Etiological Profile of Acute Onset Hemiparesis in Children Admitted at a Tertiary Care Teaching Hospital of Northern India

Verma S

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OJHAS Vol. 20, Issue 3: (July-September 2021)

Original Article
Etiological Profile of Acute Onset Hemiparesis in Children Admitted at a Tertiary Care Teaching Hospital of Northern India

Authors:
Animesh Saxena, Senior Resident, Department of Pediatrics,
Chandra Kanta, Professor, Department of Pediatrics,
Sciddhartha Koonwar, Professor Junior Grade, Department of Pediatrics,
Sanjeev Verma, Associate Professor, Department of Pediatrics,
Anit Parihar, Professor, Department of Radio-diagnosis,
King George Medical University, Lucknow.

Address for Correspondence
Dr. Sanjeev Verma,
Associate Professor,
Department of Pediatrics,
King George Medical University,
Lucknow, India.
E-mail: drsanjeev78@gmail.com.

Citation
Saxena A, Kanta C, Koonwar S, Verma S, Parihar A. Etiological Profile of Acute Onset Hemiparesis in Children Admitted at a Tertiary Care Teaching Hospital of Northern India. Online J Health Allied Scs. 2021;20(3):8. Available at URL: https://www.ojhas.org/issue79/2021-3-8.html

Submitted: Sep 28, 2021; Accepted: Oct 5, 2021; Published: Oct 31, 2021

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This work is licensed under a Creative Commons Attribution-No Derivative Works 2.5 India License

Abstract: Introduction: Acute hemiparesis, weakness of either half of the body is a common nonspecific neurological response of the central nervous system to a varying of infective/non-infective aetiologies noted among admitted children. There is a paucity of data on etiologies of this condition, from this part of the Indian subcontinent, so this study was planned to describe the etiological profile of hemiparesis in children. Method: This prospective observational study was done from September 2017 to August 2018 at a tertiary care teaching hospital in northern India. Consecutive children of age 2 months to 14 years, admitted with acute onset hemiparesis or developed hemiparesis during hospital stay were enrolled in the study. Data was collected in a predesigned proforma after obtaining consent. Results: 65 children (57% male) who were admitted with hemiparesis, were enrolled. The mean age at presentation was 5.7 ± 3.5 years. Central nervous system infection (CNS) was the most common cause (69%) followed by pediatric stroke (19%). Intracranial space-occupying lesions (SOL), cerebral palsy, and acute disseminated meningoencephalitis (ADEM) were the other important causes of hemiparesis. Among CNS infections, acute encephalitis was found in 43% and tuberculous meningitis in 26% of patients. Japanese encephalitis 9.2%, inflammatory granuloma & abscess (5%), chikungunya (1.5%) and rickettsial infections (1.5%) were other CNS infections identified. In 12 cases of pediatric stroke, 9 were ischemic infarct and the rest were hemorrhagic. Among ischemic infarction 3 were with the prothrombotic state each 1 case of protein C, S & antithrombin III deficiency. 3 children were comorbid with heart diseases (2 cases of valvular heart disease with infective endocarditis & one case of tetralogy of Fallot). Conclusion: This study shows that, in Uttar Pradesh, India, CNS infection and pediatric stroke (non-infective) are the most common cause of acute onset hemiparesis in children.
Key Words: Infectious etiology, Pediatric stroke, Hemiplegia, Northern India

Introduction:

Hemiparesis (hemiplegia means complete loss of power in stricter sense, but mostly used almost exchangeably with hemiparesis) means weakness of one vertical side of the body which can involve any side either right or left. Rather than being one disease entity it should be understood as a non-specific response of the central nervous system (CNS) caused by a variety of infectious /non-infectious insults to parts of the brain that control movements of the limbs, trunk, face, etc. A number of conditions including congenital malformations, infections (meningitis, encephalitis, brain abscess), intracranial space-occupying lesions (ICSOL), trauma, and systemic conditions like anaemia, procoagulant states, valvular and cyanotic heart diseases with or without infective endocarditis, may result in hemiparesis¹. Pediatric stroke (PS) is a relatively uncommon condition, defined as sudden onset, occlusion, or rupture of artery or veins resulting in focal cerebral damage. The incidence of PS is 1.2 to 13 per 100,000 children under 18 years of age^2,3. Among the various causes of PS arterial ischemic stroke, cerebral sino-venous thrombosis and hemorrhagic strokes are commonly found, and the mean age of diagnosis is 6-10 years^3,4. A prompt and precise etiological diagnosis of acute pediatric hemiplegia/hemiparesis is required for timely management. There is a paucity of data from the Indian subcontinent regarding pediatric hemiparesis/hemiplegia (mostly used interchangeably), so this study was planned to look into various causes of hemiparesis in this part of the world⁵.

