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Bacterial meningitis in children: Neurologic complications

Bacterial meningitis in children: Neurologic complications
Literature review current through: Jan 2024.
This topic last updated: Jun 24, 2019.

INTRODUCTION — Bacterial meningitis continues to result in substantial morbidity and mortality despite the availability of effective antimicrobial therapy. The risk of dying or of developing complications is related to the age and underlying condition of the patient, the causative pathogen, the severity and duration of illness at the time of presentation, and, occasionally, to delays in the initiation of antibiotic therapy. (See "Bacterial meningitis in children older than one month: Treatment and prognosis".)

The neurologic complications of bacterial meningitis in children will be discussed here. The neurologic complications of bacterial meningitis in neonates and adults, and the prevention of neurologic complications in children, are discussed separately. (See "Bacterial meningitis in the neonate: Neurologic complications" and "Neurologic complications of bacterial meningitis in adults" and "Bacterial meningitis in children: Dexamethasone and other measures to prevent neurologic complications".)

OVERVIEW — Complications of bacterial meningitis can be divided into systemic and neurologic. Systemic complications, such as septic shock, disseminated intravascular coagulation, acute respiratory distress syndrome, and septic or reactive arthritis are usually the consequence of the bacteremia that frequently accompanies meningitis. (See "Bacterial meningitis in children older than one month: Clinical features and diagnosis".)

The neurologic complications of meningitis may be sudden or gradual in onset and can appear at any time after the onset of symptoms, including after the completion of therapy. Although many neurologic complications are severe and readily apparent, others, such as hearing loss, may be subtle or inapparent during the early phases of infection. The neurologic complications of meningitis include:

Impaired mental status

Cerebral edema and increased intracranial pressure

Seizures

Focal deficits (eg, hearing loss, cranial nerve palsies, hemiparesis or quadriparesis)

Ataxia

Cerebrovascular abnormalities

Neuropsychologic impairment, developmental disability

Subdural effusion or empyema (image 1 and picture 1)

Hydrocephalus

Hypothalamic dysfunction

Neurologic complications can develop at any time during the course of bacterial meningitis. Impaired mental status is seen in most patients at presentation, and seizures are more often seen during the acute episode. (See "Bacterial meningitis in children older than one month: Clinical features and diagnosis".)

Although also occurring early, sensorineural hearing loss is typically not appreciated until the patient has recovered from the acute illness or, in young children, when a hearing assessment is performed [1]. (See "Bacterial meningitis in children older than one month: Treatment and prognosis", section on 'Hearing evaluation'.)

EPIDEMIOLOGY

Incidence — Most studies of the incidence of neurologic complications of bacterial meningitis have been undertaken in children [2,3]. The incidence of complications in these studies has varied widely depending upon the time of the study and the duration of follow-up. In a meta-analysis of 45 prospective studies (1955 to 1993) including 4920 children, neurologic sequelae that persisted or developed after hospital discharge occurred in 16 percent of survivors in developed countries and 26 percent in developing countries [2]. Among the 19 reports of prospective studies from developed countries, the most common sequelae were:

Deafness – 11 percent, including bilateral severe or profound deafness in 5 percent

Intellectual disability (formerly referred to as mental retardation) – 4 percent

Spasticity and/or paresis – 4 percent

Seizure disorder – 4 percent

In a literature review of published reports (1970 to 2010), approximately one-half of 1433 survivors of pediatric meningitis beyond the neonatal period had at least one sequela at ≥5 years of follow-up [3]. Intellectual/behavioral deficits (eg, cognitive impairment, academic limitations, attention deficit hyperactivity disorder) accounted for 78 percent of the reported sequelae, neurologic deficits (seizures, motor deficits, cerebral palsy) for 14 percent, hearing loss for 7 percent, and vision deficits for 3 percent.

Microbiology — In the literature review cited above, the distribution of bacterial etiologies (when specified) among children with sequelae was as follows [3]:

Haemophilus influenzae (37 percent)

Tuberculosis (12 percent)

Streptococcus pneumoniae (4 percent)

Neisseria meningitidis (3 percent)

Among children with pneumococcal meningitis, there appears to be an increased incidence of certain complications (particularly empyema and hemiparesis) in the post-13-valent pneumococcal conjugate vaccine (PCV13) era. In one study, empyema occurred in 1 percent (1 of 67) of children with pneumococcal meningitis in the three years prior to PCV13 compared with 16 percent (9 of 58) of children during the three years after PCV13 introduction [4]. Similarly, hemiparesis was noted in 1 percent (1 of 76) of children in the pre-PCV13 period compared with 12 percent (8 of 69) of children the post-PCV13 period. The reasons for the increased rates of empyema and hemiparesis after PCV13 are not understood. In a separate report that bridged the pre- and post-PCV13 eras, pneumococcus was the most common pathogen among 16 pediatric patients with bacterial meningitis complicated by ischemic stroke [5].

