Introduction

• Rare cause of neurological disease → rapid cerebral dysfunction.
• In contrast to the high incidence in man, intracerebral hemorrhage resulting from spontaneous rupture of vessels is rare in dogs.
• Cause: trauma (subarachnoid or intracranial hemorrhage), rupture of congenital vascular abnormalities, primary or secondary brain tumors, vasculitis, systemic hypertension, intravascular lymphoma, hemorrghagic infarction, impaired coagulation.
• Predisposed to by hypertension ( → sub-arachnoid bleeding), hypothyroidism, thromboembolic disease, coagulopathy, vasculopathy, radiation therapy.
• Signs: acute onset, diverse neurological deficits depending on site and type of hemorrhage.
• Diagnosis: imaging techniques, cerebrospinal fluid (CSF) analysis.
• Prognosis: depends upon the extent of hemorrhage and the area of the nervous system involved.
• See cerebral concussion/contusion Brain: cerebral concussion / contusion.

Pathogenesis

Etiology

• Rupture of congenital vascular abnormalities.
• Primary or secondary brain tumor Brain: neoplasia.
• Vasculopathy, eg secondary to radiation therapy Radiotherapy., intravascular lymphoma, vasculitis.
• Hypothyroidism Hypothyroidism.
• Thrombosis, infarction and hemorrhage can occur spontaneously, secondary to drug therapy (L-asparaginase, anticoagulants), with thrombocytopenia and other bleeding disorders Hemostatic disorder: acquired , with trauma Brain: trauma , hypertension Hypertension , hyperthyroidism, hyperadrenocorticism Hyperadrenocorticism , and atherosclerosis from hypothyroidism Hypothyroidism , and with infection (septic emboli) Lung: pulmonary thromboembolism , Kidney: thromboembolism.
• Hemorrhage may also occur secondary to brain trauma.
• Intraparenchymal hemorrhage is most common, although subdural hematoma is possible.

Predisposing factors

General

• Coagulopathies Hemostatic disorder: acquired.
• Thromboembolic disease Lung: pulmonary thromboembolism , Kidney: thromboembolism.
• Hypertension Hypertension.

• Radiation therapy Radiotherapy.

Pathophysiology

• Blood leaks directly into the brain, forming a hematoma within the brain parenchyma, or into the subarachnoid or subdural space, leading to physical disruption of the tissue and pressure on the surrounding brain. This alters CNS volume/pressure relationships, with the possibility of increasing intracranial pressure (ICP) and decreasing cerebral blood flow (CBF).
• As a hematoma develops, ICP may remain constant due to a system of compensation. Within the skull, a change in the volume of one intracranial component (brain tissue, arterial blood, venous blood, CSF) will be balanced by a compensatory change in another.
• Exhaustion of the compensating mechanisms for an intracranial space occupying lesion results in further increases in the volume of the hematoma, producing massive elevations in ICP.
• Due to mechanical autoregulation, CBF remains constant even though cerebral perfusion pressure (CPP) may vary between 40 and 120 mmHg.
• The normal autoregulation of CBF may be impaired following intracranial bleed, causing blood flow to damaged regions to become directly dependent on systemic blood pressure. Such animals may be unable to compensate for reductions in mean arterial pressure, causing decreased CPP in the presence of increased ICP.
• In these circumstances, systemic hypotension can result in inadequate perfusion of the brain, which leads to cerebral ischemia and secondary neuronal injury.
• Raised intracranial pressure Intracranial pressure measurement ultimately leads to brain herniation Brain: tentorial herniation.

Types of brain herniation

• Subfalcal.
• Caudal transtentorial.
• Foramen magnum (can cause respiratory depression).
• Rostral transtentorial.
• Intracranial disease processes may result in mechanical disruption of intracranial tissues (primary injury). This primary injury may initiate a number of secondary pathophysiological sequelae such as:
  • Metabolic alterations in neuronal or glial cells.
  • Impairment of vascular supply to normal tissue (ischemia).
  • Impairment of cerebrovascular autoregulation.
  • Hemorrhage (intraparenchymal, intraventricular, extradural or subdural).
  • Irritation (seizure generation).
  • Obstruction of the ventricular system.
  • Edema formation.
  • Production of physiologically active products.
  • Increased intracranial pressure (ICP).
• See pathophysiology of brain trauma Brain: trauma.

Diagnosis

Treatment

Outcomes