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The Canadian Veterinary Journal logoLink to The Canadian Veterinary Journal
. 2004 Feb;45(2):153–155.

Headshaking in a 10-year-old Thoroughbred mare

Angela JM Bell 1
PMCID: PMC548606  PMID: 15025153

Abstract

A 10-year-old Thoroughbred mare was presented with a 2.5-week history of headshaking. Based on a thorough physical examination, blood analysis, and a fine needle aspirate of an enlarged thyroid gland, a tentative diagnosis of seasonal idiopathic headshaking was made. Treatment with cyproheptadine was attempted.


A 10-year-old Thoroughbred mare was presented with a history of headshaking of 2.5 weeks duration. During this time, the horse also had frequent episodes of snorting and sneezing and, periodically, was observed rubbing its head against the stall boards and standing with its muzzle immersed under water. Headshaking tended to wax and wane, with a maximum frequency of 1 to 2 times/min at rest. Headshaking had also been observed for approximately 1 mo during the previous spring.

The mare had been regularly vaccinated and treated with anthelmintics for internal parasites. She received occasional light exercise on a lunge line but, after the onset of headshaking, had refused to trot when exercised and appeared agitated. The diet consisted of grass hay and free access to 2 acres of grass pasture. Since winter, the mare’s appetite had decreased and subsequent weight loss had occurred. However, she shared a stall with another horse during this time, which may have contributed to the problem. After the onset of clinical signs, the mare had spent more time indoors than in previous years.

Possible differential diagnoses considered on the basis of the history were uveitis, corneal ulceration, retinal lesions or iris cysts, cranial nerve dysfunction, guttural pouch mycosis, dental abnormalities, ear mite infestation, otitis interna, and allergic and vasomotor rhinitis (1,2). Accordingly, a physical examination was conducted, which included ophthalmic, otoscopic, neurologic, and dental examinations. These procedures included a complete blood cell (CBC) count, serum biochemical profile, determination of thyroid hormone levels, fine needle aspirate of the thyroid gland, and swabs of the external ear canal for cytologic examination.

The most obvious abnormalities noted included unilateral enlargement of the thyroid gland, a point on the 1st left premolar of the upper dental arcade, and several moderately sharp molar teeth on both buccal surfaces. The right lateral lobe of the thyroid gland was mobile, oval, and approximately 5 cm long. Results from otoscopic and cranial nerve examinations were unremarkable. No ocular or nasal discharge was observed. The ocular examination revealed no evidence of anterior uveitis, retinal lesions, or iris cysts, and corneal lesions were not observed with the fluorescein dye test; however, the right eye retained an overall mild hazy appearance due to a slight uptake of green dye. An increased sensitivity to light and touch during examination of the right eye was also noted.

The CBC count revealed no significant abnormalities. The ear swab was negative for mites, bacteria, and yeast. No neoplastic cells were detected in the thyroid aspirate, which had a histological appearance consistent with thyroid gland hyperplasia (Animal Health Laboratories, Guelph, Ontario). Table 1 shows results of the serum biochemical profile and thyroid tests. Total thyroxine (T4) was elevated, but free T4 by equilibrium dialysis ruled out the possibility of hyperthyroidism.

Table 1.

Results of serum biochemistry profile and thyroid hormone assays in a 10-year-old thoroughbred mare showing signs consistent with idiopathic headshaking

Analyte Result Reference range
Fibrinogen (g/L) 2.0 1.6–2.9
Calcium (mmol/L) 3.1 2.75–3.25
Phosphorus (mmol/L) 1.01 0.73–1.7
Magnesium (mmol/L) 0.8 0.6–1.0
Sodium (mmol/L) 137 136–144
Potassium (mmol/L) 5.4 3.1–4.3
Chloride (mmol/L) 100 95–104
Carbon dioxide (mmol/L) 25 25–36
Total protein (g/L) 67 58–75
Albumin (g/L) 31 30–37
Globulin (g/L) 36 26–41
Albumin:globulin ratio 0.86 0.8–1.3
Urea (mmol/L) 5.8 4.2–8.9
Creatinine (μmol/L) 75 80–130
Glucose (mmol/L) 4.2 3.7–6.7
Cholesterol (mmol/L) 1.83 1.70–2.70
Total bilirubin (μmol/L) 14 21–57
Conjugated bilirubin (μmol/L) 3 2–3
Free bilirubin (μmol/L) 11 18–55
Alkaline phosphatase (U/L) 146 119–329
Gamma glutamyl transferase (U/L) 15 7–54
Aspartate aminotransferase (U/L) 281 259–595
Creatine kinase (U/L) 312 108–430
Glutamate dehydrogenase (U/L) 5 1–7
Haptoglobin (g/L) 0.81 0.1–1.7
Total T4 (nmol/L) 58 10–49
Free T4 equilibrium dialysis (nmol/L) 22.9 19–40

T4 — thyroxine

The working diagnoses generated from the physical examination included dental disease, guttural pouch mycosis, and seasonal headshaking. Although the teeth were floated, clinical signs remained unchanged a week later. Guttural pouch mycosis could not be ruled out without an endoscopic examination; however, an endoscope was not available. Accordingly, a tentative diagnosis of seasonal idiopathic headshaking was made.

