Autonomic Nervous System Effects Research Articles

Autonomic nervous system and viscera-related responses to manual therapy: A narrative overview

BackgroundManual therapy (MT) has long-held that it physiologically impacts autonomic nervous system (ANS) and viscera-related function. This narrative review is intended to serve as a consolidated interdisciplinary resource of original studies related to physiological effects of MT as it relates to the ANS for MT clinicians and researchers new to this MT-related topic. ObjectiveThis review seeks to identify ANS and viscera-related physiological responses to MT interventions using search terms commonly used by chiropractic, massage, osteopathic, physical therapy, and structural integration clinicians and to provide a quick reference resource of original MT-related studies investigating ANS effects. MethodsFor this interdisciplinary review, the search was limited to the largest and most commonly used database (PubMed) between years 2000 and 2024, with a focus on direct ANS-related physiological outcomes. Unlike systematic reviews, assessment of scientific rigor and potential bias of included articles was beyond the scope and purpose of the current work. ResultsOriginal MT-related studies provide mixed evidence with regards to immediate and/or short term ANS and/or viscera-related responses on blood pressure, heart rate variability, skin conductance/temperature, respiratory and lymphatic changes. ConclusionsThis review identified a large number of MT and ANS-related original research in PubMed. Careful study of original MT-related research is needed with particular attention focused on the standardization of MT methodological approaches, appropriate controls, study design, appropriate populations, MT techniques, and anatomical site delivery so as to design more rigorous studies in order to arrive at definitive conclusions regarding direct effects of MT on the ANS.

Pulsed Field Ablation to Treat Atrial Fibrillation: Autonomic Nervous System Effects

BackgroundDuring atrial fibrillation ablations using thermal energy, the treatment effect is attributed to not just pulmonary vein isolation (PVI), but also to modulation of the autonomic nervous system by ablation of cardiac ganglionated plexi (GP). ObjectivesThis study sought to assess the impact of pulsed field ablation (PFA) on the GP in patients undergoing PVI. MethodsIn the retrospective phase, heart rate was assessed pre- versus post-PVI using PFA, cryoballoon ablation, or radiofrequency ablation. In the prospective phase, a pentaspline PFA catheter was used in a protocol: 1) pre-PFA, high-frequency stimulation (HFS) identified GP sites by vagal effects; 2) PVI was performed assessing for repetitive vagal effects over each set of PF applications; 3) mapping defined PVI extent to identify those GP in the ablation zone; and 4) repeat HFS at GP sites to assess for persistence of vagal effects. ResultsBetween baseline and 3 months, heart rates in the retrospective radiofrequency ablation (n = 40), cryoballoon (n = 40), and PFA (n = 40) cohorts increased by 8.9 ± 11.4, 11.1 ± 9.4, and −0.1 ± 9.2 beats/min, respectively (P= 0.01 PFA vs radiofrequency ablation; P= 0.01 PFA vs cryoballoon ablation). In the prospective phase, pre-PFA HFS in 20 additional patients identified 65 GP sites. During PFA, vagal effects were noted in 45% of first PF applications, persisting through all applications in 83%. HFS post-PFA reproduced vagal effects in 29 of 38 sites (76%) in low-voltage tissue. ConclusionsPFA has minimal effect on GP. Unlike with thermal ablation, the mechanism by which PFA treats atrial fibrillation is mediated solely by durable PVI.

Nonclinical cardiovascular safety assessment of thioridazine: Impact of autonomic tone, body temperature, and choice of species

