Cerebral malaria is associated with long-term mental health disorders: a cross sectional survey of a long-term cohort

Abstract

Background: Cerebral malaria (CM) and severe malarial anaemia (SMA) are associated with neuro-developmental impairment in African children, but long-term mental health disorders in these children are not well defined.

Methods: A cohort of children previously exposed to CM (n = 173) or SMA (n = 99) had neurologic assessments performed and screening for behaviour difficulties using the Strengths and Difficulties Questionnaire (SDQ) a median of 21 months after the disease episode. These findings were compared to concurrently recruited community children (CC, n = 108). Participants with SDQ total difficulties score ≥ 17 had a mental health interview with the child and adolescent version of the Mini-International Neuropsychiatric Interview (MINI-KID) and a sample had brain magnetic resonance imaging (MRI).

Results: Fifty-five children had SDQ score ≥ 17. On the MINI-KID, these children were classified as having no difficulties (n = 18), behaviour difficulties only (n = 13) or a mental health disorder (n = 24). Behaviour difficulties were seen in similar frequencies in CM (3.5%), SMA (4.0%) and CC (2.8%). In contrast, mental health disorders were most frequent in CM (10.4%), followed by SMA (4.0%) and CC (1.8%). Externalizing disorders (conduct, oppositional defiance and attention deficit hyperactivity) were the most common mental health disorders. The median total coma duration was 72 (IQR 36.0-115.0) h in patients with mental health disorders compared to 48 (IQR 28.5-78.7) h in those without, p = 0.039. Independent risk factors for mental health disorder included neurologic deficit at discharge (OR 4.09 (95% CI 1.60, 10.5) and seizure recurrences during hospitalization, (OR 2.80, 95% CI 1.13, 6.97). Brain MRI findings consistent with small vessel ischaemic neural injury was seen in over half of these children.

Conclusions: Cerebral malaria may predispose children to mental health disorders, possibly as a consequence of ischaemic neural injury. There is urgent need for programmes of follow-up, diagnosis and interventions for these children.

Keywords: Behaviour; Cerebral malaria; Children; Disorder; Mental health; Psychiatric.

Fig. 1

This is a distribution of total difficulties scores on the SDQ by study group

Fig. 2

This is a set of brain MRI images of a 7 year old boy who suffered cerebral malaria at the age of 4 years. On discharge he only had hyperreflexia. His neurologic examination 3 years later was normal but the mental health assessment demonstrated oppositional defiant disorder. The brain MRI had bilateral wide spread punctate T1 weighted (T1W) hypointensities (a) and T2W hyperintensities (b) and (c) in the white mater and most marked in the parietal and temporal areas. There are associated with periventricular hyperintensities around the posterior horns of the lateral ventricles the largest of which measures 6 mm and widening of the sulcal spaces in the frontal and parietal lobes. The lesions exhibit no diffusion restriction on diffusion weighted imaging (DWI), (d). The changes suggest bilateral wide spread small vessel ischemia and cerebral atrophy. T1W T1 weighted imaging, T2W T2 weighted imaging, DWI diffusion weighted imaging

Fig. 3

This is a set of brain MRI images of a 5 years old boy who suffered cerebral malaria at the age of 3 years and 3 months. On discharge he had severe neurological sequelae with motor, visual, hearing, and speech deficits and later developed epilepsy. At the time of imaging 20 months later, the visual, speech and motor difficulties had markedly improved but he had developed conduct problems and attention deficit and hyperactivity disorder with violent and aggressive behaviour. The images show generalized widening of sulcal spaces and sylvian fissures in both cerebral hemispheres. There are numerous bilateral T1 W hypointense foci showing confluence in some areas (a); hyper-intense foci in the grey mater and sub cortical regions of the frontal occipital and temporal lobes on T2 W (b and c) and fluid fluid-attenuated inversion recovery (FLAIR) images. There was no restriction of water diffusion on DWI, (d)