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Idiopathic intracranial hypertension in children
S Youroukos1, F Psychou, S Fryssiras
1First Department of Pediatrics, Athens University, Greece. sotel@hol.gr
Insights
Idiopathic intracranial hypertension in children often has identifiable causes like middle-ear infections or obesity. Prompt treatment with acetazolamide and corticosteroids can resolve this condition, but visual impairment is a risk.
Area of Science:
- Pediatric Neurology
- Ophthalmology
Background:
- Idiopathic intracranial hypertension (IIH) is a neurological condition affecting children, characterized by increased pressure within the skull.
- Diagnosis can be challenging due to a wide spectrum of clinical presentations.
Purpose of the Study:
- To investigate the causes, clinical features, and outcomes of IIH in pediatric patients.
- To evaluate the effectiveness of different treatment modalities for IIH in children.
Main Methods:
- Prospective study of 36 pediatric patients (3.5 months to 14 years) with IIH.
- Etiological investigation, clinical assessment including fundoscopy, and cerebrospinal fluid pressure measurement.
- Analysis of treatment responses to acetazolamide and corticosteroids.
Main Results:
- Etiology identified in 77.7% of cases, with middle-ear infection and obesity being common predisposing factors.
- Classic symptoms (headache, papilledema, elevated CSF pressure) present in 26 patients; variations observed in others.
- Effective resolution achieved with acetazolamide (8/17) and corticosteroids with acetazolamide (22/24).
- Permanent visual impairment occurred in 2 of 10 patients with initial visual deficits.
Conclusions:
- IIH in children has diverse etiologies and clinical presentations, necessitating thorough investigation.
- Combination therapy with acetazolamide and corticosteroids is highly effective.
- Visual function loss is the primary serious complication, emphasizing the need for timely diagnosis and treatment.
Abstract:
We studied prospectively the etiology, clinical presentation, and outcome of idiopathic intracranial hypertension in 36 patients (20 boys and 16 girls) aged 3.5 months to 14 years. The etiology was identified in 28 (77.7%) patients. The most common predisposing factor was middle-ear infection, followed by obesity. Of the 36 cases seen, 26 presented with the classic picture of headaches, papilledema, and elevated cerebrospinal fluid pressure; 8 children had intracranial hypertension in the absence of papilledema and 2 had fundoscopic evidence of papilledema with normal cerebrospinal fluid pressure initially. In four children resolution of intracranial hypertension occurred with removal of the causative agent or appropriate treatment of the underlying condition. In 8 of 17 patients intracranial hypertension resolved with acetazolamide therapy and in 22 of 24 patients it resolved with corticosteroids in combination with acetazolamide. Subnormal visual acuity, narrowing of visual fields, or both were present on the initial examination in 10 patients; 2 of them, who presented with loss of vision, have permanent visual impairment. Four additional patients presented a transient, mild impairment of visual acuity during treatment. Our study confirms the wide clinical spectrum and the difficulties encountered in diagnosis of idiopathic intracranial hypertension. A wide variety of etiologic associations should be investigated to provide definitive therapy. Loss of visual function is the only serious complication.