Neurologists use a variety of tests to detect subtle upper motor neuron lesion causing a mild motor impairment of the upper limb. The forearm and index finger rolling tests are some of these. Their sensitivity varies, but in general these tests appear to be more likely to be abnormal in mild motor impairment of the arm and hand due to a cortico-spinal tract lesion than tests of power, muscle tone or reflexes. Thumb rolling involves more distal limb segments than forearm rolling and distal limb segments are typically more affected than proximal limb segments after cerebral lesions to the cortico-spinal tract.

Thumb rolling was tested, in comparison to pronator drift, forearm rolling and index finger rolling, for its sensitivity to detect a cerebral lesion of the cortico-spinal tract in 17 consecutive patients with mild pure motor stroke affecting only one arm and hand.

Thumb rolling is more sensitive (88%) than pronator drift (47%), forearm rolling (65%) and index finger rolling (65%) to detect a cerebral lesion of the cortico-spinal tract in mild pure motor stroke of the upper limb.

The thumb rolling test may be a valuable adjunct clinical test to detect a subtle lesion of the cortico-spinal tract causing mild pure motor stroke of the arm and hand when the remainder of routine neurological examination is unremarkable.

Epileptic seizures may be misdiagnosed if they manifest as psychiatric symptoms or seizures occur in patients with known psychiatric illness.

We present clinical profiles of six patients with epilepsy (three male, mean age 39 ± 12 years) that presented with prominent psychiatric symptoms.

Two patients had pre-existing psychiatric illnesses. Three patients were initially diagnosed with panic attacks, two with psychosis, and one with schizophrenia. Five patients had temporal lobe epilepsy (TLE) while the sixth patient was subsequently found to have absence status epilepticus (SE). Cranial computed tomogram (CT) including contrast study was unremarkable in five patients and showed post-traumatic changes in one patient. Cranial magnetic resonance imaging (MRI) revealed dysembryoplastic neuroepithelial tumour (DNET) in one patient, cavernous hemangioma in one, and post-traumatic changes plus bilateral mesial temporal sclerosis in another patient but it was normal in two TLE patients. Routine electroencephalography (EEG) revealed absence SE in one patient but it was non-diagnostic in the TLE patients. Video-EEG telemetry in the epilepsy monitoring unit (EMU) was necessary to establish the diagnosis in four TLE patients. None of the patients responded to medications aimed at treating psychiatric symptoms alone. Two patients required surgery while the other four required treatment with anti-epileptic drugs. All the patients had favorable response to the treatment of their epilepsy.

This case series illustrates that epileptic patients may experience non-convulsive seizures that might be mistaken as primary psychiatric illnesses. In this subset of patients, evaluation by an epileptologist, MRI of the brain, and/or video-EEG telemetry in an EMU was necessary to confirm the diagnosis of epilepsy if routine EEGs and cranial CT are normal.

Axon growth is crucial for injured neural tissue to recover; however it is difficult to achieve in general. Axon outgrowth is inhibited by the activation of the Nogo receptor (NgR) by one of three different ligands. The present study aimed to suppress the inhibitory effect of the three inhibitory proteins to facilitate axon outgrowth.

A lentiviral vector, siNgR199 (that has the capacity to interfere with the gene of NgR expression), was constructed for suppressing the gene transcription of NgR. Rat cortex neurons and oligodendrocytes were prepared to observe the effect of siNgR199 on facilitating axon outgrowth.

After transfection, the lentiviral siRNA of NgR remained in target neurons for almost two weeks whereas the conventional siRNA of NgR remained in neurons less than five days. Lentivirus-mediated delivery of exogenous small interfering RNA (siNgR199) targeting NgR significantly reduced the expression of this receptor and promoted axon outgrowth. In contrast, provision of naked siRNA targeting NgR (NgRsiRNA) showed less inhibitory effect on NgR protein expression and did not affect axon outgrowth.

Lentiviral siRNA of NgR effectively suppresses the expression of NgR in cultured neurons that facilitates the axon outgrowth. The data implicate that lentiviral siRNA of NgR has therapeutic potential in facilitating the recovery of injured neural tissue.

Some reports demonstrated vascular alterations in brain magnetic resonance imaging (MRI) in migraineurs and a relationship between circle of Willis (Circle) variants and lacunar brain infarcts. We examined anomalies of the whole circle of Willis and their relationship with vascular brain lesions in migraineurs, to identify any possible vascular mechanism in migraine.

We studied, with a cohort controlled study, the circle of Willis in migraineurs seen consecutively in our Headache Center, and in non-headache controls, using angio-MRI of the brain. Statistical analysis used ANOVA, Scheffè's criterion, t-student test.