Pending updates to ICH S7B/E14 guidelines will enable the substitution of human TQT studies with support from concomitant negative hERG and non-rodent CV studies. This retrospective analysis compared the effects of thioridazine (THD) (5–20 mg/kg) on heart rate (HR), blood pressure (BP), body temperature (Tc), and QT in the dog (n = 6), cynomolgus monkey (n = 4), and Goettingen minipig (n = 4) with data from previously completed studies employing crossover designs. As QT measurements are confounded by HR and Tc changes, QT effects were individually corrected for changes in HR (QTca) and Tc (QTcaT). THD-induced hemodynamic changes seen in humans were most accurately reflected in the monkey and, to a lesser extent, the dog, but not in the minipig. The minipig was most sensitive to THD QTc effects. When QTca was adjusted for THD-associated Tc decreases in minipigs and monkeys, the minipig revealed a lessened but pronounced QTcaT increase (48 ms). In the monkey, a persistent QTca increase was reduced to only a transient (0.5–3 h) QTcaT increase (20 ms). The dog's lack of THD QTca effects triggered co-administration of atenolol (AT) to attenuate THD-induced HR increases in the dog and monkey. THD + AT revealed peak QTcaT increases of 32 ms in the dog and 40 ms in the monkey, suggesting potential autonomic nervous system (ANS) interference in detecting repolarization changes. These results highlight critical species-specific differences in the outcome of parallel safety investigations. Species selection for nonclinical safety studies should consider the potential impact of Tc and ANS effects to avoid false-negative or overly positive outcomes.

Amyotrophic Lateral Sclerosis and Cardiac Function: How can we do with Hummingbird’s Racing Hearts?

Amyotrophic lateral sclerosis (ALS) is a degenerative disease that classically affects the motor neuron, causing paralysis, flaccidity and death. However, although its etiopathogenesis is not fully elucidated, it is known that its involvement is not only motor, but also has a strong interaction with the autonomic nervous system, with cardiovascular, gastrointestinal and sleep effects, for example. The disease, which leads to death mainly from respiratory complications, also has underestimated cardiovascular effects, like increased heart rate variability, malignant arrhythmias and sudden death.

Computerized dynamic pupillometry as a screening tool for evaluation of autonomic activity

ObjectivesDynamic pupillometry is a simple screening tool for quantifying pupillary light reflex (PLR), to indicate autonomic nervous system (ANS) activity. Heart rate variability (HRV) is the gold standard method for assessing ANS effects on the heart. The present study aimed to compare ANS activity as measured using dynamic pupillometry (DP) with short term HRV in healthy volunteers. MethodsThe study includes 200 participants aged between 20–60 years. PLR was measured using infrared videography and categorized into different quantitative parameters that reflect ANS activity. Simultaneously, Lead II ECG was recorded for 5 min to evaluate the short term HRV of time and frequency domain parameters. The data obtained from the two methods were compared with each other to provide the relationship between PLR and HRV. ResultsStudy participants’ mean age was 36.95 ± 9.45 years. The different pupillary indices of PLR and all the HRV parameters were within the range of normative data. Several PLR indicators of the parasympathetic function include mean constriction velocity (MCV; r = 0.60, P < 0.001), absolute constriction amplitude (ACA; r = 0.57, P < 0.001) baseline pupil diameter (BPD; r = 0.44, p < 0.001), and minimum pupil diameter (MPD; r = −0.35, p < 0.001) were significantly correlated with high-frequency power (HF in normalized units) of HRV signal. ConclusionPLR variables showed a significant relationship to HRV indices. Dynamic pupillometry can be a complementary tool to HRV for evaluating ANS activity.

Electromagnetic hypersensitivity (EHS, microwave syndrome) – Review of mechanisms

Electromagnetic hypersensitivity (EHS), known in the past as “Microwave syndrome”, is a clinical syndrome characterized by the presence of a wide spectrum of non-specific multiple organ symptoms, typically including central nervous system symptoms, that occur following the patient's acute or chronic exposure to electromagnetic fields in the environment or in occupational settings. Numerous studies have shown biological effects at the cellular level of electromagnetic fields (EMF) at magnetic (ELF) and radio-frequency (RF) frequencies in extremely low intensities. Many of the mechanisms described for Multiple Chemical Sensitivity (MCS) apply with modification to EHS. Repeated exposures result in sensitization and consequent enhancement of response. Many hypersensitive patients appear to have impaired detoxification systems that become overloaded by excessive oxidative stress. EMF can induce changes in calcium signaling cascades, significant activation of free radical processes and overproduction of reactive oxygen species (ROS) in living cells as well as altered neurological and cognitive functions and disruption of the blood-brain barrier. Magnetite crystals absorbed from combustion air pollution could have an important role in brain effects of EMF. Autonomic nervous system effects of EMF could also be expressed as symptoms in the cardiovascular system. Other common effects of EMF include effects on skin, microvasculature, immune and hematologic systems. It is concluded that the mechanisms underlying the symptoms of EHS are biologically plausible and that many organic physiologic responses occur following EMF exposure. Patients can have neurologic, neuro-hormonal and neuro-psychiatric symptoms following exposure to EMF as a consequence of neural damage and over-sensitized neural responses. More relevant diagnostic tests for EHS should be developed. Exposure limits should be lowered to safeguard against biologic effects of EMF. Spread of local and global wireless networks should be decreased, and safer wired networks should be used instead of wireless, to protect susceptible members of the public. Public places should be made accessible for electrohypersensitive individuals.

