Cerebral Infarction

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Definition

• Cerebrovascular disease refers to a group of disorders that result from a pathological process that compromises blood supply to the brain.

  • Such disorders may be either ischemic or hemorrhagic.

• Infarction is a local tissue injury or necrosis from reduced or absent blood flow to a specific part of the body, including the brain.

• Cerebral infarction (cerebral infarct, cerebrovascular accident [CVA], or stroke) is usually a focal ischemic event with an acute onset of asymmetric clinical signs that are progressive for a short time.

• Global brain ischemia can also occur (eg, anesthetic accidents, cardiopulmonary arrest).

• By definition, clinical signs must be present for at least 24 hours to be considered a stroke.^1,2

• Transient ischemic attack (TIA) is the term used to describe a cerebrovascular disorder in which clinical signs resolve within 24 hours following transient ischemia.

Pathophysiology

• There is little energy reserve in the brain, so it is dependent on continuous delivery of oxygen and glucose for energy; it is capable of only aerobic metabolism.¹

• The brain receives 20% of cardiac output and accounts for 15% of oxygen consumption, despite comprising only 2% of body weight.¹

• Infarcts can be described based on their underlying pathophysiology or location and size.

Underlying Pathophysiology^2,3

• Ischemic infarct is secondary to lack of oxygen delivery caused by blood vessel obstruction; this is the most common form of cerebral infarct in dogs and cats.

• Hemorrhagic infarct is secondary to ruptured blood vessels leading to hemorrhage within the brain parenchyma.

Location & Size^1,3

• Territorial infarct is a large area of tissue damage secondary to obstruction of one of the major arteries to the brain (eg, middle cerebral artery, rostral cerebellar artery).

• Lacunar infarct is a smaller area of tissue damage from obstruction of small superficial or deep penetrating arteries.

Signalment

• Infarction can occur at any age but is typically diagnosed in middle-aged to geriatric dogs and cats.^4-6

• No apparent gender predisposition.

• They can occur in all breeds of dogs and cats, but the following breeds may be at increased risk^6-10:

  • Greyhounds: Especially cerebellar infarcts; these are often idiopathic but may be hypertension-related.

  • Cavalier King Charles spaniels: Possibly related to local alterations in intracranial pressure secondary to Chiari-like malformation.

  • Miniature schnauzers: Possibly related to hyperlipidemia.

  • Brachycephalic breeds: Increased risk for global ischemia, especially with ketamine anesthetic protocols.

Risk Factors

• The three most common risk factors for cerebral infarction are hypertension, hypercoagulability, and hyperviscosity.

Predisposing Conditions^2,4,6,11

• The most common predisposing causes are idiopathic hypertension, chronic kidney disease, and hyperadrenocorticism.

• A predisposing condition is identified in just over half of dogs with MRI evidence of infarction.

• See Predisposing Conditions for Cerebral Infarction.

History

• Patients are usually presented for evaluation following peracute to acute onset of neurologic signs that are non-progressive after 24 hours.

  • Rarely, progression may occur at 48-72 hours because of secondary cerebral edema.^1,2

• Common clinical signs noted by owners include vestibular dysfunction, seizures, altered mental status, paresis, or ataxia.

Physical Examination

• General examination may be normal or demonstrate changes consistent with a predisposing condition (eg, cranial abdominal organomegaly, thin hair coat).

• Retinal fundic examination is recommended.

  • Hypertension may cause enlarged or tortuous retinal vessels.

  • Papilledema may be present if increased intracranial pressure.

  • Concurrent chorioretinitis or infiltrative disease (eg, lymphoma)further suggests presence of a concurrent, predisposing condition.

Neurologic Examination

• As with all neurologic disorders, neurologic signs reflect lesion location and extent rather than cause.

• Common signs based on lesion location include:

  • Cerebrum: Seizures, mental obtundation, circling, pacing, inappropriate elimination

  • Thalamus: Signs of cerebral disease as above or vestibular dysfunction (possibly from damaged thalamic relay centers associated with cerebellar and vestibular nuclei; damage to the medial longitudinal fasciculus; input of vestibular information to the thalamus; or diaschisis, a sudden change in function in one area of the brain from damage in a distant location).

  • Brainstem: Altered mental status, cranial nerve deficits, vestibular dysfunction, paresis, ataxia.

  • Cerebellum: Paradoxical central vestibular dysfunction, hypermetria, cerebellar (intention) tremors, truncal sway/ataxia.

Diagnosis

Definitive Diagnosis

• Definitive diagnosis requires histopathology at necropsy.

  • CT- or MRI-guided stereotactic biopsy may not provide a definitive diagnosis of infarction but may help rule out other possible causes (eg, neoplasia, encephalitis).

• A presumptive diagnosis can be made via advanced imaging and exclusion of other potential causes.

Differential Diagnoses

• Intracranial neoplasia

• Immune-mediated, non-infectious encephalitis (eg, granulomatous meningoencephalomyelitis, necrotizing encephalitis)

• Infectious encephalitis

• Traumatic brain injury

Laboratory Findings

• Minimum database includes CBC, serum chemistry panel, thyroid hormone analysis, and urinalysis.

• Serial systolic blood pressure measurements should be obtained to rule out systemic hypertension.

• Thoracic radiographs and abdominal ultrasound are recommended to screen for neoplasia and predisposing conditions.

• Ancillary diagnostics should be performed based on the type of infarction present (Table 1).

