Chronic exposure of rats to cognition enhancing drugs produces a neuroplastic response identical to that obtained by complex environment rearing.

Recent data suggest that Alzheimer's patients who discontinue treatment with cholinesterase inhibitors have a significantly delayed cognitive decline as compared to patients receiving placebo. Such observations suggest cholinesterase inhibitors to provide a disease-modifying effect as well as symptomatic relief and, moreover, that this benefit remains after drug withdrawal. Consistent with this suggestion, we now demonstrate that chronic administration of tacrine, nefiracetam, and deprenyl, drugs that augment cholinergic function, increases the basal frequency of dentate polysialylated neurons in a manner similar to the enhanced neuroplasticity achieved through complex environment rearing. While both drug-treated and complex environment reared animals continue to exhibit memory-associated activation of hippocampal polysialylated neurons, the magnitude is significantly reduced suggesting that such interventions induce a more robust memory pathway that can acquire and consolidate new information more efficiently. This hypothesis is supported by our findings of improved learning behavior and enhanced resistance to cholinergic deficits seen following either intervention. Furthermore, the level of enhancement of basal neuroplastic status achieved by either drug or environmental intervention correlates directly with improved spatial learning ability. As a combination of both interventions failed to further increase basal polysialylated cell frequency, complex environment rearing and chronic drug regimens most likely enhanced cognitive performance by the same mechanism(s). These findings suggest that improved memory-associated synaptic plasticity may be the fundamental mechanism underlying the disease modifying action of drugs such as cholinesterase inhibitors. Moreover, the molecular and cellular events underpinning neuroplastic responses are identified as novel targets in the search for interventive drug strategies for the treatment of neurodegenerative and neuropsychiatric disorders.     

Socio-economic burden of permanent incisor replantation on children and parents

Abstract – This study describes the socio‐economic burden and attitudes of children and their parents following replantation of avulsed incisors. Records of 80 patients with 99 avulsion injuries treated in a teaching hospital clinic from 1988 to 1999 were reviewed. Mean age at time of injury was 10.6 years (range = 6.6–17.7 years). Complete records for a minimum of 1 year were obtained for 43 patients with 60 replanted incisors. Mean treatment procedures provided during the first year included 5.5 diagnostic periapical radiographs, 1.9 occlusal radiographs, 1.3 pulpectomies, and 2.7 pulp medicament applications. The mean estimated treatment cost and direct time (dentist) for first‐year post‐trauma management was $1465 CAD and 7.2 h, respectively. Treatment costs were significantly higher during the first year post‐trauma for patients who had their incisors extracted (P = 0.04), but there was no significant difference in direct treatment time between the two groups (P = 0.19). Twenty‐one patient–parent pairs were surveyed for a number of qualitative factors. Ninety per cent of patients and 86% of parents reported that school and work time was lost. Even after having gone through the painful experience of replantation, the demands of recall, and in some cases, extraction, the majority of patients (67%) and parents (81%) stated that they would have still made the same (replantation) decision. Patient and parent responses were not statistically different (P = 0.453). Almost half the parents stated they would be willing to pay over $2000 CAD to save an incisor. Patients rated retention of an incisor as significantly more important than infraocclusion. This is the first study to quantify the treatment burden of replantation of avulsion injuries exclusively in the pediatric population. This study describes the socio‐economic burden and responsibilities of patient/parent and dentist and their role in informed consent.     

Palatal implants: a new approach for the treatment of obstructive sleep apnea.

OBJECTIVE: To evaluate the short-term safety and efficacy of palatal implants in patients with mild and moderate obstructive sleep apnea (OSA). STUDY DESIGN AND SETTING: A prospective, non-randomized study conducted at 5 clinical sites. Three polyester implants were placed in the soft palate under local anesthesia during a single-stage office procedure. Polysomnography was conducted at baseline and 90 days post-procedure. Subjective quality of life data were collected. RESULTS: Fifty-three patients were evaluated; the apnea hypopnea index (AHI) decreased from 25.0 +/- 13.9 to 22.0 +/- 14.8 events/hour (P = 0.05). The Epworth Sleepiness Scale (ESS) decreased from 11.0 +/- 5.1 to 6.9 +/- 4.5 (P < 0.001), and the snore score decreased from 7.9 +/- 2.1 to 4.0 +/- 3.0 (P < 0.001). No serious complications occurred during the study. CONCLUSION: Palatal implants can be an effective initial low morbidity treatment option for patients diagnosed with mild to moderate OSA.     