The Association between Long-Term Air Pollution and Urinary Catecholamines: Evidence from the Multi-Ethnic Study of Atherosclerosis.

Background:Autonomic nervous system effects have been hypothesized as a mechanism of air pollutant health effects, though scant prior epidemiologic research has examined the association between air pollutants and catecholamines.Objectives:To examine the association of long-term air pollutants with three urinary catecholamines: dopamine (DA), epinephrine (EPI), and norepinephrine (NE). As a secondary aim, we also examined the association between short-term (or acute) exposure to fine particulate matter [particulate matter with aerodynamic diameter ()] and those catecholamines.Methods:We used data from the Multi-Ethnic Study of Atherosclerosis (MESA) and two of its ancillary studies, the MESA Air Pollution Study and the MESA Stress Study, to provide exposure and outcome data. DA, EPI, and NE from urine samples were collected from 2004 to 2006 from 1,002 participants in the New York, New York, and Los Angeles, California, study sites. Spatiotemporal models incorporated cohort-specific monitoring and estimated annual average pollutant concentrations (, , and black carbon) at participants’ homes the year prior to urine collection. Secondarily, short-term was evaluated (day of, day prior, and 2- to 5-d lags prior to urine collection). Several covariates were considered confounders (age, race, sex, site, socioeconomic status, cardiovascular disease risk factors, psychosocial stressors, and medication use) in linear regression models.Results:A higher annual concentration was associated with 6.3% higher mean EPI level [95% confidence interval (CI): 0.3%, 12.6%]. A 2- higher annual ambient concentration was associated with 9.1% higher mean EPI (95% CI: 3.2%, 15.3%) and 4.4% higher DA level (95% CI: 1%, 7.9%). , black carbon, and short-term exposures were not significantly associated with any of the catecholamines.Conclusions:We found an association between EPI and long-term concentrations of and and an association between DA and long-term ambient . These novel findings provide modest support for the hypothesis that air pollutant exposures are related to sympathetic nervous system activation. https://doi.org/10.1289/EHP3286

Medical Correlates of Chronic Multisymptom Illness in Gulf War Veterans

BackgroundChronic multisymptom illness (CMI) is more prevalent among deployed than nondeployed veterans from the first Gulf War. Objective physiologic markers of CMI are lacking. The purpose of this study is to determine whether measurable abnormalities in the autonomic nervous system or hypothalamic-pituitary adrenal axis would distinguish CMI cases (CMI+) from controls (CMI-) among deployed veterans of the 1990-1991 Gulf War. MethodsThis is a cross-sectional case-control cohort study that examined deployed veterans who participated in the Phase III study: National Health Survey of Gulf War Veterans and Their Families. Autonomic nervous system and hypothalamic-pituitary adrenal axis function-related measures included: 24-hour heart-rate variability, urinary catecholamines and cortisol, hypertension, insulin sensitivity, dyslipidemia, body fat, bone mineral density, and ultrasensitive C-reactive protein. ResultsVeterans of the first Gulf War with CMI (n = 73) and without the condition (n = 111) were studied. Sociodemographic characteristics were similar. Veterans with CMI reported poorer mental and physical functioning, greater use of prescription medications, and more nonroutine clinic visits. These veterans were also more likely to have fibromyalgia syndrome, irritable bowel syndrome, metabolic syndrome, and among males, a larger waist-to-hip ratio. Lower values for a nonlinear heart-rate-variability parameter—the short-term fractal scaling exponent (DFA1), reflecting an increased randomness of beat-to-beat changes in heart rate—were observed in veterans with CMI than those veterans without it (1.28±0.16vs 1.35±0.15; p=0.005). Hypothalamic-pituitary-adrenal axis function measures were similar between the two groups. ConclusionIn this cohort of deployed veterans from the first Gulf War, we identified abnormal heart-rate variability in veterans with CMI compared to veterans without the condition, which suggests abnormal functioning of the autonomic nervous system and possible long-term cardiovascular effects.

