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Herniations:
The volume of the intracranial contents is fixed by the skull. as a result, the introduction of additional tissue or fluid (as may occur in a space-occupying lesion, cerebral oedema, or hydrocephalus) raises intracranial pressure, which may lead to life-threatening herniation of the brain through openings of the skull. The major herniations are as follows:
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Subfalcine: cingulate gyrus herniates under the falx (may compromise the anterior cerebral artery).
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Transtentorial: medial temporal lobe (uncus) passes over the free edge of the tentorium (may lead to distortion of the adjacent midbrain and pons and tearing of feeding vessels [Duret haemorrhages] or compress the posterior cerebral artery)
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Tonsillar: cerebellar tonsils herniate through the foramen magnum (may result in compression of the medulla and compromise cardio-respiratory centres)
Subfalcine herniation: occurs in a supratentorial intracerebral expanding lesion; expansion of a unilateral cerebral hemisphere lesion results in the cingulate gyrus herniating under the free margin of the falx cerebri above the corpus callosum.
Transtentorial herniation: is the most important herniation associated with a supratentorial-expanding lesion. The medial part of the ipsilateral temporal lobe (anteromedial hippocampus) is squeezed through the tentorial opening.
Depending on the supratentorial pressure several sequelae may be seen:
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Uncal notch: a definite notch forms on the inferior aspect of the brain due to compression of the herniating brain against the edge of the tentorium cerebella.
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Fixed dilated pupil: (unilateral or bilateral) with oculomotor nerve (III) may be damage.
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Compression of the posterior cerebral artery: close proximity to the tentorium and herniating portion of the brain lumen may be obliterated infarction occurs in the medial occipital lobe (unilateral or bilateral).
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Contralateral midbrain compression: midbrain pushed against contralateral ridge edge of the tentorium (forms groove – Kernohan’s notch on midbrain)
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Compression of the aqueduct: distortion and partial obstruction of the lumen of the aqueduct CSF accumulates within the ventricles which exacerbates the problem ( pressure).
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Midbrain herniation: rapidly expanding supratentorial mass shifts the midbrain down through the incisura; causes shearing of vessels Duret haemorrhages (upper pons and midbrain), associated compromised vital centres and rapid death.
Upward transtentorial herniation: occurs with space occupying lesions in the posterior fossa (i.e. cerebellar lesions). The midbrain and cerebellar hemispheres move upwards through the incisura aqueduct becomes distorted and compressed, blocking CSF outflow supratentorial pressure
Cerebellar tonsillar herniation: cerebellar tonsils move downward through the foramen magnum; caused by:
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Subtentorial expanding lesion (posterior fossa mass)
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Transmitted supratentorial pressure
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Coning – post lumbar puncture in the patient with raised intracranial pressure
Intracranial pressure is increased with the obstruction of CSF through the fourth ventricle and exit foramina; the tonsils compress the medulla and interfere with the cardio-respiratory centres rapid demise of the patient.
Transcalverial herniation: herniation of the brain through any defect in the skull (usually seen in severe penetrating injuries of the skull and brain)
Category: Medicine Notes , Pathology Notes
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1 comments:
One marker for high IOP (other than the danger signs like blown pupils and directly measuring it) is by checking for spontaneous venous pulsations in the back of the eye at the optic nerve.
The ocular contents and the brain CSF are seperated by only a small layer of tissue called the lamina cribosa through which the arteries and veins of the retina pass through. If you can see venous pulsating with the heartbeat at this level, then you know the two compartments have similar pressure and that the ICP probably isn't too high.
To see a video of what this looks like, check out:
spontaneous venous pulsations
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