OBJECTIVE AND IMPORTANCE: Focal or diffuse corpus callosal changes can occur in patients with active hydrocephalus who undergo shunting procedures. The neural compression caused by active hydrocephalus and the conditions that follow ventricular shunting may contribute to the development of these changes. CLINICAL PRESENTATION: Two patients who underwent successful shunting for hydrocephalus subsequently developed thickening and diffuse signal changes in the corpus callosum, which were revealed by magnetic resonance imaging. The abnormal signal intensity extended laterally and linearly along the callosal fiber tracts and was not associated with mass effect. These changes persisted despite clinical improvement after the shunts were implanted. INTERVENTION: Detailed neuropsychological testing showed no evidence of residual cognitive impairment or any interruption of the interhemispheric transfer of information. It has been proposed that the impingement of the corpus callosum by the rigid falx may contribute to symptomatic hydrocephalus. Impingement may cause partial hemispheric disconnection, resulting from callosal axonal dysfunction. Our patients showed radiographic evidence of dramatic changes within the corpus callosum after ventricular shunting, consistent with a transcallosal demyelinating process. Patients demonstrated neither clinical nor neuropsychological evidence of callosal disconnection, even though the callosal changes persisted. In these two patients, it is reasonable to assume that the relative sparing of the splenium accounts for the lack of neuropsychological deficits. CONCLUSION: Based on our findings, conservative management, rather than a stereotactic biopsy or other forms of intervention, seems reasonable when these characteristic changes of the callosum are noted by magnetic resonance imaging after a shunt for hydrocephalus has been implanted in the patient.
OBJECTIVE AND IMPORTANCE: Focal or diffuse corpus callosal changes can occur in patients with active hydrocephalus who undergo shunting procedures. The neural compression caused by active hydrocephalus and the conditions that follow ventricular shunting may contribute to the development of these changes. CLINICAL PRESENTATION: Two patients who underwent successful shunting for hydrocephalus subsequently developed thickening and diffuse signal changes in the corpus callosum, which were revealed by magnetic resonance imaging. The abnormal signal intensity extended laterally and linearly along the callosal fiber tracts and was not associated with mass effect. These changes persisted despite clinical improvement after the shunts were implanted. INTERVENTION: Detailed neuropsychological testing showed no evidence of residual cognitive impairment or any interruption of the interhemispheric transfer of information. It has been proposed that the impingement of the corpus callosum by the rigid falx may contribute to symptomatic hydrocephalus. Impingement may cause partial hemispheric disconnection, resulting from callosal axonal dysfunction. Our patients showed radiographic evidence of dramatic changes within the corpus callosum after ventricular shunting, consistent with a transcallosal demyelinating process. Patients demonstrated neither clinical nor neuropsychological evidence of callosal disconnection, even though the callosal changes persisted. In these two patients, it is reasonable to assume that the relative sparing of the splenium accounts for the lack of neuropsychological deficits. CONCLUSION: Based on our findings, conservative management, rather than a stereotactic biopsy or other forms of intervention, seems reasonable when these characteristic changes of the callosum are noted by magnetic resonance imaging after a shunt for hydrocephalus has been implanted in the patient.