Seizures in dogs and cats: reactive, structural and idiopathic causes
A seizure in a dog or cat comes from abnormal, excessive brain activity, and its cause falls into one of three groups: reactive seizures from a systemic metabolic or toxic insult acting on a normal brain, structural epilepsy from disease within the brain, or idiopathic epilepsy.[1]
Confirming the sign
The first question is whether the event was an epileptic seizure at all. Syncope, vestibular attacks, movement disorders and other paroxysmal events can look similar on a phone video, and the international task force sets out criteria for telling them apart, such as the presence of autonomic signs, altered consciousness and a postictal phase.[2] Ask for video, the time of day, the duration, what the pet was doing beforehand, and how long it took to return to normal. A syncopal collapse tends to follow exertion or excitement and ends with a quick recovery, while an epileptic seizure is often followed by a period of disorientation.[2]
Reactive (metabolic and toxic) differentials
Intoxication[3]
Supports it:A known or possible exposure, acute onset, and other signs such as tremors, hypersalivation or vomiting. Intoxications were the most common cause of reactive seizures in a series of 96 dogs.
Argues against it:No plausible access to a toxin and a normal minimum database.
Next test:A detailed exposure history and toxicology testing where available.
Hypoglycemia, including insulinoma[3,4]
Supports it:A low blood glucose at the time of signs. In dogs with insulinoma under primary care, seizures, weakness, collapse and muscle fasciculations were the signs reported most often.
Argues against it:A normal glucose measured during or soon after the event.
Next test:Blood glucose first, repeated if borderline, then a search for the cause.
Hypocalcemia and other electrolyte disorders[3]
Supports it:A low ionized calcium; hypocalcemia was the most frequent electrolyte cause of reactive seizures in dogs.
Argues against it:Normal ionized calcium and electrolytes.
Next test:Ionized calcium and an electrolyte panel.
Hepatic encephalopathy[5,6,2]
Supports it:A young dog with a suspected portosystemic shunt, or a patient with known liver disease, and raised ammonia or bile acids.
Argues against it:Normal pre- and postprandial bile acids. Note that raised ammonia after a seizure does not always mean a shunt; hyperammonemia without shunting or liver failure has been described in dogs with seizures.
Next test:Bile acids and ammonia, then imaging for a shunt if they are abnormal.
Uremia, hypoxia and other systemic causes[3]
Supports it:Severe azotemia, hypoxia, hyperglycemia or hypothyroidism found on the work-up; each appeared in the reactive seizure series.
Argues against it:A normal minimum database.
Next test:CBC, chemistry, urinalysis and oxygenation as the case requires.
Structural differentials
Structural epilepsy (intracranial disease)[2]
Supports it:Seizure onset before six months or after six years of age, neurologic deficits between seizures that localize to the forebrain, or status epilepticus or cluster seizures at onset.
Argues against it:A normal interictal neurologic examination in a dog within the typical idiopathic age range, though this does not exclude brain disease.
Next test:Brain MRI with an epilepsy protocol and CSF analysis, once reactive causes are excluded.
Structural and other causes in cats[7]
Supports it:Cats have a broad range of differentials for epileptic seizures, so the feline work-up relies on a careful history, physical and neurologic examination and stepwise testing rather than assuming idiopathic epilepsy.
Argues against it:A complete work-up with no abnormality found.
Next test:Minimum database, then MRI and CSF analysis guided by the examination.
Idiopathic epilepsy
Idiopathic epilepsy (dogs)[2]
Supports it:Two or more unprovoked seizures at least 24 hours apart, onset between six months and six years of age, a normal interictal physical and neurologic examination, and a normal minimum database; this is the tier I level of confidence.
Argues against it:Any of the structural red flags above, or an abnormal minimum database.
Next test:Tier II adds normal bile acids, brain MRI and CSF analysis; tier III adds characteristic EEG findings.
