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Nervous System
Motion Sickness
Overview of Motion Sickness
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Sections in Veterinary Professionals
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Chapters in Nervous System
  • Nervous System Introduction
  • Congenital and Inherited Anomalies of the Nervous System
  • Demyelinating Disorders
  • Diseases of the Peripheral Nerve and Neuromuscular Junction
  • Diseases of the Spinal Column and Cord
  • Dysautonomia
  • Facial Paralysis
  • Hypoxic Ischemic Encephalopathy
  • Limb Paralysis
  • Meningitis, Encephalitis, and Encephalomyelitis
  • Motion Sickness
  • Neoplasia of the Nervous System
  • Paraneoplastic Disorders of the Nervous System
  • Polioencephalomalacia
  • Bovine Spongiform Encephalopathy
  • Chronic Wasting Disease
  • Scrapie
  • Equine Viral Encephalomyelitis
  • Louping Ill
  • Pseudorabies
  • Rabies
  • Teschovirus Encephalomyelitis
  • Sporadic Bovine Encephalomyelitis
  • Equine Protozoal Myeloencephalitis
  • CNS Diseases Caused by Helminths and Arthropods
  • Tick Paralysis
Topics in Motion Sickness
  • Overview of Motion Sickness
         
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        Overview of Motion Sickness

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        Motion sickness is characterized by nausea, excessive salivation, and vomiting. Affected animals may have other signs referable to stimulation of the autonomic nervous system and may yawn, whine, or show signs of uneasiness and apprehension; severely affected animals may also develop diarrhea. Motion sickness is seen during travel by land, sea, or air, and signs usually disappear when vehicular motion ceases. The principal causative mechanism involves stimulation of the vestibular apparatus in the inner ear, which has connections to the emetic center in the brain stem. The chemoreceptor trigger zone (CRTZ) and H1-histaminergic receptors are involved in this pathway in dogs, but apparently are less important in cats. Recent evidence has revealed that the neurokinin 1 substance P receptors (NK1) in the emetic center play a major role in motion sickness in both dogs and cats and are more important than the receptors in the CRTZ. Fear of the vehicle may also become a contributory factor in dogs and cats that develop a conditioned response to the event; signs may be seen even in a stationary vehicle.

        In some cases, motion sickness can be overcome by conditioning the animal to travel. In others, ataractic and antinausea drugs can be used with good results. Antihistamines (such as diphenhydramine hydrochloride, dimenhydrinate, meclizine, and promethazine hydrochloride) prevent motion sickness, provide sedation, and inhibit drooling. The centrally acting phenothiazine derivatives (such as triethylperazine, chlorpromazine, prochlorperazine, and acepromazine maleate) have antiemetic as well as sedative effects. Cats have no histamine receptors in the CRTZ; therefore, antihistamines are ineffective in treating motion sickness in this species. Motion sickness in cats probably is best treated with an α-adrenergic antagonist (eg, chlorpromazine) instead of a pure H1-histaminergic antagonist.

        Maropitant, an NK1 receptor antagonist, is effective in treating motion sickness in dogs. NK1 receptors are located in the emetic center of the brain stem, which is the source most responsible for the vomiting and nausea of motion sickness. Blocking these receptors is more effective than inhibiting the CRTZ. Therefore, maropitant is probably the drug of choice to treat motion sickness in dogs. Another benefit is that treatment is given once daily. The drug is available in tablet and injectable forms. Although it is not labeled for use in cats, it appears to be safe and effective for the treatment of motion sickness in the cat.

        Phenobarbital and diazepam can be used to produce a general sedative effect if anxiety is a problem. Oral administration of one of these drugs several hours before departure should reduce or eliminate the signs of motion sickness. (Also see Systemic Pharmacotherapeutics of the Digestive System: Drugs to Control or Stimulate Vomiting (Monogastric).)

        Last full review/revision July 2011 by T. Mark Neer, DVM, DACVIM

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