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Case complexity and resistance to change have the potential to derail the successful treatment of child conduct problems in part through the effects they have on therapists. This chapter examines therapist competencies for responding to complexity and resistance to change in the evidence-based treatment of such problems. Key dimensions of case complexity among families of children referred for conduct problems are outlined, along with principles for adapting treatment plans based on these dimensions. A reflective practice model for overcoming resistance to change is then detailed. This process model, which draws heavily on principles from family therapy and research into parental resistance during the treatment of conduct problems, is designed to promote a shared therapeutic agenda and empower parents in the change process. Case examples and practical illustrations are presented throughout
This chapter highlights the key competencies required to deliver effective evidence-based cognitive behavioural therapy (CBT) for youth with anxiety disorders and their families. A number of generic competencies and specific CBT competencies are important for a clinician to master. Generic competencies include the ability to conduct a competent assessment and understanding relevant child and adolescent characteristics, whereas specific CBT competencies include competence in delivering key CBT strategies, such as cognitive restructuring and exposure. Clinicians also need to consider the role of family factors in maintaining youth anxiety. This chapter addresses the factors that clinicians need to consider when making a decision about the type and extent of parental involvement in therapy. Finally, some of the common obstacles to successful CBT intervention for youth anxiety and strategies for overcoming them are considered.
Cannabis is the most widely used illicit drug worldwide, and it is estimated that up to 30% of people who use cannabis will develop a cannabis use disorder (CUD). Demand for treatment of CUD is increasing in almost every region of the world and cannabis use is highly comorbid with mental disorders, where sustained use can reduce treatment compliance and increase risk of relapse. In this narrative review, we outline evidence for psychosocial and pharmacological treatment strategies for CUD, both alone and when comorbid with psychosis, anxiety or depression. Psychosocial treatments such as cognitive behavioural therapy, motivational enhancement therapy and contingency management are currently the most effective strategy for treating CUD but are of limited benefit when comorbid with psychosis. Pharmacological treatments targeting the endocannabinoid system have the potential to reduce cannabis withdrawal and cannabis use in CUD. Mental health comorbidities including anxiety, depression and psychosis hinder effective treatment and should be addressed in treatment provision and clinical decision making to reduce the global burden of CUDs. Antipsychotic medication may decrease cannabis use and cannabis craving as well as psychotic symptoms in patients with CUD and psychosis. Targeted treatments for anxiety and depression when comorbid with CUD are feasible.
The Roma people are one of the most unknown and interesting nations in Europe. Although they are severely marginalised within European societies, they have greatly influenced European culture. Despite this fact, there is a deep prejudice against them. In the region of East Macedonia and Thrace, a significant proportion of the population are Roma. Their marginalisation leads to many problems and also affects their mental health. Their psychopathological manifestations differ from the majority population. They express more somatic complaints and higher overall stress in a histrionic background. The main obstacles regarding their mental health issues and treatment appear to be the following: gender inequality, illiteracy and lack of cultural sensitivity in healthcare system. Although all of these obstacles must be removed, some are easier to remove than others. Cultural sensitivity could be applied by using more culturally sensitive diagnostic tools, improving overall training for mental health professionals and treating Roma wherever they seek help, because they often have a nomadic style of living. Telemedicine can be quite useful in serving this goal. Improving their educational status and addressing gender inequalities issues, on the other hand, are more difficult and long-term goals.
Medical care is predicated on ‘do no harm’, yet the urgency to find drugs and vaccines to treat or prevent COVID-19 has led to an extraordinary effort to develop and test new therapies. Whilst this is an essential cornerstone of a united global response to the COVID-19 pandemic, the absolute requirements for meticulous efficacy and safety data remain. This is especially pertinent to the needs of pregnant women; a group traditionally poorly represented in drug trials, yet a group at heightened risk of unintended adverse materno-fetal consequences due to the unique physiology of pregnancy and the life course implications of fetal or neonatal drug exposure. However, due to the complexities of drug trial participation when pregnant (be they vaccines or therapeutics for acute disease), many clinical drug trials will exclude them. Clinicians must determine the best course of drug treatment with a dearth of evidence from either clinical or preclinical studies, where at least in the short term they may be more focused on the outcome of the mother than of her offspring.
