Feline hippocampal and piriform lobe necrosis as a consequence of severe cluster seizures in two cats in Finland

Abstract

Feline hippocampal and piriform lobe necrosis (FHN) has been reported from several countries worldwide and is considered an important aetiology for feline epileptic seizures. The aetiology of FHN remains unclear, however it is suspected that FHN might occur secondary to intense epileptic activity as described in humans and dogs although this has not yet been documented in cats. The purpose of our report is to describe the first cases of FHN in Finland diagnosed by magnetic resonance imaging (MRI) and histopathology. The two cases we describe had a well documented history of pre-existing seizures with normal brain MRI at the onset of cluster seizures but MRI done when the cats exhibited clinical deterioration secondary to severe seizure activity, revealed lesions in the hippocampus and piriform lobes typical of FHN. Our report confirms that feline hippocampus and piriform lobe necrosis does occur in the Finnish cat population and should therefore be considered as a differential diagnosis in cats with seizures. In addition, the presentation, clinical findings, results of MRI and/or histopathology shows that cats may develop FHN secondary to severe seizure activity.

Recurrent seizures in cats: Diagnostic approach – when is it idiopathic epilepsy?

“…Feline hippocampal necrosis (FHN) is a severe structural abnormality in the brain that has been associated with seizures in cats. 7,20,[50][51][52][53][54] it is uncertain whether this hippocampal pathology serves as an epileptogenic focus to cause seizures or if the FHN occurs secondarily to severe seizure activity. 7,51 Hippocampal neurons are very sensitive to hypoxia, hypoglycemia, hyperglycemia and glutamate excitotoxicity, potentially leading to ischemic injury and necrosis following severe seizures.…”

“…7,51 Hippocampal neurons are very sensitive to hypoxia, hypoglycemia, hyperglycemia and glutamate excitotoxicity, potentially leading to ischemic injury and necrosis following severe seizures. 7,50,[52][53][54] in humans and dogs, prolonged seizure activity can cause hippocampal ischemia that is initially reversible but can be perpetuated by ongoing seizure activity, leading to necrosis. 50,51,54 Hippocampal sclerosis has a strong association with temporal lobe epilepsy in humans.…”

Uremic encephalopathy in a rhesus macaque (Macaca mulatta): A case report and a brief review of the veterinary literature

“…Uremia results in inappropriate activation of excitatory NMDA receptors and concomitant inhibition of inhibitory GABA neurotransmitters, resulting in excitatory neurotoxicity, and is one of the accepted mechanisms of uremic encephalopathy [17]. Neuronal excitotoxicity has also been proposed as a mechanism of neuronal necrosis in cats with chronic seizure [18, 19], and resulted in lesions similar those observed in this macaque. Although the underlying toxic metabolite has not been identified, human patients with uremic encephalopathy typically show improved neurological symptoms after dialysis treatment [20].…”

Deleted in colorectal cancer (netrin‐1 receptor) antibodies and limbic encephalitis in a cat with hippocampal necrosis

“…From these MRI findings, feline hippocampal necrosis (FHN) and limbic encephalitis (LE) were suspected. [1][2][3][4][5][6][7] After MRI, in addition to ZNS (serum level was 15.3 μg/mL), prednisolone (1 mg/kg, PO q24h for 4 days, then 0.5 mg/kg PO q24h for After euthanasia, the brain was removed and histopathologically examined. However, a full necropsy was not allowed by the owner.…”

“…A cerebrospinal fluid tap was not performed due to suspected increased intracranial pressure indicated by narrowing sulci, ventricles (on transverse and dorsal planes), and cisterna magna (on sagittal plane) (not shown). From these MRI findings, feline hippocampal necrosis (FHN) and limbic encephalitis (LE) were suspected …”