Transient ischemic attacks (TIAs), a common finding in people, are defined as temporary, focal brain (or retinal) deficits
secondary to vascular disease. In most cases, symptoms associated with TIA resolve completely in just a few minutes, and they
tend to recur over time.
TIAs represent brief periods of inadequate perfusion in a territory of the carotid or ventrobasilar arteries. In people, thrombi
or vasospasm related to systemic hypertension, atherosclerosis or diabetes mellitus represent the typical causes of TIA.
Although frequently described in people, TIA associated with hypertension was not described in dogs. Recently, however, clinical
and neurologic signs associated with a presumed TIA were reported in a 9-year-old spayed female Australian shepherd.1
The neurologic signs reported in this dog consisted of a peracute onset of vomiting, ptyalism, incoordination, pelvic limb
ataxia and frequent falling. The results of an abdominal radiographic examination, complete blood count, serum chemistry profile,
urinalysis and bile acid assays were within accepted range limits. The dog was clinically normal after one night of hospitalization
and treatment with intravenous fluids.
Six weeks later, the dog was readmitted because of two episodes similar to the first admission. Findings on physical and neurologic
examinations were unremarkable. A further neurologic episode occurred two days later while the dog was exercising vigorously
outside. Neurologic examination revealed a head tilt to the left, nystagmus and normal responsiveness. The neurologic signs
resolved completely within 30 minutes.
An additional episode lasting 20 minutes was induced by a 25-minute period of vigorous exercise; this episode was characterized
by a peracute onset of vestibular signs, staggering to the left, a head tilt to the left, wide-based positioning of the pelvic
limbs, vertical nystagmus, positional ventral strabismus in the left eye and adequate mentation.
Results of thyroid testing were within the reference range. Systolic arterial blood pressure recorded by Doppler ultrasonography
ranged between 180 and 200 mm Hg. An ACVIM Consensus Statement has ranked the risk for target-organ damage in hypertension
Table 1: Classification of blood pressure in dogs and cats based on risk for future target-organ damage*
The results of additional neurologic diagnostic tests—magnetic resonance imaging (MRI) of the brain, cerebrospinal fluid analysis,
abdominal ultrasonography, echocardiography—were unremarkable, with the exception of mild mitral regurgitation. Primary hypertension
Treatment and follow-up
Treatment consisted of the administration of amlodipine and enalapril, and the owner was instructed to avoid strenuous exercise
until the systemic hypertension was well-controlled.
An additional episode of neurologic signs occurred one month after the onset of treatment when the dog's systolic arterial
blood pressure was 163 mm Hg. The dose of antihypertensive medications was adjusted until the systolic arterial blood pressure
ranged from 120 to 130 mm Hg.
Elevated blood pressure (over 200 mm Hg) was sometimes recorded in relation with excitement. Four episodes of vestibular signs
occurred during an eight-month period. As of 19 months after the final event, the dog's systolic arterial blood pressure ranged
from 120 to 130 mm Hg, and the owner reported no further neurologic problems (total follow-up time of 30 months).
TIA and cerebrovascular accident (CVA) may be associated with similar or identical neurologic signs. CVA may require immediate
and aggressive treatment to reduce progression of cerebral tissue damage, whereas TIA associated with hypertension is treated
with long-term medications. Diagnostic tests (particularly imaging of the brain) should, therefore, be performed without delay
in all cases. Diffusion-weighted imaging, an advanced MRI technique, has revolutionized the early detection of CVAs in people.
MRI sequences, particularly diffusion-weighted imaging, is the most reliable method for early detection of cerebral ischemia,
for the definition of infarct core and for the differentiation of acute ischemia from other disease processes that mimic stroke.3
A vascular cause was suspected in the dog in this report based on the occurrence of the episodes upon exercise and during
periods of uncontrolled hypertension. Lack of evidence for CVA on MRI and occurrence of episodes upon exercise and during
periods of uncontrolled hypertension support this conclusion.
Hypertension may be primary or associated with chronic kidney disease, untreated hyperadrenocorticism, aortic stenosis, diabetes
mellitus and pheochromocytoma. Diagnostic tests are indicated for a definitive diagnosis of hypertension and specific, directed
Antihypertensive drugs should be considered whenever systolic arterial blood pressure is 150 mm Hg or greater and there is
evidence of ocular or CNS target-organ damage.
1. Bentley RT, March PA. Recurrent vestibular paroxysms associated with systemic hypertension in a dog. J Am Vet Med Assoc 2011;239(5):652-655.
2. Brown S, Atkins C, Bagley R, et al. Guidelines for the identification, evaluation, and management of systemic hypertension
in dogs and cats. ACVIM Consensus Statement. J Vet Intern Med 2007;21(3):542-558.
3. Fung SH, Roccatagliata L, Gonzalez RG, et al. MR diffusion imaging in ischemic stroke. Neuroimaging Clin N Am 2011;21(2):345-377.