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V. Larson, M.A., M.D., M.P.H.
Vice Chair, Texas Tech University Health Sciences Center Paul L. Foster School of Medicine
Resting-state functional magnetic resonance imaging data was also acquired for all participants. Future studies with an increased number of female participants is required to address potential sex differences in connectivity patterns related to symptoms of depression and anxiety. Abstract: E-cigarette use has increased dramatically among adolescents in the past 5 years alongside a steady increase in daily use of marijuana. This period coincides with a historic rise in depression and suicidal ideation among adolescents. In this study, we describe the associations between e-cigarette and marijuana use and depressive symptoms and suicidality in a large nationally representative sample of high school students. We used data from the 2 most recent waves (2015 and 2017) of the Youth Risk Behavior Survey. Our sample (n = 26,821) included only participants with complete information for age, sex, race/ethnicity, and exposure to e-cigarettes and marijuana (89. We performed multivariate logistic regressions to explore the associations between single or dual use of ecigarette and marijuana and depressive and suicidal symptoms in the past year adjusting for relevant confounders. Youth with single and dual e-cigarette and marijuana use had increased odds of reporting depressive symptoms and suicidality compared to youth who denied use. There is a need for effective prevention and intervention strategies to help mitigate adverse mental health outcomes in this population. Study quality was assessed using the Research Triangle Institute item bank on risk of bias and precision of observational studies. In the studies selected, depression was diagnosed according to the third or fourth editions of Diagnostic and Statistical Manual of Mental Disorders or by using scales with predetermined cutoff points. After screening 3142 articles, 269 articles were selected for full-text review, 35 were selected for further review, and 11 studies comprising 23317 individuals were included in the quantitative analysis. Although individual-level risk remains moderate to low and results from this study should be confirmed in future adequately powered prospective studies, the high prevalence of adolescents consuming cannabis generates a large number of young people who could 135 develop depression and suicidality attributable to cannabis. This is an important public health problem and concern, which should be properly addressed by health care policy. She told me that nearly all her patients had used marijuana heavily, many at the times of their crimes. Marijuana drives a surprising amount of psychosis, and psychosis-besides being a terrible burden for sufferers and their families-is a shockingly high risk for violent crime. People with schizophrenia commit violent crime at rates far higher than healthy people - their homicide rates are about 20 times as high. Since cannabis causes paranoia-not even advocates dispute that fact-and psychosis, it is not surprising that it would drive violent crime. And in fact there are a number of good studies showing that users have significantly higher violence rates than non-users. Further, in researching the book, I found many, many cases where the causation appeared clear. In some cases it was as simple and obvious as, this person-with no history of violence-smoked, became psychotic, and committed a homicide. Of the potential 2449 articles that were screened for eligibility, 12 studies were analyzed using a random-effect meta-analysis. These findings are clinically relevant for violence prevention/management and highlight the necessity of further investigations with methodologically-sound studies. We estimated the prevalence of physical abuse during pregnancy, we analyzed the main risk factors and described the relationship between physical violence, psychological wellbeing and pregnancy outcome. Methods We used a national representative sample of births, in all public and private maternity units, in 2016 in France. Women were interviewed after delivery, on their living conditions and occurrence of physical violence at least once during pregnancy. The study of risk factors and pregnancy outcome was done with multivariable logistic regressions.
The final Constant score was compared in the patients with a conversion procedure and in patients with specific procedures. While both groups significantly improved as -Within a ten-year period, since 2003, we reported 5. Anterior shoulder prosthetic instability has most often been attributed to disruption of the repaired subscapularis tendon 19 and has been linked to inferior outcomes 3,13,18,23. Nevertheless the most frequently identified cause for instability in our study was subscapularis tendon rupture (10/27). One argument is that a glenoid metal-backed component (which is thicker than a cemented glenoid component) could lead to subscapularis and/or massive rotator cuff tendon rupture and consequently to anterior instability or to a devastating anterior-superior escape of the humeral head 31. Type B2 and C glenoid dysplasia - which is one of the major causes for post-operative instability 11,21 - is not rare in patients with shoulder osteoarthritis and represents 2432. That is the reason why soft-tissue failure in our study may be due to overstraining of the soft tissue during correction of posterior dysplasia in four out of nine cases (44. Those results highlight the fact that the amount of bone block to be placed in order to prevent a posterior instability from happening has to be quantified. Inability to correct posterior glenoid Walch B2 or C deformities with regular cemented glenoid components has been associated with high rate of loosening whichever be the technique used: 152 Paris Shoulder Course 2019 Currents Concepts in Shoulder Arthroplasty 153 either augmentation with polymethylmetacrylate cement to fill the posterior defect or bone grafting which may lead to thermal necrosis during cement setting 7. Although anteverting the humeral component to compensate for glenoid retroversion is relatively simple and has been advocated by many investigators 1,5,8 19,20,26,32 it does not increase the stability of a shoulder replacement with a retroverted glenoid component 12,25. Soft-tissue imbalance is present in most cases of instability following shoulder arthroplasty, and component malpositioning plays an additional role in some cases. Sanchez-Sotelo showed