Idiopathic intracranial hypertension

Kleinschmidt, Julia J.; Digre, Kathleen B.; Hanover, Rita

doi:10.1212/wnl.54.2.319

Cited by 109 publications

(76 citation statements)

References 16 publications

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“…Two previous studies have shown IIH to be associated with poorer scores on SF-36 when compared with healthy controls [19,20]. With the possible exceptions of the subscales Pain and Change in Health, the values in this study appeared similar to normal scores from population studies.…”

Section: Protocol Compliancesupporting

confidence: 78%

A randomised controlled trial of treatment for idiopathic intracranial hypertension

et al. 2010

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The cause of idiopathic intracranial hypertension (IIH) remains unknown, and no consensus exists on how patients should be monitored and treated. Acetazolamide is a common treatment but has never been examined in a randomised controlled trial. The objectives of this pilot trial are to prospectively evaluate the use of acetazolamide, to explore various outcome measures and to inform the design of a definitive trial in IIH. Fifty patients were recruited from six centres over 23 months and randomised to receive acetazolamide (n = 25) or no acetazolamide (n = 25). Symptoms, body weight, visual function and health-related quality-of-life measures were recorded over a 12-month period. Recruited patients had typical features of mild IIH and most showed improvement, with 44% judged to have IIH in remission at the end of the trial. Difficulties with recruitment were highlighted as well as poor compliance with acetazolamide therapy (12 patients). A composite measure of IIH status was tested, and the strongest concordance with final disease status was seen with perimetry (Somers' D = 0.66) and optic disc appearance (D = 0.59). Based on the study data, a sample size of 320 would be required to demonstrate a 20% treatment effect in a substantive trial. Clinical trials in IIH require pragmatic design to involve sufficiently large numbers of patients. Future studies should incorporate weighted composite scores to reflect the relative importance of common outcome measures in IIH.

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Section: Protocol Compliancesupporting

confidence: 78%

A randomised controlled trial of treatment for idiopathic intracranial hypertension

et al. 2010

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“…43 Patients with PTC also appear to have depression and anxiety to a greater extent than weight-matched controls and healthy controls. 44 Health-related quality-of-life scores are also affected in PTC, with patients reporting significantly lower general health than controls and patients with other neuro-ophthalmologic conditions. 31 Restoration of visual acuity and resolution of papilledema constitute the primary goals of management in PTC and the benchmark of relative success of a treatment technique.…”

mentioning

confidence: 99%

Pseudotumor Cerebri: Brief Review of Clinical Syndrome and Imaging Findings

Degnan

Levy

2011

AJNR Am J Neuroradiol

239

179

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SUMMARY: PTC is a clinical entity of uncertain etiology characterized by intracranial hypertension. The syndrome classically manifests with headaches and visual changes in women with obesity. Traditionally, imaging ruled out secondary causes of elevated CSF pressure but now may reveal findings frequently seen in patients with PTC, including the following: flattening of the globe, an empty sella, an enlarged ONS, protrusion and enhancement of the optic nerve head, and increased tortuosity of the optic nerve. Novel imaging methods, including MR venography, have additionally identified sinovenous stenosis as a potential indicator of PTC.ABBREVIATIONS: BMI ϭ body-mass index; CN ϭ cranial nerve; HIV ϭ human immunodeficiency virus; ICP ϭ intracranial pressure; IIH ϭ idiopathic intracranial hypertension; ISF ϭ interstitial fluid; MRI ϭ MR imaging; ONS ϭ optic nerve sheath; ONSF ϭ optic nerve sheath fenestration; IOP ϭ intraocular pressure; PCOS ϭ polycystic ovary syndrome; PTC ϭ pseudotumor cerebri syndrome

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“…Interestingly, patients with idiopathic intracranial hypertension, a neurological disorder characterized by nontraumatic elevations in ICP, exhibited higher rates of developing depression and anxiety, as compared to matched control patients (Kleinschmidt, Digre, & Hanover, 2000). These clinical findings suggested post-traumatic elevations in ICP could directly induce psychiatric co-morbidities.…”

Section: Discussionmentioning

confidence: 96%

Therapeutic Targeting of P2X7 after TBI

Kimbler¹

2012

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Public reporting burden for this collection of information is estimated to average 1 hour per response, including the time for reviewing instructions, searching existing data sources, gathering and maintaining the data needed, and completing and reviewing this collection of information. Send comments regarding this burden estimate or any other aspect of this collection of information, including suggestions for reducing this burden to Department of Defense, Washington Headquarters Services, Directorate for Information Operations and Reports (0704-0188), 1215 Jefferson Davis Highway, Suite 1204, Arlington, VA 22202-4302. Respondents should be aware that notwithstanding any other provision of law, no person shall be subject to any penalty for failing to comply with a collection of information if it does not display a currently valid OMB control number. PLEASE DO NOT RETURN YOUR FORM TO THE ABOVE ADDRESS. REPORT DATE (DD-MM-YYYY) SPONSOR/MONITOR'S REPORT NUMBER(S)N10-P10 DISTRIBUTION / AVAILABILITY STATEMENTApproved for public release; distribution unlimited SUPPLEMENTARY NOTESN/A ABSTRACTTraumatic brain injury (TBI) is a leading cause of death and disability worldwide. Cerebral edema, the abnormal accumulation of fluid within the brain parenchyma, contributes to elevated intracranial pressure (ICP) and is a common life-threatening neurological complication following TBI. Unfortunately, neurosurgical approaches to alleviate increased ICP remain controversial and medical therapies are lacking due in part to the absence of viable drug targets. In the present study, genetic inhibition (P2X7-/-mice) of the purinergic P2x7 receptor attenuated the expression of the pro-inflammatory cytokine, interleukin-1β (IL-1β) and reduced cerebral edema following controlled cortical impact, as compared to wild-type mice. Similarly, brilliant blue G (BBG), a clinically nontoxic P2X7 inhibitor, inhibited IL-1β expression, limited edemic development, and improved neurobehavioral outcomes after TBI. The beneficial effects of BBG followed either prophylactic administration via the drinking water for one week prior to injury or via an intravenous bolus administration up to four hours after TBI, suggesting a clinically-implementable therapeutic window. Notably, P2X7 localized within astrocytic end feet and administration of BBG decreased the expression of glial fibrillary acidic protein (GFAP), a reactive astrocyte marker, and attenuated the expression of aquaporin-4 (AQP4), an astrocytic water channel that promotes cellular edema. Together, these data implicate P2X7 as a novel therapeutic target to prevent secondary neurological injury after TBI, a finding that warrants further investigation. SUBJECT TERMS AbstractTraumatic brain injury (TBI) is a leading cause of death and disability worldwide. Cerebral edema, the abnormal accumulation of fluid within the brain parenchyma, contributes to elevated intracranial pressure (ICP) and is a common life-threatening neurological complication following TBI. Unfortunately, neurosurgical approaches ...

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Idiopathic intracranial hypertension

Abstract: This study supports previous reports that link obesity and psychosocial difficulties, but obesity alone is not the explanation for the higher levels of depression and lower levels of quality of life.

Cited by 109 publications

References 16 publications

A randomised controlled trial of treatment for idiopathic intracranial hypertension

A randomised controlled trial of treatment for idiopathic intracranial hypertension

Pseudotumor Cerebri: Brief Review of Clinical Syndrome and Imaging Findings

Therapeutic Targeting of P2X7 after TBI

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