Intracranial Arachnoid Cysts: Are They Clinically Significant?

Intracranial arachnoid cysts constitute 1% of space-occupying lesions in humans.1 The incidence of the condition in dogs is unknown. Only 6 reports describing radiographic findings of 13 affected dogs and 1 cat have been published, but detailed information about the clinical presentation of these patients is lacking.2–7 The present report describes the clinical history, diagnostic findings, and longterm outcomes of 2 dogs in which the presence of arachnoid cysts was considered incidental. Treatment options for arachnoid cysts include medical management or surgical intervention. In humans, surgical treatment consists of cyst fenestration or shunting and results in variable success rates.8,9 In 5 dogs, fenestration was performed, and in 1 dog a shunt was implanted.2,3,6,7 Clinical improvement was reported in 4 of the 5 dogs, with follow-up periods ranging from 2 months to 3.5 years.2,3,6,7 One patient required a second fenestration procedure due to clinical deterioration after initial improvement. The dog that did not respond to surgery was euthanized after recurrent seizure activity. In humans, cysts have been reported as incidental findings at the time of autopsy. Intracranial arachnoid cysts also may be incidental findings in veterinary medicine, and affected patients should be evaluated carefully before surgical treatment is selected. A 5-year-old male Shih Tzu dog was referred to the Ontario Veterinary College (OVC) with a 24-hour history of focal seizures characterized by facial twitching and excessive drooling. Before presentation, results of routine CBC and blood chemistry tests done by the referring veterinarian were within reference range. At that time, the dog was treated with IV fluids and methocarbamola (22 mg/kg q8h). At admission to OVC, left-sided facial twitching was observed, and the dog reacted excessively to stimulation. Anisocoria, with the right pupil smaller than the left, was noted, with normal pupillary light reflexes. Fundic examination did not disclose any abnormalities. The seizures indicated a right-sided thalamocortical lesion, but the size of the right pupil could not be explained by this neuroanatomic localization and presumably was related to loss of left cortical inhibition over the right parasympathetic nucleus of the oculomotor nerve, indicating a left-sided lesion. Alternatively, irritation of the right parasympathetic nuclei could have resulted in anisocoria that, in combination with seizure activity, indicated a multifocal disorder. Cerebrospinal fluid (CSF) analysis identified a moderate pleocytosis with a