Risk factors — Factors related to the outcome of bacterial meningitis in children include [6]:

The age of the patient (the younger the child, the worse the prognosis) [7-9]

The etiologic agent (S. pneumoniae is associated with worse outcome compared with other pathogens) [2,10-13]

The duration and/or progression of illness before effective antibiotic therapy [7]

The number of organisms or the quantity of polysaccharide material present in the cerebrospinal fluid (CSF) at the time of diagnosis [14,15]

The rapidity with which the CSF is sterilized [16]

The adequacy of the host response to infection

A number of studies have attempted to identify predictors of adverse outcome in children with bacterial meningitis. Clinical features that have been associated with increased risk of neurologic complications or sequelae include:

Seizures that are prolonged, complicated, or begin >72 hours after admission [17,18]

Low CSF glucose concentration [7,10]

≥2 days of symptoms before admission [10,19]

Ataxia [10,20-22]

≥107 colony forming units (CFU)/mL of CSF [14,15,23]

Focal neurologic deficits in patients who are not postictal [18]

S. pneumoniae infection [2,10-13]

Among the subset of children requiring mechanical ventilation, a Pediatric Risk of Mortality score ≥20 within the first 24 hours [24]

The increased risk of adverse outcome with pneumococcal meningitis may result in part from the persistence of potent biologic activity in the debris of killed bacteria. The debris may stimulate the host inflammatory response, which in turn contributes to tissue damage. (See "Pathogenesis and pathophysiology of bacterial meningitis".)

MAJOR NEUROLOGIC COMPLICATIONS

Cerebral edema — Cerebral edema can be caused by vasogenic, cytotoxic, or interstitial mechanisms [25]. The net effect of these processes is an increase in the total fluid volume of the brain, leading to a rise in intracranial pressure (ICP).

Vasogenic cerebral edema usually results from increased permeability of the blood-brain barrier, especially in the choroid plexus endothelium and the endothelium of the cerebral microvasculature.

Cytotoxic factors released from neutrophils, microglia, and astrocytes can directly produce cerebral edema.

The inflammation produced by the infection can impede the normal absorption of cerebrospinal fluid (CSF) from the subarachnoid space via the arachnoid villi.

Cerebral perfusion pressure, normally maintained by an autoregulatory mechanism, becomes dependent upon peripheral blood pressure during meningitis because autoregulation is impaired [26,27]. Cerebral edema itself can increase the ICP and secondarily reduce cerebral blood flow.

Cerebral edema and elevated ICP initially manifest with headache, confusion, irritability, nausea, and vomiting. Papilledema may be appreciated on physical examination. More severe intracranial hypertension is characterized by severely depressed mental status (coma); cranial nerve palsy, particularly involve the abducens (VI) nerve; and bradycardia with hypertension (the Cushing reflex). In the most severe cases, this can progress to herniation of the cerebellar tonsils, leading to death.

The possibility of cerebral edema should be considered in all critically ill patients with meningitis, particularly those with severely depressed mental status, asymmetric pupillary examination, or other cranial nerve palsy. The diagnosis is confirmed with neuroimaging, though urgent empiric treatment may be warranted if there are highly concerning clinical findings. Management of elevated ICP is discussed in greater detail separately. (See "Elevated intracranial pressure (ICP) in children: Management".)

Careful attention to fluid management is an important aspect of care in children with bacterial meningitis, and avoiding excessive fluid administration may reduce the risk of cerebral edema. Fluid management in children with bacterial meningitis is discussed separately. (See "Bacterial meningitis in children older than one month: Treatment and prognosis", section on 'Fluid management'.)