Vasodepressor reactions after orthotopic cardiac transplantation: Relationship to reinnervation status

Ventricular vagal nerve endings are thought to trigger vasodepressor syncope. Reports of vasodepressor reactions associated with donor bradycardia after cardiac transplantation have led to speculation that vagal reinnervation occurs. We assessed reinnervation status in seven patients 23–36 months (median 24 months) post-transplantation. Heart rate responses to vagal manoeuvres (respiration, Valsalva) and sympathetic stimuli (exercise and injection of tyramine into the coronary artery supplying the sinus node) were measured. All patients underwent 60 min of 60° head-up tilt with foot plate support. During tilt four of the seven had vasodepressor reactions with a fall in mean arterial pressure of 20–90 mmHg. During vasodepression two patients had falls in donor heart rate of 13 and 40% relative to peak heart rate during tilt. These two patients had evidence of functional sympathetic reinnervation. By contrast the two patients without donor bradycardia during vasodepression had only limited or no evidence of sympathetic reinnervation. No patient had consistent evidence of parasympathetic reinnervation as judged by the heart rate response to vagal manoeuvres. Headup tilt can thus produce vasodepressor reactions with donor bradycardia after cardiac transplantation in the absence of consistent evidence of vagal reinnervation. Left ventricular nerve endings may not be the only mediators of tilt-induced vasodepressor reactions in man. Donor bradycardia during vasodepression may reflect sympathetic withdrawal and not vagal reinnervation.     

Auditory evoked potential index: a quantitative measure of changes in auditory evoked potentials during general anaesthesia

We describe a novel index derived from the auditory evoked potential, the auditory evoked potential index, and we compare it with latencies and amplitudes related to clinical signs of consciousness and unconsciousness. Eleven patients, scheduled for total knee replacement under spinal anaesthesia, completed the study. The initial mean (SD) value of the auditory evoked potential index was 72.5 (11.2). During the first period of unconsciousness it decreased to 39.6 (6.9) and returned to 66.8 (12.5) when patients regained consciousness. Thereafter, similar values were obtained whenever patients lost and regained consciousness. Latencies and amplitudes changed in a similar fashion. From all parameters studied, Na latencies had the greatest overlap between successive awake and asleep states. The auditory evoked potential index and Nb latencies had no overlap. The consistent changes demonstrated suggest that the auditory evoked potential index could be used as a reliable indicator of potential awareness during propofol anaesthesia instead of latencies and amplitudes.     

Influence of hypothermic cardiopulmonary bypass on atrial natriuretic factor levels

Atrial natriuretic factor (ANF) is a peptide released from the heart in response to atrial distension. This peptide causes diuresis, vasodilatation, decreased blood pressure, and antagonizes the renin-aldosterone and antidiuretic hormone neuraxes. The influence of cardiopulmonary bypass and cardiac surgery on the circulation and release of ANF is unknown. Plasma ANF concentrations were therefore determined in patients undergoing coronary artery revascularization (CABG) and mitral valve replacement (MVR). Peptide levels were unchanged following anaesthetic induction. Plasma ANF concentrations decreased significantly during hypothermic (less than or equal to 28 degrees C) cardiopulmonary bypass in both patient groups. After 60 minutes of cardiac bypass, ANF declined from (mean +/- SEM) 512 +/- 132 to 20 +/- 6 pg.ml-1 (P less than 0.05) during MVR, and from 178 +/- 41 to 110 +/- 48 pg.ml-1 during CABG (P less than 0.05). Rewarming during bypass was associated with an increase in ANF concentration in both groups. Heparin anticoagulation and protamine reversal had no effect on immunoreactive ANF levels. In patients undergoing CABG, there was a linear relationship between plasma ANF concentration (pg.ml-1) and right atrial pressure (mmHg) prior to cardiopulmonary bypass (r = 0.86, P less than 0.005). However, one and three hours after cardiopulmonary bypass there was no significant relationship between right atrial pressure and ANF plasma levels. These results suggest that reduction in plasma ANF concentration occurs during hypothermic cardiopulmonary bypass. Furthermore, the proportional relationship between atrial distension and circulating ANF concentration was altered following cardiac surgery.