Background: Cerebral palsy (CP) is a non-progressive disorder. The global incidence of neonatal CP is 1-5 per 1000 live births where 45% of children with CP have a comorbid intellectual disability (ID). This affects the quality of life and reduces life expectancy of affected individuals. Methods and findings: With an aim to study the efficacy and safety of autologous bone marrow mononuclear cells (BMMNCs) transplantation in CP with ID, we administered a 17-year-old boy with BMMNCs along with neurorehabilitation. On follow up after 6 months, clinical improvements were recorded in speech, fine motor skills, ambulation, oromotor skills, social awareness, cognitive skills, memory and attention. Comparative Positron Emission Tomography- Computer Tomography scan of brain before and six months after cell transplantation revealed improved metabolism in the anterior cingulate cortex, left caudate head, thalamus, medial temporal cortex, cerebellum. Intelligent Quotient improved from 21 to 29. Social age according to the Vineland Social Maturity Scale was increased by 1 year. Functional Independence Measure and Gross Motor Functional Measure increased from 22 to 26 and 74.65 to 76 respectively. On Gross Motor Functional Classification System, he improved from IV to III. Conclusion: These changes suggest that BMMNCs transplantation along with neurorehabilitation was effective for this child suffering from CP with ID. Keywords Cerebral palsy; Intellectual disability; Autologous bone marrow mononuclear cells; Cell transplantation; Positron emission tomography-computer tomography

Background: Psychiatric side effects of mefloquine, an antimalarial drug, are well known (agitation, depression and suicidal ideation, psychosis with paranoia and hallucinations). Case Presentation: We report the case of a 30-year-old man without psychiatric antecedents, who developed acute psychosis and depression with suicidal ideation after five weeks of treatment with mefloquine. The symptomatology decreased rapidly a few days later, under antipsychotic drug (olanzapine) and benzodiazepines (lorazepam) and the treatment doses were diminished after one week. However, three weeks later, the same symptomatology reappeared and the treatment doses of both psychotropic drugs had to be increased once again. The antidepressant escitalopram was also introduced. Three months were necessary to definitively suppress the psychotropic drugs. Plasma mefloquine clearance was monitored by a validated liquid-chromatography mass-spectrometric method and confirmed the very long half-life of the drug, which is estimated at 14.5 days. Conclusions: The pathophysiological mechanisms of these psychiatric side effects probably involve a toxic limbic encephalopathy. Mefloquine is highly lipophilic and may accumulate in the limbic system. In conclusion, due to the very long half-life of mefloquine, psychiatric symptoms can persist for weeks, necessitating an appropriate psychotropic treatment. Chronic symptoms resulting from permanent neurotoxicity may also occur.

Altered mental status is a frequent reason for consult for neurology and psychiatry services. Multiple causes can be considered including: Wernicke’s, hepatic encephalopathy, metronidazole-induced encephalopathy, and acute demyelination. We present the case of a 49-year-old Hispanic female with end stage liver disease admitted for altered mental status. Neurology and Psychiatry were consulted.

Objectives:There is growing evidence of both hypothalamic-pituitary-adrenal (HPA) axis and immune system dysfunction in schizophrenia. Additionally, accumulating evidence has linked dysfunction in the kynurenine pathway to schizophrenia as well as to stress and inflammation. The current pilot tested changes in immune, cortisol and kynurenine and kynurenic acid responses to a psychosocial stressor in people with schizophrenia and healthy controls.Methods:Ten people with schizophrenia/schizoaffective disorder and 10 healthy controls were included. Participants completed the Trier Social Stress Test (TSST) and cortisol, cytokines (IL-6 & TNF-α), kynurenine and kynurenic acid were measured in the plasma at baseline 15, 30, 60 and 90 minutes following the TSST.Results:Compared to baseline, at 30 minutes post TSST, mean cortisol levels had increased by 7.6 ng/ml (11%) in healthy controls but decreased by 16.3 ng/ml (25%) in schizophrenia (F=4.34, df=3,38.2, p=0.010). While people with schizophrenia had a lower TNF-α level at baseline (χ2(1)=10.14, p=0.001), no decreases or increases occurred after the TSST in either group. Both groups had a similar increase in IL-6 at 15 minutes post TSST (F=4.17, df=3, 16.3, p=0.023) demonstrating an immune response to the stress in both groups. A trend towards increased kynurenine from baseline was found immediately after the TSST followed by a decrease at 60 minutes in healthy controls but no change was found in people with schizophrenia (F=2.46, df=3, 49.1, p=0.074).Conclusion:People with schizophrenia showed a decrease in cortisol from baseline following the TSST as compared to an elevation from baseline seen in healthy controls, supporting HPA axis dysfunction in schizophrenia. An immediate inflammatory response with IL-6 was seen in both groups following the TSST. Larger studies should examine psychosocial stress response in schizophrenia and the relationship of immune function and kynurenine pathway.

