PEDIATRICS Vol. 39 No. 2 February 1967, pp. 227-237
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BENIGN INTRACRANIAL HYPERTENSION IN CHILDREN

Arthur Rose M.D., C.L.B., D.C.H.1 and Donald D. Matson M.D.2

1 The Department of Neurology, Children's Hospital Medical Center and Harvard Medical School, Boston, Massachusetts
2 The Department of Neurosurgery, Children's Hospital Medical Center and Harvard Medical School, Boston, Massachusetts

The clinical features of 23 cases of benign intracranial hypertension occurring in childhood have been reviewed. Eight cases followed minor bacterial or viral infections, four cases occurred in association with head or neck injury, four cases occurred with otitis media, and one case followed sudden cessation of corticosteroid treatment. There were no apparent associated clinical factors in the remaining six cases. Benign intracranial hypertension thus emerges as a clinical syndrome of varied etiology, generally with a short course, good prognosis, little tendency to recurrence, and only rarely requiring surgical intervention. Clinical evidence suggests that, in addition to otitis media, cerebral venous thrombosis may, in certain circumstances, follow head injury, trauma to the jugular vein, and thrombosis in the pterygoid venous plexus. Therefore, it is suggested that complete visualization of the venous cerebral circulation should be attempted in the investigation of patients with benign intracranial hypertension.

In view of the occurrence of the syndrome following gastroenteritis, upper respiratory tract infections, and chickenpox, diagnostic virological studies, including culture of cerebrospinal fluid, are of special interest. Other precipitating causes of this clinical syndrome are discussed. The occurrence of benign intracranial hypertension as an initial manifestation of two well defined endocrine abnormalities is described. It is possible in the future that systematic endocrine study of patients, particularly pre-pubertal females, will reveal other hormonal defects.

It appears probable that transient generalized cerebral edema of any type may be responsible for the occurrence of this syndrome. The elucidation of its pathophysiology will probably have to wait more accurate and safe methods of clinical measurement of intra- and extra-cellular fluid shifts within the brain, as well as more reliable understanding of cerebrospinal fluid and cerebral blood flow alterations.

Submitted on May 20, 1966
Accepted on September 14, 1966




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