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INTRODUCTION

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Increased intracranial pressure (ICP) often requires invasive monitoring and emergent treatment. Pseudotumor cerebri is the common name for the idiopathic form, which may be due to cerebral venous sinus thrombosis and associated with papilledema and visual loss. The opposite clinical syndrome is intracranial hypotension, which is one of the causes of new daily persistent headache. The magnetic resonance imaging (MRI) shows a sagging brain and pachymeningeal enhancement. Myelography using either computed tomography (CT) or MRI imaging is used to find the cerebrospinal fluid (CSF) leak, sometimes cured with a blood patch. Brain herniation is a complication of increased ICP requiring emergent treatment. False localizing signs are seen due to compression of the contralateral Kernohan notch.

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Hydrocephalus can be associated with the normal pressure form, diagnosed by a high-volume lumbar puncture (LP), and treated with ventriculoperitoneal or lumboperitoneal shunting.

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White matter diseases include acute disseminated encephalomyelitis, progressive multifocal encephalopathy caused by the John Cunningham (JC) virus, multiple sclerosis, and central pontine myelinolysis.

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PART 1—INCREASED INTRACRANIAL PRESSURE (ICP)

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The total volume of the adult intracranial content is 1400–1700 mL, of which the brain is 80% (1200 mL), and the cerebrospinal fluid (CSF) and the blood are each 10% (150 mL). The choroid plexi form CSF at a rate of 20 mL/hour or 450–500 mL/day. The arachnoid granulations lie along the superior sagittal sinus and return the CSF into the venous system via a one-way valve.

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The Monro-Kellie hypothesis states the skull is inelastic, containing a fixed volume. This applies to both intracranial hypertension and hypotension.

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What are the symptoms of increased ICP?

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  • Headache (HA) that is worse upon awakening and exacerbated with coughing/sneezing/bending.

  • Visual changes may include diplopia and transient visual obscurations (TVOs).

  • Weakness, sensory changes, and myelopathy (compression at the cervical–medullary junction).

  • Altered breathing patterns, cardiac dysrhythmia, and hiccups.

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What are the causes and noted imaging modalities?

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  • CT: tumor, stroke, hydrocephalus, subarachnoid hemorrhage (SAH), cysts, abscess, herniation, hematoma, loss of gray–white junction, congenital or developmental anomalies, and lateral displacement of the calcified pineal body

  • MRI: above plus encephalitis, meningitis, shear, empty sella, edema, and prominence of the optic nerve sheath (optic nerve hydrops)

  • MRV (venous): cerebral venous thrombosis (do not overlook this important and treatable etiology that is not seen on routine imaging, unless there is associated cerebral venous infarction) (Figure 18-1)

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Figure 18-1

(A) Initial MR venography demonstrated partial thrombosis of the superior sagittal sinus, torcula, and proximal transverse sinuses (arrows). (B) Follow-up MR venography at the time of visual worsening showed improvement in venous flow, with mild residual thrombosis. (C) Fast-spin echo T2-weighted axial imaging demonstrated reversed optic nerve cupping in the right eye with posterior scleral flattening and protrusion of optic nerve papilla into the globe (arrow) (subsequent image on MRI demonstrated similar findings in the ...

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