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Fever commonly produces tachypnea out of proportion to the increase in metabolic acid production associated with illness, resulting in a respiratory alkalosis that may be profound. The excessive motor activity of generalized convulsions, especially generalized convulsive status epilepticus (GCSE), can raise core temperature. Central stimulant intoxication produces both seizures and hyperthermia. The clinician must distinguish febrile seizures from other types of seizures that may be triggered by fever. There are some epilepsies for which febrile exacerbation is characteristic, such as generalized epilepsy with febrile seizures plus, and severe myoclonic epilepsy of infancy (Dravet syndrome). Lowering the temperature of patients who are markedly febrile in the setting of status epilepticus involves termination of seizure activity as well as external cooling and treatment of any underlying condition producing fever, such as infection. Induced hypothermia is gaining attention as a potential therapy for refractory status epilepticus.
Dakshin Gullapalli, Department of Neurology, University of Virginia School of Medicine, Charlottesville, VA, USA,
Thomas P. Bleck, Neuroscience Intensive Care Unit, University of Virginia School of Medicine, Charlottesville, VA, USA
Infections of the central nervous system (CNS) are notable for rapid progression resulting in death or permanent damage in a very short time (Baraff et al., 1993; Grimwood et al., 1995). CNS infections share many distinct characteristics, which distinguish them from systemic infections. The CNSis confinedanatomically within abonycasement which allows little room for expansion following inflammatory responses; the resulting increase in intracranial pressure may cause severe damage to the structures within. The CNS also lacks awell-developed conventional immune system to defend against offending pathogens, and thus infections are more difficult to eradicate than in the periphery. Because of the presence of the blood–brain barrier (BBB), delivery of antimicrobial agents in adequate concentrations is difficult. As vital tissues are involved, CNS infections can cause devastating sequelae, and in some cases may result in both neurologicalandmedicalemergencies. Understanding their pathophysiological mechanisms, neuroanatomical principles, clinical manifestations and neuroaradiological features is essential to providing effective treatment.
Infections can primarily occur either within the brain parenchyma or in the spaces between the different layers of the brain called meninges. Between the dura mater and the arachnoid lies the subdural space, through which the veins course from the brain surface to the venous sinuses. The dura mater is tightly bound to the inner table of skull, and hence intracranially the epidural space is a potential space; along the spinal column, the dura is separated from bone by fat and other structures. The subarachnoid space refers to the space between the pia mater and the arachnoid membrane which contains CSF and the mediumsized arteries supplying blood to the brain. CSF in the ventricles is in continuity with the CSF in the subarachnoid space through the foramina of Luschka and Magendie.The CSF is finally absorbed by the arachnoid granulations to drain into the venous sinuses.
Bacterial meningitis is an inflammatory response to infection of the pia-arachnoid and the CSF of the subarachnoid space. Since the subarachnoid space is continuous throughout the neuraxis, this inflammation extends throughout the subarachnoid space as well as ventricles. When there is accompanying obvious brain involvement, it is more appropriately called meningoencephalitis. Histologically, most meningitides include some parenchymal involvement, but when clinical signs of meningeal inflammation predominate one traditionally refers to the condition as meningitis. Knowledge of the anatomic details and CSF flow pathways is important to understand the pathophysiologic manifestations.
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