Atrial Cardiopathy and Sympatho-Vagal Imbalance in Cryptogenic Stroke: Pathogenic Mechanisms and Effects on Electrocardiographic Markers.

Recently, atrial cardiopathy has emerged as possible pathogenic mechanism in cryptogenic stroke and many electrocardiographic (ECG) markers have been proposed in order to detect an altered atrial substrate at an early stage. The autonomic nervous system (ANS) plays a well-known role in determining significant and heterogeneous electrophysiological changes of atrial cardiomyocytes, that promote atrial fibrillation episodes in cardioembolic stroke. Conversely, the role of ANS in atrial cardiopathy and cryptogenic stroke is less known, as well as ANS effects on ECG markers of atrial dysfunction. In this paper, we review the evidence linking ANS dysfunction and atrial cardiopathy as a possible pathogenic factor in cryptogenic stroke.

Effect of swearing on strength and power performance

ObjectivesSwearing aloud increases pain tolerance. The hypothesis that this response may be owed to an increase in sympathetic drive raises the intriguing question as to whether swearing results in an improvement in strength and power. DesignEmploying repeated measures designs, we evaluated the effect of repeating a swear word v. a neutral word on strength and power during anaerobic and isometric exercise through two experiments. MethodExperiment #1 (n = 29) employed the Wingate Anaerobic Power Test (WAnT). Experiment #2 (n = 52) employed an isometric handgrip test. ResultsGreater maximum performance was observed in the swearing conditions compared with the non-swearing conditions for WAnT power (Experiment #1; dz = 0.618, p = 0.002) and hand grip strength (Experiment #2; dz = 0.962, p < 0.001). However, swearing did not affect cardiovascular or autonomic function assessed via heart rate, heart rate variability, blood pressure and skin conductance. ConclusionsData demonstrate increased strength and power performance for swearing v. not swearing but the absence of cardiovascular or autonomic nervous system effects makes it unclear whether these results are due to an alteration of sympathovagal balance or an unknown mechanism.

The Association Between Air Pollution And Stress Hormones: Evidence From The Multi-Ethnic Study Of Atherosclerosis

Introduction: Autonomic nervous system effects have been hypothesized as a mechanism of air pollutant health effects, though scant prior epidemiologic research has examined the association between air pollutants and catecholamines. Methods: We examined the association between air pollutants and urinary catecholamines in the Multi-Ethnic Study of Atherosclerosis (MESA), a cohort study with participants from six US areas. Data from two ancillary studies, the MESA Air Study and the MESA Stress Study, provide exposure and outcome data. Dopamine (DA), epinephrine (EPI), norepinephrine (NE) data were collected from 2004 – 2006 from 1002 white, black and Hispanic participants from the New York and Los Angeles study sites. Urinary analyte concentrations were adjusted for creatinine and log-transformed for analysis. Spatio-temporal models incorporated cohort-specific monitoring and modeled estimated annual average pollutant concentrations (PM2.5 and NOx) at participant's homes the year prior to urine collection. Several covariates were considered confounders: age, race, sex, site, socioeconomic status, cardiovascular disease risk factors (smoking, second hand smoke, BMI, alcohol use and hypertension) and psychosocial stressors (depression, social support, anxiety, anger and chronic stress) and linear regression models were employed. Results: Preliminary models show a 40 ppb higher NOx concentration was associated with 10% higher NE (95% confidence interval (CI): 4%, 20%) and 17% higher EPI level (95% CI: 3%, 33%). A 5 µg/m3 higher PM2.5 concentration was associated with 23% higher EPI (95% CI: 8%, 41%) and 14% higher DA level (95% CI: 5%, 23%). Conclusions: We found a cross-sectional association between several urinary catecholamines and long-term residential concentrations of PM2.5 and NOx. These novel finding support the hypothesis that air pollutant exposures are related to sympathetic nervous system activation; however, additional investigation is warranted.

