We present an update of the literature concerning long-term neuropsychological outcomes following surgery for refractory temporal lobe epilepsy (TLE). A thorough search was conducted through the PubMed and Medline electronic databases for studies investigating neuropsychological function in adult patients undergoing resective TLE surgery and followed for a mean/median > five years period. Two independent reviewers screened citations for eligibility and assessed relevant studies for the risk of bias. We found eleven studies fulfilling the above requirements. Cognitive function remained stable through long-term follow up despite immediate post-surgery decline; a negative relation between seizure control and memory impairment has emerged and a possible role of more selective surgery procedures is highlighted.

Purpose: Multiple system atrophy (MSA) is a progressive neurodegenerative disease characterized by postural instability, autonomic failure, cerebellar ataxia, and cognitive deficits. There is currently no effective cure. Transcranial direct current stimulation (tDCS), offers promise in amendment of motor, and cognitive performance in advanced Parkinson’s disease. Case description: We estimated the effect of anodal tDCS on motor and cognitive function in a 66-year-old woman with moderate MSA. For the evaluation of the motor function, we used the Unified MSA Rating Scale II, the Unified Parkinson’s Disease Rating Scale Part III (UPDRS III), and the Timed Up and Go test (TUG). The battery of neuropsychological tests included the Rey’s Auditory Verbal Learning Test (RAVLT) and the Digit Symbol Substitution Test-Wechsler Adult Intelligence (DSST-WAIS-III), the Trail Making Test (TMT-A). tDCS was applied in 10 sessions. Clinical evaluations were performed at baseline, day 11, day 30, and at day 90. Results: Anodal stimulation was associated with improvement in UPDRS III and the TUG test. A positive effect was also seen in RAVLT the DSST-WAIS-III and the TMT-A. Conclusions: Our results suggest that tDCS has a beneficial effect mainly on motor performance in MSA, which lasts beyond the duration of the treatment.

Introduction. There is an emerging interest in the literature about MOGHE (Mild Malformation of Cortical Development with Oligodendroglial Hyperplasia and Epilepsy). We report the case of an epileptic patient with MOGHE. Case Report. A 33-year-old male patient was suffering from refractory focal epilepsy since adolescence. MRI demonstrated increased T2/FLAIR signal intensity of right frontal lobe. Presurgical evaluation led to definition of epileptogenic network in a specific area of right frontal lobe. The resected specimen revealed MOGHE. Discussion. MOGHE appears to be a brain entity which shares some unique histopathological features. Review of the literature is in accordance with our patient’s findings. The major neuropathological finding consists of areas with blurred gray-white matter boundaries due to heterotopic neurons in white matter and increased numbers of subcortical oligodendroglial cells with increased proliferation. MR abnormalities are present in T2/FLAIR sequences. It concerns patients with refractory frontal lobe epilepsy and appears to associate with unfavourable postsurgical outcome in seizure control. Conclusion. More cases are needed in order to establish more data about this distinct entity in frontal lobe epilepsy. This could be valuable knowledge to patients and doctors concerning expectations or management of undesirable outcome in frontal lobe epilepsy surgery.

In this review, we explore current literature and assess evidence linking secondary (acquired) alexithymia to aberrant humor processing, in terms of their neurobiological underpinnings. In addition, we suggest a possible common neuropathological substrate between secondary alexithymia and deficits in humor appreciation, by drawing on neurophysiologic and neuroradiological evidence, as well as on a recent and unique single-case study showing the cooccurrence of secondary alexithymia and deficit in humor appreciation. In summary, what emerges from the literature is that the cortical midline structures, in particular the medial prefrontal cortex (mPFC), the anterior cingulate cortex (ACC), and the insular cortex, seem to play a crucial role in the expression of both alexithymia and defective humor processing, while though to a lesser extent, a right hemisphere and bilateral frontoparietal contribution becomes evident. Neurobiological evidence of secondary alexithymia and aberrant humor processing points to the putative role of ACC/mPFC and the insular cortex in representing crucial processing nodes whose damage may produce both the above clinical conditions. We believe that the association of secondary alexithymia and aberrant humor processing, especially humor appreciation deficit, and their correlation with specific brain regions, mainly ACG/mPFC, as emerged from the literature, may be of some heuristic importance. Increased awareness on this topic may be of aid for neurosurgeons when accessing emotion-relevant structures, as well as for neuropsychologists to intensify their efforts to plan evidence-based neurorehabilitative interventions to alleviate the deleterious effects of such interpersonal communication deficits.