Drugging our kids, Suicide & homicide effects CASPER. MR NEWS

I’d like to share a very interesting and informative YouTube presentation.  While lengthy in its presentation it gives one much to think about. 

http://www.youtube.com/watch?v=5bu1uApqIr4&feature=player_embedded

Warmly,

Herb
vnsdepression@gmail.com
http://www.vnstherapy-herb.blogspot.com/

J Clin Sleep Med. 2011 Aug 15;7(4):401-7.

Obstructive sleep apnea and respiratory complications associated with vagus nerve stimulators.

Parhizgar F, Nugent K, Raj R.

Source

Department of Internal Medicine, Texas Tech University Health Sciences Center, Lubbock, TX.

Abstract

Intermittent vagus nerve stimulation can reduce the frequency of seizures in patients with refractory epilepsy. Stimulation of vagus nerve afferent fibers can also cause vocal cord dysfunction, laryngeal spasm, cough, dyspnea, nausea, and vomiting. Vagus nerve stimulation causes an increase in respiratory rate, decrease in respiratory amplitude, decrease in tidal volume, and decrease in oxygen saturation during periods of device activation. It usually does not cause an arousal, or a change in heart rate or blood pressure. Most patients have an increase in their apnea-hypopnea index (AHI). Patients with VNS can have central apneas, obstructive hypopneas, and obstructive apneas. These respiratory events can be reduced with changes in the vagus nerve stimulator operational parameters or with the use of CPAP. In summary, there are complex relationships between epilepsy and obstructive sleep apneas. In particular, patients with refractory epilepsy need assessment for undiagnosed and untreated obstructive sleep apnea before implantation of vagus nerve stimulator devices. Patients with vagus nerve stimulators often have an increase in apneic events after implantation, and these patients need screening for sleep apnea both before and after implantation. CITATION: Parhizgar F; Nugent K; Raj R. Obstructive sleep apnea and respiratory complications associated with vagus nerve stimulators. J Clin Sleep Med 2011;7(4):401-407.

PMID:

21897779

[PubMed - in process]

http://www.ncbi.nlm.nih.gov/pubmed/21897779

Dev Med Child Neurol. 2011 Aug 31. doi: 10.1111/j.1469-8749.2011.04103.x. [Epub ahead of print]

Autonomic effects of refractory epilepsy on heart rate variability in children: influence of intermittent vagus nerve stimulation.

Jansen K, Vandeput S, Milosevic M, Ceulemans B, VAN Huffel S, Brown L, Penders J, Lagae L.

Source

Department of Pediatric Neurology, University Hospitals Leuven, Leuven, Belgium.  Department of Electrical Engineering, ESAT KU Leuven, Leuven, Belgium.  Epilepsy Center, Pulderbos, Belgium.  Holst Center/IMEC, Eindhoven, the Netherlands.

Abstract

Aim  Vagus nerve stimulation (VNS) is a therapeutic option for individuals with refractory epilepsy. Individuals with refractory epilepsy are prone to dysfunction of the autonomic nervous system. Reduced heart rate variability is a marker of dysfunction of the autonomic nervous system. Our goal was to study heart rate variability in children with refractory epilepsy and the influence of VNS on this parameter. Methods  In 17 children (13 male; four female; mean age 7y 6mo; age range 3-16y) with refractory epilepsy, electroencephalographic and electrocardiographic data were obtained before and after implantation of VNS during stage 2 and slow-wave sleep. Time and frequency domain parameters were calculated and the results were compared with an age- and sex-matched group of individuals without refractory epilepsy. Results  Our results show that autonomic cardiac control is affected in individuals with refractory epilepsy. There is a striking reduction in vagal tone during slow-wave sleep and modulation capacity is smaller than in individuals without refractory epilepsy. Implantation of VNS induces a shift in sympathovagal balance towards sympathetic predominance and an improvement in autonomic modulation. Interpretation  Heart rate variability is affected in children with refractory epilepsy, and changes after implantation of VNS. The observed changes could be of importance in the cardiac complications of individuals with epilepsy and should be explored in more detail.
© The Authors. Developmental Medicine & Child Neurology © 2011 Mac Keith Press.

PMID:

21883174

[PubMed - as supplied by publisher]

http://www.ncbi.nlm.nih.gov/pubmed/21883174

Prescrire Int. 2011 May;20(116):128-33.

