Walsh & Hoyt: Headache Attributable to Nonvascular Intracranial Disorders

Both increased and decreased intracranial pressure (ICP) can result in headache. The causes of elevated ICP include intracranial mass lesion causing obstructive hydrocephalus, meningeal processes (meningitis, meningeal carcinomatosis) resulting in impaired absorption at the arachnoid villi, elevated cerebral venous sinus pressure (venous sinus thrombosis, superior vena cava syndrome), overproduction of CSF (from a choroid plexus papilloma), certain toxins and metabolic disturbances, and idiopathic intracranial hypertension (IIH). In many of these conditions, the mechanism of headache is multifactorial, with increased ICP playing a small or large role. In IIH, and similar conditions, the elevated ICP plays a more dominant role in pain generation. Intracranial hypotension results from excessive drainage of CSF; this is due to either an iatrogenic (postlumbar puncture or postneurosurgical) or a spontaneous CSF leak. Patients with headaches related to high or low ICP often describe a positional component: i.e., the headache is worse when erect (low pressure) or supine (high pressure). Although not always present, a positional headache should raise concern about elevated or decreased ICP. Early morning headache, and early morning nausea and emesis, suggest increased ICP. A classic cause of positional headache is a colloid cyst of the third ventricle. The presumed mechanism is a ""ball-valve effect"" when the patient suddenly changes position the tumor obstructs the third ventricle and causes a rapid increase in ICP. Intracranial masses and meningitis often have accompanying neurologic symptoms, including focal deficits, meningismus, altered level of consciousness, or seizures.