Meningitis as a cause of stroke

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Meningitis denotes the inflammation of the leptome-ninges, which consist of the pia mater and arachnoid mater. These layers ensheath the spinal cord and brain and confine the subarachnoidal space, which contains cerebrospinal fluid (CSF). Infection of the meninges by bacteria or fungi leads to an inflammatory response which causes the typical clinical symptoms, headache and nuchal rigidity. Depending on the time course, meningitis can be classified as acute or chronic.

Acute bacterial meningitis is prevalent worldwide and accounts for an estimated 1.2 million cases with 185 000 deaths per year. Patients present with fever, nuchal rigidity, and lethargy or confusion. Other less frequent symptoms are photophobia, seizures, petechial bleeding, and arthritis. The disease occurs in all age groups, but the causative organisms vary depending on age (Table 18.5). If left untreated, the disease is fatal.

Diagnosis is based on clinical symptoms, CSF analysis and microbiological testing. Empiric antimicrobial treatment needs to be initiated as early as possible with antimicrobials that reach adequate bactericidal concentrations in the CSF. The choice of antimicrobial therapy needs to be reconsidered when the causative organism is identified and susceptibility testing results become available.

Table 18.5. Acute bacterialmeningitis: age groups and most common causative organisms.

Age group

Main pathogens


Enterobacteriaceae, Streptococcus

(<1 month)

agalactiae (group B

streptococcus), coagulase-

negative staphylococci

(in preterm infants)

Children (1 month

Haemophilus influenzae, Neisseria

to 15 years)

meningitidis, Streptococcus


Adults (>15 years)

Streptococcus pneumoniae,

Neisseria meningitides

Common complications of acute bacterial meningitis include raised intracranial pressure, seizures, and hyponatremia. Stroke is most prevalent in infants (less than 1 year of age) with an incidence of up to 10%, which is attributed to a more susceptible brain tissue.

Research into the molecular pathogenesis of stroke in meningitis has been scarce. Most likely, the spreading inflammation involves intracranial vessels and leads to thrombosis and subsequent ischemia or hemorrhage [17].

Chronic meningitis lasts for more than 4 weeks, has a subacute onset, and is often accompanied by fever, headache, and vomiting. There are many infectious and non-infectious causes of chronic meningitis and despite advances in diagnostic techniques, such as PCR, about 30% of cases are idiopathic. In the following sections we will discuss several organisms that cause chronic meningitis with a high incidence of stroke.

Tuberculous meningitis

Tuberculous meningitis is caused by Mycobacterium tuberculosis, a hardy slow-growing bacterium whose only natural reservoir is the human. It is taken up by inhalation, phagocytosed by alveolar macrophages and transported to the lung tissue, where an exudative inflammation is initiated. During the first couple of weeks, mycobacteria are undetected by the cellular immune system and spread to the draining hilar lymph nodes. There they slowly proliferate and the host immune system finally mounts a T-cell response. Depending on the capacity of the host immune system the infection can be cleared or mycobacteria survive within granulomata.

Granulomata are caseous foci with a fibrotic capsule that enwraps viable mycobacteria. They are formed by the host immune system to keep the bacteria contained and prevent further spread of infection. However, they allow the pathogen to persist within its host for decades, until the conditions for growth become more favorable, e.g. when the host immune system is impaired.

The granuloma at the site of initial infection and the swollen hilar lymph nodes together are called the primary complex, a typical feature of early tuberculosis. From there lymphogenous and hemato-genous spread may occur to various distant organs, e.g. the meninges, where further granulomata are formed.

When reactivation of the disease occurs, the center of a granuloma liquefies, mycobacteria proliferate and the granuloma ruptures. Bacteria are released into the surrounding tissue, which leads, in the case of a meningeal granuloma, to tuberculous meningitis.

In tuberculous meningitis, the meningeal inflammation produces a basilar, gelatinous inflammatory exudate in the subarachnoid space. The walls of small and medium-sized arteries that traverse the exudate are invaded by inflammatory cells. Furthermore, disturbance of CSF circulation leads to an increased intracranial pressure.

