The electrical discharge of neurons associated with seizure activity stimulates a marked rise in cerebral metabolic activity. Estimates from animal experiments indicate that energy utilization during seizures increases by more than 200", while tissue adenosine triphosphate (ATP) levels remain at more than 95" of control, even during prolonged status epilepticus. The brain generally withstands the metabolic challenge of seizures quite well because enhanced cerebral blood flow delivers additional oxygen and glucose. Mild to moderate degrees of hypoxemia that commonly accompany seizures are usually harmless. However, severe seizures and status epilepticus can sometimes produce an imbalance between metabolic demands and cerebral perfusion, especially if severe hypotension or hypoglycemia is present. A marked increase in glutamate release, which occurs during a prolonged seizure, is likely to result in the activation of all types of glutamate receptors. Although kainic acid produces seizures in the immature brain, it produces little cytotoxicity.

Recent advancements in molecular genetics have expanded our understanding of the etiology of many neurological diseases and neurodevelopmental abnormalities. Having a comprehensive understanding of genetics is essential in treating patients with metabolic epilepsies. Genetic counseling has been defined as a process of helping people understand and adapt to the medical, psychological, and familial implications of genetic contributions to disease. Some of the components of a genetic counseling interaction include interpretation of family and medical histories to assess the chance of disease occurrence or recurrence; education about inheritance, testing, management, prevention, resources, and research; and counseling to promote informed choices and adaptation to the risk or condition. The genetic counselor may also educate patients and their families about the underlying genetics of their epilepsy and the relevance of a genetic cause of epilepsy for family members, including recurrence risk, reproductive options and the possible teratogenic effect of antiepileptic drugs.

This chapter presents a brief review of the enzymes, transporters, and cofactor producers of the urea cycle. Seizures have long been associated with urea cycle disorders (UCDs), thought to be caused by high levels of ammonia. Furthermore, the brain damage obtained during metabolic crisis has been thought to damage critical structures, leading to epilepsy after the conclusion of the crisis. The first and most critical step of successful treatment of UCDs is recognition. Neurologic monitoring is an essential part of the emergency management of UCDs. The neurological abnormalities observed in patients with urea cycle defects are vast. Controlling ammonia levels by dialysis and complementary medication are needed. EEG monitoring should be initiated early, as this may be very useful for clinical management and indication of untreated metabolic crises. Furthermore, aggressive treatment of clinical and subclinical seizure activity may be helpful in optimizing outcomes for these patients.

Clinical neurophysiology (CNP) is a time-honored medical specialty that continues to make great strides, bolstered by rapid advances in neuroscience, biomedical engineering, and computer technology. It encompasses a wide range of methods and techniques for recording, presenting, and analyzing neurophysiologic signals in order to diagnose sensory, motor, autonomic, and central nervous system disorders. Testing performed in CNP or procedures used in current neurological practice include a variety of modality-specific and mixed-modality tests. Modality-specific CNP tests are performed to assess specific functional modalities using biomedical instruments that measure changes in neurophysiologic signals that occur spontaneously or with activation. Mixed-modality CNP tests utilize two or more test modalities to assess complex states (e.g., sleep, coma), to track multiple physiologic parameters, or to obtain more accurate results. CNP tests are classified based on functional anatomy or neural pathway tested. This chapter discusses artifact recognition and presents sources of artifacts in clinical neurophysiologic testing.

This chapter promotes a better understanding of women’s experience of abuse. It articulates strategies used in victim advocacy, and addresses the experiences and needs of female victims of intimate partner violence. The chapter examines common practices used and issues faced by victim advocates–who are often trained social workers–who work with women who have been victimized by a male intimate partner. It also highlights firsthand experiences of a victim advocate for female victims of intimate partner violence. Many women continue to be victims of intimate partner violence, and the work of victim advocates who serve these women is challenging. Advocates must be able to assess the needs of victims, refer them to appropriate services, protect their rights, empower them, and help them navigate the criminal and civil justice systems. These responsibilities require advocates to possess various personal and professional skills and to collaborate with many different professionals.