Material and Methods:

This prospective observational study was planned at the Department of Pediatrics, King George Medical University, Lucknow, Uttar Pradesh, India. The children of 2 months to 14 years of age; presenting with hemiplegia in pediatric emergency ward or developing hemiplegia during hospital stay, over a period of one year (September 2017-August 2018) were included after a written informed consent was obtained from the parents / attendants coming as legal guardians. Excluding criteria were a history of peri-natal insult, pre-existing neurological disease, traumatic neurological injury, suspected hemiplegic migraine and Todd’s paralysis. A detailed clinical history, examination and due diligence in neuro-imaging and extensive lab work-up to look for the etiology of the event, was exercised. An MRC (Medical Research Council) scale grade 4 or less was criteria for defining hemiparesis²⁶. Ethical clearance was obtained from the Institutional Ethics Committee, before starting the study (Ref. code-88^thECM IIB-Thesis/P22). Data were entered in a predesigned format and managed and analysed using Microsoft excel and epi info 7.0 software.

Results:

A total of 5056 children were admitted during the study period; of the 65 children (1.29%) had recent onset hemiplegia. All were enrolled and 37 among them were male, mean age at presentation was 5.7 ± 3.5 years, while 72 % of the children were between 2-10 years of age. Sixty cases were acute or subacute onset while 5 were stuttering. The majority (73%) belonged to lower-middle or upper-lower socioeconomic status on basis of the modified Kuppuswamy scale. Also, 55% cases were of left-sided hemiparesis, and fever, altered sensorium, headache vomiting were the most common complaints and among clinical findings, hypertonia, brisk DTRs, seizures, and abnormal breathing pattern were seen in descending order of frequency (Table 1).

Table 1: Clinico-epidemiological characteristics of hemiplegia cases (N=65)
Characteristics	Groups	N (%)
Age	<24 months	12 (18.5)
	24- 59 months	22 (33.8)
	60-119 months	25 (38.5)
	>120 months	6 (9.2)
Symptoms	Weakness of limbs	65 (100.0)
	Altered Sensorium	44 (67.7)
	Fever	42 (64.6)
	Headache	28 (43.1)
	Vomiting	28 (43.1)
	Seizure	19 (29.2)
	Abnormal breathing pattern	18 (27.7)
Co-morbidities	Heart disease	3 (4.6)
Co-morbidities	Renal disease	1 (1.5)
General physical examination	Pallor	28 (43.1)
	Cyanosis	1 (1.5)
	Clubbing	3 (4.6)
	Significant Lymphadenopathy	10 (15.4)
Glasgow Coma Scale (GCS)	<7	18 (27.7)
	7-10	24 (36.9)
	11-15	23 (35.4)
Neurological signs/deficits	Meningeal Signs positive	10 (15.4)
	Cranial Nerve Palsy	11 (16.9)
	III cranial Nerve	2 (3.1)
	VII cranial nerve	9 (13.8)
Side of hemiparesis	Right	29 (44.6)
Side of hemiparesis	Left	36 (55.4)
Motor power of affected side at enrollment	Grade 3	10 (15.4)
	Grade 2	38 (58.5)
	Grade 1	17 (26.2)
	Grade 0	0 (0)
Deep Tendon reflex on affected side	Exaggerated	44 (67.7)
	Normal	7 (10.8)
	Not elicit able	14 (21.5)
	Abnormal Tone	48 (73.8)
	Hypertonia	38 (58.5)
	Hypotonia	10 (15.4)
Comorbidities	CVS	3 (4.6)
Comorbidities	Renal	1 (1.5)

Among the etiologies, infections accounted for 69% of pediatric hemiplegia cases, including 43% acute encephalitis syndrome cases, followed by tubercular meningitis 26%. Among the non-infective causes of stroke in 19%, cerebral palsy (6%), space-occupying lesions (5%) and acute disseminated encephalomyelitis (1.5%) were identified as causes (Table 2). CSF examination was done in 45 cases and showed pleocytosis and high protein in 40% of the cases.

Neuroimaging was possible in 60 cases (35 CTs & 39 MRIs) and abnormalities were detected in 49 cases. Multiple abnormalities detected in 22 of cases. Neuroimaging abnormalities were detected in the ventricular, frontoparietal, brain stem, corona radiata areas. MR Angiography was done in 12 cases with 5 cases of middle cerebral artery, 1 case of anterior cerebral artery involvement and 6 cases had normal MR angiographic findings (Table 2).

