Congenital heart disease (CHD) is the commonest birth defect, and children may present at all ages with variably corrected lesions for both elective and emergency surgery. No single anaesthetic approach can be recommended in this heterogeneous group of children, so a general strategy is presented based on applied physiology and the available evidence. Pathophysiological patterns are presented along with the common physiological consequences of cardiac disease in children: cardiac failure, cyanosis, pulmonary hypertension and arrhythmias. Children with congenital heart disease presenting for non-cardiac surgery are at increased perioperative risk compared to their unaffected peers. Risk factors are identified, and a scoring system to predict in-hospital mortality is presented. Preoperative assessment encompasses consideration of the optimal location for surgery as well as specific considerations, including echocardiography, infectious endocarditis prophylaxis and pacemaker/ defibrillators. In general, a balanced anaesthetic technique including controlled ventilation and opioids to reduce volatile exposure is preferred. However, with appropriate understanding of the underlying physiology, most anaesthetic techniques can be used safely and successfully in children with CHD.

Tremor, which is defined as an oscillatory and rhythmic movement of a body part, is the most common movement disorder worldwide. The most frequent tremor syndromes are tremor in Parkinson’s disease, essential tremor, and dystonic tremor syndromes, whereas Holmes tremor, orthostatic tremor, and palatal tremor are less common in clinical practice. The pathophysiology of tremor consists of enhanced oscillatory activity in brain circuits, which are ofen modulated by tremor-related afferent signals from the periphery. The cerebello-thalamo-cortical circuit and the basal ganglia play a key role in most neurologic tremor disorders, but with different roles in each disorder. Here we review the pathophysiology of tremor, focusing both on neuronal mechanisms that promote oscillations (automaticity and synchrony) and circuit-level mechanisms that drive and maintain pathologic oscillations.

Tics are brief, sudden, non-rhythmic, repetitive movements. Tics can be motor or vocal. Further, both motor and vocal tics can be either simple or complex. Simple tics typically involve only one group of muscles and are brief and meaningless, whereas complex tics may last longer and appear more purposeful. Tic disorders usually begin in childhood and are classified according to the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) into four groups: (1) provisional tic disorder, (2) chronic motor or vocal tic disorder, (3) Tourette disorder (or Gilles de la Tourette syndrome), (4) tic disorder not otherwise specified. As tics can resemble almost any other movement disorder, phenotypic analysis alone is insufficient and patients must be questioned whether the execution is preceded by a premonitory sensation (urge to do, urge to move) and whether a temporary control of the movement can be achieved. Also, relief following execution of the tic is frequently reported. There are no biomarkers available for tics and diagnosis therefore remains strictly clinical.

"Ataxia" refers to both the neurologic syndrome of motor coordination and to a large and diverse group of diseases that have motor coordination impairment as their main clinical feature. The brain structure most consistently affected is the cerebellum. Although many different brain diseases may manifest with ataxia, the vast majority of slowly progressive ataxias are genetic diseases. Indeed, genetic molecular analysis has become the cornerstone of both diagnosis and classification of this complex group of conditions. In this overview, the basics of the clinical features and the classification of these diseases, as well as common conditions, and recently defined novel forms of ataxia are discussed.

This chapter provides a review for post-traumatic stress disorder (PTSD). It starts by presenting the epidemiological data as well as the risk factors in the development of PTSD. It then defines the diagnosis of PTSD, by using both DSM-5 and ICD-11 criteria, and provides a clinical approach on how to clarify differential diagnoses and comorbidities. It then reviews the pathophysiology and pathogenesis of PTSD by looking at neuroanatomic, neuroendocrine, neurochemical, and genetic changes in brain neural networks. It concludes by presenting the current evidence-based options for the treatment and management of PTSD that include psychotherapy and pharmacotherapy.

Mood disorders are among the most prevalent and potentially severe mental disorders. These conditions are associated with important psychological morbidity and functional impact, as well as elevated rates of suicide. While the past several decades have produced valuable contributions to the understanding of the pathophysiology of mood disorders, currently available treatments at times fail to produce full remission and restore patient’s premorbid level of function. Nevertheless, promising new agents and novel therapeutic targets are currently under investigation. The twenty-first century is looking at an individualized approach for the management of mood disorders, with the proper integration of evidence-based, effective biological and psychosocial therapeutic modalities.

‘Psychotic disorders’ is an umbrella term for psychiatric conditions featuring psychosis, including mood disorders. Despite the prominence of psychotic symptoms across the psychotic spectrum, a distinction between schizophrenia and affective psychoses has been historically established. Findings from genetic studies support the aetiological overlap between affective and non-affective psychosis, although poor characterisation of the schizoaffective population still poses a challenge. Likewise, literature points to shared environmental risk factors between bipolar disorder and schizophrenia. Neuroimaging evidence suggest significant similarities in the pathophysiology of the brain between affective and non-affective psychosis. An overlap is also observed in other biological and behavioural illness markers, as well as in the pharmacotherapy of psychotic disorders. Current diagnostic entities may not accurately delineate the aetiology and pathophysiology of these conditions. Modern classification approaches, such as the RDoC framework, propose the adoption of aetiological factors and pathophysiological evidence to characterise patients, rather than categorical diagnoses based on symptoms.

