Recovery-based practice: do we know what we mean or mean what we know?

The concept of recovery is now widely promoted as the guiding principle for the provision of mental health services in Australia and overseas. While there is increasing pressure on service providers to ensure that services are recovery oriented, the way in which recovery-based practice is operationalized at the coalface presents a number of challenges. These are discussed in the context of five key questions that address (i) the appropriateness of recovery as a focus for service delivery, (ii) the distinction between recovery as a process and an outcome, (iii) the assessment of recovery initiatives, (iv) the alignment of recovery with current service delivery models, and (v) the risks associated with recovery-based practice. It is argued that these questions provide a framework for a debate that must extend beyond patients and providers of mental health services to the broader public, whose attitudes will ultimately determine the possibilities and limits of recovery-oriented practice.     

Childhood epilepsy: what is the evidence for what we think and what we do?

This article reviews the strength of the evidence that underlies the current approach to the management of childhood epilepsy. The authors reviewed published, peer-reviewed English literature accessed through PubMed and Cochrane reviews with evidence rated as Class 1 (strongest) to Class 4 (weakest). There is considerable inaccuracy in the diagnosis of seizures and epilepsy syndromes. Sound information supports the consensus that the diagnosis of epilepsy should await two unprovoked seizures. Population-based studies indicate that remission from childhood onset epilepsy occurs in at least 50% of children. It is easier to predict a good seizure outcome than a poor one. Absence of concomitant neurologic handicap and onset before about 12 years of age are the most consistent predictors of remission. Intractability is poorly defined and difficult to predict until several antiepilepsy drugs have been used and failed to control the seizures. Most epilepsy syndrome diagnoses do not yield an accurate prognosis. Social outcome appears unsatisfactory in about 50% of cases without intellectual handicap. Death is rare in childhood epilepsy. Those without severe neurologic handicaps have the same mortality as the general population. We identified only 27 published randomized trials of antiepilepsy drugs in children that compare the efficacy of antiepilepsy drugs, offer treatment of syndromes currently without successful treatment, or have negative effects. There is a pressing need for better definitions of seizures and epilepsy syndromes. The causes of poor social outcome are unclear. Intractability needs a clear definition and randomized trials comparing treatment regimes are sadly lacking.     

Pediatric stroke: what do we know and what do we need to know?

Stroke is a heterogeneous disorder and an important cause of mortality and chronic morbidity in children. Estimates of international incidence rates for childhood stroke have varied widely. Arterial ischemic stroke is reported to be more common than hemorrhagic stroke in children. The clinical presentation of stroke in children differs according to the child's age and stroke type and location. Several risk factors for ischemic and hemorrhagic stroke in children have been reported and include cardiac disorders, blood disorders, vasculopathies, viral infections, and arteriovenous malformations. Current treatment recommendations for stroke in children are based on small nonrandomized trials, adult stroke studies, case series, or consensus or individual expert opinion. Over half of children with stroke will develop lifelong cognitive or motor disability, and up to a third will have a recurrent stroke. International studies have provided important information on stroke in children, but major gaps in our knowledge of the disorder still exist. Currently, there is a need for prospective cohort studies in diverse populations, which utilize a consensus pediatric stroke classification system and a standard evaluation of risk factors and outcome, so that treatment and prevention strategies can be developed.     

Measuring anxiety: are we getting what we need?

This article discusses several studies describing either the reevaluation and validation of existing scales for measuring anxiety (i.e., the Spielberger Trait Anxiety Inventory, the Liebowitz Social Anxiety Scale for adults and for children and adolescents, the Clinical Global Impression Scale, the Self-Rating Inventory for Posttraumatic Stress Disorder, and the Yale-Brown Obsessive Compulsive Scale Symptom Checklist), or the development and validation of new scales (i.e., the Social Thoughts and Beliefs Scale, the Social Phobia Diagnostic Questionnaire, the Aberdeen Trauma Screening Index and the Health Anxiety Inventory). As an increasing number of rating scales have been developed over the past several years, a critical review of their usefulness and psychometric properties seems pertinent and prudent.     

Migraine prophylaxis: what is new and what we need?

A wide array of options are now available for migraine prophylaxis. Conventional treatments include beta-blockers, anticonvulsants, antidepressants, calcium antagonists and antiserotoninergic drugs. Emerging medications such as ACE inhibitors, sartans and nutritional supplements are gaining favour for migraine prophylaxis. Botulinum toxin type A is a promising therapeutic tool for chronic migraine. Tonabersat is likely to be a step forward for the treatment of migraine with aura. However, much work is needed to identify predictive clinical features of successful responsiveness and to better define the duration of prophylaxis.     

Animal models of the ketogenic diet: what have we learned, what can we learn?

