Incidence and outcomes of childhood status epilepticus in Kano, northern Nigeria

Abstract

Objective

Convulsive status epilepticus (CSE) is a major neurological emergency in childhood, but population‐based data from low‐ and middle‐income countries remain limited. We estimated the incidence, mortality, neurological outcomes, and predictors of adverse outcomes among children with CSE in Kano, northern Nigeria.

Methods

We conducted a review of one‐year surveillance data on childhood CSE across eight hospitals and a random sample of eight primary health centers in the Kano metropolis. Cases were identified using standardized definitions and weighted to account for sampling at primary health centers. Demographic and clinical data were collected at presentation and during hospitalization. Logistic regression analysis was used to identify predictors of mortality and new‐onset neurological deficits.

Results

A total of 972 children with CSE were identified at participating hospitals, with additional cases detected at primary health centers. After weighting, an estimated 1921 CSE cases occurred during the study period, corresponding to an annual incidence of 98 per 100 000 children aged 1 month–14 years. Incidence was highest among infants (175 per 100 000). Among hospitalized children, in‐hospital mortality was 24.7%, with more than half of the deaths occurring within 24 h of admission. New‐onset neurologic deficits were observed in 9.6% of hospitalized survivors. In multivariable analysis, hypoglycemia at presentation, presumed meningoencephalitis, and CSE lasting longer than 30 min were independently associated with increased odds of death. Neurological deficits were associated with multiple CSE episodes, prolonged seizures, and presumed meningoencephalitis.

Significance

Childhood CSE in Kano is associated with a high incidence and substantial mortality, particularly among infants. Hypoglycemia, central nervous system infections, and prolonged seizures are key predictors of adverse outcomes. These findings highlight the need for improved early recognition and strengthened emergency seizure management in resource‐limited settings.

Plain Language Summary

Convulsive status epilepticus is a dangerous type of prolonged seizure in children. In this study from Kano, Nigeria, many children developed this condition and about one in four hospitalized patients died. Low blood sugar, suspected brain infections, and long seizures increased the risk of poor outcomes. Improving early treatment and emergency care may help reduce these deaths.

Key points.

• We estimated an overall incidence of CSE in Kano Metropolis at 98 episodes per 100 000 population per year, which is more than 4 times higher than reports from high‐income countries.

• CSE associated in‐hospital mortality in Kano was 24.7%, and it is highest among infants.

• Hypoglycemia, presumed meningoencephalitis, and CSE lasting longer than 30 min were the modifiable predictors of in‐hospital mortality identified.

• New‐onset neurologic deficit was associated with multiple episodes of CSE, presumed meningoencephalitis, and CSE longer than 30 min.

1. INTRODUCTION

Status epilepticus (SE) is a life‐threatening emergency manifested by prolonged seizures, with an increased risk of long‐term morbidity and mortality as consequences of SE‐induced neuronal death and neuronal injury with alteration of neuronal networks, sometimes exacerbated by hypoxia associated with respiratory depression, aspiration, and trauma from falls. SE has been operationally defined as a seizure lasting longer than 5 min or a cluster of seizures lasting longer than 5 min without return to baseline between clinical seizures. ¹ There are few studies of childhood convulsive SE (CSE) incidence, with reported CSE incidence rates ranging from 3 to 42 episodes per 100 000 population per year. ² Studies utilizing more rigorous case‐finding and sampling methods have reported higher incidence rates, which may be higher in Africa's low‐ and middle‐income countries (LMICs). ³ , ⁴

CSE‐associated mortality in children varies between high‐income countries and LMICs. A recent review estimates a CSE‐associated mortality range of 3%–11% ² in high‐ and middle‐income countries, while CSE‐associated mortality in LMICs has been reported to be higher. For example, CSE‐associated in‐hospital mortality in Germany has been documented at 3% ³ and CSE‐associated in‐hospital mortality in rural Kenya has been reported to be 15%. ⁴ Although CSE associated with malaria is common in Africa's LMICs, the degree to which malaria contributes to higher CSE‐associated mortality is not known, and even less is known about potentially modifiable risk factors for CSE‐associated mortality.