Treatment-resistant depression: no panacea, many uncertainties. Adverse effects are a major factor in treatment choice.

[No authors listed]

Abstract

At least 50% of patients with depression do not enter remission after several weeks of antidepressant therapy. To determine the treatment options and their respective risk-benefit balances in this setting, we reviewed the literature using the standard Prescrire methodology. Clinical trials and epidemiological studies show that depression should only be considered drug-resistant after at least 6 weeks of therapy. After assessing residual symptoms and their impact on the patient's quality of life, a search should be made for factors responsible for the persistence of depression, such as the patient's environment, a psychiatric or somatic disorder, and drug intake or addiction. Increasing the dose of the first-line antidepressant is only based on weak evidence. Trials comparing continuing the first-line antidepressant versus switching to another pharmacological class have yielded conflicting results. A switch may benefit some patients, but the elimination half-life of the discontinued drug must be taken into account to limit the risk of interactions during the transition. Combining two antidepressants mainly increases the risk of adverse effects, without a tangible clinical benefit. Two meta-analyses suggest that adding a so-called atypical neuroleptic to ongoing antidepressant therapy leads to 1 extra remission per 7 to 10 treated patients, but also to treatment cessation due to adverse effects in 8% to 9% of cases. Older neuroleptics have not been properly evaluated in this setting. Comparative trials suggest that lithium may have a certain antidepressant effect in this setting, but there is no firm evidence that adding lithium increases the chances of remission. Lithium has a narrow therapeutic margin and overdose can be fatal; the blood lithium concentration must therefore be monitored. Adding an antiepileptic or a psychostimulant is more harmful than beneficial. Adding a thyroid hormone, a benzodiazepine, buspirone or pindolol has no proven antidepressive effect. Four trials, each including fewer than 20 patients, have assessed the efficacy of psychotherapy in patients with treatment-resistant depression. Two of them provided positive results. Electroconvulsive therapy is probably effective for some patients with refractory depression but it necessitates general anaesthesia and carries a risk of memory disorders. Vagal nerve electrostimulation has no proven efficacy. Transcranial magnetic stimulation seems to have some efficacy and few adverse effects, but its optimal modalities remain to be determined. In practice, when the patient and doctor decide to attempt second-line therapy for treatment-resistant depression, adverse effects must be taken into account in the choice of drug(s). Maintaining a good quality relationship between patient and doctor may be more important than attempting to obtain remission "at any cost".

PMID:

21648180

[PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/21648180

J Neurosurg Pediatr. 2011 Jun;7(6):671-5.

Vagal nerve stimulator infection: a lead-salvage protocol.

Wozniak SE, Thompson EM, Selden NR.

Source

Department of Neurological Surgery, Oregon Health & Science University, 3303 SW Bond Avenue, Portland, OR 97239, USA.

Abstract

OBJECT:

Vagal nerve stimulator (VNS) hardware infections are fraught with difficult management decisions. As with most implanted medical device-related infections, standard practice traditionally involves complete hardware removal, systemic antibiotic therapy, and subsequent reimplantation of the device. To avoid the potential morbidity of 2 repeat left carotid sheath surgical dissections, the authors have implemented a clinical protocol for managing VNS infections that involves generator removal and antibiotic therapy without lead removal.

METHODS:

A prospective, single-surgeon database was compared with hospital billing records to identify patients who underwent primary implantation or reimplantation of a VNS lead, generator, or both, from January 2001 to May 2010, at Oregon Health & Science University. From these records, the authors identified patients with VNS hardware infections and characterized their management, using a lead salvage protocol.

RESULTS:

In their review, the authors found a matching cohort of 206 children (age 3 months-17 years) who met the inclusion criteria. These children underwent 258 operations (including, in some children, multiple operations for generator end of life and/or lead malfunction). Six children experienced a single postimplantation infection (2.3% of the 258 operative cases), and no child experienced repeated infection. A lead-salvage protocol was used in 4 of 6 infected patients and was successful in 3 (75%), with clinical follow-up ranging from 10 months to 7.5 years. The fourth patient subsequently underwent lead removal and later reimplantation in standard fashion, with no adverse sequelae.

CONCLUSIONS:

Vagal nerve stimulator lead salvage is a safe and potentially advantageous strategy in the management of VNS-related infection. Further study is necessary to validate appropriate patient selection, success rates, and risks of this approach.