Autonomic effects of music in health and Crohn's disease: the impact of isochronicity, emotional valence, and tempo.

BackgroundMusic can evoke strong emotions and thus elicit significant autonomic nervous system (ANS) responses. However, previous studies investigating music-evoked ANS effects produced inconsistent results. In particular, it is not clear (a) whether simply a musical tactus (without common emotional components of music) is sufficient to elicit ANS effects; (b) whether changes in the tempo of a musical piece contribute to the ANS effects; (c) whether emotional valence of music influences ANS effects; and (d) whether music-elicited ANS effects are comparable in healthy subjects and patients with Crohn´s disease (CD, an inflammatory bowel disease suspected to be associated with autonomic dysfunction).MethodsTo address these issues, three experiments were conducted, with a total of n = 138 healthy subjects and n = 19 CD patients. Heart rate (HR), heart rate variability (HRV), and electrodermal activity (EDA) were recorded while participants listened to joyful pleasant music, isochronous tones, and unpleasant control stimuli.ResultsCompared to silence, both pleasant music and unpleasant control stimuli elicited an increase in HR and a decrease in a variety of HRV parameters. Surprisingly, similar ANS effects were elicited by isochronous tones (i.e., simply by a tactus). ANS effects did not differ between pleasant and unpleasant stimuli, and different tempi of the music did not entrain ANS activity. Finally, music-evoked ANS effects did not differ between healthy individuals and CD patients.ConclusionsThe isochronous pulse of music (i.e., the tactus) is a major factor of music-evoked ANS effects. These ANS effects are characterized by increased sympathetic activity. The emotional valence of a musical piece contributes surprisingly little to the ANS activity changes evoked by that piece.

INFLUENCE OF IVABRADYN ON HEART RATE VARIABILITY IN PATIENTS WITH HYPERTENSION AND ASSOCIATED HEART

58 patients, sick with arterial hypertension of the third stage with concomitant heart failure of II A stage were and studied. The patients were divided into two groups: the first group (30 persons) received basic therapy, and patients of the second group (28 persons) in addition to basic therapy additionally were treated with a selective inhibitor of if-channels cells of heart sinus node “ivabradine”. Parameters of temporal and frequency analysis of heart rate variability were studied. It has been established that using ivabradine ogainst a background of basic therapy significante reduces sympathetic and increases parasympathetic autonomic nervous system effects on heart and normalizes its bio-reflex regulation.

Cardiac autonomic modulation and sleepiness: Physiological consequences of sleep deprivation due to 40 h of prolonged wakefulness

The autonomic nervous system (ANS) is modulated by sleep and wakefulness. Noninvasive assessment of cardiac ANS with heart rate variability (HRV) analysis is a window for monitoring malfunctioning of cardiovascular autonomic modulation due to sleep deprivation.This study represents the first investigation of dynamic ANS effects and of electrophysiological and subjective sleepiness, in parallel, during 40h of prolonged wakefulness under constant routine (CR) conditions. In eleven young male healthy subjects, ECG, EEG, EOG, and EMG chin recordings were performed during baseline sleep, during 40h of sleep deprivation, and during recovery sleep. After sleep deprivation, slow-wave sleep and sleep efficiency increased, whereas HRV – global variability and HRV sympathovagal balance – was reduced (all p<0.05). Sleep-stage-dependent analysis revealed reductions in the sympathovagal balance only for NREM sleep stages (all p<0.05). Comparison of the daytime pattern of CR day one (CR baseline) with that of CR day two (CR sleep deprivation) disclosed an increase in subjective sleepiness, in the amount of unintended sleep, and in HRV sympathovagal balance, with accompaniment by increased EEG alpha attenuation (all p<0.05). Circadian rhythm analysis revealed the strongest influence on heart rate, with less influence on HRV sympathovagal balance. Hour-by-hour analysis disclosed the difference between CR sleep deprivation and CR baseline for subjective sleepiness at almost every single hour and for unintended sleep particularly in the morning and afternoon (both p<0.05). These findings indicate that 40h of prolonged wakefulness lead in the following night to sleep-stage-dependent reduction in cardiac autonomic modulation. During daytime, an increased occurrence of behavioral and physiological signs of sleepiness was accompanied by diminished cardiac autonomic modulation. The observed changes are an indicator of autonomic stress due to sleep deprivation — which, if chronic, could potentially increase cardiovascular risk.

