Birth asphyxia and the resulting neonatal encephalopathy (NE) in neonates remains a critical condition causing significant mortality and long-term morbidities, including cerebral palsy, epilepsy, and global developmental delay. The incidence of birth asphyxia is approximately 2–4 cases per 1,000 live births in high-income countries (HICs), and up to 30 per 1,000 live births in low- and middle-income countries (LMICs). Currently, therapeutic hypothermia (TH) is the only proven treatment for NE in HICs, but its role in LMICs remains debated. However, up to 29% of these treated neonates still develop abnormal outcome. Research on adjunct treatments is ongoing to improve the outcome of these neonates. In the meantime, to prevent or limit further brain injury, supportive therapies and maintenance of homeostasis remain a cornerstone of the daily management of these neonates.

Premature birth remains a major cause of morbidity and mortality. Although there have been marked improvements in the survival of preterm infants, this has not been matched by a corresponding improvement in morbidity. Although there is some evidence for modest improvements in survival without disability in modern cohorts, others report no apparent improvement and even increases in disability after extremely preterm (<25 weeks’ gestation) birth. Traditionally, brain injury in preterm infants was thought to reflect a fundamental vulnerability of the developing periventricular white matter to damage. However, recent evidence suggests a much more complex picture. In the present chapter, we will critically dissect the neuropathology of preterm brain injury, including the timing of injury, the association of hypoxia–ischemia and infection/inflammation with adverse outcomes, and the importance of impaired maturation and late evolving injury of both white and gray matter regions, and highlight key unresolved issues.

The possibility of achieving an accurate and early diagnosis of cerebral palsy has become a reality and is now considered the standard of care. The shift toward early diagnosis has catalyzed the initiation of numerous clinical trials within the first 2 years of life, yielding emerging data on effective interventions. This research confirms the long-held belief in the critical importance of specialist intervention beginning before 6 months of age. The accumulation of evidence is rapidly reshaping the landscape of cerebral palsy diagnosis and early intervention knowledge, ultimately influencing child outcomes. Parents harbor hope that this earlier targeted treatment approach will yield improved outcomes for their children, and emerging data suggest that this optimism is well founded. As we continue to advance our understanding and refine our practices, the future holds promise for further enhancing the lives of individuals affected by cerebral palsy.

Neonatal encephalopathy (NE) encompasses a range of disorders presenting with altered brain function in neonates, often leading to long-term neurodevelopmental deficits. Characterized by symptoms such as altered consciousness, poor tone, and seizures, NE occurs in 1–6 per 1,000 live term births and is a major cause of neurodevelopmental disabilities. Although many cases relate to hypoxic–ischemic injury, other causes include metabolic disorders, infections, and congenital anomalies. The introduction of therapeutic hypothermia (TH) has improved outcomes for infants with hypoxic–ischemic encephalopathy (HIE), significantly reducing the incidence of severe neurodevelopmental disabilities. However, variations in practices and results persist, and adjunct therapies such as erythropoietin have not shown effective benefits. The chapter discusses the spectrum of neurocognitive impairments following HIE, predictors of outcomes based on brain injury patterns, and highlights ongoing research to understand the long-term impact of these interventions on affected individuals.

Obstetrics claims accounted for 62% of all clinical claims by value received in the year, highlighting the underlying impact of the financial costs of maternity indemnity payments, alongside the impact of harm on patients, families and healthcare staff. CTG misinterpretation contributes substantially to claims pertaining to mismanagement of labour and cerebral palsy. Medical negligence involves establishing causation and liability. Presence of abnormal CTG, low Apgar score, low cord arterial pH, assisted ventilation, admission to neonatal intensive care, moderate or severe neonatal encephalopathy and subsequent neurological damage point to asphyxia as a possible cause. However, several intrinsic fetal disorders cause neurological disability and an abnormal CTG may have been coincidental. Causation is best determined by neuroradiologist and paediatric neurologist based on the areas of scarring within the brain on MRI. The thalamus, basal ganglia injury show scarring, reflecting acute profound hypoxia while prolonged partial hypoxia results in bilateral cortical atrophy. Expert opinion is requested to judge whether the care provided fell short of what was expected (Bolam principle).

It is very much hoped that this book, which has moved away from the illogical, unscientific and potentially dangerous ‘nNormal, suspicious, pathological’ classification from its first publication in 2017, and is based on the principles of physiological interpretation of CTG, in line with the International Expert Consensus Statement published by more than 50 CTG experts from over 20 countries in 2024, will continue our journey to reduce avoidable harm to women, birthing people, their babies and the families. We owe this to women, birthing people, their babies and families who have placed in their trust in us to provide evidence-based clinical care, which is based on scientific foundations and the application of the knowledge of fetal pathophysiology.

Cerebral palsy (CP) refers to a heterogeneous group of neurological conditions appearing in early childhood, causing permanent motor dysfunction, and affecting muscle tone, posture or movement. These conditions are caused by abnormalities of the developing fetal or infant brain and are non-progressive in nature. They are often accompanied by cognitive and sensory impairments. While forms such as spastic quadriplegia and dyskinesia are notably associated with fetal hypoxia, existing evidence indicates that intrapartum events contribute to only 10–20% of all CP cases. Establishing a causal relationship between CP and events arising during labour requires multiple criteria to be met. Recent advancements in neuroimaging and diagnostic laboratory techniques have shed some light on the diverse pathways leading to brain injury. However, further research is still necessary to evaluate the impact of intrapartum fetal monitoring and obstetric interventions on the incidence of CP.