Ischemic stroke is a relatively frequent complication of tuberculous meningitis and occurs in about 30% of cases [18]. Most cerebral infarcts occur in the anterior circulation. Strangulation and spasm of blood vessels by an intense inflammatory exudate, periarteriitis or necrotizing panarteritis, and stretching of blood vessels by increased intracranial pressure are pathogenic mechanisms. Compression of the M1 or M2 segment of the middle cerebral artery by the exudate causes large artery infarctions, whereas multiple infarcts are most likely due to secondary thrombosis.

When tuberculous meningitis is suspected in a patient, the diagnosis needs to be confirmed by microbiological techniques, i.e. direct microscopic examination, culture, or PCR-based techniques, before a long-lasting drug therapy is initiated.

Cryptococcal meningitis

The fungus Cryptococcus neoformans is a soil pathogen with a high potential to invade the central nervous system. It causes an often fatal disease, despite antimycotic therapy. Especially immunocompromised individuals with a defect in cellular immunity (e.g. AIDS patients) are at risk of developing cryptococcal disease. The frequency of ischemic complications is unknown, but stroke is associated with a worse outcome [19, 20].


Coccidioides immitis is a fungal pathogen restricted to the deserts of south-western USA and Central and South America. Inhalation of contaminated soil normally leads to asymptomatic infection or mild pulmonary symptoms. Fewer than 2% of patients develop a disseminated disease within weeks to months after exposure. Most common extrapulmonary sites of infection are skin and subcutaneous soft tissue, the meninges and the skeleton.

Patients with basilar, coccidioidal meningitis have a 40% risk of developing cerebral infarcts and they often develop communicating hydrocephalus. A long course of antifungal drug treatment is required and there is a significant risk of relapse [21].

Neurosyphilis and neuroborreliosis

Other bacterial infections that have been implicated in stroke are the spirochetes Treponema pallidum and Borrelia burgdorferi. Meningovascular syphilis, caused by T. pallidum, is now a rare complication, since syphilis is most often recognized and treated at an earlier stage.

Stroke in syphilis develops as a result of inflammatory infiltration of medium to large arteries. Most often the middle cerebral artery and to a lesser extent basilar arteries are involved [22]. Typically, the onset of stroke is subacute. A diagnosis is based on serological testing of cerebrospinal fluid. Additionally, syphilis can cause stroke by other mechanisms, e.g. compression of the left carotid artery by a large aneurysm of the thoracic aorta has been reported [23].

Chronic meningitis in neuroborreliosis, an infection with B. burgdorferi, rarely causes stroke [24].


Neurocysticercosis is the most common parasitic central nervous system infection. The pork tapeworm Taenia solium is prevalent worldwide, especially in developing countries. In the human, the definite host, Taenia solium lives as a tapeworm in the small intestine and sheds eggs with the feces. The cystic larval

form (termed cysticercus) is usually found in the pig. However, when humans ingest shed tapeworm eggs invasive larvae may develop in the intestines, penetrate the mucosa, enter the bloodstream, migrate to the tissues and mature into cysticerci.

Cysticerci have a predilection for neural tissue and can settle in the brain, subarachnoid space, and ventricle. Symptoms depend on localization and size of the larvae and include seizures, headache, visual problems, confusion, and hydrocephalus. About 50% of patients develop arteriitis with associated lacunar infarcts. Erosion of large vessels can occasionally lead to a large artery stroke, preferentially in the territory of the middle cerebral artery.

The diagnosis in non-endemic areas can be difficult and is generally made by a combination of clinical, radiographic, and serological criteria. Cysticerci normally die within 5-7 years after arrival in the brain, a process which can be accelerated by antipar-asitic drug treatment. In many cases of symptomatic disease, drug treatment is not sufficient and neuro-surgical procedures are required.

Chronic meningitis, caused by, for example, tuberculosis, neurosyphilis or neuroborreliosis, can lead to stroke when the spreading inflammation involves intracranial vessels and leads to thrombosis.

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  • oreste
    How does meningitis cause stroke?
    2 years ago
  • Terttu Paija
    Can menegitis causes stroke?
    2 years ago
  • francis
    How bacterial meningitis causes stroke?
    2 years ago
  • sanni tervo
    Does cryptococcus meniningitis cause stokes?
    1 year ago
    Can meningitis lead to left lacuner stroke?
    1 year ago
  • daisy whitfoot
    How can meningitis causw stroke?
    1 year ago
  • markus
    How long can you have strokes after meningitis?
    10 months ago
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    How does meningitis cause cerebral infarction?
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