We recruited 270 migraineurs (204 without aura (MWOA), 66 with aura (MWA) and 159 controls. Migraineurs presented an anatomical variant in 108 (40%) cases with 34 controls (21.4%) presenting a variant. We found a significant association between MWOA and variants (OR=2.4 CI95% [1.5 to 3.9]) and between MWA and variants (OR=3.2 CI95% [1.6 to 4.1]). Unilateral posterior variants with basilar hypoplasia are statistically associated only with MWA compared to controls (OR=9.2, CI95% [2.3 to 37.2]). Thirty-three percent of MWOA and 24% of MWA sufferers present some kind of brain lesion, included 2% of infra-tentorial lesions. We did not find any statistical association between the presence of Circle variants and ischemic lesions on MRI (OR=1.5 CI95% [0.68; 1.94]), or with infratentorial lacunar lesions (OR=1.58 CI95% [0.48 to 5.24]).

Anatomical variants of the Circle of Willis are significantly more frequent in migraineurs; posterior anomalies are more frequent in MWA, suggesting a vascular mechanism provoking changes in cerebral blood flow, thereby stimulating cortical spreading depression.

An abnormal central nervous system excitability level was found in patients with migraine. Whether it is hyper- or hypo-excitable is still debated. This study aimed to compare the somatosensory high-frequency oscillations (HFOs), which reflected subcortical excitability (early phase) and intracortical inhibition (late phase), between patients with migraine and control subjects.

HFOs were recorded from C3'-Fz, using a 500-1000 Hz frequency filter after stimulation at right median nerves at the wrists, and divided into early and late phases based on the N20 peak. Fifty-nine untreated patients (n=24 during ictal period; n=35, interictal) and 22 controls finished the study.

In early HFOs, patients both during ictal and interictal periods had higher maximal amplitudes (p =0.039) and area-under-curve (p =0.029) than those of the controls. Regarding the late HFOs, there were no significant differences among these groups.

Our study suggests a hyper-excitable state in the subcortical regions in patients with migraine both during interictal and ictal periods.

To compare a specialized interprofessional team approach to community-based stroke rehabilitation with usual home care for stroke survivors using home care services.

Randomized controlled trial of 101 community-living stroke survivors (<18 months post-stroke) using home care services. Subjects were randomized to intervention (n=52) or control (n=49) groups. The intervention was a 12-month specialized, evidence-based rehabilitation strategy involving an interprofessional team. The primary outcome was change in health-related quality of life and functioning (SF-36) from baseline to 12 months. Secondary outcomes were number of strokes during the 12-month follow-up, and changes in community reintegration (RNLI), perceived social support (PRQ85-Part 2), anxiety and depressive symptoms (Kessler-10), cognitive function (SPMSQ), and costs of use of health services from baseline to 12 months.

A total of 82 subjects completed the 12-month follow-up. Compared with the usual care group, stroke survivors in the intervention group showed clinically important (although not statistically significant) greater improvements from baseline in mean SF-36 physical functioning score (5.87, 95% CI -3.98 to 15.7; p=0.24) and social functioning score (9.03, CI-7.50 to 25.6; p=0.28). The groups did not differ for any of the secondary effectiveness outcomes. There was a higher total per-person costs of use of health services in the intervention group compared to usual home care although the difference was not statistically significant (p = 0.76).

A 12-month specialized, interprofessional team is a feasible and acceptable approach to community-based stroke rehabilitation that produced greater improvements in quality of life compared to usual home care. Clinicaltrials.gov identifier: NCT00463229

The association of genetic polymorphism of mitochondrial aldehyde dehydrogenase 2 (ALDH2) and Alzheimer's disease (AD) has been controversial and has been investigated only in several small-sample studies. In the present study, we performed a meta-analysis to evaluate the cross-sectional association of ALDH2 variants and AD risk in East Asian populations.

Trials were retrieved through MEDLINE, EMBASE, J-STAGE and the China National Knowledge Internet databases (from January 1, 1994 to November 1, 2010) without any restriction on language. Data were abstracted by a standardized protocol.

We found four studies of 821AD patients and 1380 healthy controls that qualified for the analysis. The variant ALDH2 genotype GA/AA was not associated with increased AD risk (odds ratio (OR) = 1.35; 95% confidence interval (CI) = 0.75-2.42; p = 0.32), even after stratification for the status of apolipoprotein E epsilon 4 allele. However, in the subgroup analyses, the association was significant for men (OR = 1.72; 95% CI = 1.10-2.67; p = 0.02).

This study adds to the evidence that ALDH2 GA/AA genotype increases the risk of AD among East Asian men, although the effect size is moderate.