Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0027497 (nausea)
23,468 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 20 year old male naval crew-member suffering from sea sickness was treated with transdermal scopolamine (TS). After 5 months of continuous treatment, he developed scopolamine intoxication followed by the appearance of recurrent classic migraine attacks. He had never suffered from headache or migraine prior to TS intoxication. The migraine attacks comprised a prodrome of apathy, bad mood and loss of appetite lasting several hours. An aura of scintillating spots, left arm numbness and paresthesias lasting several minutes was followed by a severe throbbing unilateral headache with photophobia, sonophobia and nausea. After one year of repeated follow-up examination, he continued to suffer from the attacks once every 10 to 14 days, with no identified precipitating factors. We are not aware of similar cases in the medical literature. Although it is not possible to establish TS intoxication as a causal effect of the appearance of classic migraine in our patient, the temporal association and clinical course are very supportive of this assumption. Central nervous system neurotransmitter imbalance of cardiovascular alterations may possibly be implicated.
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PMID:Recurrent classic migraine attacks following transdermal scopolamine intoxication. 207 97

"Motion sickness" is the general term describing a group of common nausea syndromes originally attributed to motion-induced cerebral ischemia, stimulation of abdominal organ afferents, or overstimulation of the vestibular organs of the inner ear. Seasickness, car sickness, and airsickness are commonly experienced examples. However, the identification of other variants such as spectacle sickness and flight simulator sickness in which the physical motion of the head and body is normal or even absent has led to a succession of "sensory conflict" theories that offer a more comprehensive etiologic perspective. Implicit in the conflict theory is the hypothesis that neural and (or) humoral signals originate in regions of the brain subserving spatial orientation, and that these signals somehow traverse to other centers mediating sickness symptoms. Unfortunately, our present understanding of the neurophysiological basis of motion sickness is incomplete. No sensory conflict neuron or process has yet been physiologically identified. This paper reviews the types of stimuli that cause sickness and synthesizes a mathematical statement of the sensory conflict hypothesis based on observer theory from control engineering. A revised mathematical model is presented that describes the dynamic coupling between the putative conflict signals and nausea magnitude estimates. Based on the model, what properties would a conflict neuron be expected to have?
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PMID:Motion sickness: a synthesis and evaluation of the sensory conflict theory. 217 53

Seasickness is usually induced by conflicting sensory cues. However, very little is known about the neural pathways and processes which play a role in the development of nausea. Since the symptoms, for example, pallor, sweating and vomiting are all of parasympathetic origin, the common antiemetic drugs are anticholinergically efficient. More recently, additional drugs and modified forms of application have been introduced to reduce the soporific side effects. It is pointed out that onboard behaviour and even choice of vessel can be of more importance than use of antivertiginous drugs. Besides attention to the individual adaptation to the atypical seagoing environment, simple behaviour patterns such as fixation on the horizon, avoiding of head movements and reduction of conflicting sensory cues can be very effective in reducing symptoms.
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PMID:[Causes and treatment of seasickness]. 288 37