Subdural effusion — Subdural effusions occur in 10 to 33 percent of children with acute bacterial meningitis [28-30]. In a multicenter pneumococcal meningitis study, subdural effusions were noted in approximately 20 percent of patients [4]. Clinical manifestations of subdural effusions are often subtle or absent. In very young children, bulging fontanelles may be a sign of this complication, while in older children, subdural effusions can rarely produce increased intracranial pressure and a shift of intracranial structures. In most children, subdural effusions produce few symptoms and require no treatment [30]. However, development of subdural empyema requires drainage (picture 1 and image 1).

Seizures — Seizures occur in 20 to 30 percent of children with acute bacterial meningitis [6,12]. The pathogenesis of seizures in meningitis is not well understood. Although fever may be a cofactor in very young children, cerebrovascular inflammation or secondary neurochemical changes are presumably the cause of most seizures. In one study, as an example, the occurrence of seizures correlated with bacterial counts of greater than 107 CFU/mL in the CSF sample prior to treatment [23].

The two most common types of seizures in children with bacterial meningitis are partial, generalized seizures with focal predominance and partial seizures with secondary generalization [18]. Seizures occurring before or at the time of presentation are usually generalized, whereas seizures occurring ≥72 hours after admission are usually focal.

Seizures that occur early in the course of bacterial meningitis and that are easily controlled are rarely associated with permanent neurologic sequelae. In contrast, seizures that are prolonged, difficult to control, or begin more than 72 hours after hospitalization are more likely to be associated with neurologic sequelae, suggesting that a cerebrovascular complication may have occurred [12,18,31]. Persistent neurologic deficits are the major independent predictor of late afebrile seizures in children [18]. (See 'Cerebrovascular complications' below.)

Hearing loss — Hearing loss after bacterial meningitis may be transient or permanent. Transient hearing loss may be secondary to a conductive disturbance in many affected patients [32]. However, sensorineural hearing loss (transient or permanent) can result from damage to the eighth cranial nerve, cochlea, or labyrinth, induced by direct bacterial invasion and/or the inflammatory response elicited by the infection [32-36].

Permanent sensorineural hearing loss occurs in 5 to 10 percent of children with bacterial meningitis overall and up to 30 percent of those with pneumococcal meningitis [2-4]. In the largest cohort since the 1980s, hearing loss developed in 7 percent of cases, one-quarter of which were detected after the routine follow-up period had ended [10]. All of the children with hearing loss had one or more of the following risk factors at presentation:

Symptoms for ≥2 days before admission

Absence of petechiae

CSF glucose concentration ≤10.8 mg/dL (0.6 mmol/L)

S. pneumoniae infection

Ataxia

Hearing loss is two to three times more common in children with pneumococcal meningitis than with other forms of bacterial meningitis [10,33]. In a multicenter study of 161 children with pneumococcal meningitis treated in the United States from 2007 through 2013 (three years before and after the introduction of the 13-valent pneumococcal conjugate vaccine), 31 percent developed hearing loss [4]. Ataxia is commonly associated with hearing loss in children, since both are related to bacterial labyrinthitis [10,20-22].

Cranial nerve palsy — Cranial nerve palsies can result from compression due to brain swelling or perineuritis due to the adjacent meningeal inflammatory reaction [37]. The VI nerve is the cranial nerve most commonly affected in meningitis, probably because its long intracranial segment adjacent to the brainstem is highly vulnerable to elevated intracranial pressure and the inflammatory reaction that can occur with meningitis. Cranial nerves III, IV, and VII also may be affected. Cranial nerve deficits related to meningitis are usually transient. (See "Third cranial nerve (oculomotor nerve) palsy in children" and "Fourth cranial nerve (trochlear nerve) palsy" and "Facial nerve palsy in children" and "Sixth cranial nerve (abducens nerve) palsy", section on 'Clinical manifestations'.)

Bacterial meningitis can induce arachnoiditis around the optic nerve, which can lead to transient or permanent visual loss. Optic atrophy that results in irreversible total blindness is a rare complication of severe meningitis [38].

Motor deficits — Hemiparesis, quadriparesis, and other motor deficits can complicate bacterial meningitis. Most motor deficits improve or resolve with successful treatment of the meningitis, but long-term disability can occur [2,3,6,18].

Paresis typically results from an intracranial abnormality (eg, cortical vein or sagittal vein thrombosis, cerebral artery spasm, subdural effusion or empyema, hydrocephalus, cerebral infarct or abscess, cerebral edema).

Paresis resulting from meningitis generally improves with time. In a review of 235 children with bacterial meningitis, hemiparesis or quadriparesis was noted in 30 patients (12 percent) shortly after discharge, but persisted in only 5 (2 percent) one year after discharge [6].

