ISSN 2398-2950      

Feline ischemic encephalopathy

ffelis

Synonym(s): Idiopathic feline cerebral infarction


Introduction

  • Feline ischemic encephalopathy has been described as a distinct syndrome of cerebral infarction, which is poorly understood. Although in some parts of the USA, cerebral infarction may be due to the aberrant migration of a parasite such as Cuterebra, in most cases an underlying cause is not found and so suspected cases should be investigated thoroughly for systemic diseases, which may predispose to such a condition.

Pathogenesis

Etiology

  • The precise etiology is unknown. It may be a common end point for many different disease processes such as infection, neoplasia, hypertension and renal disease. At least a subset of cats with this disorder in the USA have been found to have aberrant parasitic (Cuterebra larva) migration in the CNS.
  • Focal ischemia can be caused by arterial thrombosis or embolism.
  • A thrombus is a blood clot developing within a vessel that causes vascular obstruction at the site of formation.
  • Embolism is occlusion of a vessel by a fragment of a blood clot or other substance that has flowed to the site of the obstruction from a distant site.

Predisposing factors

General

  • Commonly seen during the summer months in the north-east USA (July September).

Pathophysiology

  • Owing to its high metabolic demands, the central nervous system depends on a constant supply of oxygen and glucose from the circulation.
  • Homeostatic mechanisms normally maintain adequate blood flow over a wide range of blood pressure. If there is a decrease in blood flow that exceeds the ability of autoregulatory mechanisms, the nervous system is deprived of the necessary oxygen and glucose, resulting in ischemia (a reduction in the blood flow to a level so severe and prolonged that an area of necrosis ensues).
  • The primary mechanism responsible for the damage following infarction is a deranged energy metabolism.
  • Deficient energy leads to a loss of ion pumping across the cell membranes of the nervous system resulting in cytotoxic edema as well as lactic acidosis, increased intracellular calcium levels and activation of proteases and phospholipases, which combined, lead to disruption of cellular integrity and necrosis.
  • The duration and the degree of the interrupted blood flow are important to the development of an infarction. In cats, when the cerebral blood flow is reduced to approximately one half of normal levels, the neuronal activity ceases but the neurons do not die off. Cellular ion homeostasis is lost when cerebral blood flow drops to about one third of normal level. Up to this point however, neuronal changes are potentially reversible if blood flow is restored rapidly. Complete occlusion of the middle cerebral artery for less than 3 hours causes transient neurologic deficits and a minimum infarction, whereas occlusion for longer than 5 hours causes permanent neurologic deficits associated with infarction.
  • Pathological lesions are most commonly unilateral and located along the distribution of the middle cerebral artery.
  • Bilateral cerebral lesions and brainstem lesions may occur.
  • Primary vascular lesions such as thromboembolism or vasculitis, are uncommon.
  • Pathological studies have associated the disease with the presence and aberrant migration of Cuterebra larva in the USA. This has not been reported in the UK or Europe and so this type of FIE does not occur and overall the disease is less common than in the USA.
  • When due to Cuterebra, cats become infected with the first stage larva, which are 1-2 mm in length, and penetrate the skin or mucous membranes. The larva that migrates to the brain is thought to enter the nasal cavity and pass through the cribriform plate of the ethmoid bone.
  • The parasite is purported to induce vasospasm of brain arteries in a poorly documented manner which results in ischemia and infarction.

Timecourse

  • The clinical onset of the disease is peracute.
  • Clinical signs may continue to progress in cats infected with the Cuterebra larva if the parasite survives and continues to migrate in the brain.

Epidemiology

  • Cats of any age and gender may be affected most commonly in the late summer months in the north-east USA.

Diagnosis

This article is available in full to registered subscribers

Sign up now to start a free trial to access all Vetlexicon articles, images, sounds and videos, or Login

Treatment

This article is available in full to registered subscribers

Sign up now to start a free trial to access all Vetlexicon articles, images, sounds and videos, or Login

Prevention

This article is available in full to registered subscribers

Sign up now to start a free trial to access all Vetlexicon articles, images, sounds and videos, or Login

Outcomes

This article is available in full to registered subscribers

Sign up now to start a free trial to access all Vetlexicon articles, images, sounds and videos, or Login

Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Glass E N, Cornetta, A M, de Lahunta A et al (1998) Clinical and Clinicopathological features in 11 cats with Cuterebra larvae myiasis of the central nervous system. J Vet Int Med 12 (5), 365-368 VetMedResource.
  • Williams K J, Summers B A, de Lahunta A (1998) Cerebrospinal cuterebriasis in cats and its association with feline ischemic encephalopathy. Vet Pathol 35 (5), 330-343 PubMed.
  • Shell L G (1996) Feline ischemic encephalopathy (cerebral infarct). Feline Pract 24 (5), 32-33 VetMedResource.
  • King J M (1991) Feline ischemic encephalopathy. Vet Med 86 (11), 1062 VetMedResource.
  • Bernstein N M, Fiske R A (1986) Feline ischemic encephalopathy in a cat. J Am Anim Hosp Assoc 22 (2), 205-206 VetMedResource.
  • Zaki F A, Nafe L A (1980) Ischaemic encephalopathy and focal granulomatous meningoencephalitis in the cat. J Small Anim Pract 21 (8), 429-438 PubMed.

Other sources of information

  • De Lahunta A (1977) Feline ischemic encephalopathy - a cerebral infarction syndrome. In: Current Veterinary Therapy VII. Kirk K W (ed). pp 906-908.

Can’t find what you’re looking for?

We have an ever growing content library on Vetlexicon so if you ever find we haven't covered something that you need please fill in the form below and let us know!

 
 
 
 

To show you are not a Bot please can you enter the number showing adjacent to this field