Kano, the largest city in northern Nigeria, is representative not only of northern Nigeria, with a population of over 110 million, half of whom are children, ⁵ but also of urban areas in the Sahel region of Africa, which has been under‐represented in medical research, including research on status epilepticus. The Sahel has a very high incidence of febrile illnesses, a high burden of malaria, and typically lacks ambulance services for emergencies, among other factors that could influence the incidence and outcomes of childhood SE. We set out to estimate the incidence of CSE in children in metropolitan Kano, northern Nigeria, to determine CSE‐associated in‐hospital mortality and new‐onset neurologic deficits, and to identify potentially modifiable risk factors for these adverse outcomes.

2. METHODS

2.1. Study design

This was a retrospective, facility‐based surveillance study of children presenting with CSE in Kano metropolis, Nigeria, conducted between September 1, 2018, and August 31, 2019.

2.2. Study setting

The study was conducted in Kano metropolis, northern Nigeria, with an estimated population of 4.5 million, predominantly of Hausa/Fulani ethnicity. ⁵ The healthcare system includes 146 community‐based primary healthcare centers (PHCs), which refer patients to secondary and tertiary facilities.

Participating hospitals included Aminu Kano Teaching Hospital (AKTH), Murtala Mohammed Specialist Hospital (MMSH), Hasiya Bayero Paediatric Hospital (HBPH), Sir Muhammad Sanusi General Hospital (SMSGH), Sheikh Muhammad Jidda General Hospital (SMJGH), and Kumbotso Comprehensive Health Centre (KCHC). Eight PHCs were randomly selected from the 146 PHCs in the metropolis.

2.3. Participants

All children aged 1 month to 14 years presenting with CSE to participating facilities during the study period were eligible.

Inclusion criteria:

• Presentation with convulsive status epilepticus as defined below.

• Seen at any participating hospital or selected PHC during the study period.

Exclusion criteria:

• Incomplete clinical records preventing confirmation of CSE diagnosis.

• For children with multiple presentations, only the first episode was included. Patients referred between facilities were counted once.

2.4. Variables

The primary outcomes were:

• In‐hospital mortality.

• New‐onset neurologic deficits.

Secondary variables included:

• Demographic characteristics (age, sex).

• Clinical features (seizure duration, seizure type, fever).

• Etiology (e.g., malaria, meningitis, epilepsy).

• Laboratory findings (blood glucose, malaria tests, CSF analysis).

• Treatment variables (antiseizure medicines administered).

2.5. Data sources and measurement

A standardized case report form for status epilepticus was implemented across all study sites prior to study initiation. Healthcare workers were trained on the recognition, management, and documentation of SE.

Five trained community health workers (CHWs) ⁶ abstracted data from medical records using REDCap®. ⁷ Training included SE diagnosis, research ethics, and electronic data capture.

Seizure duration was estimated using caregiver report, supported by contextual time markers (e.g., duration of routine daily activities) where precise timing was unavailable.

Laboratory measurements were conducted using standard methods:

• Malaria: microscopy or rapid diagnostic test. ⁸

• Blood glucose: glucometer (Accu‐Chek® Active).

• Blood culture: BACTEC system.

• CSF analysis: standard microbiological techniques.

2.6. Bias

To minimize misclassification and information bias:

• Standardized definitions and data collection tools were used across all sites.

• Healthcare workers received uniform training prior to and during the study.

• Regular CME sessions reinforced adherence to protocols.

• Use of contextual time estimation reduced recall bias for seizure duration.

Selection bias was minimized by including all eligible cases presenting to participating facilities during the study period.

2.7. Study size

The study included all eligible cases of CSE presenting during the 12‐month surveillance period. For PHC estimates, data from eight randomly selected PHCs were weighted to represent all 146 PHCs in the metropolis.