Cerebrovascular complications — Thrombosis, vasculitis, acute cerebral hemorrhage or infarction, and aneurysm formation of cerebral vessels are potential complications of bacterial meningitis [17,39-42]. These diverse processes can manifest similarly as a focal abnormality, such as hemiparesis or focal seizures [42].

Intellectual and behavioral disabilities — Survivors of childhood meningitis are at increased risk for developmental delays, learning difficulties, and behavioral problems [3,43,44]. This is true even for those who do not have acute neurologic complications during the acute illness. Caregivers and schoolteachers should be aware of possible language deficits and problems understanding language-based material [6,45]. Early identification and intervention may help to minimize the long-term impact of these problems [44].

Intellectual disability — Intellectual disability is a well-recognized complication of bacterial meningitis in children and can range from mild to severe [9,46-52]. However, few studies have utilized appropriate controls and sufficient follow-up to assess the risk. In a meta-analysis of 19 prospective studies of bacterial meningitis in children from developed countries, intellectual disability (defined by intelligence quotient [IQ] ≤70) occurred in 4 percent of survivors [2].

Several studies have evaluated the IQ of survivors of bacterial meningitis compared with their siblings or other control children [6,45,53,54]. Although not all of the studies found a difference in the mean IQ compared with controls (usually siblings), a greater proportion of children who had meningitis had IQ <70 [6,46,54].

In a report of a cohort of 130 children who were evaluated 7 and 12 years after meningitis, after adjustment for sociodemographic variables, scores on measures of intelligence, learning, and neuropsychologic skills were consistently below those of age- and grade-matched controls, even though meningitis survivors achieved scores within the normal range [9,46]. Onset of meningitis before 12 months of age was associated with decreased performance on tests requiring language and executive skills [9]. The occurrence of acute neurologic complications and duration of symptoms before diagnosis were not predictors of outcome at 12 years.

In a case-control study of a British cohort of 461 teenagers who had bacterial meningitis in infancy and 289 matched controls (recruited when the cases were five years old), 8 percent of cases attended special schools (compared with none of the controls); this rate is more than four times the national average [47,51]. One-quarter of cases did not pass any General Certificate of Secondary Education examination compared with 7 percent of controls.

In a population-based Danish cohort, by age 35 years, survivors of childhood meningitis were less likely to have completed high school, attain higher education, or achieve economic self-sufficiency than the comparison cohort [55].

Behavioral problems — Survivors of childhood bacterial meningitis may have increased behavior problems over time (eg, somatic complaints, mood problems, social problems, thought problems, attention problems, and delinquent behavior) [3,48,49,56,57]. Whether the frequency of behavior problems varies according to pathogen is not clear; one retrospective review found the prevalence of behavior problems among survivors of non-H. influenzae type b meningitis to be similar to that in the general population [58].

UNUSUAL COMPLICATIONS — A variety of unusual neurologic complications can occur in children with meningitis. These unusual complications are rare and include:

Spinal cord complications, such as transverse myelitis or infarction, presumably as a direct result of local vascular changes with secondary cord ischemia [59-61] (see "Transverse myelitis: Etiology, clinical features, and diagnosis")

Brain abscesses – Brain abscesses are rare in patients with meningitis due to S. pneumoniae, H. influenzae, and N. meningitidis but occur with higher frequency with certain rare pathogens, such as Enterobacter sakazakii (also known as Cronobacter [62]) or Citrobacter spp [33] (see "Pathogenesis, clinical manifestations, and diagnosis of brain abscess")

Severe permanent hydrocephalus (see "Hydrocephalus in children: Physiology, pathogenesis, and etiology")

Aneurysm formation of focal intracranial vessels, presumably secondary to inflammatory changes in the blood vessel wall [63]

Cortical visual impairment [40,64-66]

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Bacterial meningitis in infants and children".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or email these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient education" and the keyword[s] of interest.)

Basics topic (see "Patient education: Bacterial meningitis (The Basics)")

SUMMARY

Permanent neurologic sequelae occur in up to one-half of children with bacterial meningitis. The most common sequelae include (see 'Major neurologic complications' above):

Intellectual and behavioral disabilities (see 'Intellectual and behavioral disabilities' above)

Seizures (see 'Seizures' above)

Hearing loss (see 'Hearing loss' above)

Motor deficits (including spasticity and/or paresis) (see 'Motor deficits' above)

Clinical features that have been associated with increased risk of neurologic sequelae include prolonged, complicated, or late-onset seizures, low cerebrospinal fluid (CSF) glucose concentration, ≥107 colony forming units/mL of CSF, and focal neurologic deficits. (See 'Risk factors' above.)