Stroke is the fifth major cause of death in the United States. Eighty seven percent of strokes are ischemic and thirteen percent are hemorrhagic. The incidence of cerebral edema in ischemic stroke is reported to be about 10% to 15% in large retrospective case studies. Cerebral edema in ischemic and hemorrhagic stroke remains a significant complication/sequel of the underlying disease and prompt diagnosis and management remains of utmost importance. Time tested medical management has not changed significantly over the past two decades. However, the use of minimally invasive surgery could change the paradigm for the surgical management for intracerebral hemorrhage. The use of hemicraniectomy for malignant middle cerebral artery infarcts complicated by life-threatening edema remains the best treatment in selected patients. More research is needed to explore the role of potential molecular targets for the management of cerebral edema in patients after acute stroke.

Cardiac complications following ischemic and hemorrhagic stroke occur frequently. The time frame for these complications includes the days following the event. In addition, patients who suffer from stroke also have an increased risk of cardiovascular morbidity and mortality in the months and years following stroke. Complications include myocardial infarction and cardiac arrhythmias. This chapter discusses the frequency of these events, their diagnosis, and potential prevention. Potential mechanisms underlying myocardial injury and electrical abnormalities detected on ECG include hypothalamic–pituitary–adrenal axis alteration, alterations in immune system function, and gut microbiome dysbiosis. Prevention of arrhythmias after stroke has not been studied to the same extent as arrhythmias after myocardial infarction. Identification of arrhythmias immediately following stroke is accomplished by monitoring patients on telemetry. Future studies are needed to identify early interventions that may reduce the likelihood of these events.

The treatment for ischemic stroke rests upon early revascularization of occluded arteries to restore blood flow and oxygen to ischemic but salvageable cerebral tissue and prevent impending neuronal cell death. Cerebral ischemic reperfusion injury (CIRI) is the biochemical cascade that occurs as a result of recanalizing an occluded artery, causing further tissue damage that parallels and antagonizes the benefits of restoring blood flow to the ischemic tissue. CIRI can worsen brain ischemia, cause hemorrhagic transformation, blood–brain barrier (BBB) disruption with subsequent cerebral edema, and is associated with worse outcomes. Clinical management of CIRI continues to hinge on prevention, early recognition, blood pressure reduction, and optimal glucose management. As recanalization becomes more common, understanding what happens to the parenchyma, cerebrospinal fluid, microglia, BBB, and vasculature after mechanical thrombectomy and pharmacologic clot lysis is vital. CIRI will become more common and mitigating its response will become a top priority.

Any pathological process can have complications, from common cold to cancer. As with any acute illness, patients with acute stroke are at high risk of complications. Complications in the setting of acute stroke can be grouped into two broad categories: cerebral and extracerebral; or neurological and medical, respectively. Both types can place the patient at risk for death and influence functional outcomes after stroke. Complications not only measure the success and quality of care, but also underscore the necessity for proper surveillance and preventive therapy. In an acute stroke patient, physical deterioration is probably the most early and sensitive sign of disarray. Acute stroke care units are particularly proficient in recognizing and acting upon symptoms of clinical or neurological deterioration due to complications. Management of acute stroke complications depends upon the type and the number of coexisting complications.

Hemorrhagic transformation (HT) is a frequent, spontaneous, and natural consequence of infarction and reperfusion characterized by a range of ischemia-related blood extravasation. This chapter defines the physiopathology, epidemiology, classification, and risk factors involved in the incidence of HT of acute ischemic stroke (AIS) after thrombolytic therapy. It discusses different predictive tools using imaging, clinical scores, and blood markers currently under research that will be able to predict the risk of symptomatic intracerebral bleeding after thrombolytic therapy. The chapter establishes the recognition and management of symptomatic intracerebral bleeding after thrombolytic therapy. The best ways to prevent the development of symptomatic intracerebral hemorrhage is adherence to treatment guidelines. However, additional validation studies are needed to confirm the utility of these methods before they should be used in clinical practice.