There is strong evidence for a genetic contribution to epilepsy, but it is commonly assumed that this genetic contribution is limited to 'generalized' epilepsies, and that most forms of 'partial' epilepsy are nongenetic. In a linkage analysis of a single family containing 11 affected individuals, we obtained strong evidence for localization of a gene for partial epilepsy. This susceptibility gene maps to chromosome 10q, with a maximum two-point lod score for D10S192 of 3.99 at theta = 0.0. All affected individuals share a single haplotype for seven tightly linked contiguous markers; the maximum lod score for this haplotype is 4.83 at theta = 0.0. Key recombinants place the susceptibility locus within a 10 centimorgan interval.

Intravenous immune globulin (IVIg) is advocated as a safe treatment for immune-mediated neurologic disease. We reviewed the medical records of 88 patients who were given IVIg for a neurologic illness. Major complications in four patients (4.5%) included congestive heart failure in a patient with polymyositis, hypotension after a recent myocardial infarction, deep venous thrombosis in a bed-bound patient, and acute renal failure with diabetic nephropathy. Other adverse effects included vasomotor symptoms 26, headache 23, rash 5, leukopenia 4, fever 3, neutropenia 1, proteinuria (1.9 g/day) 1, viral syndrome 1, dyspnea 1, and pruritus 1. Fifty-two patients (59%) had some adverse effect of IVIg infusion, most commonly vasomotor symptoms, headaches, fever, or shortness of breath in 40 (45%), which improved with reduced infusion rate or symptomatic medications. Five (6%) had asymptomatic laboratory abnormalities and seven (8%) had other minor adverse effects. Adverse effects led to discontinuation of therapy in 16% and permanent termination of therapy in 10% of patients. There was no mortality or long-term morbidity. Although adverse effects were frequent, serious complications were rare except in patients with heart disease, renal insufficiency, and bed-bound state.

Eclampsia, defined as unexplained seizure in a woman with preeclampsia, is a life-threatening complication of pregnancy with unclear etiology. Magnesium sulfate (MgSO4) is the leading eclamptic seizure prophylactic, yet its mechanism of action remains unclear. Here, we hypothesized severe preeclampsia is a state of increased seizure susceptibility due to blood-brain barrier (BBB) disruption and neuroinflammation that lowers seizure threshold. Further, MgSO4 decreases seizure susceptibility by protecting the BBB and preventing neuroinflammation. To model severe preeclampsia, placental ischemia (reduced uteroplacental perfusion pressure; RUPP) was combined with a high cholesterol diet (HC) to cause maternal endothelial dysfunction. RUPP+HC rats developed symptoms associated with severe preeclampsia, including hypertension, oxidative stress, endothelial dysfunction and fetal and placental growth restriction. Seizure threshold was determined by quantifying the amount of pentylenetetrazole (PTZ; mg/kg) required to elicit seizure in RUPP+HC±MgSO4 and compared to normal pregnant controls (n = 6/group; gestational day 20). RUPP+HC rats were more sensitive to PTZ with seizure threshold being ∼65% lower vs. control (12.4±1.7 vs. 36.7±3.9 mg/kg PTZ; p<0.05) that was reversed by MgSO4 (45.7±8.7 mg/kg PTZ; p<0.05 vs. RUPP+HC). BBB permeability to sodium fluorescein, measured in-vivo (n = 5–7/group), was increased in RUPP+HC vs. control rats, with more tracer passing into the brain (15.9±1.0 vs. 12.2±0.3 counts/gram ×1000; p<0.05) and was unaffected by MgSO4 (15.6±1.0 counts/gram ×1000; p<0.05 vs. controls). In addition, RUPP+HC rats were in a state of neuroinflammation, indicated by 35±2% of microglia being active compared to 9±2% in normal pregnancy (p<0.01; n = 3–8/group). MgSO4 treatment reversed neuroinflammation, reducing microglial activation to 6±2% (p<0.01 vs. RUPP+HC). Overall, RUPP+HC rats were in a state of augmented seizure susceptibility potentially due to increased BBB permeability and neuroinflammation. MgSO4 treatment reversed this, increasing seizure threshold and decreasing neuroinflammation, without affecting BBB permeability. Thus, reducing neuroinflammation may be one mechanism by which MgSO4 prevents eclampsia during severe preeclampsia.

Objective: To determine whether low back pain (LBP) associates with altered postural stabilization and concomitant changes in cerebrocortical motor physiology. Methods: Ten participants with LBP and 10 participants without LBP performed self-initiated, voluntary arm raises. Electromyographic onset latencies of the bilateral internal oblique and erector spinae muscles were analyzed relative to that of the deltoid muscle as measures of anticipatory postural adjustments (APAs). Amplitudes of alpha event-related desynchronization (ERD) and of Bereitschaftspotentials (BP) were calculated from scalp electroencephalography as measures of cerebrocortical motor physiology. Results: The APA was first evident in the trunk muscles contralateral to the arm raise for both groups. Significant alpha ERD was evident bilaterally at the central and parietal electrodes for participants with LBP but only at the electrodes contralateral and midline to the arm raise for those without LBP. The BP amplitudes negatively correlated with APA onset latencies for participants with (but not for those without) LBP. Conclusions: Cerebrocortical activity becomes altered prior to arm movements requiring APAs for individuals with chronic LBP. Significance: These results support a theoretical model that altered central motor neurophysiology associates with LBP, thereby implying that rehabilitation strategies should address these neuromotor impairments.

Variability in the constituents of movement is fundamental to adaptive motor performance. A sustained decrease in the variability of anticipatory postural adjustments (APAs) occurs when performing cued arm raises following acute, experimentally induced low back pain (LBP) [Moseley and Hodges, 2006, Behavioral Neuroscience, 120, 474-476]. This observation implies these changes in variability may also be relevant to people with chronic LBP. To confirm that this reduced variability in the timing of APAs is also evident in people with chronic LBP, we examined the standard deviations of electromyographic onset latencies from the bilateral internal oblique (IO) and erector spinae muscles (relative to deltoid muscle onset) when 10 people with chronic LBP and 10 people without LBP performed 75 trials of rapid arm raises. The participants with LBP exhibited significantly less variability of their IO muscle onset latencies, confirming that the decreased variability of postural coordination that is evident following acutely induced LBP is also evident in people with chronic LBP. Thus, people with chronic LBP may be less capable of adapting their APAs to ensure postural stability during movement. Keywords low back pain; anticipatory postural adjustment; posture; variability; EMG Variability in the kinematic, kinetic, and electromyographic (EMG) components of movement is hypothesized to contribute to motor adaptation in order to preserve performance of the motor endpoint (Davids et al., 2003). Moseley and Hodges (2006) recently reported that, when performing rapid arm raises in response to cues, healthy participants decrease the variability of the ipsilateral external oblique muscle's EMG onset latency relative to that of the deltoid muscle following acute, experimentally induced low back pain (LBP). The authors noted that the activations of the external oblique muscle represent anticipatory postural adjustments (APAs), which are generated in a feed-forward capacity by the central nervous system to stabilize the body against the anticipated perturbing forces generated by limb movements (Massion, 1992). The authors also reported that the reduced variability of the external oblique muscle's onset times depended on the participants' perceived vulnerability to back pain and that the decreased variability persisted several trials after the induced pain was ceased. Based on these observations, the authors then suggested that this decrease in variability represented a change in the central neural control of the postural strategy based on the participants' perceived consequences of performing the movement. Moseley and Hodges (2006)