Seizures that are prolonged, difficult to control, or begin more than 72 hours after hospitalization are more likely to be associated with neurologic sequelae. Persistent neurologic deficits are the major predictor of late afebrile seizures in children. (See 'Seizures' above.)

Hemiparesis or quadriparesis resulting from meningitis often improves with time. (See 'Motor deficits' above.)

Permanent sensorineural hearing loss occurs in 5 to 10 percent of children with bacterial meningitis overall and up to 30 percent of those with pneumococcal meningitis. (See 'Hearing loss' above.)

Survivors of childhood meningitis are at increased risk for developmental delays, learning difficulties, and behavioral problems, even if they did not have acute neurologic complications or physical sequelae. (See 'Intellectual and behavioral disabilities' above.)

  1. Kaplan SL, Catlin FI, Weaver T, Feigin RD. Onset of hearing loss in children with bacterial meningitis. Pediatrics 1984; 73:575.
  2. Baraff LJ, Lee SI, Schriger DL. Outcomes of bacterial meningitis in children: a meta-analysis. Pediatr Infect Dis J 1993; 12:389.
  3. Chandran A, Herbert H, Misurski D, Santosham M. Long-term sequelae of childhood bacterial meningitis: an underappreciated problem. Pediatr Infect Dis J 2011; 30:3.
  4. Olarte L, Barson WJ, Barson RM, et al. Impact of the 13-Valent Pneumococcal Conjugate Vaccine on Pneumococcal Meningitis in US Children. Clin Infect Dis 2015; 61:767.
  5. Dunbar M, Shah H, Shinde S, et al. Stroke in Pediatric Bacterial Meningitis: Population-Based Epidemiology. Pediatr Neurol 2018; 89:11.
  6. Kim KS. Bacterial meningitis beyond the neonatal period. In: Feigin and Cherry’s Textbook of Pediatric Infectious Diseases, 8th, Cherry JD, Harrison GJ, Kaplan SL, et al (Eds), Elsevier, Philadelphia 2019. p.309.
  7. Herson VC, Todd JK. Prediction of morbidity in Hemophilus influenzae meningitis. Pediatrics 1977; 59:35.
  8. Anderson V, Bond L, Catroppa C, et al. Childhood bacterial meningitis: impact of age at illness and acute medical complications on long term outcome. J Int Neuropsychol Soc 1997; 3:147.
  9. Anderson V, Anderson P, Grimwood K, Nolan T. Cognitive and executive function 12 years after childhood bacterial meningitis: effect of acute neurologic complications and age of onset. J Pediatr Psychol 2004; 29:67.
  10. Koomen I, Grobbee DE, Roord JJ, et al. Hearing loss at school age in survivors of bacterial meningitis: assessment, incidence, and prediction. Pediatrics 2003; 112:1049.
  11. Kornelisse RF, Westerbeek CM, Spoor AB, et al. Pneumococcal meningitis in children: prognostic indicators and outcome. Clin Infect Dis 1995; 21:1390.
  12. Arditi M, Mason EO Jr, Bradley JS, et al. Three-year multicenter surveillance of pneumococcal meningitis in children: clinical characteristics, and outcome related to penicillin susceptibility and dexamethasone use. Pediatrics 1998; 102:1087.
  13. Oostenbrink R, Maas M, Moons KG, Moll HA. Sequelae after bacterial meningitis in childhood. Scand J Infect Dis 2002; 34:379.
  14. Feldman WE. Concentrations of bacteria in cerebrospinal fluid of patients with bacterial meningitis. J Pediatr 1976; 88:549.
  15. Feldman WE, Ginsburg CM, McCracken GH Jr, et al. Relation of concentrations of Haemophilus influenzae type b in cerebrospinal fluid to late sequelae of patients with meningitis. J Pediatr 1982; 100:209.
  16. Lebel MH, McCracken GH Jr. Delayed cerebrospinal fluid sterilization and adverse outcome of bacterial meningitis in infants and children. Pediatrics 1989; 83:161.
  17. Taft TA, Chusid MJ, Sty JR. Cerebral infarction in Hemophilus influenzae type B meningitis. Clin Pediatr (Phila) 1986; 25:177.