First diagnostics for this sign
Check blood glucose and ionized calcium immediately, then run a CBC, chemistry panel and urinalysis as the minimum database.[3,2] Add bile acids, and interpret ammonia with the caution described above.[2,6] Move to MRI and CSF analysis when the age at onset, the interictal examination or the seizure pattern points toward structural disease.[2] A patient in status epilepticus or having cluster seizures is an emergency: seizure control comes first, and the underlying cause is managed alongside it.[8]
Example: working the sign
Example. A nine-year-old dog has two generalized seizures on the same afternoon. Between them it is quiet but neurologically normal. The age at onset alone would point toward structural epilepsy and an MRI, but the point-of-care glucose taken on arrival is low.[2] The plan changes: the hypoglycemia is confirmed on a repeat sample and the search turns to its cause, with insulinoma on the list because seizures, weakness and collapse are its most commonly reported signs in dogs.[4,3] If the glucose had been normal, imaging of the brain would have been the next step.
Frequently asked questions
What are the most common reactive causes of seizures in dogs?
In a retrospective series of 96 dogs with metabolic or toxic seizures, intoxications and hypoglycemia were the two most common causes.[3]
When does a seizing dog need an MRI?
The task force recommends MRI and CSF analysis, after reactive causes are excluded, when seizures start before six months or after six years of age, when there are interictal neurologic deficits, when status epilepticus or cluster seizures occur at onset, or when a dog presumed to have idiopathic epilepsy is drug resistant.[2]
Does a high ammonia after a seizure mean the dog has a portosystemic shunt?
Not necessarily. Hyperammonemia without evident shunting or acute liver failure has been reported in dogs with epileptic seizures, so other causes should stay on the list.[6]
Are cluster seizures and status epilepticus emergencies?
Yes. The ACVIM consensus statement calls for early, rapid, stage-based treatment and management of the underlying cause alongside seizure control.[8]
Sources
- Berendt M, Farquhar RG, Mandigers PJ, et al. International veterinary epilepsy task force consensus report on epilepsy definition, classification and terminology in companion animals. BMC Vet Res. 2015;11:182. PMID 26316133 · doi:10.1186/s12917-015-0461-2
- De Risio L, Bhatti S, Munana K, et al. International veterinary epilepsy task force consensus proposal: diagnostic approach to epilepsy in dogs. BMC Vet Res. 2015;11:148. PMID 26316175 · doi:10.1186/s12917-015-0462-1
- Brauer C, Jambroszyk M, Tipold A. Metabolic and toxic causes of canine seizure disorders: A retrospective study of 96 cases. Vet J. 2011;187(2):272-275. PMID 19939714 · doi:10.1016/j.tvjl.2009.10.023
- Kraai K, O'Neill DG, Davison LJ, et al. Clinical signs, management, and survival of 278 dogs diagnosed with insulinoma under primary veterinary care in the United Kingdom. J Vet Intern Med. 2026;40(2):aalag045. PMID 41824751 · doi:10.1093/jvimsj/aalag045
- Gow AG. Hepatic Encephalopathy. Vet Clin North Am Small Anim Pract. 2017;47(3):585-599. PMID 28069286 · doi:10.1016/j.cvsm.2016.11.008
- Fors SM, Ostergard Jensen S. Hyperammonaemia in Dogs Presenting with Acute Epileptic Seizures-More than Portosystemic Shunts. Animals (Basel). 2025;15(17):2558. PMID 40941353 · doi:10.3390/ani15172558
- Sivolapenko D, Lowrie M. Epileptic seizures in cats: practical approaches to diagnosis. J Feline Med Surg. 2026;28(2):1098612X251407905. PMID 41674402 · doi:10.1177/1098612X251407905
- Charalambous M, Munana K, Patterson EE, Platt SR, Volk HA. ACVIM Consensus Statement on the management of status epilepticus and cluster seizures in dogs and cats. J Vet Intern Med. 2024;38(1):19-40. PMID 37921621 · doi:10.1111/jvim.16928