Table 1: Ancillary Diagnostics

Imaging

• MRI is the advanced imaging modality of choice given its superior soft tissue resolution.

  • The classic MRI characteristic of an ischemic stroke (Figure 1, see image gallery below) is an intra-axial lesion (often wedge-shaped) that is hyperintense (bright) on T2-weighted and fluid attenuation inversion recovery (FLAIR) images, iso- to hypointense (dark) on pre-contrast T1-weighted images, and minimal to no contrast enhancement.

  • Diffusion weighted imaging (DWI; Figure 2, see image gallery below) is the sequence of choice for acute ischemic infarction.

    • DWI detects lack of normal Brownian motion of molecules, particularly lack of intercellular water movement from cell swelling associated with cytotoxic edema.

    • An acute infarction appears as a hyperintense region.

  • The MRI appearance of hemorrhagic infarction (Figure 3, see image gallery below) varies greatly as blood cells and hemoglobin degrade (Table 2). 

    • Hemorrhagic infarcts can be difficult to distinguish from hemorrhagic brain tumors (eg, glioma, hemangiosarcoma).

    • The T2*-gradient echo (T2*GRE) sequence is best for identifying hemorrhage as it is hypointense on this sequence.

    • T2*GRE is also hypointense for mineralization, air, iron, melanin, and foreign bodies.

FIGURE 1

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FIGURE 1

MRI images of a dog with a right cerebellar infarct (A). Note the wedge-shaped intra-axial lesion in the right dorsal cerebellar gray matter (arrow) that is hyperintense on T2-weighted images (B), isointense on T1-weighted images (C), and does not contrast enhance (D).

FIGURE 1

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FIGURE 1

MRI images of a dog with a right cerebellar infarct (A). Note the wedge-shaped intra-axial lesion in the right dorsal cerebellar gray matter (arrow) that is hyperintense on T2-weighted images (B), isointense on T1-weighted images (C), and does not contrast enhance (D).

Table: MRI Characteristics of Hemorrhage

Treatment

Inpatient or Outpatient

• Patients with mild signs may be treated on an outpatient basis.

• Non-ambulatory patients with moderate to severe clinical signs, especially larger-breed dogs, may need to be hospitalized until they are able to walk with minimal to no assistance.

Acute Medical Treatment

• In general, there is no specific treatment for cerebral infarction.

• So-called clot busters or thrombolytic agents (eg, tissue plasminogen activator [tPA], streptokinase) are frequently used in human medicine.

  • These medications are infrequently used in veterinary medicine because blood clots are rarely a cause of infarction in dogs and cats, thrombolytic agents need to be given within 6 hours of infarction, and expense or limited availability preclude their use.

• Mannitol (0.5-1.0 g/kg IV over 10-15 minutes) or hypertonic saline 7.5% (3-5 mL/kg IV over 10-15 minutes) may be needed to reduce brain swelling.

  • There is a theoretical risk for exacerbating hemorrhage or cerebral edema if mannitol is given to patients with intracranial hemorrhage, but benefits likely outweigh risks.

• Hypertension should be treated to prevent ongoing damage. 

  • Initial treatment recommendations include enalapril (dogs, 0.5 mg/kg PO q12h) or amlodipine (cats, 0.625-1.25 mg per cat PO daily).

• Oxygen support is recommended in moderate to severe cases, especially if hypoventilation is present.

• Nursing care for recumbent patients is critical and includes frequent turning and thick bedding to prevent pressure sores, urinary catheterization if indicated, and physical rehabilitation (at a minimum, passive range of motion and massage).

Chronic Medical Treatment

• Underlying predisposing conditions should be treated as indicated to reduce the risk for future infarction.

• Antithrombotics may be considered if a thromboembolic disorder is proven, but their use is controversial and not proven to be beneficial.

  • Options include clopidogrel (dogs, 1 mg/kg PO q24h; cats, 18.75 mg per cat PO q24h) or aspirin (dogs, 0.5-1.0 mg/kg/q24h; cats, 40 mg [1/2 baby aspirin tab] PO q48-72h

Nutritional Aspects

• There are no specific nutritional recommendations for infarction, but diets higher in essential fatty acids and omega-3 may be helpful.¹²

• Diet recommendations should also be based on predisposing conditions, such as a low-protein diet in patients with kidney disease.

Activity

• There are no activity restrictions for this condition.

• Physical rehabilitation is highly recommended to improve recovery and shorten duration of signs.

Client Education

• Clients should be taught how to provide nursing care for recumbent animals, as well as how to treat underlying predisposing conditions.

Follow-up

Patient Monitoring

• Patients should be monitored for signs of progression that might be consistent with a diagnosis other than stroke.

  • If signs are progressive, further examination is required as that would suggest the patient did not have a stroke.

• Clients should be instructed to observe for signs of recumbency-associated aspiration pneumonia (eg, coughing, tachypnea, dyspnea).

Complications

• The most common complication is recumbency-associated aspiration pneumonia.

• Other complications may be observed depending on concurrent predisposing conditions.

In General

Relative Cost

• Diagnostic workup and acute treatment: $$$$-$$$$$

• Chronic treatment and follow-up: $$-$$$

Prognosis

• In general, the prognosis for recovery is good to excellent for patients with focal infarctions that have limited initial clinical abnormalities, if given enough time and supportive care.

• Some patients have residual clinical signs, but quality of life is acceptable for most patients.

• The prognosis for global brain ischemia is guarded to fair.