Effects of electrical muscle stimulation on cerebral blood flow

Background Electrical muscle stimulation (EMS) induces involuntary muscle contraction. Several studies have suggested that EMS has the potential to be an alternative method of voluntary exercise; however, its effects on cerebral blood flow (CBF) when applied to large lower limb muscles are poorly understood. Thus, the purpose of this study was to examine the effects of EMS on CBF, focusing on whether the effects differ between the internal carotid (ICA) and vertebral (VA) arteries. Methods The participants performed the experiments under EMS and control (rest) conditions in a randomized crossover design. The ICA and VA blood flow were measured before and during EMS or control. Heart rate, blood pressure, minute ventilation, oxygen uptake, and end-tidal partial pressure of carbon dioxide (PETCO2) were monitored and measured as well. Results The ICA blood flow increased during EMS [Pre: 330 ± 69 mL min−1; EMS: 371 ± 81 mL min−1, P = 0.001, effect size (Cohen’s d) = 0.55]. In contrast, the VA blood flow did not change during EMS (Pre: 125 ± 47 mL min−1; EMS: 130 ± 45 mL min−1, P = 0.26, effect size = 0.12). In the EMS condition, there was a significant positive linear correlation between ΔPETCO2 and ΔICA blood flow (R = 0.74, P = 0.02). No relationships were observed between ΔPETCO2 and ΔVA blood flow (linear: R = − 0.17, P = 0.66; quadratic: R = 0.43, P = 0.55). Conclusions The present results indicate that EMS increased ICA blood flow but not VA blood flow, suggesting that the effects of EMS on cerebral perfusion differ between anterior and posterior cerebral circulation, primarily due to the differences in cerebrovascular response to CO2.

Efficient high-voltage protection in the electric catfish

ABSTRACTFor thousands of years, starting with detailed accounts from ancient Egypt, the African electric catfish (Malapteruridae) has been renowned for its ability to hunt and to defend itself with powerful electric shocks. Surprisingly, the degree to which electric catfish are protected against their own or external electric shocks, how specific any protection would be to the species-specific waveform and whether a discharging catfish has to actively prepare for the onset of its high-voltage discharges has never been analysed. Here, we used digital high-speed video to record catfish during their own discharges or as they were exposed to external discharges, employing goldfish to carefully calibrate the efficiency of all discharges. Electric catfish show a remarkable degree of protection against high voltages: both self-produced and external electric shocks that heavily affected control goldfish failed to evoke involuntary muscle contraction or to affect sensorimotor processing. Even a commercial electrofishing device, set to efficiently immobilise and narcotise fish, failed to have any effect on the electric catfish. Our findings rule out several protective mechanisms and demonstrate a highly efficient and versatile shielding whose nature is presently unclear.

The shocking predatory strike of the electric eel

Electric eels can incapacitate prey with an electric discharge, but the mechanism of the eel’s attack is unknown. Through a series of experiments, I show that eel high-voltage discharges can activate prey motor neurons, and hence muscles, allowing eels to remotely control their target. Eels prevent escape in free-swimming prey using high-frequency volleys to induce immobilizing whole-body muscle contraction (tetanus). Further, when prey are hidden, eels can emit periodic volleys of two or three discharges that cause massive involuntary twitch, revealing the prey’s location and eliciting the full, tetanus-inducing volley. The temporal patterns of eel electrical discharges resemble motor neuron activity that induces fast muscle contraction, suggesting that eel high-voltage volleys have been selected to most efficiently induce involuntary muscle contraction in nearby animals.

Transcriptomic and proteomic analysis of global ischemia and cardioprotection in the rabbit heart

Cardioplegia is used to partially alleviate the effects of surgically induced global ischemia injury; however, the molecular mechanisms involved in this cardioprotection remain to be elucidated. To improve the understanding of the molecular processes modulating the effects of global ischemia and the cardioprotection afforded by cardioplegia, we constructed rabbit heart cDNA libraries and isolated, sequenced, and identified a compendium of nonredundant cDNAs for use in transcriptomic and proteomic analyses. New Zealand White rabbits were used to compare the effects of global ischemia and cardioplegia compared with control (nonischemic) hearts. The effects of RNA and protein synthesis on the cardioprotection afforded by cardioplegia were investigated separately by preperfusion with either α-amanitin or cycloheximide. Our results demonstrate that cardioplegia partially ameliorates the effects of global ischemia and that the cardioprotection is modulated by RNA- and protein-dependent mechanisms. Transcriptomic and proteomic enrichment analyses indicated that global ischemia downregulated genes/proteins associated with mitochondrial function and energy production, cofactor catabolism, and the generation of precursor metabolites of energy. In contrast, cardioplegia significantly increased differentially expressed genes/proteins associated with the mitochondrion and mitochondrial function and significantly upregulated the biological processes of muscle contraction, involuntary muscle contraction, carboxylic acid and fatty acid catabolic processes, fatty acid β-oxidation, and fatty acid metabolic processes.

