervals studied, the maximum effect was obtained at 120 min for both drugs.
An original scheme of quantitative evaluation of clinical manifestations of motion sickness has been developed. According to the scheme, eight major symptoms of motion sickness: vertigo, nausea, vomiting, sweating, paleness, headache, sleepiness, flaccidity are scored in relation to their manifestations. The scheme has been used in vestibular tests of 57 test subjects. The vestibular test used is tolerance to cross-coupled acceleration. On the basis of the scores quantitative criteria of human tolerance to vestibular exposures have been suggested. It is emphasized that the scheme can be widely used allowing statistical treatment, comparative individual and group analysis of the data obtained.
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Motion sickness is common in the population, especially in children, but its physiopathology is only partially understood and the true nature of the particular susceptibility of certain subjects remains completely unknown. Some symptoms of motion sickness, like pallor and cold sweating, are of an autonomic nature and the role of the autonomic nervous system in vasovagal syncope is well known. Our aim was therefore to study the relationship between motion sickness susceptibility and vasovagal syncope susceptibility. Questionnaires about susceptibility to motion sickness and to vasovagal syncope or presyncope in adulthood and childhood, filled in by 899 students (20.4 +/- 2.1 years, 405 men), were analysed. Motion sickness susceptibility in childhood was 31.1% and in adulthood 7.9% (p < 0.001). Vasovagal syncope susceptibility in childhood was 36.4% and in adulthood 33.9% (NS). A relationship between motion sickness susceptibility in adulthood and vasovagal syncope susceptibility in childhood and adulthood (p = 0.004 and 0.005, respectively) was found. Despite the limitations of a retrospective study this relationship between motion sickness susceptibility and vasovagal syncope susceptibility may indicate that a common mechanism exists, explaining the particular susceptibility of some subjects to both disorders. This paradigm may prove useful in better understanding the true nature of motion sickness and vasovagal syncope.
Approximately one in four patients experiences nausea and/or vomiting in anticipation of a chemotherapy treatment by the time of their fourth treatment cycle. Anticipatory nausea and vomiting is a prevalent problem of clinical significance in the total management of chemotherapy side effects. While refractory to standard antiemetic treatment, anticipatory nausea and vomiting has been successfully treated with behavioral approaches such as systemic desensitization. The present study was designed to identify the characteristics of patients at high risk for developing anticipatory side effects. Early identification of cancer patients prone to developing anticipatory side effects could lead to preventive measures. One hundred seventy-six consecutive ambulatory patients with histologically confirmed cancer who were being treated at three geographically separate hospitals of the University of Rochester Cancer Center were studied at the time of their fourth chemotherapy treatment. Patients found to experience anticipatory nausea and vomiting were significantly more likely (P less than .001) to have four or more of the following characteristics than patients who did not report anticipatory side effects: (1) less than 50 years of age; (2) the experience of nausea and/or vomiting after their last chemotherapy treatment; (3) a description of nausea after the last treatment as "moderate, severe, or intolerable"; (4) a description of vomiting after the last treatment as "moderate, severe, or intolerable"; (5) the reporting of the side effect "warm or hot all over" after their last treatment; (6) a susceptibility to motion sickness; (7) the experience of "sweating after their last treatment"; (8) and the experience of "generalized weakness after their last chemotherapy treatment." Results support a view that anticipatory side effects are conditioned and point to practical interventions for their clinical control.
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There is evidence in experimental animals for a potent vestibulosympathetic reflex, but its existence in humans is controversial. Static head-down neck flexion and off-vertical axis rotation have been shown to increase muscle sympathetic nerve activity (MSNA), but not skin sympathetic nerve activity (SSNA), whereas horizontal linear acceleration decreases MSNA in humans. However, both forms of stimuli also activate other receptors. To examine the effects of a pure vestibular stimulus on MSNA and SSNA, and its potential interaction with the baroreceptors, we used galvanic vestibular stimulation (GVS) in 12 healthy seated subjects. MSNA was recorded in ten subjects via a percutaneous microelectrode in the peroneal nerve; ECG, blood pressure, respiration, skin blood flow and sweating were also recorded. GVS (2 mA, 1 s pulse) was delivered via surface electrodes over the mastoid processes at unexpected times, triggered from the R-wave with a delay of 0, 200, 400 or 600 ms. In addition to causing robust postural illusions, GVS caused cutaneous vasoconstriction and sweat release in all subjects (due to a short-latency increase in SSNA, three subjects), but no significant change in MSNA. The failure of GVS to elicit a change in muscle sympathetic nerve activity, as documented by averaging, suggests that the vestibular system is not engaged in short-term modulation of muscle sympathetic activity. Conversely, phasic vestibular inputs do excite cutaneous sympathetic neurones, consistent with the observation that motion sickness is accompanied by pallor and sweating.
Anamnesis and clinical signs of horses form five different stables after ingestion of ionophores are reported and techniques of feed examination are described. Within a few hours or days after feeding of new types or batches of concentrates horses fell ill. They showed colic-like symptoms with intense sweating and ataxia. Most of the sick animals died within a short time span. Samples of the concentrates were analysed and different types and amounts of ionophores were detected. In four cases contamination by monensin in concentrations of less than 5 mg to 679 mg/kg feed were found. One feed sample contained monensin (8.8 mg/kg feed) as well as salinomycin (67.3 mg/kg feed). In one case lasalocid (7.9 mg/kg feed) was present. One horse from the stable where animals had obtained concentrates containing monensin (679 mg/kg feed) was necropsied. Typical signs of monensin intoxication with severe myocardial degeneration were found. Veterinarians should be alert to this rare but severe intoxication of horses.
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Space motion sickness is experienced by 60% to 80% of space travelers during their first 2 to 3 days in microgravity and by a similar proportion during their first few days after return to Earth. Space motion sickness symptoms are similar to those in other forms of motion sickness; they include: pallor, increased body warmth, cold sweating, malaise, loss of appetite, nausea, fatigue, vomiting, and anorexia. These are important because they may affect the operational performance of astronauts. Two hypotheses have been proposed to explain space motion sickness: the fluid shift hypothesis and the sensory conflict hypothesis. The fluid shift hypothesis suggests that space motion sickness results from the cranial shifting of body fluids resulting from the loss of hydrostatic pressure gradients in the lower body when entering microgravity. The cranial fluid shifts lead to visible puffiness in the face, and are thought to increase the intracranial pressure, the cerebrospinal-fluid pressure or the inner ear fluid pressures, altering the response properties of the vestibular receptors and inducing space motion sickness. The sensory conflict hypothesis suggests that loss of tilt-related otolith signals upon entry into microgravity causes a conflict between actual and anticipated signals from sense organs subserving spatial orientation. Such sensory conflicts are thought to induce motion sickness in other environments. Space motion sickness is usually treated using pharmaceuticals, most of which have undesirable side effects. Further studies elucidating the underlying mechanism for space motion sickness may be required for developing new treatments.
This literature review presents an inventory of the nature and incidence of side-effects that arise from the clinical application of monoclonal antibodies (MoAb) for the diagnosis and treatment of cancer. Most side-effects occurred during therapy. Toxic reactions, such as fever, sweating and chills, were more common than immunological skin reactions; they were observed predominantly in association with the elimination of circulating target cells. Dosage and rate of administration of the MoAb appeared to have little influence on the reactions, which disappeared quickly and did not necessitate discontinuation of treatment. Serum sickness, anaphylactic reactions and bronchospasms were not common; the patients reacted quickly to the indicated therapy. Prevention of the side-effects described here, especially during diagnostic applications, was such that they need not form a barrier to the clinical use of MoAb.