that more than one half of the shoulders remained unstable despite attempts of revision 24. On the other hand nine patients who had specific open procedures such as bone blocks, humeral or glenoid component revision, subscapularis repair, reduction or nothing had a final Constant score of 39. Finally eleven unconstraint prostheses sustained episodes of prosthetic instability without any rotator cuff deficiency whereas sixteen unconstraint prostheses had either an isolated subscapularis tendon tear (ten) or a massive rotator cuff tear (six). Consequently, we do think that, soft-tissue deficiency was the main cause for unconstraint prosthesis instability instead of component malpositioning. This platform system with a cementless glenoid had the advantage of preservation of bone stock, reconstruction of glenoid bone loss if any and easier revision 15. As opposed to previous studies we had predictable and reliable results thanks to a platform system that made the revision easier. Subscapularis function after primary tendon to tendon repair in patients after replacement arthroplasty of the shoulder. Total shoulder arthroplasty for glenohumeral arthritis associated with posterior glenoid bone loss: results of an all-polyethylene, posteriorly augmented glenoid component. Subscapularis muscle function and structure after total shoulder replacement with lesser tuberosity osteotomy and repair. Regarding "Metal-backed glenoid implant with polyethylene insert is not a viable longterm therapeutic option". Patient self-assessment of health status and function in glenohumeral degenerative joint disease. Loss of subscapularis function after total shoulder replacement: A seldom recognized problem. The effect of humeral component anteversion on shoulder stability with glenoid component retroversion. Minimum fifteen-year follow-up of Neer hemiarthroplasty and total shoulder arthroplasty in patients aged fifty years or younger. Mazzocca decoaptation is an abnormal gap between the humeral cup and glenosphere that results from insufficient deltoid tension (Figure 4). Hypertensioning can also cause permanent, resting abduction and axillary nerve damage. The range of motion between both stem inclinations was not significantly different. Further biomechanical data are needed to truly determine how altering the humeral inclination alone changes the abduction moment arm, center of rotation, and glenoid-baseplate interface. Figure 3 Medialization of the center of rotation (right) reduces posterior deltoid tension in external rotation. While some superior decoaptation is considered normal for the Grammont design, global Figure 5 Combined deltoid force requirements for maximal abduction are reduced with 135° and 155° humeral stems compared to the native state.
Syncope in an elderly, institutionalised population: prevalence, incidence, and associated risk. The postural orthostatic tachycardia syndrome: definitions, diagnosis, and management. Clinical characteristics of vasodepressor, cardioinhibitory, and mixed carotid sinus syndrome in the elderly. Syncope in advanced heart failure: high risk of sudden death regardless of origin of syncope. The utility of implantable loop recorders for diagnosing unexplained syncope in 100 consecutive patients: five-year, single-center experience. Randomized assessment of syncope trial: conventional diagnostic testing versus a prolonged monitoring strategy. Effect of patient characteristics on the yield of prolonged baseline head-up tilt testing and the additional yield of drug provocation. Prospective evaluation of day-to-day reproducibility of upright tilt-table testing in unexplained syncope. Evaluation of a single-stage isoproterenol-tilt table test in patients with syncope. Clinical evaluation of idiopathic paroxysmal kinesigenic dyskinesia: new diagnostic criteria. Hyperekplexia and stiff-man syndrome: abnormal brainstem reflexes suggest a physiological relationship. Factors determining the electroencephalogram in migraine: a study of 560 patients, according to clinical type of migraine. Visual phenomena and headache in occipital epilepsy: a review, a systematic study and differentiation from migraine. Epileptic vertigo: evidence for vestibular representation in human frontal cortex. Amygdala pathology in psychosis of epilepsy: A magnetic resonance imaging study in patients with temporal lobe epilepsy. In: Memory Disorders in Psychiatric Practice, eds G Berrios, J Hodges, 2000;187203. Further, there is a possibility of nocturnal seizures being misdiagnosed as parasomnia and vice versa. Finally, sleep disorders may aggravate epilepsy and epilepsy may aggravate certain sleep disorders. Normal sleep physiology and relationship to seizures Sleep consists of active brain states during which many biological processes occur, such as synaptic plasticity and memory consolidation1. The transition between wakefulness and sleep and between different sleep stages is often gradual and the mechanisms controlling these transitions are poorly understood. Particularly frontal lobe seizures often occur from both daytime and night-time sleep. However, if temporal lobe seizures occur during sleep, the seizures are more likely to secondarily generalise4. There may also be diurnal variation of certain types of epileptic syndromes such as juvenile myoclonic epilepsy or epilepsy with generalised tonic-clonic seizures on awakening5. The reasons for this remain unclear but it has been suggested that the increase in spike-wave activity seen after sleep deprivation may be due to more frequent fluctuations in vigilance levels both during wakefulness and sleep8. This has not been the case for control subjects or at least not to the same extent. Interestingly, changes have been seen bilaterally in patients with generalised epilepsies but only ipsilateral to seizures onset zone in patients with focal epilepsies9. The effect was most pronounced when seizures occurred during sleep but also significant when seizures occurred on the previous day. Disrupted sleep may hence contribute to the prolonged recovery time that some patients report following seizures. Differential diagnosis of paroxysmal nocturnal events Paroxysmal nocturnal events often represent a differential diagnostic challenge for the clinician. Patient recall is often poor and the bed partner is often the person instigating contact with medical professionals. Despite this, there may still be a limited history as events occur during the night when it is dark, and the witness may be asleep at the onset and miss part of the events.