Obsessive-compulsive Symptoms in Primary Dystonia: Reactive and Psychogenic or Primary and Neurophysiological?

Introduction:Primary dystonia (PDy) is an idiopathic neurological disorder causing involuntary muscle contraction. Its pathophysiology is believed to involve basal-ganglia (BG) dysfunction. A possible association with Obsessive-compulsive symptoms (OCS) is regarded as further evidence of BG involvement but remains controversial due to contradictory research data. We proposed to answer three questions:1.Do PDy patients have high OCS scores?2.Are OCS in PDy reactive?3.Does botulinum toxin treatment (BT) influence PDy psycopathology?Subjects:45 patients with blepharospasm, spasmodic torticollis, writer's cramp; 43 patients with hemifacial spasm, cervical spondilarthropathy, peripheral hand neuropathy; 27 healthy volunteers.Assessment: non-structured DSM-IV based psychiatric interview; Symptom Checklist 90 Revised (SCL-90R); Yale-Brown Obsessive-Compulsive Scale (YBOCS); Unified Dystonia Rating Scale (UDRS).Results:PDy patients scored significantly higher than controls and healthy controls on the YBOCS (11.1 ± 7.24; 5.98 ± 4.33; 2.07 ± 0.92, both p< 0.001). Controls’ mean score was also significantly higher than healthy subjects’. Controls scored higher than PDy and healthy subjects on the SCL-90R somatization scale. BT treated PDy patients had significantly lower anxiety and somatization but higher UDRS and similar YBOCS ratings compared to untreated patients.Discussion:Higher ratings of OCS but not of depression, anxiety or somatization in PDy patients suggests a neurophysiological origin for OCS in PDy. However, diseased controls also scored higher than healthy subjects, suggesting that OCS may nevertheless be partly reactive in PDy. BT may decrease anxiety/depressive symptoms but not OCS, lending further strength to a possible neurophysiological aetiology for OCS in PDy.

Graphospasm - clinical presentation, etiology and the course of disease: Analysis of 30 cases

INTRODUCTION Dystonia, as prolonged, involuntary muscle contraction, causes torsion, repetitive movements and abnormal body position. In so far only a part of body is affected by dystonic movement, it is the question of focal dystonia, which is called writer's cramp if the arm is involved. OBJECTIVE The objective of the study was to present the specific clinical features of patients with task-specific dystonia, who were diagnosed, treated and followed up at the Institute of Neurology, Clinical Center of Serbia, Belgrade. MATERIAL AND METHODS In the period 1995-2003, 30 patients with task-specific dystonia were treated at the Institute of Neurology, CCS, who met the adopted criteria for diagnosis. The severity of the diseases was tested by estimating the ability of patient to write the test sentence per time unit, as well as by means of scale for measuring different disabilities, ranging from 0-16 (Marsden-Fahn). Depression, anxiety and obsessiveness were tested by Beck's scale, Hamilton's depression and anxiety scale and Mousdly's obsessiveness scale. Thorough questionnaire focused on clinical details was also used. Besides descriptive statistics, data processing included analysis of variance and Kruskal-Wallis's test. RESULTS Thirty patients with diagnosis of task-specific dystonia were analyzed. At the onset of the disease, mean-age was 34.1 years (SD=11.4; 13-58), while the duration of disease at the moment of the examination was 10.3 years (SD=10.6; 1-39). There were 20 males and 10 females (sex ratio 2:1). None of the patients reported any history of trauma of subsequently affected region before the development of discomforts. Twelve patients used their hands for a long time during their professions (writing, playing the instrument, type-writing, etc.). Eight patients were typists (26.6%), four were musicians (13.3%), while the rest of cases (18) had some other occupations that did not necessarily imply long-term use of hands (office worker, engineer, physician, mechanical technician, etc.). Twelve patients had simple task-specific dystonia (type I) (40%), ten cases manifested progressive diseases (type II) (33.3%), while the others suffered from dystonia that was present at rest (type III). Two patients had positive family history. DYT 1 mutation was verified in one of them. Depression, anxiety and obsessiveness were not verified in our patients. Type of writer's cramp was not in correlation with any of the tested parameters except with the age at the onset of the disease, severity of disease according to Marsden's scale and degree of disability.