2.8. Quantitative variables

Age was analyzed in predefined categories. Blood glucose was categorized using a threshold of ≤2.2 mmol/L for hypoglycemia. Clinical and laboratory variables were categorized based on standard clinical definitions.

2.9. Statistical methods

Data were analyzed using Stata version 13.0 (Stata Corp, College Station, TX, USA).

• Categorical variables were compared using Pearson's chi‐squared test.

• PHC case estimates were weighted by a factor of 146/8

• Age‐specific incidence rates and 95% confidence intervals (CIs) were calculated using population estimates from the National Population Commission ⁹

CSE‐associated in‐hospital mortality and 95% CIs were estimated using cluster bootstrap methods to account for weighting.

Multivariable logistic regression models were used to identify factors associated with:

• In‐hospital mortality.

• New‐onset neurologic deficits.

Variables were selected based on clinical relevance. Adjusted odds ratios (aORs) and 95% CIs were reported.

Children who died before discharge were excluded from the analysis of neurologic outcomes.

2.10. Definitions

Convulsive status epilepticus was defined according to the 2015 International League Against Epilepsy operational definition. ¹

Other definitions:

• Multiple SE: >1 SE episode during a single hospitalization. ¹⁰

• Recurrent CSE: new SE episode after an initial event during the study period. ¹¹

• In‐hospital mortality: death between SE onset and discharge. ¹²

• New‐onset neurologic deficit: motor, cognitive, sensory, or behavioral impairment developing after SE. ¹³ , ¹⁴

• Prior epilepsy: ≥2 unprovoked seizures before SE onset. ¹⁵

• Presumed meningoencephalitis: febrile illness with encephalopathy but without laboratory confirmation of malaria or bacterial infection. ¹⁶

• Presumed malaria: presence of fever and clinical features compatible with malaria in the absence of microscopy or RDT testing, based on the clinical judgment of the attending clinician. ⁸

2.11. Ethical considerations

This study was approved by the Health Research Ethics Committees of AKTH and Kano State Ministry of Health (ethics approval numbers NHREC/21/08/2008/AKTH/EC/2404 & MOH/Off/797/TI/1111, respectively).

3. RESULTS

A total of 972 children with convulsive status epilepticus (CSE) were identified at the participating hospitals during the surveillance period, with an additional 52 cases detected at eight primary health centers (PHCs). After applying sampling weights to account for PHC ascertainment, we estimated that 949 CSE cases presented to PHCs during the study period, yielding an estimated total of 1921 children with CSE in Kano metropolis.

3.1. Demographic and clinical characteristics

Table 1 summarizes the demographic and clinical characteristics of the estimated cohort. The median age was 3 years, and 56.2% were male. Febrile illness was highly prevalent, with 88.7% of children presenting with fever‐associated CSE, reflecting the dominant contribution of infectious etiologies in this setting.

TABLE 1.

Demographic and clinical characteristics of the study population.

Demographic & clinical characteristic (n = 1921)	n (%)
Age groups (months/years)
1–11 months	180 (9.4)
12–59 months	1190 (62.0)
5–9 years	431 (22.4)
10–14 years	120 (6.2)
Fever‐associated SE
Febrile illness associated	1703 (88.7)
No febrile illness	142 (7.3)
Unknown fever status at presentation	76 (4.0)
Duration of hospitalization
Not admitted	962 (50.1)
Admitted for <24 h	134 (7.0)
Admitted for 1–3 days	254 (13.2)
Admitted for >3 days	551 (28.7)
No information available	20 (1.0)
Estimated total SE time
≤30 min	854 (44.5)
>30 min	536 (27.9)
No information available	531 (27.6)
Prior epilepsy diagnosis
Epilepsy diagnosis	162 (8.4)
No epilepsy diagnosis	1759 (91.6)
Number of status seizures during the index presentation
Single SE	1830 (95.3)
Multiple SE	73 (3.8)
No information available	18 (0.9)
Presumed meningoencephalitis
Presumed meningoencephalitis	118 (6.1)
No presumed meningoencephalitis	828 (43.1)
No information available	975 (50.8)
Hypoglycemia
Documented hypoglycemia at presentation	57 (3.0)
Normal glucose level	505 (26.3)
No information available	1359 (70.7)
Outcome of SE
Survived and discharged	1663 (86.6)
Died in the hospital	258 (13.4)
Neuro‐developmental outcome n = 732 a
New‐onset neurologic deficit	70 (9.6)
No new‐onset neurologic deficit	662 (90.4)