Table: 2: Etiological Profile of Hemiplegia in enrolled children (N= 65)
Etiology	N (%)
Infective	45 (69.0)
Acute encephalitis syndrome	28(43.1)
Japanese Encephalitis	6 (9.2)
Scrub	1 (1.5)
Chikungunya	1 (1.5)
Unknown	19 (29.2)
TBM	17 (26.2)
Brain abscess	1 (1.5)
Pediatric stroke	12 (18.5)
Ischaemic stroke	9 (75.0)
Hemaorrhagic stroke	3 (25.0)
Pro-coagulant state (etiology / comorbidity)	3 (4.6)
Protein C deficiency	1 (1.5)
Protein S deficiency	1 (1.5)
Anti-thrombin III deficiency	1 (1.5)
Valvular heart disease with Infective Endocarditis	2 (3.1)
Cyanotic heart disease (TOF)	1 (1.5)
Anemia (etiology / comorbidity)	28 (43.1)
Intracranial Space Occupying Lesions	3 (4.6)
Brain Abscess	1 (1.5)
Malignancies	2 (3.1)
Auto immune disseminated Encephalomyelitis	1 (1.5)

Of the twelve pediatric stroke cases, nine cases were of ischemic stroke and the rest were hemorrhagic stroke. Three cases had a pro-thrombotic state, one case, each of Protein C, S and Antithrombin III deficiency, within ischemic stroke group. Three cases had abnormal echocardiography findings, two cases of valvular heart disease with infective endocarditis and one case of tetralogy of Fallot.

These hemiplegic children were followed till discharge and the mortality rate was 2.2% in infective etiology cases and 5% of non-infective etiology cases.

Discussion:

This prospective study of 65 children with recent-onset hemiplegia at a teaching tertiary care hospital in Northern India has tried to elaborate on various etiologies for hemiplegia. The exact incidence of hemiplegia in children is scantly described. In this study we found 1.29% of pediatric hemiplegia, among admitted children. Another northern India hospital-based, study showed 0.55% incidence in admitted children⁵. Though this may not reflect the community picture, as both the studies were done at tertiary care referral centers. Pediatric stroke can cause hemiplegia and was considered rare in children before 1978 when studies by Schoenberg et al, 1978, Giroud et al., 1995, revealed that stroke in children is not an uncommon event^4,6. Current study has 19% cases of pediatric stroke; 0.24% incidence in admitted children per year.

Childhood hemiplegia due to any cause is a disabling condition for the affected child. Clinical and demographic features in this study of 65 children with hemiparesis showed that boys (57%) were affected more than girls for which allowance of a referral bias must not be forgotten. The most commonly affected age group was of preschool and school-going children (2-10 years), most of whom belonged to low socioeconomic status. This is supported by available literature across the world (Nagaraja et al., 1994; Obama 1994, Awada et al., 1994, P. Shivalli et al. 2014)^7-10. Right side hemiparesis was more common than on the left side though the reasons were unexplainable^9-11. In clinical presentations, fever, signs of raised intracranial pressure, abnormal breathing, brisk DTR pattern was significantly more common in children with infective causes of hemiparesis while vomiting, abnormal pupil size, and aphasia were more in the non-infective etiology patients (Table 3)

Table 3: Clinical comparison among infective and non-infective etiologies (N=65)
Clinical Presentation	Number (%)	Infective (N=45)	Non infective (N=20)	p value	Odds ratio
Age
< 2 years	12(18.5)	8 (17.8)	4(20)	0.24	NA
2-5 years	22(33.8)	12 (26.7)	10(50)	0.24	NA
5-10 years	25(38.5)	20 (44.4)	5 (25)	0.24	NA
>10 years	6 (9.2)	5 (11.1)	1 (5)	0.24	NA
Male	37 (56.9)	15 (33.3)	7 (35)	0.89	0.92
Fever	42(64.6)	35 (77.8)	7 (35)	0.001	6.50
Altered sensorium	44(67.7)	33 (73.3)	11 (55)	0.148	2.25
Headache	28 (43.1)	17 (37.8)	11 (55)	0.197	0.49
Vomiting	28 (43.1)	13 (28.9)	15 (75)	0.001	0.13
Weight loss	14 (21.5)	11 (24.4)	3 (15)	0.397	1.83
Seizures	19 (29.2)	16 (35.6)	3 (15)	0.103	3.12
Abnormal breathing	18 (27.7)	17 (37.8)	1 (5)	0.005	11.5
Cranial nerve involvement	11 (16.9)	6 (13.3)	5 (25)	0.253	0.46
Abnormal pupil size	4 (6.2)	0 (0)	4 (20)	0.007	0.26
Signs of meningeal irritation	10 (15.4)	9 (20)	1 (5)	0.153	4.75
Hypertonia	29 (44.6)	23 (51.1)	6 (30)	0.118	2.43
Hypotonia	11 (16.9)	8 (17.8)	3 (15)	0.056	3.77
Signs of raised ICP	17 (26.2)	16 (35.6)	1 (5)	0.028	10.48
Brisk DTR	21 (32.3)	19 (42.2)	2 (10)	0.019	6.57
Optic atrophy	2 (3.1)	1 (2.2)	1 (5)	0.524	0.46
Aphasia (21 conscious on presentation)	10 (15.4)	3 (25) (12 conscious)	7 (77.8) 9 conscious	0.016	0.22
Mortality	2 (3.07)	1 (2.2)	1 (5)	0.549	0.43