Despite its clinical use as a therapy for refractory epilepsy for more than 75 years, the ketogenic diet (KD) remains a therapy in search of an explanation. The mechanism of action of the KD is unclear and the optimal indications for its clinical use are incompletely defined. Animal models could help to elucidate these questions. Surprisingly, there have been very few animal studies of the KD, and those that have been performed are difficult to compare because of wide discrepancies in experimental methods. Earlier models concentrated on the effect of the KD on acute seizure threshold in normal (i.e. nonepileptic) animals. Recent studies are beginning to examine the longer term effects of the KD and its role in epileptogenesis. Some features of clinical experience have been replicated in animal models, including the role of ketosis, elevation of seizure threshold by both classic ketogenic and medium chain triglyceride diets, better effectiveness at younger ages, and rapid reversal of the seizure protective effect when the diet is discontinued. These parallels raise hope that pertinent clinical questions can be addressed in the more controlled setting of the research laboratory. As in the clinical arena, there has been a recent resurgence of interest in pursuing basic questions related to the ketogenic diet, using techniques of modern neuroscience. Experimental approaches such as brain slice neurophysiology, genetic models, dissection of metabolic pathways, and neurohistological techniques hold much promise in the effort to understand this intriguing alternative to standard anticonvulsants.     

Schizophrenia today: what do we know-and how sure are we?

The growth of our understanding of the biology and treatment of schizophrenia is still very much a work in progress. In this article, which introduces a series of papers presented at a conference entitled "Schizophrenia: Doing the Right Thing Well," held at Northcoast Behavioral Healthcare System (Cleveland, May 2000), the authors provide a short overview of what is known about schizophrenia today. He briefly reviews findings concerning epidemiology, phenomenology and course, neurobiology, and treatment, and highlights some of the most significant findings to date as well as areas needing further research. Early evaluation and treatment, in advance of the florid presentation of the illness, offer much hope, but only if our knowledge of the diagnostic specificity of prodromal and neurodevelopmental precursors can be enhanced. Significant advances in medication treatment have been made, and the newer antipsychotic medications overall have a more benign adverse-effect profile than the older agents, although the specter of endocrine/metabolic complications looms as a significant long-term concern. The authors conclude that, although many advances in our understanding of the etiology and treatment of schizophrenia have been made, much remains to be learned.     

Brain temperature: what do we know?

This review article presents a summary of recent efforts to understand brain temperature and its regulation under different conditions. Brain temperature has a crucial influence on brain processes. Its regulation is the outcome of the balance of core and arterial blood temperatures, cerebral blood flow, brain metabolism, functional conditions, and external temperature. However, the relationship between these factors is not fully understood and several uncertainties remain. There are no satisfactory normative data on temperatures throughout the brain, but new technologies promise to fill this gap. Brain temperature changes with brain functional activation and under pathological conditions in ways that are not understood. A full understanding of brain temperature control is mandatory to optimize attempts at brain cooling during clinical conditions such as stroke and head injury.     

Stroke trials: what have we learned?

We reviewed the recent, major, therapeutic trials of intravenous thrombolytic therapy and ancrod for ischemic stroke. Randomized, controlled studies of acute ischemic stroke treatment were reviewed. Several post-FDA approval intravenous tPA studies were reviewed to understand the experience of this medication in practice. STAT trial was the major study using ancrod. Of multiple intravenous thrombolytic studies, the NINDS study of intravenous tPA was the only study to demonstrate a significantly higher percentage of patients with complete recovery or minimal deficit at three months. Studies in communities utilizing intravenous tPA for stroke illustrate the need for close adherence to the NINDS study protocol or else the risk of tPA use may exceed the benefits.     

Sleep deprivation in depression: what do we know, where do we go?

Manipulations of the sleep-wake cycle, whether of duration (total or partial sleep deprivation [SD]) or timing (partial SD, phase advance), have profound and rapid effects on depressed mood in 60% of all diagnostic subgroups of affective disorders. Relapse after recovery sleep is less when patients are receiving medication; it may be prevented by co-administration of lithium, pindolol, serotonergic antidepressants, bright light, or a subsequent phase advance procedure. Diurnal and day-to-day mood variability predict both short-term response to SD and long-term response to antidepressant drug treatment. These mood patterns can be understood in terms of a "two-process model of mood regulation" based on the model well established for sleep regulation: the interaction of circadian and homeostatic processes. The therapeutic effect of SD is postulated to be linked to changes in disturbed circadian- and sleep-wake-dependent phase relationships and concomitant increase of slow-wave-sleep pressure; additionally, SD-induced sleepiness may counteract the hyperarousal state in depression. This model has the advantage of providing a comprehensive theoretical framework and stringent protocols ("constant routine," "forced desynchrony") to dissect out specific disturbances. Many aspects tie in with current serotonergic receptor hypotheses of SD action. A treatment inducing euthymia in severely depressed patients within hours is an important therapeutic option that has come of age for clinical use.