Medical advancements have encouraged minimally invasive surgical repair of congenital heart defects such as ventricular septal defects (VSDs), and the diagnostic process can now be carried out using non-traditional techniques such as pulse oximetry. This, in turn, has improved clinical outcomes with reduced complication rates post-surgery. However, the variations in type of VSDs, age of patient, comorbidities, and access to closure devices may limit the efficacy of surgical advancements.
Articles were identified amongst Scopus, MEDLINE, and PubMed using various relevant search strings using PRISMA guidelines. Of the 115 articles initially extracted, 10 were eventually reviewed after duplicates and irrelevant studies were removed.
Of the 24 eligible articles, 10 papers were selected for analysis. Minimally invasive approaches to VSD repair was associated with satisfactory short-term outcomes when compared to open repair. For diagnosis of congenital VSD, whilst recent advances such as pulse oximetry method and genome analysis are more sensitive, the limited availability and access to such investigatory methods must be recognised.
Pulse oximetry and fetal echocardiography are established non-invasive diagnostic tools for VSD. The recent advances in minimally invasive treatment options including periventricular approach and transcatheter techniques have improved patient outcomes, yet at the expense of higher residual rates. Careful patient selection for each technique and follow-up should be planned through multidisciplinary team meetings.
With the exception of near-occlusion, CEA is of overall benefit for selected patients with recent symptomatic carotid stenosis =50% (NASCET method), provided surgical stroke/death risk is low. The benefit is greater with greater stenosis, men, the elderly (aged =75y), most recent ischaemic event within 2w, irregular plaque surface, and impaired cerebral perfusion reserve. Patients with recent symptomatic carotid territory ischaemic events should be screened by Doppler ultrasonography, MRA, or CTA, confirming substantial stenosis with a second non-invasive investigation. Catheter angiography may be required to confirm uncertain results. The surgical peri-operative stroke and death rate (7% in RCTs) is higher in women, hypertension, peripheral arterial disease, and occlusion of the contralateral ICA or ipsilateral ECA. The experience of the surgeon and hospital are crucial, and audited peri-operative complication rates should be publically available. Carotid stenting is less invasive than CEA and causes fewer local complications (cranial neuropathy and neck haematoma), but carries a higher procedural risk of stroke. Stenting should be considered in younger patients, or those at increased risk from CEA. While stenting is of high risk for intracranial vertebral artery stenosis, risk is low for extracranial stenosis and should be considered for recurrent symptoms despite optimal medical therapy.
More than 20,000 patients have participated in clinical trials of more than 100 neuroprotective therapies, but no study has provided convincing evidence of benefit. Several improvements to the rigor of preclinical agent qualification have been identified to increase the likelihood of success in human clinical trials: stringent randomization and blinding techniques to mitigate observer bias; assessment in in time periods achievable in the clinical setting; testing in older animals with comorbidities; and robust and reproducible benefit magnitudes. Human clinical trials should start agents hyperacutely, in the first minutes and hours after onset, when treatment effect would be maximal; target enrolment of patients likely to have transient rather than permanent ischaemic exposure; and use factorial and platform trial designs that would permit efficient testing of combinations of agents able to block multiple ischaemic injury-mediating pathways concurrently, including both anti-necrotic and anti-apoptotic interventions. For agents that allow cells to endure ischaemic stress, human trial delivery approaches include: prehospital initiation; initiation immediately upon brain imaging in patients destined for endovascular intervention; and initiation at outside hospitals in patients undergoing transfer to a neurothrombectomy center. For agents that mitigate reperfusion injury, treatment start before or concurrent with reperfusion, including intra-arterial administration via catheter immediately after endovascular thrombectomy, should be pursued.
Aneurysmal SAH is a severe disease, and the post-haemorrhage period fraught with potential complications that must be recognized and treated early for favourable outcome. While diagnosis of SAH is often straightforward from clinical history and initial CT, some patients will require cerebrospinal fluid evaluation. The aneurysm must be secured urgently to reduce rerupture and clinical worsening. Endovascular coiling is preferable when feasible, but surgical clipping is sometimes needed based on patient or aneurysmal characteristics, or presence of intraparenchymal haemorrhage requiring evacuation. Treatment of symptomatic hydrocephalus with CSF diversion is also crucial. Patients with aneurysmal SAH should be managed by a team of nurses and physicians with neurocritical care, neuroendovascular, and neurosurgical expertise, preferably in a dedicated neurosciences intensive care unit. Early complications include aneurysmal rebleeding, hydrocephalus, and neurogenic cardiopulmonary injury. In the subacute phase, delayed cerebral ischaemia and hyponatremia are more commonly seen. With optimal multidisciplinary management, many patients can return to their previous level of function only weeks after the aneurysm rupture. Still, most treatments in SAH are based on insufficient evidence, and more collaborative research from the bench to the bedside is necessary to continue improving patient outcomes.
