Motion Sickness in Small Animals: Pathophysiology & Treatment

The body detects motion through 3 sources: vestibular, visual, and proprioceptive input to the CNS.^1-3 Motion sickness can occur when there is conflicting or inconsistent input (vestibular, visual, or proprioceptive) processed within a multimodal sensory system whose function is to ascertain a patient's motion in relation to environment.^1,3

The nausea and vomiting associated with motion sickness is a result of overstimulation of the labyrinth (ie, inner ear) apparatus. The labyrinth has 3 semicircular canals, responsible for maintaining equilibrium.^1,3 Postural adjustments are made when the brain receives nerve impulses initiated by the fluid in canals.^1,3 Motion sickness occurs with acceleration in a direction perpendicular to the longitudinal axis of the body, which explains why head movements in the opposite direction of the body's movement are so stimulating. This type of motion is common when riding in the car, on a boat, or in an airplane. During motion sickness, impulses from the vestibular center in the labyrinth of the inner ear are thought to travel through the chemoreceptor trigger zone (CRTZ) to the vomiting center in the medulla oblongata.^1,2 A number of medications have been successfully used to prevent or minimize motion sickness by interrupting signaling pathways between the vestibular apparatus and the vomiting center.

Related Article: GI Roundtable: Current Approaches to Vomiting in Cats and Puppies

Phenothiazines
Dopamine-2 receptor (adrenergic) antagonists that also have weak antihistaminic and anticholinergic effects, which may contribute to their efficacy. Bonus: α-1 antagonistic effects cause sedation.^2,4

• Adverse effects: Hypotension, CNS stimulation, bradycardia, rarely extrapyramidal signs in cats (eg, tremors, shivering, rigidity, loss of the righting reflexes).⁴
• Contraindications: Hypotension or severe dehydration.⁴
• Dosing: For chlorpromazine, dogs at 4–8 mg per dog (not >0.5 mg/kg) PO q 12 h, cats at 2 mg per cat (not >0.5 mg/kg) q12h. For acepromazine, which is more sedating, dogs and cats at 0.55–2.2 mg/kg PO.

For promethazine (Phenergan), dogs at 0.2–0.5 mg/kg q6–8h.

Antihistamines
Blockade of histaminic receptors in vomiting center.^2-5 Poor efficacy in cats.

• Adverse effects: CNS depression (sedation), anticholinergic effects (eg, dry mouth, urinary retention). ^2,4
• Contraindications: Angle closure glaucoma, GI or urinary obstruction⁴
• Dosing: Administer 30 min before departure; may need redosing q4–6h. For meclizine (Antivert, Bonine) dogs at 4 mg/kg PO q24h. For diphenhydramine (Benadryl), dogs at 2–4 mg/kg PO q8h. For dimenhydrinate (Dramamine), dogs at 4–8 mg/kg PO q8h.

Related Aritlce: Preventing Motion-Elicited Vomiting in Dogs

Neurokinin-1 (NK1) Receptor Antagonists
Maropitant (Cerenia) affects NK1 receptors in the GI tract, CRTZ, and vomiting center; at high doses, maropitant also prevents vestibular-induced travel sickness in dogs and cats.^5-7 Substance P is a neurotransmitter that is involved in the regulation of mood, anxiety, stress, respiratory rhythm, pain, nausea, and vomiting, and it is found in the highest concentrations in the vomiting center.^4-7 The receptor for substance P is NK1. NK1 receptors are found in both the CRTZ and the emetic center. When substance P binds to the NK1 receptor vomiting occurs. By blocking the binding of substance P to NK1 receptors, vomiting stimuli are interrupted.^4-7

• Adverse effects (rare): Weakness, lethargy, decreased appetite, mild neutropenia, decreased heart rate, and prolonged QT intervals (in toxicity trials).⁴
• Contraindications: Avoid in patients with hepatic dysfunction and those receiving calcium-channel blockers (eg, diltiazem, amlodipine), β-blockers (atenolol, propranolol), or a potassium channel blocker (sotalol) as it may contribute to dysrhythmias.⁴ It is now labeled for use in both cats and dogs 16 weeks and older.
• Dosing: For maropitant, dogs at 8 mg/kg PO 2 hours before travel for up to 2 consecutive days, cats at 1 mg/kg PO.