^a n = number of SE survivors in hospitals.

Approximately 30% of children had laboratory‐confirmed malaria, while an additional 20% were treated for presumed malaria without confirmatory testing. Presumed meningoencephalitis was identified in 6.1% (118 cases); however, microbiological confirmation was limited, with positive cerebrospinal fluid cultures in 9.3% and positive blood cultures in 4.2% of these cases.

Assessment of metabolic abnormalities at presentation was incomplete. Blood glucose was measured in 29.3% of cases (562 children), among whom 10.1% had hypoglycemia. Only 8.4% of children had a prior diagnosis of epilepsy, indicating that most CSE episodes occurred in children without previously recognized epilepsy. Multiple episodes of SE during the same hospitalization occurred in 3.8% of cases.

3.2. Incidence of childhood CSE

The estimated annual incidence of childhood CSE among children aged 1 month to 14 years in Kano was 98 per 100 000 children. Incidence varied substantially by age group (Table 2). Infants had the highest incidence (175 per 100 000), nearly twice the overall rate, and also demonstrated the highest incidence of prolonged CSE lasting more than 30 min (85 per 100 000). These findings indicate that the burden of CSE in this population is concentrated in the youngest age groups, consistent with the known epidemiology of symptomatic seizures in early childhood.

TABLE 2.

Age‐specific Incidence of CSE.

Age group (in months/years)	SE episode	Population	Incidence rate (per 100 000)	95% CI
Age‐specific incidence rate of CSE in Kano, northern Nigeria
1–11 months	180	102 827	175	123–256
12–59 months	1190	623 189	190	77–394
5–9 years	431	658 067	65	39–98
10–14 years	120	580 974	20	12–35
Overall	1921	1 960 057	98	49–180
Age‐specific incidence rate of CSE (lastin >30 min) in Kano, northern Nigeria
1–11 months	87	102 827	85	55–126
12–59 months	231	623 189	37	31–45
5–9 years	151	658 067	23	18–30
10–14 years	66	580 974	11	7–19
Overall	535	1 960 057	27	22–36

Abbreviations: CI, confidence interval; CSE, convulsive status epilepticus.

3.3. Mortality

Among the 972 children treated at the study hospitals, 240 died, corresponding to an in‐hospital mortality of 24.7%. Mortality occurred early in the course of hospitalization: 53% of deaths occurred within the first 24 h, and 81.7% within 72 h of admission.

When population weighting was applied, the estimated CSE‐associated in‐hospital mortality rate for children in Kano metropolis was 13 deaths per 100 000 children (95% CI: 11–16). Mortality was markedly higher among infants, reaching 61 deaths per 100 000 (95% CI: 47–77) (Table 3).

TABLE 3.

In‐hospital mortality and new‐onset neurologic deficit incidence rates.

