Acute bacterial meningitis and stroke

Abstract

Introduction. Acute bacterial meningitis remains a common disease, especially in developing countries. Although advances over the last century have improved mortality and morbidity, the neurological adverse effects remain high. Specifically, acute ischaemic stroke is a serious comorbidity that represents both disease severity and poor prognosis. This review presents the clinical connection between meningitis and stroke, and discusses the neuroinflammatory components that have direct ties between these diseases. State of the art. Ischaemic stroke is the direct result of the inflammatory response produced to eradicate infectious pathogens. Bacterial virulence factors and pathogen-associated molecular patterns cause direct damage to the blood-brain barrier and trigger leukocytes to react to the infection. Cytokines are released that cause further destruction of the blood-brain barrier, lead to neuronal death, and recruit the prothrombotic effects of the coagulation cascade through the complement system. Unfortunately, this inflammatory response causes vasculopathy and hypercoagulation of the cerebral blood vessels, leading to cerebral ischaemia. Clinical implications. Pharmacological attempts to mitigate this inflammatory response have produced both positive and negative results. On the one hand, corticosteroids have been shown to improve mortality if given early in patients with bacterial meningitis, particularly pneumococcal meningitis. On the other hand, corticosteroids have been linked to delayed cerebral infarction and other adverse effects. Future directions. New targets for specific inflammatory markers have shown success in rodent models, but have not yet been proven beneficial in humans. Genetic markers are on the horizon, and may serve as individualised targets for diagnosis and therapy.

Understanding the Role of Oxidative Stress, Neuroinflammation and Abnormal Myelination in Excessive Aggression Associated with Depression: Recent Input from Mechanistic Studies

“…Notably, both an aggressive experience and the expectation of an aggressive event are associated with increases in inflammatory cytokines, which can be the result of sympathetic activation and HPA axis activation [ 146 , 147 ]. Aside from stress which contributes to glial activation, neuroinflammation may be caused by such factors as viral or bacterial diseases of the CNS [ 148 , 149 , 150 ], as well as systemic inflammation caused both by infection [ 151 ] or aseptic condition, as in case of type 1 and 2 diabetes [ 152 ]. Alimentary factors, e.g., “Western diet” [ 153 , 154 ], as well as environmental toxicity, e.g., metal toxicity, may also contribute to neuroinflammation [ 155 ].…”

Surgical Treatment for Refractory Aggression after Bacterial Meningitis Complicated by Stroke: Case Report

“…In cases of systemic hypotension, a reduction in brain irrigation and tissue ischemia occur. 3 The interaction and synergy of the events described above can cause focal or diffuse irreversible damage to the brain. It has been long believed that diffuse brain lesions result in psychic changes.…”

“…2 One of the complications of this group of diseases is cerebral ischemia, an important indicator of severity and an independent predictor of poor prognosis. 3 Among the main repercussions of bacterial meningitis are hearing loss, language disorders, mental retardation, motor abnormalities, and visual disturbances. 4 Although no articles describing the evolution from bacterial meningitis to aggressive pathological behavior have been found, it is already known that, in many cases, pathological aggressiveness is the result of brain abnormalities in individuals with mental illnesses.…”

Stroke in Patients with Bacterial Meningitis: A Cohort Study and Meta‐Analysis

“…A reduced level of consciousness at the time of admission and a low white blood cell count in the cerebrospinal fluid (CSF) might be predictive factors for cerebral infarction after bacterial meningitis 10 . Cerebral infarction in bacterial meningitis can be caused by increased cerebral vasospasm, vasculitis, affection of the coagulation cascade, infective endocarditis, and systemic inflammatory responses 11 . However, the exact pathophysiological background and possible differences between these factors are not yet sufficiently well understood.…”

“…10 Cerebral infarction in bacterial meningitis can be caused by increased cerebral vasospasm, vasculitis, affection of the coagulation cascade, infective endocarditis, and systemic inflammatory responses. 11 However, the exact pathophysiological background and possible differences between these factors are not yet sufficiently well understood.…”