- Section 1 ICU organization and management
- Section 2 Pharmacotherapeutics
- Section 3 Resuscitation
- Section 4 The respiratory system
- Section 5 The cardiovascular system
- Section 6 The gastrointestinal system
- Section 7 Nutrition
- Section 8 The renal system
- Section 9 The neurological system
- Part 9.1 Anatomy and physiology
- Part 9.2 Neurological monitoring
- Part 9.3 Sleep disturbance
- Part 9.4 Agitation, confusion, and delirium
- Part 9.5 The unconscious patient
- Part 9.6 Seizures
- Chapter 231 Pathophysiology and causes of seizures
- Chapter 232 Assessment and management of seizures in the critically ill
- Part 9.7 Intracranial hypertension
- Part 9.8 Stroke
- Part 9.9 Non-traumatic subarachnoid haemorrhage
- Part 9.10 Meningitis and encephalitis
- Part 9.11 Non-traumatic spinal injury
- Part 9.12 Neuromuscular syndromes
- Section 10 The metabolic and endocrine systems
- Section 11 The haematological system
- Section 12 The skin and connective tissue
- Section 13 Infection
- Section 14 Inflammation
- Section 15 Poisoning
- Section 16 Trauma
- Section 17 Physical disorders
- Section 18 Pain and sedation
- Section 19 General surgical and obstetric intensive care
- Section 20 Specialized intensive care
- Section 21 Recovery from critical illness
- Section 22 End-of-life care
(p. 1098) Pathophysiology and causes of seizures
- Chapter:
- (p. 1098) Pathophysiology and causes of seizures
- Author(s):
Thomas P. Bleck
- DOI:
- 10.1093/med/9780199600830.003.0231
Seizures result from imbalances between excitation and inhibition, and between neuronal synchrony and dyssynchrony. Current models implicate the cerebral cortex in the genesis of seizures, although thalamic mechanisms (particularly the thalamic reticular formation) are involved in the synchronization of cortical neurons. Often, the precipitants of a seizure in the critical care setting are pharmacological. Several mechanisms linked to critical illness can lead to seizures. Failure to remove glutamate and potassium from the extracellular space, functions performed predominantly by astrocytes, occurs in trauma, hypoxia, ischaemia, and hypoglycaemia. Loss of normal inhibition occurs during withdrawal from alcohol and other hypnosedative agents, or in the presence of GABA. Conditions such as cerebral trauma, haemorrhages, abscesses, and neoplasms all produce physical distortions of the adjacent neurons, astrocytes, and the extracellular space. Deposition of iron in the cortex from the breakdown of haemoglobin appears particularly epileptogenic. Although acute metabolic disturbances can commonly produce seizures in critically-ill patients, an underlying and potentially treatable structural lesion must always be considered and excluded.
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- Section 1 ICU organization and management
- Section 2 Pharmacotherapeutics
- Section 3 Resuscitation
- Section 4 The respiratory system
- Section 5 The cardiovascular system
- Section 6 The gastrointestinal system
- Section 7 Nutrition
- Section 8 The renal system
- Section 9 The neurological system
- Part 9.1 Anatomy and physiology
- Part 9.2 Neurological monitoring
- Part 9.3 Sleep disturbance
- Part 9.4 Agitation, confusion, and delirium
- Part 9.5 The unconscious patient
- Part 9.6 Seizures
- Chapter 231 Pathophysiology and causes of seizures
- Chapter 232 Assessment and management of seizures in the critically ill
- Part 9.7 Intracranial hypertension
- Part 9.8 Stroke
- Part 9.9 Non-traumatic subarachnoid haemorrhage
- Part 9.10 Meningitis and encephalitis
- Part 9.11 Non-traumatic spinal injury
- Part 9.12 Neuromuscular syndromes
- Section 10 The metabolic and endocrine systems
- Section 11 The haematological system
- Section 12 The skin and connective tissue
- Section 13 Infection
- Section 14 Inflammation
- Section 15 Poisoning
- Section 16 Trauma
- Section 17 Physical disorders
- Section 18 Pain and sedation
- Section 19 General surgical and obstetric intensive care
- Section 20 Specialized intensive care
- Section 21 Recovery from critical illness
- Section 22 End-of-life care