Interventions to decrease the morbidity and mortality associated with implantable cardioverter-defibrillator shocks

Implantable cardioverter-defibrillator (ICD) implantation is the standard of care for secondary prevention in patients with previous cardiac arrest and for primary prevention in appropriately selected patients with cardiomyopathy. However, ICD therapies and the arrhythmias that trigger these therapies cause decreased quality of life as well as increased morbidity and mortality. In this review, we summarize the recent evidence for interventions that may prevent ICD therapies. Pharmacologic therapy remains central to prevent ICD shocks, but there is limited new evidence for drug therapies. Programming techniques continue to evolve which decrease the risk of inappropriate shocks. Cardiac resynchronization therapy (CRT) improves quality of life and decreases mortality, at least in part because of decreased arrhythmia burden. Procedures such as catheter ablation of ventricular tachycardia and procedures to modulate the autonomic nervous system can help minimize ICD therapy. Pharmacologic therapy and appropriate device programming remain essential to the overall care of ICD patients. The role of CRT continues to grow as we gain a better understanding of its benefits. Advancements in the fields of catheter ablation and new understanding of the autonomic nervous system's effects on ventricular arrhythmias allow interventions to decrease the frequency of ICD shocks.

Out-of-Hospital Cardiac Arrest

Sudden cardiac death (SCD), which is responsible for approximately 300 000 deaths in the United States, refers to an unexpected death from a cardiovascular cause in a person with or without preexisting heart disease. Most studies include cases that are associated with death occurring within 1 hour of an acute change in clinical status or an unexpected death that occurred within the previous 24 hours,1 but this definition is not specific for sudden arrhythmic death. The most common sequence of events leading to arrhythmic SCD is the degeneration of ventricular tachycardia (VT) into ventricular fibrillation (VF), often followed by asystole or pulseless electric activity. The transition of shockable rhythms (VT/VF) to more ominous rhythms such as asystole or pulseless electric activity depends on various factors, but is highly dependent on time; the longer the time interval, the more likely the VT/VF degenerates to pulseless electric activity or asystole. Although VF and VT together represent the initial rhythm in half of all outpatient cardiac arrests, data suggest that with each passing minute of untreated VF, the likelihood of survival is reduced by 7% to 10%.2 Preexisting coronary artery disease and its sequelae (eg, acute myocardial ischemia, scarring from previous myocardial infarction, heart failure) are manifest in 80% of SCDs.3 Dilated nonischemic and hypertrophic cardiomyopathies account for the second largest number of SCDs, whereas other cardiac disorders such as congenital heart disease and underlying genetically determined ion channel anomalies account for 5% to 10% of SCDs.3 Although the cascade of events triggering SCD are complex and are currently active areas of investigation, the general goals of reducing SCD are focused on (1) identifying and preventing sudden death in high-risk individuals by using efficacious therapies such as medications and implantable cardioverter defibrillators (ICDs), (2) organizing resuscitation services to improve …

QT-RR hysteresis is caused by differential autonomic states during exercise and recovery

QT-RR hysteresis is characterized by longer QT intervals at a given RR interval while heart rates are increasing during exercise and shorter QT intervals at the same RR interval while heart rates are decreasing during recovery. It has been attributed to a lagging QT response to different directional changes in RR interval during exercise and recovery. Twenty control subjects (8 males, age 51 ± 6 yr), 16 subjects with type 2 diabetes (12 males, age 56 ± 8 yr), 71 subjects with coronary artery disease (CAD) and preserved left ventricular ejection fraction (LVEF) (≥50%) (51 males, age 59 ± 12 yr), and 17 CAD subjects with depressed LVEF (<50%) (13 males, age 57 ± 10 yr) underwent two 16-min exercise tests followed by recovery. In session 2, parasympathetic blockade with atropine (0.04 mg/kg) was achieved at end exercise. QT-RR hysteresis was quantified as: 1) the area bounded by the QT-RR relationships for exercise and recovery in the range of the minimum RR interval at peak exercise to the minimum RR interval + 100 ms and 2) the difference in QT interval duration between exercise and recovery at the minimum RR interval achieved during peak exercise plus 50 ms (ΔQT). The effect of parasympathetic blockade was assessed by substituting the QT-RR relationship after parasympathetic blockade. QT-RR hysteresis was positive in all groups at baseline and reversed by parasympathetic blockade (P < 0.01). We conclude that QT-RR hysteresis is not caused by different directional changes in RR interval during exercise and recovery. Instead, it is predominantly mediated by differential autonomic nervous system effects as the heart rate increases during exercise vs. as it decreases during recovery.

