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Critically ill patients admitted to the intensive care unit (ICU) may exhibit signs and symptoms of primary or secondary neurological disorders. Factors such as altered mental status, agitation, pain, sedation, neuromuscular blockade, hypothermia, metabolic disturbances, intubation/mechanical ventilation, and surgical or traumatic lesions of the extremities may complicate the interpretation of the neurological assessment in the ICU. Nevertheless, neurological signs in the critically ill have been established as prognostic indicators and markers of severity. Subsequently, a proper neurological assessment of the critically ill patient remains a central aspect of care, diagnosis, and prognosis [1].
Acute confusional state (ACS) is very common in the intensive care unit (ICU) setting. Most often, it is one of the main reasons a neurology consult is requested in the surgical or medical ICU. Acute confusional states are often used interchangeably when describing metabolic encephalopathy, delirium, ICU psychosis, or septic encephalopathy. Encephalopathy is defined as a subacute global brain dysfunction that is gradual in onset with very broad clinical symptoms, whereas delirium is often described as an acute process. The list of potential causes (Table 32.1) of ACS could be summarized using “Vitamin E” as a mnemonic. In this chapter, we will only focus on management of delirium and toxic metabolic encephalopathy.
Antibody-associated disorders of the central nervous system (CNS) are divided into two broad categories: classic paraneoplastic disorders and autoimmune disorders (i.e. autoimmune encephalitis) [1]. Autoimmune encephalitis is associated with antibodies that bind to cell surface determinants of membrane-associated proteins on neuronal cells (neuronal surface antibody syndrome –NSAb), whereas paraneoplastic syndromes are associated with intracellular neuronal antigens. It can be challenging at times to differentiate between the two syndromes. Patients with NSAb usually present with an acute or subacute symptom onset, with short duration to nadir, and a very good response to immunotherapy [2]. Table 18.1 summarizes some of the characteristics of each. In this chapter, we will focus on the diagnosis and management of autoimmune encephalitis (AE).