In‐hospital mortality for the hospital population only
Age group (months/years)	No death	Study population	Mortality rate (per 100)	95% CI
1–11 months	63	143	44.1	35.7–51.8
12–59 months	116	478	24.3	20.5–28.2
5–9 years	42	267	15.7	11.6–20.2
10–14 years	19	84	22.6	14.3–32.1
Overall	240	972	24.7	22.0–27.5

In‐hospital mortality: Estimates for the Kano population
Age group (months/years)	No death	Kano population	Mortality rate (per 100 000)	95% CI
1–11 months	63	102 827	61.3	46.7–76.8
12–59 months	134	623 189	21.5	16.2–28.9
5–9 years	42	653 067	6.4	4.6–8.4
10–14 years	19	580 974	3.3	1.9–4.8
Overall	258	1 960 057	13	11–16

New‐onset neurologic deficit: Estimates for the hospital population
Age group (months/years)	No cases	Hospital SE survivors	New‐onset neurologic deficit rate (per 100)	95% CI
1–11 months	7	80	8.8	2.6–14.9
12–59 months	30	362	8.3	5.4–11.1
5–9 years	27	225	12.0	7.8–16.2
10–14 years	6	65	9.2	2.2–16.3
Overall	70	732	9.6	7.4–11.7

New‐onset neurologic deficit: Estimates for the Kano population
Age group (months/years)	No cases	Kano population	New‐onset neurologic deficit rate (per 100 000)	95% CI
1–11 months	7	102 827	6.8	2.0–12.6
12–59 months	30	623 189	4.8	3.2–6.6
5–9 years	27	653 067	4.1	2.6–5.8
10–14 years	6	580 974	1.0	0.3–1.9
Overall	70	1 960 057	3.6	2.8–4.4

Abbreviations: CI, confidence interval.

3.4. Neurological outcomes

Among surviving children, 70 cases (9.6% of hospitalized cases) developed new‐onset neurological deficits at hospital discharge, corresponding to 3.6% of the estimated total cohort. Age‐specific mortality and neurological deficit rates are presented in Table 3.

3.5. Predictors of mortality

Multivariable logistic regression analysis identified several factors independently associated with in‐hospital mortality (Table 4). These included:

• Hypoglycemia at presentation.

• Presumed meningoencephalitis.

• CSE duration >30 min.

TABLE 4.

Predictors of CSE associated—In‐hospital mortality and new‐onset neurologic deficit.

Clinical predictors	Odd ratio	p value	95% confidence interval
Predictors of in‐hospital mortality
Hypoglycemia	9.4	<0.001	4.5–19.5
Presumed meningoencephalitis	4.0	<0.001	1.8–8.6
SE > 30 min	2.3	<0.001	1.6–3.3
Age (years)	0.9	0.01	0.9–1.0
Female sex	1.0	>0.9	0.7–1.4
Duration of hospitalization (days)	0.7	<0.0001	0.5–0.8
Multiple SE	1.5	>0.3	0.6–3.5
Malaria	0.6	0.1	0.3–1.1
Predictors of new‐onset neurologic deficit
Multiple SE	7.8	<0.001	5.0–19.3
Presumed meningoencephalitis	2.8	0.03	1.1–6.9
SE > 30 min	2.5	0.003	1.4–4.6
Hypoglycemia	1.4	0.8	0.1–16.7
Age (years)	1.1	0.3	1.0–1.1
Malaria	0.8	0.5	0.4–1.6

In contrast, sex, malaria infection, multiple CSE episodes, and sepsis were not independently associated with mortality.

Age and duration of hospitalization were associated with a protective effect. Each additional year of age reduced the odds of death (OR: 0.92 per year), while a longer hospital stay was associated with reduced mortality (OR: 0.66 per day), reflecting the concentration of deaths early after admission.

3.6. Predictors of neurological deficits

New‐onset neurological deficits were independently associated with:

• Multiple episodes of CSE.

• Presumed meningoencephalitis.

• CSE lasting more than 30 min.

Neurological deficits were not associated with age, hypoglycemia, malaria infection, or prior epilepsy diagnosis.

4. DISCUSSION

This study provides population‐based estimates of the incidence and outcomes of childhood convulsive status epilepticus in Kano, northern Nigeria, using surveillance data collected across both hospital and community health facilities. Three principal findings emerge.

