86 years Male (DOB:1/27/1930)Reason: hydrocephalus History: gait issuesPROVIDER/ATTENDING NAME: PETER C WARNKE PETER C WARNKE Since prior examination the patient has undergone right frontal burr hole placement. Since prior examination a septation hasn't developed along the anterior aspect of the third ventricle posterior to the infundibular recess and anterior to the foramen of Monro.Since prior exam the patient is developed some dural thickening adjacent to the right frontal bone. Since the prior exam the patient is developed the small extra-axial 5 mm focus of T2, T1 and FLAIR signal hyperintensity behind and adjacent to the right occipital lobe measuring about 4 mm in diameter.There is an 8 x 6 mm sagittal dimension nonenhancing lesion just above the tectal plate associated with some depression of the tectal plate and narrowing of the aqueduct. This could be a source of obstructive hydrocephalus. It abuts the junction of the vein of Galen and internal cerebral veins on one side and the tectal plate on the other side is associated with punctate foci of signal loss and has heterogeneous signal on T2 imaging. The adjacent portion of the aqueduct is nearly obliterated.There is a couple punctate foci of signal hyperintensity on diffusion-weighted imaging which are not associated with diffusion restriction. These are located in the left occipital lobe and in the left middle frontal gyrus subcortical white matter. These could not be identified on the prior MRI.There is redemonstration of ventriculomegaly. Biventricular diameter is 50 mm on the current exam and was 50 mm on the prior exam. The third ventricle width is 11 mm on the current exam and 11 mm on the prior exam.There are subdural effusions present bilaterally which were also present on the prior exam. These are also stable.There is a mild degree of periventricular and subcortical punctate hyperintense white matter lesions present identified on the FLAIR and T2 images. Punctate focus of T2 and FLAIR signal hyperintensity is present in the right basal ganglia. Several punctate foci of signal hyperintensity are present in the pons.Normal vascular flow voids are present in the distal carotid and vertebral arteries, the basilar artery and the proximal anterior, middle and posterior cerebral arteries as well as the internal cerebral veins and superior sagittal sinus.The visualized portions of the paranasal sinuses are clear. The visualized portions of the mastoid air cells are clear. The visualized portions of the orbits are intact. The eyeball lenses are thin.
1.Since the prior exam the patient is undergone right sided burr hole placement for stereotactic third ventriculostomy. There are now some septations present within the third ventricle. The size of the lateral ventricles and third ventricles remain unchanged.2.The prior exam the patient is developed a couple new extra-axial collections adjacent to the right frontal lobe and right occipital lobe. These are relatively small in size. One possibility is that there postoperative nature they do not have any significant mass effect.3.A couple new punctate foci of diffusion abnormality are present which do not appear to represent diffusion restriction. These could represent new vascular events which no longer have diffusion restriction.4.There is redemonstration and no change of a small calcified lesion interposed between the tectal plate and the junction of the vein of Galen and internal cerebral veins. The aqueduct is narrowed immediately adjacent to this lesion. This could potentially represent pineal gland but its location is rather odd. Signal characteristics indicated that they may be associated with calcifications. Its location suggesting may be a potential cause for significant narrowing of the aqueduct and explain the patient's ventriculomegaly. It is associated with near obliteration of the aqueduct at its site.5.Periventricular and subcortical white matter lesions of a mild degree and scattered lesions in the brainstem and right basal ganglia are nonspecific. At this age they are most likely vascular related. 6.Subdural effusions are stable compared to the prior exam. This could be related to atrophy.