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Albino P. Bricolo and Roberta P. Glick

reported experience 28, 47 in which high-dose barbiturate therapy has led to the control and normalization of ICP in three-fourths of patients exhibiting resistant intracranial hypertension. Despite this experimental and clinical evidence, neurosurgeons are cautious in advocating the wide-spread use of barbiturate therapy. 6, 28, 39, 40, 44 The indication relied on for initiation of this treatment has been the presence of elevated ICP not controlled by so-called “standard measures.” Two important questions arise: is the treatment initiated too late to avoid

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Steven L. Wald and Robert L. McLaurin

I ntracranial hypertension is a potentially fatal complication of many conditions of the central nervous system. Beneficial effects on both morbidity and mortality have been reported in several clinical studies with aggressive management of cerebral edema. 4, 33, 41 The introduction of intracranial pressure (ICP) monitoring devices has promoted intensive study of various drugs and drug regimens for the treatment of intracranial hypertension, and has allowed for a rational approach to many pharmacological decisions. Management of traumatic intracranial

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Hiroshi Yokota, Takahiko Eguchi, Misato Nobayashi, Toshikazu Nishioka, Fumihiko Nishimura and Yuji Nikaido

A depressed skull fracture overlying the major venous sinuses may lead to sinus injury, venous thrombosis, and infection. If no vital sign is in crisis, the generally accepted strategy is conservative treatment. Flow disturbance in the posterior part of the SSS compressed by a depressed skull fracture is a rare condition; however, persistent intracranial hypertension may result in late signs and symptoms requiring delayed surgical bone elevation. A review of the literature showed that the symptoms are non-specific and the clinical courses are variable and

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Robbin de Goederen, Iris E. Cuperus, Robert C. Tasker, Bianca K. den Ottelander, Marjolein H. G. Dremmen, Marie-Lise C. van Veelen, Jochem K. H. Spoor, Koen F. M. Joosten and Irene M. J. Mathijssen

I ntracranial hypertension is a major concern in children with syndromic craniosynostosis (sCS), and in Apert and Crouzon syndromes the incidence is as high as 53%. 5 , 21 There are many complications of prolonged intracranial hypertension, with the most severe being irreversible visual loss. 5 Intracranial hypertension may also impair neurodevelopment and impact behavior and learning. 20 , 21 Initially, surgeons thought that limited growth of the cranial vault was the main reason for intracranial hypertension in children with craniosynostosis. Treatment

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Eisha A. Christian, Thomas A. Imahiyerobo, Swathi Nallapa, Mark Urata, J. Gordon McComb and Mark D. Krieger

S ince Renier et al. 27 published their landmark report in 1982, the association between untreated craniosynostosis and elevated intracranial pressure (ICP) has been an extensively debated entity. Renier and colleagues showed that one-third of patients with untreated multisuture synostosis had intracranial hypertension (IH). Other groups have since confirmed these findings of elevated ICP, which differ according to the site of the affected suture—8% in metopic, 13% in sagittal, 16% in unicoronal, and 31% in bicoronal synostosis. 3 , 4 , 20 , 26 There is

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Justin S. Cetas, Morad Nasseri, Targol Saedi, Anna A. Kuang and Nathan R. Selden

D elayed intracranial hypertension may occur after cranial reconstruction for syndromic cranial synostosis but has been reported less frequently in patients with nonsyndromic cranial synostosis. 1 , 7 , 15 , 16 Delayed intracranial hypertension may result in developmental delay, visual loss, or death. 4 , 6 , 9 , 17 , 21 Persistence of the original pathological synostotic process, deficient venous drainage, and unexpected sequela of the original surgical procedure are all possible causes of delayed intracranial hypertension. 2 , 7 Regardless of origin

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Mustafa Uzan, Nejat Çiplak, S. G. Reza Dashti, Hakan Bozkus, Pamir Erdinçler and Canan Akman

the depressed bone fragments were not elevated. By obliterating the sinus lumen and disrupting normal flow, bone fragments can cause an acute or chronic increase in intracranial pressure, and patients may be readmitted to the hospital with related symptoms. 4 Here we present the case of a man who had a depressed skull fracture located over the superior sagittal sinus (SSS). Initially the case had been managed conservatively and the patient was readmitted to the hospital with symptoms and signs of benign intracranial hypertension. Treatment choices and indications

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Daniel F. Kelly, Rouzbeh K. Kordestani, Neil A. Martin, Tien Nguyen, David A. Hovda, Marvin Bergsneider, David L. McArthur and Donald P. Becker

The relationship between CBF and intracranial hypertension after head injury is equally unclear. 5, 24 Earlier investigations by Bruce, et al. , 9 and Obrist, et al. , 33 indicated that hyperemia was the principal cause of elevated intracranial pressure (ICP) in many patients with head injuries. More recent studies, however, have shown little or no relationship between CBF and intracranial hypertension. 6, 30, 35 Elevations in systemic blood pressure or cerebral perfusion pressure (CPP) have not been associated with intracranial hypertension in the majority of

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Acute intracranial hypertension and auditory brain-stem responses

Part 1: Changes in the auditory brain-stem and somatosensory evoked responses in intracranial hypertension in cats

Seigo Nagao, Peter Roccaforte and Robert A. Moody

C erebral evoked responses (somatosensory, visual, auditory, and auditory brain-stem responses) have recently been employed for monitoring severe head injury in humans. 14, 17, 26 Despite this potential for the evaluation of patients with head injury, few basic studies with detailed analysis of these responses have been carried out, especially in the condition of intracranial hypertension and head injury. 4, 18, 27, 29 Since every component of the evoked responses is considered to relate to topographically specific neural structures, it is possible that the

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Mónica Rivero-Garvía, F. Javier Márquez-Rivas, Antonia García-Iglesias and Raquel Gutiérrez-González

hearing loss. Signs of intracranial hypertension may be the result of jugular foramen stenosis together with hyperostosis of the cranial vault and compression of the superior sagittal sinus. 2–6 We present 2 rare cases of intracranial hypertension of multifactorial origin treated using different therapies. Summary of Cases In this paper we present 2 patients with CMD who were treated at the Department of Pediatric Neurosurgery of Virgen del Rocío Hospital in Seville, Spain. Both patients showed distinctive craniofacial features of CMD: wide nasal bridge