PMID:

21631207

[PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/21631207

J Neurosurg Pediatr. 2011 Jun;7(6):671-5.

Vagal nerve stimulator infection: a lead-salvage protocol.

Wozniak SE, Thompson EM, Selden NR.

Source

Department of Neurological Surgery, Oregon Health & Science University, 3303 SW Bond Avenue, Portland, OR 97239, USA.

Abstract

OBJECT:

Vagal nerve stimulator (VNS) hardware infections are fraught with difficult management decisions. As with most implanted medical device-related infections, standard practice traditionally involves complete hardware removal, systemic antibiotic therapy, and subsequent reimplantation of the device. To avoid the potential morbidity of 2 repeat left carotid sheath surgical dissections, the authors have implemented a clinical protocol for managing VNS infections that involves generator removal and antibiotic therapy without lead removal.

METHODS:

A prospective, single-surgeon database was compared with hospital billing records to identify patients who underwent primary implantation or reimplantation of a VNS lead, generator, or both, from January 2001 to May 2010, at Oregon Health & Science University. From these records, the authors identified patients with VNS hardware infections and characterized their management, using a lead salvage protocol.

RESULTS:

In their review, the authors found a matching cohort of 206 children (age 3 months-17 years) who met the inclusion criteria. These children underwent 258 operations (including, in some children, multiple operations for generator end of life and/or lead malfunction). Six children experienced a single postimplantation infection (2.3% of the 258 operative cases), and no child experienced repeated infection. A lead-salvage protocol was used in 4 of 6 infected patients and was successful in 3 (75%), with clinical follow-up ranging from 10 months to 7.5 years. The fourth patient subsequently underwent lead removal and later reimplantation in standard fashion, with no adverse sequelae.

CONCLUSIONS:

Vagal nerve stimulator lead salvage is a safe and potentially advantageous strategy in the management of VNS-related infection. Further study is necessary to validate appropriate patient selection, success rates, and risks of this approach.

PMID:

21631207

[PubMed - indexed for MEDLINE]

Electrical stimulation outside the heart

"In the previous paragraphs, we have discussed the application of electrical stimulation on the heart, which has the advantage of avoiding possible adverse side-effects as regularly encountered with pharmacological therapies. The therapies discussed below are applied outside the heart and usually are applied continuously throughout the cardiac cycle (see Fig. 1). Their benefit may be that the stimulation is affecting a much more integrated system. Studies of these therapies clearly show cardiac benefit, but in most cases, the exact mechanism is unknown. This is likely due to multi-organ and central nervous system pathways.

Vagal nerve stimulation

There has been extensive research demonstrating that acute vagus nerve stimulation results in a decrease in various measures of ventricular function including contractility. Lewis et al. showed that in the human and pig heart, stimulation of the left vagus nerve can profoundly decrease contractility of the left ventricular myocardium, independent of its braducardic effect [54]. This decrease in ventricular contractility during vagal stimulation (VNS) appears to be mediated by the parasympathetic ganglia located in the cranial medial ventricular fat pad [55, 56]. However, at low sympathetic tone, the negative inotropic effect of vagal stimulation is attributable primarily to its negative chronotropic effect [57]. This suggests that the effect of VNS on contractility is mediated via an interaction with the sympathetic system.

It may seem counterintuitive that a reduction in contractility by VNS may be beneficial to patients with heart failure. However, several pre-clinical studies have shown benefit in chronic vagus nerve stimulation in models of systolic heart failure [58]. Recently, Zhang et al. evaluated VNS in a canine high-rate pacing-induced model of heart failure. VNS at an intensity that reduced sinus rate by approximately 20 bpm was delivered in the VNS group. After 4 and 8 weeks, both left ventricular end-diastolic and end-systolic volumes were lower, and left ventricular EF was higher in the VNS group than in the control group [59]. Li et al. showed that VNS markedly improved the long-term survival of chronic heart failure rats through the prevention of pumping failure, remodeling, and increasing contractility [60]. Very recently, the same group showed that VNS applied immediately after MI attenuated LV remodeling, which may be related to the decreased acute inflammatory response or to the reduction in infarct size induced by VNS [61], since the remodeling process increases with a larger infarct."

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3074071/