First, childhood CSE incidence in Kano is substantially higher than that reported in high‐income settings. Second, mortality following CSE is extremely high, with nearly one quarter of hospitalized children dying. Third, metabolic and infectious factors—particularly hypoglycemia, presumed meningoencephalitis, and prolonged seizure duration—were key predictors of poor outcomes.

4.1. High incidence of CSE

The estimated incidence of 98 per 100 000 children is approximately three to four times higher than rates reported in high‐income countries. ³ , ¹⁷ Importantly, this study included ascertainment of cases presenting to primary health centers, which may partly explain the higher incidence compared with studies restricted to tertiary hospitals.

The markedly elevated incidence among infants is consistent with previous epidemiological studies. ² , ³ , ⁴ , ¹⁸ Several mechanisms likely contribute to this pattern, including the high burden of infectious diseases in early childhood, the natural history of genetic or metabolic diseases, and/or increased incidence of new‐onset seizures in infants.

The very high prevalence of febrile illness among children with CSE in Kano underscores the role of infectious disease in shaping the epidemiology of status epilepticus in this region. More than 80% of cases were associated with fever, and approximately half of the children had confirmed or suspected severe malaria. Seasonal variation in cases also corresponded with periods of increased malaria transmission, supporting the contribution of infectious diseases to seizure emergencies, including children older than 5 years in this setting. ¹⁹ , ²⁰

4.2. Mortality following CSE

The in‐hospital mortality of 24.7% observed in this study is markedly higher than the 3%–11% mortality reported in high‐income settings. ² , ³ , ¹⁸ , ²¹ However, it is consistent with findings from other low‐ and middle‐income countries, including studies from India and Nigeria reporting mortality rates of approximately 23%–30%. ²² , ²³

Notably, more than half of the deaths occurred within 24 h of admission, suggesting that many children arrived at the hospital with advanced physiological deterioration. Although pre‐hospital factors were not directly measured in this study, the timing of deaths highlights the likely importance of early recognition of prolonged seizures, timely transport, and rapid initiation of treatment in improving outcomes.

4.3. Predictors of mortality

Our findings identify hypoglycemia, presumed meningoencephalitis, and prolonged seizure duration as independent predictors of death. These factors have been consistently reported in previous studies of childhood CSE in both high‐income and resource‐limited settings. ⁴ , ¹⁰ , ²⁴

Hypoglycemia represents a particularly important and potentially modifiable risk factor. In our study, approximately 10% of children tested had hypoglycemia, and its presence was strongly associated with mortality. Similar associations have been reported in studies from the United States and Nigeria. ²³ , ²⁴ Early recognition and correction of metabolic abnormalities may therefore represent an important opportunity to reduce mortality.

Presumed meningoencephalitis was also associated with increased mortality, reflecting the severe neurological injury and systemic complications associated with central nervous system infections. Limited microbiological confirmation in this study likely reflects the diagnostic challenges faced in many LMIC settings, including delayed presentation and limited laboratory capacity.

Interestingly, malaria infection was not independently associated with mortality, despite being the most common infectious comorbidity. This finding may reflect early empirical treatment with parenteral artesunate in suspected severe malaria cases.

4.4. Neurological outcomes

Approximately 10% of hospitalized children developed new‐onset neurologic deficits at discharge, a rate within the range reported in previous studies. ⁴ , ²¹ , ²⁵ , ²⁶ , ²⁷ However, this estimate is likely conservative because neurological outcomes were evaluated clinically rather than with formal neuropsychological testing.

Predictors of neurological deficits in this study included recurrent CSE episodes, prolonged seizures, and presumed meningoencephalitis, findings consistent with prior research demonstrating that seizure burden and underlying neurological injury are key determinants of long‐term morbidity. ⁴ , ²³ , ²⁸

4.5. Implications for health systems and future research

Although this study did not directly assess pre‐hospital care, the high incidence of prolonged seizures and the concentration of deaths early after admission suggest opportunities for strengthening seizure emergency care systems.

Potential priorities include:

• Improving community recognition of prolonged seizures.

