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Cerebral Infarction

Mark Troxel, DVM, DACVIM (Neurology), Massachusetts Veterinary Referral Hospital, Woburn, Massachusetts

Neurology

|August 2015|Peer Reviewed

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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 Pathophysiology2,3

  • 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 & Size1,3

  • 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 risk6-10:
    • 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 Conditions2,4,6,11

  • 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.

Predisposing Conditions for Cerebral Infarction

  • Aberrant parasite migration (eg, Cuterebra spp, Dirofilaria immitis)
  • Angiostrongylus vasorum infection
  • Atherosclerosis
  • Cardiac disease
  • Coagulopathy
  • Chronic kidney disease
  • Extension of CNS infection
  • Hyperadrenocorticism
  • Hyperlipidemia
  • Hypertension
  • Hypothyroidism
  • Increased blood viscosity (eg, polycythemia, multiple myeloma)
  • Intravascular neoplasia (eg, lymphoma, hemangiosarcoma)
  • Liver disease
  • Protein-losing nephropathy
  • Sepsis and bacterial thromboembolism
  • Vasculitis

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

Ischemic infarction Hemorrhagic infarction
  • Urine protein:creatinine ratio if proteinuria
  • Endocrine testing for hyperadrenocorticism (eg, ACTH stimulation test, dexamethasone suppression testing)
  • Serum antithrombin III activity
  • D-dimer tests
  • Echocardiography and electrocardiography if underlying cardiac condition
  • Rickettsial disease testing
  • Clotting studies: buccal mucosal bleeding time, prothrombin time (PT), activated partial thromboplastin time (APTT)
  • von Willebrand factor analysis
  • Testing for Angiostrongylus vasorum in endemic regions

 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.

Table 2

MRI Characteristics of Hemorrhage

Stage Time frame Hemoglobin state T2-weighted T1-weighted
Peracute <24 hrs Oxyhemoglobin   Hyperintense Isointense
Acute 1-3 days Deoxyhemoglobin   Hypointense Isointense
Early subacute 3-7 days Intracellular methemoglobin Hypointense Hyperintense
Late subacute >7 days Extracellular methemoglobin Hyperintense Hyperintense
Chronic >14 days Hemosiderin   Hypointense Iso- to hypointense

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

Cost Key

$ = up to $100    

$$ = $101-$250    

$$$ = $251-$500

$$$$ = $501-$1000

$$$$$ = more than $1000

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.

References

For global readers, a calculator to convert laboratory values, dosages, and other measurements to SI units can be found here.

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