Intracerebral haemorrhage and subarachnoid haemorrhage are associated with considerable morbidity and mortality. Too often the focus is on acute treatment after a haemorrhage has occurred, instead of primary and secondary prevention. Medical therapies to control hypertension, achieve tobacco abstinence, and avoid excessive alcohol consumption can confer broad reductions in haemorrhage risk across pathophysiological subtypes. Judicious restriction of antiplatelet and anticoagulant therapies to only those individuals and those intensities for which they are indicated also can substantially reduce haemorrhagic stroke frequency. Specific endovascular and surgical therapies, judiciously employed, will further reduce risk of first or recurrent haemorrhage from structural vascular anomalies, including arteriovenous malformation, cavernous malformations, and saccular aneurysms. For unruptured intracranial aneurysms, features that favour consideration of preventive occlusion include include younger patient age, prior subarachnoid haemorrhage from a different aneurysm, familial intracranial aneurysms, large aneurysm size, irregular shape, basilar or vertebral artery location, and aneurysm growth on serial imaging. Among individuals who are technical candidates for either coiling or clipping, endovascular coiling is associated with a reduction in procedural morbidity and mortality but has a higher risk of recurrence.
Non-invasive brain stimulation to stimulate neuroplasticity, enhance recovery, and improve mood after stroke has made substantial technical advances in the past two decades. The most common neuromodulatory techniques are transcranial direct current stimulation (tDCS), applying a weak electrical current across the brain, and transcranial magnetic stimulation (TMS), inducing an electrical field within the brain. Currently, the only non-invasive brain stimulation technique and indication for which there is a sufficiently strong evidence base to support routine use in clinical practice is transcranial magnetic stimulation to improve mood in post-stroke depression. TMS applied to dorsolateral prefrontal cortices can substantially reduce depressive symptoms, though not increase complete remission. TMS is a reasonable second-line intervention in patients with post-stroke depressed mood who have been resistant to pharmacotherapy. For several additional indications in post-stroke patients, both TMS and tDCS have shown signals of potential benefit in randomized trials. The strongest evidence is for enhancement of recovery of upper extremity motor function and hand dexterity with TMS. In addition, there is suggestive evidence for possible benefit in improving recovery of function after stroke in walking (TMS), activities of daily living (tDCS), aphasia (both), hemispatial neglect (both), and swallowing (both). However, for these and potentially other recovery-enhancing applications, substantial additional larger trials are needed.
In broad, relatively unselected patients with acute ischaemic stroke, immediate high-dose anticoagulation therapy to avert early stroke progression or recurrence reduces recurrent ischaemic stroke compared with control during the treatment period but this benefit is offset by an increase in intracranial haemorrhage (ICH) and extracranial haemorrhage (ECH). Immediate antiplatelet therapy has similarly efficacy as anticoagulation in averting early stroke progress or recurrence, and is safer when used as an immediate agent (see Chapter 9). In acute ischaemic stroke patients with atrial fibrillation, after start of antiplatelet therapy on presentation, early switchover to anticoagulation therapy 2 -14 days after stroke onset is reasonable, but caution should be taken in certain subgroups of patients with high risk of bleeding. In broad, relatively unselected ischaemic stroke patients, low-dose, venous prophylaxis anticoagulation compared with control reduces the occurrence of asymptomatic deep venous thrombosis (DVT) and shows a tendency to reduce pulmonary embolism, but also shows off-setting tendencies to increase ICH and ECH, without conferring a clear net clinical benefit. Low-molecular-weight heparins (LMWH) or heparinoids, compared with unfractionated heparin, appear to further decrease the occurrence of DVT and PE but potentially further increase ICH, but there are too few data to provide reliable information.