Role of piracetam in treatment of cerebral palsy disease

The term cerebral palsy (CP) refers to neurological disorders that appear in infancy or early childhood and permanently affect body movement and muscle coordination. Piracetam is a compound chemically related to gamma-aminobutyric acid (GABA). It crosses the blood-brain barrier but does not produce any overt central or autonomic nervous system effects. The aim of this prospective study was to evaluate and compare the effect of different doses of Piracetam on clinical status and intellectual power of cerebral palsy patient. The study was carried out on 40 cerebral palsy patients; 22 out of them were females, aged from 1 to 4.75 years old; from outpatient clinic at Beni Suef University Hospital. Patients were divided into four equal groups. Group A received dose 40mg/kg/day, group B received dose 80mg/kg/day, group C received dose 120mg/kg/day and group D was the control group, did not receive any Piracetam. Patients were treated and followed up for 6 month. They were represented by full history taking and clinical examination. The Intelligence quotient (IQ) test was done for every patient to evaluate mental development before starting piracetam treatment and every month for six months. There was an improvement in general health of children after therapy and quotient. Dose 120mg/kg/day of piracetam was found to be the most effective dose piracetam in the treatment of cerebral palsy disease as shown by improved scores of IQ test. The best improvement in mental and motor development was greatly observed in group C. Dose 40mg/kg/day of piracetam showed insignificant effect on improving the IQ of the patients.

What science says about khat (Catha edulis Forsk)? Overview of chemistry, toxicology and pharmacology

Catha edulis (khat) is a plant grown commonly in the horn of Africa. The leaves of khat are chewed by the people for its stimulant action. Khat is an evergreen shrub, which is cultivated as a bush or small tree. The leaves have an aromatic odour. The taste is astringent and slightly sweet. The plant is seedless and hardy, growing in a variety of climates and soils. Khat contains more than 40 alkaloids, glycosides, tannins, amino acids, vitamins and minerals. Many different compounds are found in khat including alkaloids, terpenoids, flavonoids, sterols, glycosides, tannins, amino acids, vitamins and minerals. The phenylalkylamines and the cathedulins are the major alkaloids which are structurally related to amphetamine. The major effects of khat include those on the gastro-intestinal system and on the nervous system. Constipation, urine retention and acute cardiovascular effects may be regarded as autonomic (peripheral) nervous system effects; increased alertness, dependence, tolerance and psychiatric symptoms as effects on the central nervous system. The main toxic effects include increased blood pressure, tachycardia, insomnia, anorexia, constipation, general malaise, irritability, migraine and impaired sexual potency in men. The purpose of this review is to summarize the chemistry, pharmacology, toxicology of khat (Catha edulis Forsk).

Inotropes and Vasopressors

Inotropic and vasopressor agents have increasingly become a therapeutic cornerstone for the management of several important cardiovascular syndromes. In broad terms, these substances have excitatory and inhibitory actions on the heart and vascular smooth muscle, as well as important metabolic, central nervous system, and presynaptic autonomic nervous system effects. They are generally administered with the assumption that short- to medium-term clinical recovery will be facilitated by enhancement of cardiac output (CO) or vascular tone that has been severely compromised by often life-threatening clinical conditions. The clinical efficacy of these agents has been investigated largely through examination of their impact on hemodynamic end points, and clinical practice has been driven in part by expert opinion, extrapolation from animal studies, and physician preference. Our aim is to review the mechanisms of action of common inotropes and vasopressors and to examine the contemporary evidence for their use in important cardiac conditions.