11. Clinical manifestations of increased intracranial pressure. Herniations. Flashcards
Monro-Kellie principle
The sum of volumes of brain, CSF, and intracranial blood is constant. An increase in one should cause a decrease in one or both of the remaining two
Pathophys. of cerebral blood flow
Cerebral blood flow is maintained by diff. in arterial and venous pressure = cerebral perfusion pressure. Intracranial and cerebral venous pressure is always equal, so an increase in one leads to the rise of the other – and cerebral perfusion pressure decrease. Cerebral arterioles dilate to maintain cerebral blood flow, increasing intracerebral blood volume, which in turn increase ICP even more. This is called vasodilatory cascade, eventually leading to global cerebral ischemia
Physicologic intracranial pressure
around 10 mmHg
Physiologic regulation of intracranial pressure
Production and absorption of the cerebrospinal fluid. Slow mechanism.
Compensatory mechanism of increased ICP
- Displacement of CSF via foramen magnum into spinal canal (valsalva maneuver)
- Decrease of cerebral volume (artificially activate hyperventilation, barbiturate narcosis, hypothermia)
Causes of increased ICP
- Space occupying lesions (tumor, abscess, hemorrhage)
- CSF disorders (occlusive hydrocephalus)
- Cerebral edema (vasogenic, cytotoxic, interstitial)
- CNS infections
Clinical manifestation of increased ICP
- Progressive headache
- Vomiting
- Papilledema + blurred vision
- Global cerebral dysfunction (due to ischemia): drowsiness, alt. behaviour
Treatment of ICP
- Treat underlying cause
- Omsodiuretics (mannitol, glycerol)
- Loop diuretics (decrease CSF production)
- Decompressive craniectomy
Four types of brain herniations
Subfalcial, central, transtorial and tonsillar
Subfalcial herniation
Cingular gyrus pressed under falx. May compress circumferential branches of anterior cerebral artery.
Symptoms of subfalcial herniation
- Contralateral leg paralysis
- Increased intracranial pressure (papilledema, headache)
- Increased risk of transtentorial herniation, central herniation, or both
Central herniation
Both temporal lobes herniate through the tentorial notch due to bilateral mass/diffuse brain edema
Symptoms of central herniation (early- and late phase, general symp)
Early: indifference, concentration, memory problems, decerebrate
Late: (further compromise to midbrain) drowsiness, unconciousness, loss of decerebrate posture, positive babinski
General: symmetric, contstricted and reactive pupils. Increased muscle tone.
Transtentorial herniation
Medial tempiral lobe squeezed under the tentorium. Compression of CN III, PCA, cerebral peduncle, upper brainstem and thalamus.
Symptoms of transtentorial herniation
- CN III: ipsilateral fixed pupil and anisocoria
- PCA: contralateral homonymous hemianopsia
- Brainstem: unconciousness and decerebrate posture (incr. extensor muscle tone)
- Cerebral peduncle: hemiparesis