In acute ischaemic stroke, cerebral blood flow autoregulatory mechanisms may be disrupted so that cerebral perfusion becomes reliant on systemic blood pressure. Too low blood pressure may lead to progression of the infarction and too high blood pressure may cause cerebral oedema or haemorrhagic transformation of the infarct. In patients with BP = 220/120 mm Hg who do not receive intravenous thrombolysis, it is reasonable to lower BP by 15% during the first 24 hours after stroke onset. Patients who have elevated blood pressure and are otherwise eligible for treatment with intravenous rt-PA should have their blood pressure lowered so that systolic blood pressure is < 185 mm Hg and their diastolic blood pressure is < 110 mm Hg before thrombolytic treatment is administered. Acute stroke patients should be assessed for dehydration and a fluid balance chart should be kept. Underlying causes of hypotension should be treated rapidly. There is no beneficial effect of hemodilution treatment for acute ischaemic stroke. Fibrinogen-depleting agents that reduce viscosity may marginally reduce risk of recurrent ischaemic stroke, but more greatly increases symptomatic intracranial haemorrhage. Methylxanthine derivatives such as pentoxyphylline and propenofylline that reduce viscosity and produce vasodilation have insufficient evidence to support their use.
Long-term (>1 year) single antiplatelet therapy with aspirin is effective in reducing the risk of any early recurrent stroke by about one-sixth compared with no antiplatelet therapy. Clopidogrel monotherapy is marginally but significantly more effective than aspirin in reducing major vascular events. Cilostazol is also more effective than aspirin in Asian patients, and its therapeutic efficacy may be augmented by the addition of probucol in patients with ischaemic stroke and high risk of cerebral haemorrhage. The safety and effectiveness of cilostazol in non-Asian patients is not known. Prasugrel monotherapy (3.75 mg daily) is not non-inferior to clopidogrel monotherapy among Japanese patients with non-cardioembolic ischaemic stroke. Dual antiplatelet therapy with aspirin and extended-release dipyridamole is more effective than aspirin monotherapy and equally effective as clopidogrel monotherapy in preventing recurrent stroke. Dual antiplatelet therapy with aspirin and clopidogrel is more effective than aspirin monotherapy in preventing recurrent ischaemic stroke and myocardial infarction in high vascular risk patients, but it also increases the risk of major bleeding which may offset its benefits. Dual antiplatelet therapy with cilostazol added to aspirin or clopidogrel is more effective, and as safe as, aspirin or clopidogrel monotherapy in Japanese patients with non-cardioembolic ischaemic stroke.
Pre-clinical studies provide clear and consistent evidence that a variety of centrally acting drugs affecting specific neurotransmitters can either facilitate or interfere with functional recovery after brain injury. Although at least some clinical trials suggest similar effects in humans, results have been inconsistent. The impact of important factors such as drug dose, duration, and intensity of physiotherapy, and timing between injury and treatment are difficult to translate from preclinical studies. Issues related to variability in stroke severity, location of injury, and comorbid conditions further complicate trial design and could obscure a true treatment effect. Because of these and other issues, the design of efficacy trials assessing putative neuro-restorative interventions is not trivial. Although a proven pharmacological approach resulting in a clinically meaningful improvement in post-stroke recovery remains elusive, it is reasonable to avoid medications that may have harmful effects in patients who have had a stroke. It is also important to control for these possible harmful effects in future clinical trials assessing the outcomes of stroke patients after the acute period.
Language and cognitive impairments are common consequences of stroke. These difficulties persist with 60% of stroke survivors continuing to experience memory problems, 50% attention deficits and 61% communication problems long after the onset of the stroke-related impairments. Such deficits are ‘invisible’ – evident only through patient report, behavioural observation or formal assessment. The impacts of such deficits are considerable and can include prolonged hospital stays, poorer functional recovery and reduced quality of life. Effective and timely rehabilitation of language (auditory comprehension, expressive language, reading and writing) and cognitive abilities (memory, attention, spatial awareness, perception and executive function) are crucial to optimise recovery after stroke. In this chapter we review the current evidence base, relevant clinical guidelines relating to language and cognitive impairments and consider the implications for stroke rehabilitation practice and future research. Speech and language therapy offers benefit to people with aphasia after stroke; intensive intervention, if tolerated, likely augments the benefits. Interventions for deficits in all non-language cognitive domains exist, but need refining and evaluating more thoroughly with a wider range of methodologies.
