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Obesity is highly prevalent and disabling, especially in individuals with severe mental illness including bipolar disorders (BD). The brain is a target organ for both obesity and BD. Yet, we do not understand how cortical brain alterations in BD and obesity interact.
We obtained body mass index (BMI) and MRI-derived regional cortical thickness, surface area from 1231 BD and 1601 control individuals from 13 countries within the ENIGMA-BD Working Group. We jointly modeled the statistical effects of BD and BMI on brain structure using mixed effects and tested for interaction and mediation. We also investigated the impact of medications on the BMI-related associations.
BMI and BD additively impacted the structure of many of the same brain regions. Both BMI and BD were negatively associated with cortical thickness, but not surface area. In most regions the number of jointly used psychiatric medication classes remained associated with lower cortical thickness when controlling for BMI. In a single region, fusiform gyrus, about a third of the negative association between number of jointly used psychiatric medications and cortical thickness was mediated by association between the number of medications and higher BMI.
We confirmed consistent associations between higher BMI and lower cortical thickness, but not surface area, across the cerebral mantle, in regions which were also associated with BD. Higher BMI in people with BD indicated more pronounced brain alterations. BMI is important for understanding the neuroanatomical changes in BD and the effects of psychiatric medications on the brain.
Transient neurological symptoms often present a difficult diagnostic dilemma. It is often difficult to tell if the transient symptoms were due to ischemia or due to something else (see Chapter 1). Usually, by the time the physician sees the patient, the neurological exam has returned to normal. On the other hand, it is critically important not to miss the diagnosis of transient ischemic attack (TIA). TIAs may provide an opportunity for physicians to intervene and prevent an ischemic stroke and subsequent disability, and must be taken seriously. The search for an etiology must be done expeditiously. Just as angina may serve as a warning for future myocardial infarction, a TIA is often a warning sign of an impending stroke.
As acute stroke therapies have developed, the context in which stroke care is provided has become more important. Creating and maintaining the organization of stroke care within a region or even a hospital requires much commitment and effort. High-quality stroke care requires coordination and communication between multiple stakeholders in the prehospital and in-hospital settings in what the American Heart Association (AHA) and American Stroke Association (ASA) term the “stroke chain of survival” (Table 14.1).
It is never too early to begin to educate the patient and family about lifestyle changes and medical treatments to prevent another stroke. These need to be reinforced throughout the hospital and rehabilitation stay, and in the outpatient stroke clinic.
After a major stroke, both the family and the patient go through a grief reaction that at first includes denial and disbelief, and sometimes anger. In particular, the need to insert a PEG is often a crisis point when the family finally comes to terms with the severe disability and prolonged recovery that lies ahead. At this stage, which is usually when the patient is in the acute stroke unit, mainly supportive measures are indicated.
In this chapter, we discuss mainly secondary prevention for stroke, although many of the measures, especially control of risk factors and lifestyle changes such as not smoking, controlling blood pressure, etc., are also important measures to avoid a first stroke.
Initially, we discuss a tailored diagnostic work-up, then general measures for secondary prevention of ischemic stroke, and finally recommendations for specific conditions that are associated with a high risk of recurrent stroke.
The following initial measures apply to all stroke patients. They are necessary to stabilize and assess the patient, and prepare for definitive therapy. All current and, probably, future stroke therapies for both ischemic and hemorrhagic stroke are best implemented as fast as possible, so these things need to be done quickly. This is the general order to do things, but in reality, in order to speed the process, these measures are usually dealt with simultaneously. They are best addressed in the ED, where urgent care pathways for stroke should be established and part of the routine (see Chapter 14).
This chapter covers the diagnosis and management of spontaneous subarachnoid hemorrhage due to rupture of intracranial aneurysms. At the end of the chapter we also discuss unruptured intracranial aneurysms. Much SAH management is not based on good-quality evidence. Much of what is recommended here comes from published practice guidelines and what is commonly practiced. Options for therapy might be limited by the availability and experience of persons performing surgery, endovascular therapy, and neurointensive care.
In this chapter, we consider spontaneous hemorrhage into the brain parenchyma and ventricles (intracerebral hemorrhage, ICH). Non-traumatic bleeding into the subarachnoid space (subarachnoid hemorrhage, SAH) is covered in Chapter 13. Traumatic subdural and epidural hemorrhages are not covered in this book.
Intracerebral hemorrhage is associated with very high morbidity and mortality. It is important to realize that, as with acute ischemic strokes, time is of the essence in ICH. The reason for this is that the blood accumulates rapidly, and the volume of the hematoma is the most important determinant of outcome.
Cerebral venous sinus thrombosis (CVST) is the thrombosis of dural venous sinuses and/or cerebral veins. It accounts for 0.5% of all strokes. It occurs predominantly in the younger population (usually < 50 years old, median age of 37). Female-to-male ratio is 3 to 1, likely secondary to sex-specific thrombogenic states including pregnancy, puerperium, oral contraceptive pill use, and hormonal therapy.
When used alone, intravenous and intra-arterial thrombolysis have yielded low recanalization rates of proximal large-vessel occlusions (LVO). The endovascular trials utilizing first-generation devices such as the Merci retriever and the Penumbra aspiration system were essentially neutral and failed to demonstrate superiority of mechanical thrombectomy over IV tPA (MR RESCUE, SYNTHESIS, IMS-III). In 2015, however, six trials – MR CLEAN, EXTEND-IA, SWIFT PRIME, ESCAPE, REVASCAT, and THRACE – led to a fundamental shift in how we acutely manage LVOs today. All six trials compared endovascular thrombectomy (EVT) to IV tPA alone and demonstrated clear superiority of thrombectomy in patients presenting within 6 hours from the time they were last known well (LKW) if they met specific imaging criteria.
This chapter discusses the four main components of acute ischemic stroke care. The sections on prevention of complications, and recovery and rehabilitation, are applicable to both ischemic and hemorrhagic stroke patients.
Although, classically, stroke symptoms are maximal at onset and patients gradually recover over days, weeks, and months, patients sometimes deteriorate. People have termed the phenomenon stroke progression, stroke in evolution, stroke deterioration, and symptom fluctuation. There is no consistent terminology. The phenomenon occurs from different causes and is incompletely understood. Although the typical definition of a significant neurological deterioration in trials has been a gain of ≥ 1 point on item 1a (level of consciousness) or ≥ 4 points in the motor items of the NIHSS, any detectable deterioration should prompt careful assessment and a tailored work-up.