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INTRODUCTION

Increased intracranial pressure can be secondary to intracranial masses (eg, neoplasm, infection, hematoma, infarction), to generalized brain swelling (eg, anoxia/ischemia, Reye syndrome, hypertensive encephalopathy), or to increased venous pressure (eg, congestive heart failure, cerebral venous thrombosis). It can also be the result of impaired cerebrospinal fluid (CSF) circulation.

Disorders of CSF dynamics include obstructive hydrocephalus, normal pressure hydrocephalus, intracranial hypotension, and pseudotumor cerebri.

CSF pressure is normally 100–180 mm H2O in adults and 30–60 mm H2O in children. CSF volume ranges from 70–160 mL, and about 500 mL are formed each day; it thus turns over several times daily. It is principally made in the choroid plexus of the lateral, third, and fourth ventricles, and it exits the ventricles through the foramina of Magendie and Luschka, which connect the fourth ventricle with the subarachnoid space. CSF is principally absorbed through arachnoidal villi, which are invaginations of arachnoid membrane into the dural sinuses and veins of the cerebral convexities, the base of the brain, and the spinal nerve roots. When resorption cannot keep up with production, CSF pressure rises.

OBSTRUCTIVE HYDROCEPHALUS

ESSENTIALS OF DIAGNOSIS

  • In infants: head enlargement, mental retardation, visual loss

  • Acute in adults: headache, obtundation

  • “Occult” in adults: unsteady or “magnetic” gait, altered mentation, urinary incontinence

General Considerations

Obstructive, or tension, hydrocephalus is the result of obstruction of CSF flow either within the ventricles (including the foramen of Monro connecting the third ventricle to the lateral ventricles and the midbrain aqueduct connecting the third ventricle to the fourth ventricle), at the foramina of Luschka and Magendie, or at the subarachnoid space at the base of the brain (the basal cisterns). (In the past a distinction was made between “communicating hydrocephalus,” in which the ventricles remained in communication with subarachnoid space, and “noncommunicating hydrocephalus,” in which they did not. This distinction is no longer considered meaningful, for in tension hydrocephalus obstruction is never total. Such an occurrence would be rapidly fatal.)

One or both foramina of Monro can be blocked by a third ventricular colloid cyst or other tumor. The aqueduct can be blocked by either congenital or acquired lesions, including mumps ependymitis, hemorrhage, or neoplasm. The foramina of Magendie and Luschka can be blocked by congenital failure of opening (Dandy-Walker syndrome), and the basal cisterns can be blocked by fibrosing posthemorrhagic or postinflammatory meningitis.

Whether tension hydrocephalus can result from obstruction of arachnoidal villi over the cerebral hemispheres is controversial. The weight of evidence is against such an occurrence. Radiographic enlargement of the subarachnoid spaces over and between the cerebral hemispheres is usually attributable to meningeal cysts or subdural hygromas.

In hydrocephalus secondary to nonprogressive disease, CSF absorption can equilibrate with CSF production; absorption increases because of increased CSF pressure, and production decreases because of compression of the ...

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