Cerebral Palsy

BACKGROUND: Migraine is associated with vascular risk factors and white matter abnormalities (WMA). Cerebral hypoperfusion is known to be one mechanism underlying WMA and a few studies have shown that an incomplete circle of Willis (CW) may predispose to cerebral hypoperfusion. This study assessed the relationship between the morphologic characteristics of the CW and migraine. METHODS: This case-control study was carried out in the Amiens University Hospital. Patients undergoing 3-dimensional time of flight magnetic resonance angiography of the CW from January 1 to June 30, 2006 were included (n = 124). A definitive diagnosis of migraine was established in 47 patients: 23 (48.9%) experienced migraine without aura and 24 (51.1%) migraine with aura. The remaining 77 patients with other neurologic disorders constituted the control group. The posterior CW was graded as complete when both posterior communicating arteries and the P1 segments of the posterior cerebral artery were present on visual examination and incomplete when one of these vessels was missing (interobserver agreement: K(total) = 0.746). RESULTS: Incomplete posterior CW was significantly more common in migraineurs than in the control group (49% vs 18%; P < .001). On multivariate analysis, incomplete posterior CW was the sole independent factor associated with migraine (OR: 6.5; 95% CI: 2.6-16.2; P < .001). No difference was found between migraineurs with and without aura. CONCLUSIONS: Despite some methodological limitations, our results showed that incomplete posterior CW was associated with migraine.

The mechanisms underlying white matter changes in psychiatric disease are not known. We aimed to characterise the differential protein expression in deep white matter from the dorsolateral prefrontal cortex from 35 schizophrenia, 35 bipolar disorder, and 35 control subjects, from the Stanley Array Collection. We used 2-D DIGE to profile for protein expression changes in the brain. We found 70 protein spots to be significantly differentially expressed between disease and control subjects (ANCOVA, p<0.05), 46 of which were subsequently identified by LC-MS/MS. The proteins identified included novel disease candidates as well as proteins that have previously been reported as abnormal in schizophrenia, thus reinforcing their association with the disease. Furthermore, we confirmed the direction of change for three proteins using ELISA, namely neurofilament-light, amphiphysin II, and Rab-GDP-alpha, in a subset of the Stanley Array Collection. In addition, altered expression of neurofilament-light, amphiphysin II, and Rab-GDP-alpha was not observed in the cortex of mice chronically treated with haloperidol, making it less likely that these alterations are a consequence of neuroleptic medication. The data presented here strongly suggest disruption of the cytoskeleton and its associated signal transduction proteins in schizophrenia, and to a lesser extent in bipolar disorder.

We aimed to assess whether allelic variants of dopamine receptor, glutamate receptor, and serotonin transporter genes are associated with the appearance of impulse control and related behaviors (ICRB) in Parkinson’s disease (PD) with dopamine replacement therapy (DRT). We surveyed ICRB in consecutive Korean patients with PD who were treated with stable DRT using modified Minnesota Impulsive Disorders Interview over a period of 4 months. In the 404 patients who completed the interview and the 559 Korean healthy normal controls, genotyping was performed for variants of the DRD3 p.S9G, DRD2 Taq1A, GRIN2B c.366C>G, c.2664C>T and c.-200T>G, and the promoter region of the serotonin transporter gene (5-HTTLPR). Behavioral abnormalities suggestive of ICRB including compulsive buying, gambling, sexual behavior and eating, and punding, were present in 14.4% of the patients. Variants of DRD2 and 5-HTTLPR were not associated with the risk of developing ICRB. However, the AA genotype of DRD3 p.S9G and the CC genotype of GRIN2B c.366C>G were more frequent in patients with ICRB than in nonaffected patients (odds ratio [OR] = 2.21, P = 0.0094; and 2.14, P = 0.0087, after adjusting for age and sex). After controlling for clinical variables in the multivariate analysis, carriage of either AA genotype of DRD3 or CC genotype of GRIN2B was identified as an independent risk factor for ICRB (adjusted OR: 2.57, P = 0.0087). Variants of DRD3 p.S9G and GRIN2B c.366C>G may be associated with the appearance of ICRB in PD. (c) 2009 Movement Disorder Society.