Feline ischemic encephalopathy in Cats (Felis) | Vetlexicon
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Feline ischemic encephalopathy

ISSN 2398-2950

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  • 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.

Presenting signs

  • Peracute onset of focal brain dysfunction.
  • Lateralizing cerebral signs such as circling and lateralizing brain stem signs such as head tilt and hemiparesis.In >70% it is the left side which is affected.
  • Behavior changes, visual dysfunction, seizures Seizures (25%).

Acute presentation

  • Seizures, hemiparesis, non-progressive forebrain signs.

Geographic incidence

  • North-eastern USA.
  • Rest of world due to causes other than Cuterebra larval migration.

Age predisposition

  • All ages (7 months-11 years).

Breed/Species predisposition

  • No breed predilection.

Public health considerations

  • None.

Cost considerations

  • The diagnosis can be expensive as it will require an intensive investigation into the cats general health as well as an exhaustive investigation of the nervous system to rule out the multiple differentials.
  • Nursing care for the cat after the onset of the signs may be expensive as the convalescence can be protracted.

Special risks

  • Due to the potential involvement of the brainstem in this CNS circulatory disorder, there is a risk of deterioration under anesthesia and upon recovery from this intervention.



  • 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


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


  • 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.


  • 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.


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


Presenting problems

  • Peracute onset of focal, often asymmetric neurologic deficits.
  • Cerebral disorders are most commonly seen; seizures, abnormal behavior, depression, ipsilateral circling, contralateral hemiparesis (with forebrain lesions normal gait but abnormal postural reactions) and contralateral visual field blindness with normal pupillary light reflexes.
  • Brainstem lesions are less commonly seen but include vestibular dysfunction and ipsilateral gait deficits.

Client history

  • Sudden onset from a normal state of neurological and physical health.
  • Asymmetrical; focal or generalized seizure activity, change in behavior, propulsive circling.
  • Non-progressive if due to a Cuterebra migration - recent upper respiratory signs, sneezing.

Clinical signs

  • Asymmetrical forebrain dysfunction.
  • Seizures, behavior change.
  • Non-progressive.

Diagnostic investigation

  • History (see above).
  • Advanced imaging will confirm cerebral infarction. Computed tomography (CT) Computed tomography (CT): uses and indications reveals multifocal regions of decreased attenuation and abnormal enhancement. Some lesions are hyperattenuating, which may indicate acute hemorrhage. MRI Magnetic resonance imaging: brain reveals hypointense lesions on T1-weighted images and hyperintense on T2-weighted images, which dont often contrast enhance.
  • CSF Cerebrospinal fluid: cytology will rule out inflammatory causes; generally in this condition, the CSF will be normal or may show a mild increase in protein.With Cuterebra migration there may be eosinophils.

Confirmation of diagnosis

Discriminatory diagnostic features

Definitive diagnostic features

  • The only definitive mechanism to diagnose the presence of this disease is with histopathology.

Gross autopsy findings

  • Asymmetric cerebral damage.
  • No gross abnormalities outside of the CNS; within the CNS, there are locally extensive areas of malacia, often with yellow discoloration compatible with superficial necrosis, often affecting the olfactory bulbs and peduncles.
  • In cats necropsied many weeks after the ischemic event there may be severe atrophy of the affected area.

Histopathology findings

  • In cats necropsied many weeks after the ischemic event: severe atrophy with parenchymal degeneration, astrocytosis, gliosis, phagocytic macrophages, in addition to frank cerebral necrosis consistent with an infarct especially in the frontal and parietal lobes. The foci of necrosis are often cavitated, and the pre-existing parenchyma is replaced by numerous macrophages (gitter cells) with abundant foamy cytoplasm. Numerous prominent reactive blood vessels are found at the margins of the areas of necrosis. In those cats with appreciable atrophy of the cortex, similar vessels extend into the remaining tissue.
  • If associated with Cuterebra there are five characteristic features:
  • Parasitic track lesion.
  • Superficial laminar cerebrocortical necrosis.
  • Cerebral infarction (see very common findings).
  • Subependymal rarefaction and astrogliosis with or without ependymal cell loss and
  • Subpial astrogliosis.
  • Changes 2-5 occur throughout the parenchyma unassociated with the parasitic track lesion or the parasite in the affected tissue. The larvae are recovered most commonly in the region of the olfactory bulbs and peduncles, optic nerves and cribriform plate, suggesting entry from the nasal cavity. The ventricular system may be involved especially if there is a parasitic association with changes exhibited in the ependymal lining cells and subependymal parenchyma. The changes are typified by locally extensive areas of marked ependymal cell attenuation to scattered foci of ependymal cell loss.The lateral ventricles are most commonly involved and usually in a bilateral manner. The third ventricle can also be involved, and less so the fourth ventricle.

Differential diagnosis

  • CNS inflammatory disease.
  • Metabolic or toxic encephalopathy in cases of just seizures; idiopathic epilepsy Epilepsy: idiopathicin case of seizures alone.


Initial symptomatic treatment

  • Anticonvulsant medication such as IV or per rectum diazepam Diazepam. Followed by introduction of oral maintenance dosing of diazepam and or phenobarbital Phenobarbital.

Standard treatment

  • There is no standard medical treatment for this condition besides supportive care.
  • Therapy fo rCuterebra (Ivermectin Ivermectin + corticosteroids and antihistamines - latter 2 to avoid allergic reaction that may occur related to the dead parasite).


  • Vital signs should be monitored for at least the first 2 days.
  • Neurological examination should be repeated at least every 4 hours; the main points to focus on include:
  • Level of mentation.
  • Pupillary response to light stimulation.
  • Oculocephalic reflex (physiologic nystagmus).
  • Gait if possible.
  • Water and food intake should be monitored as cats may not be self sufficient.

Subsequent management


  • Continued supportive care including bladder and skin care and fluid and caloric supplementation.
  • Seizure frequency and severity; liver enzyme levels if initiated on diazepam; Phenobarbital levels after 14 days.


  • Repeat neurologic examinations over a 2-3 month period.
  • Repeat serum Phenobarbital levels over the first few months until seizure control is established, then every 6 months.



  • None.
  • Where Cuterebra intracranial migrations occur, keep the cats indoors.


  • None.

Group eradication

  • None.



  • The prognosis is guarded for survival and is determined by the amount of cerebral damage due to the initial infarction.
  • Some cats can live with just seizure activity for months after the event and their prognosis is determined by the ability to control the activity.

Expected response to treatment

  • Improvement may be seen over the first 2-3 months with the majority seen within a month. If there is deterioration, consider other differentials. If no improvement at all in 7 days may consider poor prognosis.
  • Motor function should improve but personality changes may be the most likely residual signs.

Reasons for treatment failure

  • SEVERE parenchymal destruction due to the original infarction.
  • Supportive care not initiated early enough.

Further Reading


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.