Canine noise aversion and motion sickness: Underdiagnosed and undertreated
Canine noise aversion and motion sickness are two common conditions that are both underdiagnosed and undertreated. The failure to diagnose and treat these conditions not only impacts the dog’s quality of life but can stress the human animal bond.
Noise aversion, a serious medical condition, affects over 1/3 of the dogs in the US.1 The fear and anxiety that is triggered by noise aversion is initiated in the locus coeruleus (LC), a cluster of noradrenergic nuclei in the brainstem that utilizes norepinephrine (NE) as the main neurotransmitter. The LC mediates arousal, but repeated exposure to acute traumatic stress can cause a maladaptive response of the LC-NE system and the development of anxiety disorders.2,3 In the case of dogs with noise aversion, noise triggers cause activation of LC – NE system, which facilitates the physiological and behavioral responses, manifesting as fight, flight, or avoidance (freezing behavior).
Inhibition of LC-NE system would be an ideal target for the treatment of noise aversion. Dexmedetomidine inhibits release of norepinephrine within the locus coeruleus. Drugs used to treat noise aversion include, dexmedetomidine oromucosal gel, trazadone, fluoxetine and clonidine. Environmental management and behavior modification may be required to effectively treat noise aversion.
Like noise aversion, canine motion sickness can also disrupt the human-animal bond. In a recent study, 46% of pet owners stated canine motion sickness weakened the relationship with their dog and 83% would travel more with their dogs if they did not get motion sickness4. Additionally, there is a disconnect between how veterinarians and dog owners perceive its occurrence. Veterinarians state 3% of their patients have canine motion sickness, however owners said it was 17%, accounting for nearly 7.3MM dogs5.
Signs of canine motion sickness include vomiting, drooling, panting, swallowing, and lip-licking.5 It is caused by conflicting sensory signals to the emetic center between the inner ear and visual cortex, combined with input from the cerebral cortex regarding fear or anxiety related to a previous experience. 7,8 The primary neurotransmitter responsible for vomiting is the neuropeptide Substance P, which binds to NK-1 receptors. These receptors are found in high concentrations within the (CRTZ) and the emetic center, where all emetic stimuli ultimately converge.
Because owners infrequently initiate the conversation regarding their dog’s noise aversion or motion sickness, the veterinary health care team must be proactive and inquire if each canine patient suffers from either of these conditions. Once a diagnosis is made, treatment can be initiated to relieve signs and restore the human animal bond.
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References
1. Based on online survey conducted by Harris Poll on behalf of Zoetis in November 2013 among 784 dog owners. 2. Aston-Jones G, Cohen JD. An integrative theory of locus coeruleus-norepinephrine function: adaptive gain and optimal performance. Annul Rev Neurosci 2005; 28:403–450. 3. Goddard AW, Ball SG, Martinez J, et al. Current perspectives of the roles of the central norepinephrine system in anxiety and depression. Depress Anxiety 2010; 27:339–350. 4. ZMR- Cerenia US Market Research Report 2017 5. ZMR- Cerenia US Market Research Report 2012 6. Conder GA, et al. Efficacy and safety of maropitant, a selective neurokinin 1 receptor antagonist, in two randomized clinical trials for prevention of vomiting due to motion sickness. J Vet Pharmacol Ther. 2008;31(6):528-532 7.Yates B, et al. Physiological basis and pharmacology of motion sickness: An update. Brain Research Bulletin, 1998 47(5), pp.395-406. 8. Encarnación H, et al. Vomiting. Compendium: Continuing Education for Veterinarians. March 2009