The behavioral variant of Frontotemporal dementia (bvFTD) is an insidious neurodegenerative disease associated with progressive degeneration of the frontal lobes, anterior temporal lobes, or both [1]. Alterations in social cognition represent the core symptoms of bvFTD resulting in emotional disengagement and socially inappropriate responses or activities [2,3]. As is apparent in revised consortium criteria, additional neuropsychiatric symptoms including apathy and stereotypical and impulsive behavior are prominent in the clinical presentation [4]. Consequently, both neurodegenerative diseases and primary psychiatric disorders are crucial in the challenging differential diagnosis. The differentiation between bvFTD and Alzheimer’s disease (AD) has become easier by the use of biomarkers that are able to identify underlying AD pathology, such as the amyloid-β (Aβ) and tau [1,5]. However, to distinguish bvFTD from psychiatric disorders can still be difficult, particularly since biomarkers for bvFTD are less robust [6]. Previous studies indicated that as a result of symptomatic overlap between bvFTD and psychiatric disorders, bvFTD patients are clinically often mistaken for psychiatric patients and vice versa [7-10]. The current clinical criteria for bvFTD require that “if behavioral disturbance is better accounted for by a psychiatric diagnosis, a diagnosis of bvFTD has to be excluded” [4]. Despite clinical overlap, bvFTD patients do not often fulfill formal criteria for a psychiatric diagnosis, suggesting that it is valuable to apply formal criteria for psychiatric disorders [11]. Careful clinical phenotyping of overlapping symptoms can help to distinguish bvFTD from psychiatric disorders in clinical practice (Figure 1) [12,13]. Figure 1 Overlap and differentiation between bvFTD and psychiatric disorders in clinical practice. The value of different symptom rating scales and clinical tools has been proven useful in clinical practice in case of suspected bvFTD when a psychiatric disorder is also probable (Figure 2) [11,14,15]. Figure 2 Clinical hallmarks and supportive measuring instruments in the differential diagnosis bvFTD and psychiatric disorders. According to current criteria, the diagnostic certainty of bvFTD increases when Frontotemporal abnormalities are found on neuroimaging. In a large cohort of patients with late-onset behavioral changes, MRI had a sensitivity of 70% and a specificity of 93% for a bvFTD diagnosis [4]. The additional [18F]FDG-PET, when the MRI was inconclusive, had a sensitivity of 90% at the cost of a lower specificity (68%) [16]. [18F]FDG-PET is mainly useful when Frontotemporal hypo-metabolism is absent to exclude bvFTD diagnosis. The interpretation of neuroimaging results should especially be taken with caution in cases with a psychiatric differential diagnosis where [18F]FDG-PET is the only abnormal investigation and in cases with a genetic background where both MRI and [18F]FDG-PET can show a specific abnormalities [16-18]. Genetic screening especially for C9orf72 repeat expansion is emphasized [19,20]. particularly in cases with a remarkable (prolonged) disease course. In clinical practice, bvFTD has a broad differential diagnosis including both neurodegenerative diseases and primary psychiatric disorders. The current criteria for bvFTD have clearly improved diagnostics but differentiating bvFTD from psychiatric disorders remains difficult. The challenge for the next decade is finding specific biomarkers for bvFTD on the one hand, and optimizing the neuropsychiatric diagnosis of bvFTD on the other hand. To this end, patient care for suspected bvFTD patients would be largely improved in a setting where neurologists and psychiatrists work hand in hand, ideally applying a consensus set of clinical rating scales next to their clinical expertise.

Objectives: To evaluate the frequency and the type of cognitive impairment (CI) in patients with temporal lobe epilepsy and to determine eventual risk factors for its occurrence. Methods: We have conducted across-sectional study in TLE patients and healthy controls (HC). All of them underwent neuropsychological assessment by using a large battery of tests to detect CI. EEG and Cerebral MRI were performed for all patients. Results: Thirty-two TLE patients and thirty matched HC were enrolled. The mean age of our patients was 35 ± 8.3 yrs. The rate duration of evolution epilepsy until the appearance of CI was 14 ± 10 yrs. In our study, comparative neuropsychological assessment between TLE patients and controls demonstrates that epileptic patients have an impairment of many cognitive processes. The most common CI are: alteration of reaction and processing speed (100% of cases), attention deficit (93.6% of cases), deterioration in verbal episodic memory (87.5% of cases) and visual episodic memory (78.1% of cases). Verbal fluency and working memory are impaired in respectively 3/4 and about half (53.1%) of our patients. At the opposite, executive and visual-spatial functions are rarely affected. Neuropsychological scores worsen with advanced age, long duration of epilepsy, high seizure frequency, clonazepam intake and presence of temporal lesion at cerebral MRI. However, high level of education seems to be protective. TLE patients with lesion evolving the temporal lobe of the dominant hemisphere have had lower scores, especially in tests for verbal memory. At the opposite, when the other side is affected, only the episodic visual memory is impaired. Conclusion: CI is frequent in TLE and alters the quality of patient’s life. We emphasize the importance of periodical neuropsychological assessment to detect early CI and undertake the adequate measures to prevent patient to get worse.