• Ensuring availability of benzodiazepines at primary care facilities.

• Strengthening referral pathways and emergency transport.

• Expanding access to rapid diagnostic testing for central nervous system infections.

Future prospective studies could evaluate health system interventions aimed at improving early treatment of CSE, including standardized treatment protocols and pre‐referral seizure management strategies.

4.6. Limitations

Several limitations should be acknowledged. First, the retrospective nature of the surveillance data limits causal inference. Second, diagnostic confirmation of infectious etiologies was incomplete, reflecting real‐world constraints in laboratory capacity. Third, blood glucose testing was not performed in all children, which may have resulted in an underestimation of this metabolic abnormality. Finally, neurological outcomes were assessed clinically rather than with standardized psychometric testing, which may underestimate subtle neurodevelopmental deficits.

5. CONCLUSION

Childhood convulsive status epilepticus in Kano, Nigeria, is associated with high incidence and substantial mortality, particularly among infants. Hypoglycemia, presumed meningoencephalitis, and prolonged seizure duration were major predictors of adverse outcomes. These findings highlight the need to strengthen the implementation of diagnosis and treatment protocols and to improve early care pathways in resource‐limited settings.

AUTHOR CONTRIBUTIONS

Conceptualization: Umar A. Sabo, Edwin Trevathan, Muktar H. Aliyu. Methodology: Umar A. Sabo, Zubairu Iliyasu, Aminu T. Abdullahi, Bryan E. Shepherd, Donna J. Ingles, Usman J. Wudil. Investigation: Umar A. Sabo, Halima Kabir, Aminu Wada, Halima Adamu, Abba M. Abdullahi, Binta W. Jibir, Usman J. Wudil, Jamilu Zakari, Safiya Gambo. Statistical analysis: Heather L. Prigmore, Bryan E. Shepherd, Umar A. Sabo, Edwin Trevathan, Angela R. Paolucci. Writing – original draft: Umar A. Sabo, Writing – reviewing and editing: Edwin Trevathan, Umar A. Sabo, Bryan E. Shepherd, Zubairu Iliyasu, Muktar H. Aliyu, Aminu T. Abdullahi, Angela R. Paolucci, Halima Kabir, Halima Adamu, Aminu Wada, Safiya Gambo, Binta W. Jibir, Abba M. Abdullahi, Jamilu Zakari, Donna J. Ingles. All authors read and approved the final manuscript.

FUNDING INFORMATION

This study was funded by grants (D43 TW009337; D43 TW011949; R01 NS118483) from Fogarty International Center (FIC) and National Institute for Neurological Diseases and Stroke (NINDS), National Institutes of Health (NIH), and from the Amos Christie Chair in Global Health at Vanderbilt University.

CONFLICT OF INTEREST STATEMENT

Umar A. Sabo received grant funding from FIC and NINDS at NIH (D43 TW009337; D43 TW011949; R01 NS118483). Aminu T. Abdullahi received funding from FIC and NINDS at NIH (R01 NS118483). Halima Adamu received funding from FIC and NINDS at NIH (D43 TW011949). Zubairu Iliyasu received grant funding from FIC and NINDS at NIH (D43 TW 011949). Muktar Aliyu received grant funding from FIC at NIH (D43 TW 009337). Donna J. Ingles received grant funding from FIC and NINDS at NIH (D43 TW009337; D43 TW011949; R01 NS118483). Bryan E. Shepherd served as a consultant on NIH grants. Angela Paolucci received grant funding from FIC and NINDS at NIH (D43 TW001949; R01 NS118483). Edwin Trevathan received grant funding from FIC and NINDS at NIH (D43 TW011949; R01 NS118483), and from the Amos Christie Chair in Global Health at Vanderbilt University. We confirm that we have read the Journal's position on ethical publication issues and affirm that this report is consistent with those guidelines.

DATA AVAILABILITY STATEMENT

The data that support the findings of this study are available from the corresponding author upon reasonable request.