Worldwide, stroke is a most common disabling disorder that requires rehabilitation services if curative and preventive treatments fail. There is growing evidence that intensive rehabilitation offered by a multidisciplinary team is effective to improve outcome in terms of independent daily living and health–related quality of life. This conclusion is based on systematic reviews and recent pragmatic phase III and IV trials. Although intensity of practice is an important part of effective stroke care, very early mobilization should be restricted and applied in small doses within 24 hours post-stroke. Systematic review shows that evidence-based therapies for the upper limb are constraint–induced movement therapy and upper limb robotics, whereas interventions that could be beneficial to gait include fitness training and high-intensive, task-specific training. A number of novel therapies, such as combining exercise therapy with transcranial direct current stimulation, repetitive transcranial magnetic stimulation or pharmacological interventions, and virtual reality are under way. However, the evidence for most of these therapies is still unclear and in its infancy.
Cervical artery dissection (CAD) is characterized by an intramural haematoma due to a subintimal tear and accounts for up to 25% of ischaemic strokes in young and middle-aged adults. Data regarding intravenous thrombolysis and endovascular thrombectomy in CAD are scarce and observational – both are reasonably safe and probably recommended. Based on observational evidence, antithrombotic therapy is used to prevent first or recurrent cerebral ischaaemic events in acute or subacute CAD, and event rates are low with either antiplatelet or anticoagulant therapy. The long-term rate of recurrent cerebral ischaemic events or bleeding complications in CAD patients is small while under antithrombotic treatment. Cerebral vasculitis treatment is based on observational series. When primary angiitis of the central nervous system is confirmed by biopsy, a combination of glucocorticoids and cyclophosphamide should be started. Rituximab may be used in patients who are intolerant of cyclophosphamide. In atypical, non-biopsy-proven cases, treatment should be adapted to the severity of neurological involvement. For giant cell arteritis, initial high-dose prednisolone is recommended, beginning a slow taper after 2–4 weeks and continuing at a low dose for 1–2 years. Treatment of p-ANCA-positive and -negative systemic vasculitis with cerebral involvement includes induction corticosteroid therapy followed by addition of cyclophosphamide or other glucocorticoid-sparing drugs.
Cardiogenic embolism is a common cause of recurrent ischaemic stroke. The cardiac source of embolism is usually the left atrial appendage and atrium due to atrial fibrillation (AF). Other sources include the left ventricle, heart valves and venous system or right atrium, via a patent foramen ovale.The most effective thromboprophylactic is oral anticoagulation, which reduces the risk of recurrent stroke by about two thirds, compared to no anticoagulation. Four target-specific, direct-acting non-vitamin K antagonist oral anticoagulants (NOACs) – the direct thrombin inhibitor dabigatran etexilate, and the factor Xa inhibitors rivaroxaban, apixaban and edoxaban – are at least as efficacious and safe as warfarin, and apixaban is superior to, and as safe as, aspirin, for preventing stroke among patients with AF. Other potential stroke prevention strategies include left atrial appendage occlusion for patients with AF in whom anticoagulation is contraindicated, anticoagulation for left ventricular thrombus and prosthetic heart valves, antibiotics +/– valve surgery for infective endocarditis, and transcatheter device closure of a symptomatic patent foramen ovale.
Although higher plasma cholesterol concentrations have not been reported to be associated with increased stroke risk, cholesterol lowering has been reported to decrease this risk. This decrease can be achieved with statins, which are well-tolerated, provided they are not given to patients with active liver or muscle diseases. Statin treatment in addition to a healthy lifestyle is recommended for the primary prevention of ischaemic stroke in patients with pre-existing coronary heart disease or other high-risk conditions such as diabetes and hypertension. Statins with intensive lipid-lowering effects are recommended for their positive influence on reducing the risks of stroke and cardiovascular events for patients with prior ischaemic stroke or TIA presumed to be of non-cardioembolic origin, even with an LDL-C level =100 mg/dL, with or without evidence of other clinical atherosclerotic cardiovascular diseases. Despite the good safety profile of statins, further studies are clarify safety in patients with prior cerebral haemorrhage and if they may increase brain haemorrhage to a small degree. PCSK9 inhibitors are advised, as add-on therapy to statins, for patients with a high cardiac risk not able to achieve an optimal LDL-C level, though studies with longer follow-up are needed