Paediatric orthopaedic surgery is wide-ranging in scope and complexity. Many patients have coexisting conditions, including cerebral palsy and neuromuscular diseases. Cerebral palsy presents a wide spectrum of motor dysfunction. Preoperative assessment must be guided by associated comorbidities and particularly evaluate respiratory function and any associated cardiac disease. Patients with muscular dystrophy presenting for major orthopaedic or spinal surgery have a high risk of morbidity and mortality, which must be discussed preoperatively; inhalational agents must be avoided due to the risk of rhabdomyolysis. Patients with conditions including osteogenesis imperfecta and arthrogryposis must be carefully managed and meticulously positioned for surgery. Major orthopaedic and spinal surgery can be accompanied by a significant risk of bleeding. Multimodal analgesic strategies, including the use of local anaesthetic blocks, should be used. Scoliosis may be congenital, acquired or idiopathic. Adolescent children with idiopathic scoliosis are often otherwise fit and healthy. In contrast, patients with acquired neuromuscular scoliosis often have significant comorbidities, particularly poor cardiorespiratory function, epilepsy and poor nutrition. Elective postoperative ventilation is frequently required. Intraoperative neuromonitoring is employed to detect and prevent potential spinal cord injury. Total intravenous anaesthesia is required for robust neuromonitoring of motor pathways, and muscle relaxation must be avoided intraoperatively.

Cerebral palsy (CP) is a neurological disorder that greatly affects movement and occurrence of muscle spasticity as well as other problems. Cerebral palsy significantly decreases quality of life in patients.Causes of CP are still not fully known but prenatal complications as well as trauma during pregnancy can lead to higher risk. It is recommended for expecting mothers to not overexert themselves during pregnancy and keep consistent health checkups to prevent causative factors. Current treatments to reduce spasticity and other symptoms involve botulinum toxin type A, intrathecal baclofen, dorsal rhizotomy, dantrolene, diazepam, flexeril, and tizanidine. Each method prevents some level of relief, but all come with their own existing risks and adverse effects. Patients must outweigh the risk over potential gain with the use of each treatment for pain and spasticity.

Botulinum neurotoxin (BoNT) injections are established as a standard procedure for the treatment of muscles in spastic or dystonic children. Superficial and palpable muscles are easy to inject. In contrast, exact needle placement is more difficult and less controllable in deep muscles or those that are small and difficult to selectively identify. Exact needle placement is, however, essential for optimal functional result, avoidance of side effects and evaluation of therapeutic failures. However, clinical application of BoNT without guidance techniques has been shown to be inaccurate. Several techniques are available to guide needle placement for injection. Electromyography is good, but many muscles may be simultaneously active. Electrical stimulation is uncomfortable and painful and often requires anesthesia. CT guidance necessitates exposure to radiation and is costly. By comparison, the advantages of the ultrasound-guided technique are obvious: real-time observation of the injection readily available easily applicable after a manageable learning period cost effective no serious side effects.

This chapter details the use of ultrasound for injection guidance, and discusses indirect and real-time techniques, and both parallel and perpendicular orientations, for needle placement.

Spasticity is part of the upper motor neuron syndrome produced by conditions such as stroke, multiple sclerosis, traumatic brain injury, spinal cord injury or cerebral palsy that affect upper motor neurons or their efferent pathways in the brain or spinal cord. It is characterized by increased muscle tone, exaggerated tendon reflexes, repetitive stretch reflex discharges (clonus) and abnormal spastic posturing. Late sequelae may include contracture, pain, fibrosis and muscle atrophy. The most common pattern of spasticity in the upper limb involves flexion of the fingers, wrist and elbow, adduction with internal rotation at the shoulder and sometimes thumb curling across the palm or fist. The most common pattern of spasticity in the lower limb involves extension at the knee, plantarflexion at the ankle and sometimes inversion of the foot.

Chemodenervation by intramuscular injection of botulinum toxin can reduce spastic muscle tone, normalize limb posture, ameliorate pain, modestly improve motor function and prevent contractures. This chapter uses anatomical illustrations to depict the muscles involved in common patterns of spastic posturing, using a “clinician’s eye” view to demonstrate approaches to injection points, discusses guidance techniques such as electromyography and tabulates dose ranges of the common toxin preparations for specific muscles.

Cerebral palsy is not a specific disease, but a clinical syndrome caused by a non-progressive injury to the developing brain that results in a disorder of movement and posture that is permanent but not unchanging. Spasticity is the most common movement disorder, affecting between 60% and 80% of children with cerebral palsy, and can manifest as spastic hemiplegia, spastic diplegia and spastic quadriplegia. Dystonia is characterized by involuntary sustained or intermittent muscle contractions that cause twisting and repetitive movements, abnormal postures or both. Athetosis, or intermittent writhing movement, is also very common. These movement disorders are all amenable to treatment with botulinum neurotoxin (BoNT). This chapter discusses topographical symptom distribution and illustrates the typical forms of cerebral palsy using an anatomical approach to management. Common clinical patterns of spastic posturing, the major involved, muscles and dose ranges for the different toxin preparations are tabulated.