  18. Pomeroy SL, Holmes SJ, Dodge PR, Feigin RD. Seizures and other neurologic sequelae of bacterial meningitis in children. N Engl J Med 1990; 323:1651.
  19. Kaaresen PI, Flaegstad T. Prognostic factors in childhood bacterial meningitis. Acta Paediatr 1995; 84:873.
  20. Kaplan SL, Goddard J, Van Kleeck M, et al. Ataxia and deafness in children due to bacterial meningitis. Pediatrics 1981; 68:8.
  21. Schwartz JF. Ataxia in bacterial meningitis. Neurology 1972; 22:1071.
  22. Roine I, Pelkonen T, Bernardino L, et al. Ataxia and Its Association with Hearing Impairment in Childhood Bacterial Meningitis. Pediatr Infect Dis J 2015; 34:809.
  23. Feldman WE. Relation of concentrations of bacteria and bacterial antigen in cerebrospinal fluid to prognosis in patients with bacterial meningitis. N Engl J Med 1977; 296:433.
  24. Madagame ET, Havens PL, Bresnahan JM, et al. Survival and functional outcome of children requiring mechanical ventilation during therapy for acute bacterial meningitis. Crit Care Med 1995; 23:1279.
  25. Tunkel AR, Scheld WM. Pathogenesis and pathophysiology of bacterial meningitis. Clin Microbiol Rev 1993; 6:118.
  26. Tureen JH, Dworkin RJ, Kennedy SL, et al. Loss of cerebrovascular autoregulation in experimental meningitis in rabbits. J Clin Invest 1990; 85:577.
  27. Goitein KJ, Tamir I. Cerebral perfusion pressure in central nervous system infections of infancy and childhood. J Pediatr 1983; 103:40.
  28. Taylor HG, Schatschneider C, Minich NM. Longitudinal outcomes of Haemophilus influenzae meningitis in school-age children. Neuropsychology 2000; 14:509.
  29. DODGE PR, SWARTZ MN. BACTERIAL MENINGITIS--A REVIEW OF SELECTED ASPECTS. II. SPECIAL NEUROLOGIC PROBLEMS, POSTMENINGITIC COMPLACATIONS AND CLINICOPATHOLOGICAL CORRELATIONS. N Engl J Med 1965; 272:954.
  30. Snedeker JD, Kaplan SL, Dodge PR, et al. Subdural effusion and its relationship with neurologic sequelae of bacterial meningitis in infancy: a prospective study. Pediatrics 1990; 86:163.
  31. Feigin RD, McCracken GH Jr, Klein JO. Diagnosis and management of meningitis. Pediatr Infect Dis J 1992; 11:785.
  32. Dodge PR, Davis H, Feigin RD, et al. Prospective evaluation of hearing impairment as a sequela of acute bacterial meningitis. N Engl J Med 1984; 311:869.
  33. Kaplan SL, Woods CR. Neurologic complications of bacterial meningitis in children. Curr Clin Top Infect Dis 1992; 12:37.
  34. Bhatt SM, Lauretano A, Cabellos C, et al. Progression of hearing loss in experimental pneumococcal meningitis: correlation with cerebrospinal fluid cytochemistry. J Infect Dis 1993; 167:675.
  35. Merchant SN, Gopen Q. A human temporal bone study of acute bacterial meningogenic labyrinthitis. Am J Otol 1996; 17:375.
  36. Klein M, Schmidt C, Kastenbauer S, et al. MyD88-dependent immune response contributes to hearing loss in experimental pneumococcal meningitis. J Infect Dis 2007; 195:1189.
  37. Durand ML, Calderwood SB, Weber DJ, et al. Acute bacterial meningitis in adults. A review of 493 episodes. N Engl J Med 1993; 328:21.
  38. Ellsworth J, Marks MI, Vose A. Meningococcal meningitis in children. Can Med Assoc J 1979; 120:155.
  39. Dunn DW, Daum RS, Weisberg L, Vargas R. Ischemic cerebrovascular complications of Haemophilus influenzae meningitis. The value of computed tomography. Arch Neurol 1982; 39:650.
  40. Mankhambo LA, Makwana NV, Carrol ED, et al. Persistent visual loss as a complication of meningococcal meningitis. Pediatr Infect Dis J 2006; 25:566.
  41. Chang CJ, Chang WN, Huang LT, et al. Cerebral infarction in perinatal and childhood bacterial meningitis. QJM 2003; 96:755.