These agents are almost invariably required in patients sedated with barbiturate anaesthesia. If seizures are continuing in spite of the measures taken above, the patient must be transferred to an intensive care environment. In severe established status epilepticus, intensive monitoring may be required, including: intra-arterial blood pressure, capnography, oximetry, central venous and pulmonary artery pressure monitoring. Although effective in preventing eclampsia, there is no evidence to suggest that increasing magnesium serum concentrations to supranormal levels has any benefit in status epilepticus. Indeed, such a policy can result in motor paralysis, difficulty in detecting clinical seizure activity and hypotension. Metabolic abnormalities may cause status epilepticus, or develop during its course, and biochemical, blood gas, pH, clotting, and haematological measures should be monitored. Intravenous lines should be set up for fluid replacement and drug administration (preferably with 0. Blood should be drawn for the emergency measurement of blood gases, sugar, renal and liver function, calcium and magnesium levels, full haematological screen (including platelets), blood clotting measures, and anticonvulsant levels; 50 ml of serum should also be saved for future analysis especially if the cause of the status epilepticus is uncertain. In prolonged status epilepticus, or in comatose ventilated patients, motor activity can be barely visible. The latter must be calibrated individually to register both burst-suppression and seizure activity. Burst-suppression provides an arbitrary physiological target for the titration of barbiturate or anaesthetic therapy. Drug dosing is commonly set at a level that will produce burst-suppression with interburst intervals of between 2 and 30 seconds. Continuous intracranial pressure monitoring is sometimes needed, especially in children in the presence of persisting, severe, or progressive elevated intracranial pressure. The need for active therapy is usually determined by the underlying cause rather than the status epilepticus. Intermittent positive pressure ventilation, high-dose corticosteroid therapy (4 mg dexamethasone every six hours), or mannitol infusion may be used (the latter is usually reserved for temporary respite for patients in danger of tentorial coning). Long-term, maintenance, anticonvulsant therapy must be given in tandem with emergency treatment. The choice of drug depends on previous therapy, the type of epilepsy, and the clinical setting. If phenytoin or phenobarbitone has been used in emergency treatment, maintenance doses can be continued orally (through a nasogastric tube) guided by serum level monitoring. Treatment of tonic-clonic status epilepticus Tonic-clonic status epilepticus is treated as an emergency in order to avoid both systemic complications and also cerebral damage. Cerebral damage is partly caused by physiological compromise and the consequent hypoxia/ischaemia, but it also results from excitotoxicity consequent upon continuous seizure activity. In the initial stages of a tonic-clonic seizure, there are compensatory mechanisms that result in increased cerebral perfusion. By 60-90 minutes these compensatory mechanisms fail; there is hypotension and, importantly, loss of cerebral autoregulation. In addition, at this stage, the continuous seizure activity results in intraneuronal calcium accumulation and neuronal death. These stages are: the premonitory (pre-hospital) stage, the early status epilepticus stage from 0-30 minutes, the stage of established status epilepticus from 30-60/90 minutes and then the refractory (late) stage during which substantial neuronal damage can occur. Stages in emergency drug treatment the suggested regimen for a typical new case presenting to a casualty department as an emergency is given in Table 2. These are guidelines, and obviously in some circumstances intensive care management and general anaesthesia may be required earlier. Premonitory stage In patients with established epilepsy, tonic-clonic status epilepticus seldom develops without warning. Usually, a prodromal phase (the premonitory stage), during which seizures become increasingly frequent or severe, precedes status epilepticus. Urgent drug treatment will usually prevent the evolution into true status epilepticus.