Cyproheptadine (The Veterinary Pharmacy, Guelph, Ontario), 0.3 mg/kg bodyweight (BW), PO, q12h, was administered in an apple-flavored suspension for 15 d (1). Ten days posttreatment, the frequency of headshaking had been reduced by approximately 70%. By day 15, complete resolution of clinical signs had occurred and treatment was discontinued.

Many drugs and alternative therapies have been utilized to treat headshaking in horses. Antihistamines, corticosteriods, nonsteroidal antiinflammatory drugs (3), and alternative forms of therapy, such as acupuncture (3) and chiropractic manipulation (5), have been tried without consistent success. Surgical treatment by infraorbital neurectomy has also been attempted, but effectiveness has been reported in only 30% to 40% of cases (3).

Cyproheptadine, an H-1 receptor antihistamine that also possesses serotonin antagonist properties, is believed to be efficacious for the treatment of headshaking because of its serotonergic blocking properties (1,4). Serotonin, a chemical produced in the central nervous system, plays a role in pain sensation in humans, and serotonin levels increase in the spring in response to the lengthening photoperiod (1). In a study of photic headshaking in the horse, 5 of 7 horses showed improvement with cyproheptadine treatment (5). In a more recent study, more than two-thirds of horses showed moderate to great improvement in headshaking when treated with cyproheptadine at the dosage used in this mare. Occasionally, mild depression, anorexia, or lethargy has been reported (5). Cyproheptadine is not an approved medication for use in show or performance horses. Treatment may need to be repeated at the same time each spring, as headshaking recurs in most horses for many years (1).

Mild irritation of the corneal epithelium secondary to minor trauma was the likely explanation for the slight uptake of fluorescein stain in this mare’s right eye. In the absence of ocular epiphoria, squinting, aqueous flare, corneal ulcers, or retinal abnormalities, it was considered unlikely that ocular pain was the primary cause of the headshaking. Swollen thyroid glands may be reported by owners of equine headshakers (6). The right lateral lobe of the thyroid gland was enlarged in this mare but, to date, hyperthyroidism has not been documented. Guttural pouch mycosis could not be ruled out. It has been suggested that endoscopy and radiography of the skull be part of the diagnostic work-up in cases of suspected idiopathic headshaking (1), but these techniques were unavailable in this case.

The etiology of equine headshaking in association with photoperiod is in many cases unknown (1). In a study of 100 cases, a cause was not found in nearly 90% of horses investigated (2). Often there is a peak period of onset in the spring and early summer (1), at an average of 9 y of age (2). The direction of head movement is usually vertical, frequently with sneezing and snorting (1). In most instances, no abnormalities are detected during a thorough physical examination. As a result, many theories have been developed to explain this peculiar phenomenon exhibited by horses.

One theory postulates that an intermittent or continuous burning, itching, tingling, or electric-like pain originates from the trigeminal nerve. The quick movements of the head, excessive snorting and rubbing of the head, and immersing the head in water may all be behavioral manifestations of neuropathic pain (1). If this theory is correct, cyproheptadine may be effective because its serotonin-blocking effects modify the ability of the horse to sense pain. There is evidence that may lend support to this theory: In some horses, when an object is applied to the muzzle or forelock region, clinical signs cease. This cutaneous stimulation may prevent the nerve from “firing,” as when a person blocks a sneeze by placing a finger under the nose.

Another possible explanation for the effectiveness of cyproheptadine for headshaking is its antihistamine properties. It has been postulated that most affected horses are suffering from allergic rhinitis. Many of the symptoms of seasonal hypersensitivity to inhaled allergens in humans parallel the clinical signs of idiopathic headshaking in horses, including sneezing, nasal pruritus, photophobia, throat clearing, headache, general malaise, and irritability (2). In one horse, skin allergy testing and hyposensitization therapy were attempted but failed to alter the headshaking behavior (5). In another study, an underlying allergic cause for the headshaking behavior seemed unlikely, as relatively few horses improved when treated with antihistamines and corticosteroids (7).

It is possible that the improvement in this horse was coincidental. Improvement was not noticed until 10 d after initial treatment with cyproheptadine, and the headshaking might have resolved in this time regardless of any treatment given. If the mare resumes headshaking next spring, alternative methods of control may include treatment with carbamazepine in conjunction with cyproheptadine, or application of a cloth or constricting piece of material to the muzzle (7,8). Carbamazepine is an anticonvulsant drug that has been used to treat trigeminal neuralgia in humans (8). When horses were treated for headshaking with carbamazepine in combination with cyproheptadine, 80% of them showed an 80% to 100% improvement (8). Perhaps, with further research into the pathogenesis of photoperiod-associated headshaking, it will become possible to prevent this condition, thereby improving animal comfort and client satisfaction.

Acknowledgments

The author thanks Dr. Keith Douglas for his knowledge and support. CVJ

Footnotes

Dr. Bell’s current address is Ferguson Animal Hospital, 332 Grand Avenue East, Chatham, Ontario N7O 1W6.

Dr. Bell will receive 50 free reprints of her article, courtesy of The Canadian Veterinary Journal.

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