Canis ISSN: 2398-2942

Brain: tentorial herniation

Contributor(s): Rodney Bagley, Laurent Garosi

Introduction

  • Cause: increased intracranial pressure or brain volume due to trauma Brain: trauma , infectious or immune-mediated encephalitis Encephalitis , non-traumatic intracranial hemorrhage Intracranial hemorrhage , brain edema (bilateral herniation) or neoplasia Brain: neoplasia (usually unilateral herniation).
  • Signs: pupillary changes due to dysfunction of cranial nerve III, progressive deterioration.
  • Diagnosis: signs, advanced imaging.
  • Treatment: management of seizures, steroids, mannitol, furosemide.
  • Prognosis: cause secondary compression of brain stem.

Pathogenesis

Etiology

  • Intracranial neoplasia Brain: neoplasia.
  • Brain edema.
  • Brain trauma.
  • Encephalitis.
  • Non-traumatic intracranial hemorrhage.
  • Systemic hypertension Hypertension.

Pathophysiology

  • Transtentorial herniation is the unilateral or bilateral displacement of the parahippocampal gyrus of the occipital lobe(s) beneath the tentorium cerebelli, resulting in compression of the mesencephalon and/or rostral cerebellum.
  • Brain herniations are the terminal effects of intracranial hypertension.
  • Acute and catastrophic clinical deterioration due to intracranial hypertension is usually caused by accumulation of brain edema, obstructive hydrocephalus Hydrocephalus , abnormalities of cerebral blood flow (ischemia or hemorrhage), physical displacement of intracranial parenchymal structures or combination of these mechanisms.
  • As intracranial volume increases beyond the limits of compensation, intracranial pressure can increase so precipitously that shifts of brain parenchyma (ie brain herniation) result.
  • 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.
  • The rigid cranium does not allow expansion of contents (blood, CSF and brain tissue), so brain edema → increase in intracranial pressure. Uncompensated raised intracranial pressure usually leads to brain herniation.
  • Tumor may disrupt the blood-brain barrier causing local accumulation of fluid, mostly in the white matter. This vasogenic brain edema may develop rapidly and is the most significant of the secondary effects, giving an acute clinical picture.
  • Brain neoplasia→ disrupted blood-brain barrier → local accumulation of fluid, mostly in white matter → rapidly developing vasogenic brain edema → increased intracranial pressure because rigid cranium does not allow expansion of contents (blood, CSF and brain tissue), may lead to brain herniation.
  • Brain trauma→ brain swelling or edema → worsened by increased cerebral blood flow in response to hypoxia → brain herniation.
  • Head trauma results in mechanical disruption of intracranial tissues (primary injury). This disruption of neuropil is irreversible.

Diagnosis

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Treatment

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Outcomes

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Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Walmsley G L, Herrtage M E, Dennis R, Platt S R, Jeffrey N D (2006) The relationship between clinical signs and brain herniation associated with rostrotentorial mass lesions in the dog. Vet J 172, 2258-264 PubMed.
  • Bagley R S (1996) Pathophysiologic sequelae of intracranial disease. Vet Clin North Am Small Anim Pract 26 (4), 711-733 PubMed.
  • Dewey C W, Budsburg S C & Oliver J E Jr (1993) Principles of head trauma management in dogs and cats - Part II. Comp Cont Ed 15 (2), 177-193 VetMedResource.
  • Kornegay J N, Oliver J E & Gorgacz E J (1983) Clinicopathologic features of brain herniation in animals. JAVMA 182 (10), 1111-1116 PubMed.

Other sources of information

  • Kornegay J N (1993)Pathogenesis of diseases of the central nervous system.In:Textbook of Small Animal Surgery.2nd edn. Ed D Slatter. Philadelphia: W B Saunders. pp 1022-1037.


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