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The lumbar puncture and cerebrospinal fluid (CSF) opening pressure (OP) in children remains an essential diagnostic test for children with suspected elevated intracranial pressure. Recent prospective data have revised the normative CSF OP values and described how clinical variables such as age, depth of sedation, and obesity may influence the measurements. In addition, the new normative data are now reflected in revised diagnostic criteria for idiopathic intracranial hypertension/pseudotumor cerebri syndrome. This review highlights the recently published data and provides guidance on how it may impact clinical management.

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Neuro-ophthalmologists frequently care for patients with idiopathic intracranial hypertension (IIH), although many questions remain unanswered regarding its diagnosis, pathogenesis, and treatment. The Friedman-Jacobson criteria for the diagnosis of IIH specify lumbar puncture (LP) opening pressure values that are largely based on experience with little supporting normative data. Until recently, there were sparse data to define normal values of the LP opening pressure in children. Papilledema, the sine qua non of IIH, may not always be present, but the frequency of true IIH without papilledema is controversial and the threshold for diagnosing it varies among clinicians. Concepts regarding the pathogenesis of IIH continue to evolve; venous hypertension is certainly implicated even though it is uncertain whether venous sinus stenosis is the cause or effect of increased intracranial pressure. The 2010 Jacobson Lecture discusses the evidence for some of the prevailing assumptions about normal lumbar puncture opening pressure, venous sinus stenosis, and the phenotypic continuum between chronic daily headaches and IIH.

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The author outlines the history of the development of the pseudotumor concept, first specifically formulated by Nonne in 1904 but implicit in earlier descriptions. A scheme of periodization is applied, identifying otological, neurosurgical, neurological, and neuroophthalmological periods; he relates theoretical and practical developments in the understanding of the condition to the concerns of the dominant speciality involved in diagnosis and management. Key studies from each period are discussed in relation to the issues of mechanism, origin, nomenclature, diagnosis, and treatment. During the otological period, approaches to the condition were heavily influenced by its common association with middle ear infection, often with venous sinus involvement, and this led to the idea of disturbed cerebrospinal fluid dynamics as the cause. The advent of neuroradiological systems ushered in the neurosurgical period in which the significant but unfinished debate began: which intracranial compartment is primarily implicated in the intracranial hypertension? By the time of the neurological period cerebral edema was implicated as the cause, and this coincided with the availability of appropriate treatment methods and steroidal and diuretic agents. Toward the end of this period additional major advances in investigative methods again brought the issue of mechanism into contention, although a resolution was not to follow. The neuroophthalmological period is characterized by an increased awareness of the significance of visual loss and a return to one of the original methods of treatment. Finally, the possible significance of impaired cranial venous outflow, a thread running through all periods, is considered.

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The concepts of serous meningitis, pseudotumour cerebri, hypertensive meningeal state and otitic hydrocephalus have not been considered historically as synonyms nor can they be superimposed on what is currently known as Benign Intracranial Hypertension (BIH). BIH is a syndrome of intracranial hypertension with no clinical, radiological or analytical evidence for the existence of focal or general neurological lesions or hydrocephalus, and which has a self-limiting "benign" development. At present, the diagnostic criteria usually accepted are: 1. Symptoms and signs of intracranial hypertension. 2. Absence of focal neurological symptoms and signs. 3. Absence of radiologically verified cerebral lesion. 4. C.S.F. of normal composition and high pressure. The requirement of other criteria for the diagnosis of BIH, such as angiography, to eliminate the possibility of thrombosis of venous sinuses, or continuous monitoring of C.S.F. pressure, is controversial.

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