This chapter considers how to care for patients who meet the criteria for a diagnosis of personality disorder. We reflect on the role of the psychiatrist in creating a resilient, honest and caring clinical environment, delivering interventions in a considered and coherent manner. Central to this is the relationship between doctor and patient, which includes not only direct clinical care but also the orchestration of work across the multi-disciplinary team and other agencies through clinical leadership.

We approach personality disorders as a relational problem in which the patient experiences their difficulties through their relationships with themselves and the world around them. These difficulties often, though not exclusively, are a developmental consequence of adverse childhood experiences, brought to life within the therapeutic relationship itself. This inevitably means the work is challenging, but it also means that the way we comport ourselves and lead becomes central to the therapeutic culture.

Much has been written on the challenges of working with people who are diagnosable with personality disorder, but perhaps less acknowledged is how these challenges represent not only the very material fundamental to our primary task but also the reason it is such rewarding work given the right circumstances.

Medication-related osteonecrosis of the jaw (MRONJ) is a debilitating condition, characterised by non-healing bone, with subsequent chronic infection, pain and morbidity. While osteonecrosis of the jaw can occur spontaneously in healthy patients, it most commonly occurs in patients taking medications that affect bone turnover and is precipitated by an invasive procedure such as a dental extraction. Medications that increase MRONJ risk are commonly used in the Australian population, therefore awareness of their association with MRONJ is critical in dental practice. In 2015, approximately 470,000 Australians were dispensed a medication for osteoporosis on the PBS (1). Other bone diseases that require medical treatments include Paget’s disease, and cancers that metastasise to bone such as multiple myeloma, breast, and prostate cancer. Corticosteroids contribute to MRONJ risk and are frequently used in the Australian population for acute and chronic disease. Antiangiogenic drugs are increasingly in use not just for treatment of malignancy, but also post-transplant and for autoimmune disease.

Neuropathic pain (NP) is a common complication of spinal cord injury (SCI) that is difficult to treat. Chronic NP is associated with increased levels of inflammatory mediators and ion channel dysfunction, as well as nerve damage and nerve-glia crosstalk. Recent studies have made headway in identifying novel biomarkers, including microRNA and psycho-social attributes that can predict progress from SCI to chronic NP (CNP). Conventional medical treatment has limited success, but recent studies have identified new biomarkers and promising drugs, such as baclofen and ziconotide, that can provide pain relief. However, further studies are needed to determine the safety profile of these drugs. Nonmedical interventions, such as brain sensitization and biofeedback techniques, have also shown promise in managing CNP. A multidisciplinary approach, including psycho-social support, medical and nonmedical interventions, is necessary to effectively manage CNP in SCI patients.

Suicide is a complex public health problem driven by a multitude of biopsychosocial factors and is the result of gene–environment interactions. Psychosocial variables like chronic stress and trauma have biologic ramifications and can contribute to various forms of pathophysiology, dysregulation, and degradation, represented by allostatic load (AL). AL is the wear and tear that stress exerts on the body, and it has been associated with mental health problems and suicide. Fortunately, there are pharmacological and non-pharmacological interventions that may be effective at reducing AL and reversing its effects. Incorporating AL into efforts to promote early risk identification, prevention, and treatment of suicide is an important consideration. Critical next steps are identifying which AL biomarkers are most malleable, which effective treatments reduce AL, and if these reductions of AL are associated with decreased suicide.

During your call duty, a healthy 32-year-old primigravida at 22+3 weeks’ gestation, confirmed by first-trimester sonography, presents to the obstetrics emergency assessment unit of your hospital center with new-onset, asymptomatic port-wine-colored urine with chills and an oral temperature of 39.1°C at home; she also notes a two-day history of headache, now accompanied by visual changes. Your obstetric trainee informs you that clinical history is not suggestive of an infectious etiology, although comprehensive investigations are pending. She has no obstetric complaints, and fetal viability was ascertained upon presentation. Routine prenatal laboratory investigations, aneuploidy screening, and fetal morphology survey were unremarkable. The laboratory urgently notifies you that the platelet concentration is 12 × 109/L, confirmed on manual count; other requested laboratory tests are in progress.

During your call duty, a 38-year-old G5P4 with a spontaneous dichorionic pregnancy presents to the obstetric emergency assessment unit of your tertiary center at 37+5 weeks’ gestation with dyspnea and noticeable bilateral leg edema. She has no obstetric complaints. Your colleague follows her prenatal care. Routine prenatal laboratory investigations, aneuploidy screening, fetal morphology surveys, and serial sonograms have all been unremarkable. She had four uncomplicated pregnancies and term vaginal deliveries in your hospital center.

A 37-year-old G6P3A2 at 20+3 weeks’ gestation is referred from a community hospital center for consultation at your tertiary center’s high-risk obstetrics unit for ‘anterior placenta previa with abnormal features’ reported on ultrasound evaluation of the morphologically normal female fetus. First-trimester sonography performed in the same center, integrated with maternal serum biomarkers, revealed a low risk of fetal aneuploidy.