  42. Kaplan SL, Fishman MA. Update on bacterial meningitis. J Child Neurol 1988; 3:82.
  43. Grimwood K. Legacy of bacterial meningitis in infancy. Many children continue to suffer functionally important deficits. BMJ 2001; 323:523.
  44. Marlow N, Johnson S. What the teacher needs to know. Arch Dis Child 2007; 92:945.
  45. Sell SH. Long term sequelae of bacterial meningitis in children. Pediatr Infect Dis 1983; 2:90.
  46. Grimwood K, Anderson VA, Bond L, et al. Adverse outcomes of bacterial meningitis in school-age survivors. Pediatrics 1995; 95:646.
  47. de Louvois J, Halket S, Harvey D. Effect of meningitis in infancy on school-leaving examination results. Arch Dis Child 2007; 92:959.
  48. Grimwood K, Anderson P, Anderson V, et al. Twelve year outcomes following bacterial meningitis: further evidence for persisting effects. Arch Dis Child 2000; 83:111.
  49. Fellick JM, Sills JA, Marzouk O, et al. Neurodevelopmental outcome in meningococcal disease: a case-control study. Arch Dis Child 2001; 85:6.
  50. Feldman HM, Michaels RH. Academic achievement in children ten to 12 years after Haemophilus influenzae meningitis. Pediatrics 1988; 81:339.
  51. de Louvois J, Blackbourn J, Hurley R, Harvey D. Infantile meningitis in England and Wales: a two year study. Arch Dis Child 1991; 66:603.
  52. Bedford H, de Louvois J, Halket S, et al. Meningitis in infancy in England and Wales: follow up at age 5 years. BMJ 2001; 323:533.
  53. Taylor HG, Mills EL, Ciampi A, et al. The sequelae of Haemophilus influenzae meningitis in school-age children. N Engl J Med 1990; 323:1657.
  54. Tejani A, Dobias B, Sambursky J. Long-term prognosis after H. influenzae meningitis: prospective evaluation. Dev Med Child Neurol 1982; 24:338.
  55. Roed C, Omland LH, Skinhoj P, et al. Educational achievement and economic self-sufficiency in adults after childhood bacterial meningitis. JAMA 2013; 309:1714.
  56. Halket S, de Louvois J, Holt DE, Harvey D. Long term follow up after meningitis in infancy: behaviour of teenagers. Arch Dis Child 2003; 88:395.
  57. Berg S, Trollfors B, Hugosson S, et al. Long-term follow-up of children with bacterial meningitis with emphasis on behavioural characteristics. Eur J Pediatr 2002; 161:330.
  58. Ritchi L, Jennekens-Schinkel A, van Schooneveld M, et al. Behaviour is not really at risk after surviving meningitis in childhood. Acta Paediatr 2008; 97:438.
  59. Seay AR. Spinal cord dysfunction complicating bacterial meningitis. Arch Neurol 1984; 41:545.
  60. Almasanu BP, Owensby JR, Pavlakis SG, Edwards JH. Spinal cord infarction in meningitis: polygenic risk factors. Pediatr Neurol 2005; 32:124.
  61. Haupt HM, Kurlinski JP, Barnett NK, Epstein M. Infarction of the spinal cord as a complication of pneumococcal meningitis. Case report. J Neurosurg 1981; 55:121.
  62. Iversen C, Lehner A, Mullane N, et al. Identification of "Cronobacter" spp. (Enterobacter sakazakii). J Clin Microbiol 2007; 45:3814.
  63. Perry JR, Bilbao JM, Gray T. Fatal basilar vasculopathy complicating bacterial meningitis. Stroke 1992; 23:1175.
  64. Newton NL Jr, Reynolds JD, Woody RC. Cortical blindness following Hemophilus influenzae meningitis. Ann Ophthalmol 1985; 17:193.
  65. Ackroyd RS. Cortical blindness following bacterial meningitis: a case report with reassessment of prognosis and aetiology. Dev Med Child Neurol 1984; 26:227.
  66. Tepperberg J, Nussbaum D, Feldman F. Cortical blindness following meningitis due to hemophilus influenzae type B. J Pediatr 1977; 91:434.
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