Róbert Debreczeni

Corticobasal Syndrome Due to Superficial Siderosis Caused by Thalamic Cavernoma

A 56-year-old right-handed woman with a history of hypertensionwas admitted to our department for consultation because of slowly worsening forgetfulness and word-finding problems started 1 year before her examination. She had a 2-year long history of severe headache episodes lasting approximately 2–3 weeks and occurring roughly three times in 1 year. During her previous consultations, she was diagnosed with migraine. Repeated brain CT scans showed progressive dilatation of the ventricular system without periventricular hypodensity (not shown). Repeated lumbar CSF puncture tests were performed without improvement of the symptoms; results on CSF tests were reported to be normal. During her first examination in our department, alexia, apraxia, agrammatism of the speech with mild anomia, executive dysfunction (decreased category-specific verbal fluency and concretization), hypokinesis with mild right upper limb rigidity, and postural instability and wide-based gait with decreased right upper limb synkinesis were seen. The MiniMental State Examination (MMSE) score was 26/30 points, the Addenbrooke’s Cognitive Examination (ACE) score was 79/100 points, and the Rey-Osterrieth Complex Figure Test score was 36/36 points in the copying exercise test and 19.5/36 in the evocative test. The Syndrom-Kurztest (SKT) results were over the average: immediate evocation was 11/12 points, whereas delayed evocation was 10/12 points. No response for levodopa substitution (200 mg t.i.d.) was seen. On the basis of the symptoms and no response to levodopa, our patient’s condition was clinically diagnosed as CBS fulfilling even its most recent criteria. To define the pattern of the atrophy and to rule out CSF circulation problems, MR imaging was indicated. A cavernoma under the ventricular wall in the right thalamus with signal changes suggestive of SS was found (Figure 1 [A–C]). The cavernoma was removed by way of a contralateral precentral parasagittal craniotomy after the third ventricle was opened through the corpus callosum without bleeding or any other surgical complication. Results on neuropathological examination showed aberrant vascular structureswith hemosiderin deposition and gliosis (Figure 1 [D and E]). Complete removal of the cavernoma was seen on the postoperative MR imaging scans with a small subependymal ischemic lesion around the cavernoma bed in the right thalamus (Figure 1 [F and G]). Slight improvement of the patient’s neuropsychological symptoms was seen 2 weeks after the surgery. She scored 28/30 points on theMMSE and 83/100 points on the ACE. In SKT, immediate evocation was 10/12 points, whereas delayed evocation was 8/12 points. These results did not change at 14 and 24 months after the surgery.

P31.13 Correlation between EEG central frequency (CF), flow and hemodynamic parameters during cognitive efforts

Background: Decreased power in delta-theta bands of EEG/MEG has been associated to depression, drug and alcohol abuse, and other psychiatric conditions. In a previous work, we found decreased slow activity in alcoholic patients, associated to cortical atrophy and chronicity of alcohol consumption. However, we failed in reveal a significant association of this QEEG feature with depression, in spite of previous MEG data who pointed to a focal decrease of delta power in frontobasal areas. Objective: To assess differences in intracranial distribution of decreased surface QEEG delta power between depressed and non-depressed alcoholic patients in order to find any symptom-related topographic feature of physiopathological relevance. Methods: Low-Resolution Electric Tomography (LORETA) for the delta (1–3 Hz) band of EEG spectra was estimated from 25 normal control subjects and 28 alcoholic patients, 15 with and 13 without clinical depression according to Beck depression inventory (BDI), whose QEEG showed diffusely decreased delta power. Statistical non-parametric mapping was used to compare depressed and non-depressed groups. Measures of intracranial current source density in individual patients at areas of significant differences were correlated with BDI scores. Results: Depressed alcoholics had significantly less delta activity than non-depressed alcoholics at left temporal pole, left midtemporal cortex and frontobasal areas. Intracranial current source density at anterior cingulate, left orbitofrontal cortex and left parahippocampal cortex was negatively correlated with BDI score, but no correlation was found at right parahippocampal cortex. Conclusion: LORETA localized discrete areas of diffusely decreased delta activity in alcoholics, with a differential distribution linked to the presence of clinical depression, that seems to reveal a dysfunctional neuronal state at several specific limbic and other cortical locations that have been related to a specific clini.