Abstract

Intracranial hypertension (IH) is a neurological disease characterized by increased intracranial pressure. Idiopathic intracranial hypertension (IIH) is characterized by increased intracranial pressure without an underlying neuroradiological cause (1-3). The IH associated with a reason such as a mass, hydrocephalus, or drug use, is referred to as secondary intracranial hypertension (SIH). We aimed to detect and determine whether the increased intracranial pressure causes a change in the diffusion values of the brain in the diffusion MRI images. The study includes 24 consecutive patients diagnosed with IIH and 18 consecutive patients diagnosed with secondary intracranial hypertension (SIH). The control group included 24 patients. Measurement of apparent diffusion coefficient (ADC) was performed using DWI sections obtained from subcortical white matter and the cortex of the frontal lobe in the basal ganglia plane, caudate nucleus head, thalamus, the posterior leg of the internal capsule, corpus callosum splenium; in the centrum semiovale plane, from the central white matter region. with 1.5T MRI using b=500s/mm2 and b=1000s/mm2 values both in patients and control groups. Mean ADC values were compared between IIH, SIH patients and control groups. The ADC values from the head of the caudate nucleus and the cortex were significantly higher in the IIH group compared to the control group. When the ADC values of the SIH and control groups were compared, it was found that some of the ADC measurements (subcortical white matter, cortex and semioval center) were significantly different. The comparison of the IIH and the SIH groups revealed that the ADC measurements of central white matter in the centrum semiovale, the subcortical white matter and the posterior leg of the internal capsule were significantly different. We have found increased diffusion of IIH and SIH patients, which supports the development of brain edema. Even though the mechanism of the brain edema in IIH is not entirely clear, it is thought that the mechanism is different from the brain edema caused by a mass or a sinus thrombosis.

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