Fever may be a predisposing factor as well as the symptom of disease for stroke (Giraud M et al., (1995), (Takeoka and Takahashi, 2002)^4,14. Seizure incidence was higher in children and young adults with acute hemiplegia with infective etiology (35.6%) as compared to non-infective cases (15%) though this difference was not statistically significant. About 29% children showed recurrent seizures in this study.

Isolated headache and irritability were clearly more evident as symptoms in non-infective cases than infective etiology cases, though this correlation was not statistically significant. Signs of meningeal irritation was present in 10 (15.4%) of our enrolled patients in the form of neck rigidity.

Infection related inflammation stimulates coagulation by various mechanisms including expression of thromboplastin by monocytes and macrophages, high tumour necrosis factor, expressing the pro-coagulant function of the endothelium, inhibition of protein C & S anticoagulants and increased levels of fibrinogen^12-14. All these mechanisms play together and can have a significant chance of overlap of infective and vascular etiologies, as the mechanism of stroke in intracranial infection is often some form of vascular catastrophe. The thick exudates formed in tubercular meningitis cause occlusion or arteritis of large vessels in the circle of Willis and middle cerebral artery. Arteritis of small vessels also produces micro infarction, specially in children with TBM^15-17. This is evident in this study as central nervous system infection (CNS) was the most common cause (69%) of hemiparesis, and acute viral encephalitis was found in 43% and tuberculous meningitis in 26% patients. Studies from South East Asia, India, and Pakistan had reported (Siddiqui et al.) intracranial infections as the commonest etiology of stroke¹⁸. Herpes, Mumps, HIV virus, and Varicella zoster are known to produce stroke (Takeoka and Takahashi, 2002, Shah et al., 1996) with different mechanisms like arteritis with fusiform aneurysms and arterial sclerosis with vascular occlusion^18-20.

An immediate neuroimaging, computed tomography (CT), or magnetic resonance imaging (MRI) scan of the head, following a stroke, helps to differentiate infarction from haemorrhage. Conventional cerebral angiography is a definite method to visualize extracranial and intracranial vasculature, signs of dissection, aneurysms, and signs of vasculitis. MR angiography (MRA) is a very sensitive non-invasive tool for identifying large vessel disease and to an extent small vessel and medium vessel disease. There was suspicion of vessel involvement in 18 patients, so MRA was done. In this study, nine patients (13.8%) had strokes of sudden onset in the absence of any fever, seizures, or signs and symptoms of encephalopathy and no lab evidence of infection or inflammation. In these cases, with arterial involvement, the middle cerebral artery (MCA) was most commonly involved, in 41% of our cases. Malik GK 1997, Nagaraja et al., (1994) also made similar observations^7,21. But in cases of acute ischaemic stroke of unknown cause, risk factors could be identified in only three out of nine cases, each case of Protein C, S, and antithrombin III deficiency. Three other cases (4.6%) had cardiac co-morbidities. Cardiac abnormalities can cause strokes following embolism or vascular events due to high blood viscosity, arrhythmias or structural defects and in cyanotic heart diseases the incidence of stroke is found to be 1.6% ^5,22.

Overall, the outcome of children with hemiplegia was found to be good, as recovery pattern in 55 (84.6%) discharged children showed 12 children with full recovery in the motor power (21%), 43 children showed partial recovery and 2 children (3.5%) did not show any improvement in power at the time of discharge. Two children expired, one case was of acute viral encephalitis and the other of acute infarct. Chou YH & Wang PJ reported 21% mortality in their study of 57 patients with acute hemiplegia^23,24.

The limitation of the study was a short follow-up and patients who left against medical advice (8 cases) and other reasons may have impacted the true picture of the outcome of these children. We could not study metabolic defects (dyslipidemia), the effect of minor trauma on hemiparesis, as none of our stroke patients gave a history of trauma. Goraya et al (2018) studied stroke after minor head trauma in infants and young children with basal ganglia calcification²⁵.

Conclusion

To conclude, intracranial infection is the commonest cause of recent onset pediatric hemiplegia. Pediatric stroke leading to hemiparesis is the second most common non- infective cause found in this study. Most of the patients of hemiplegia recovered from the acute neurological insult. With the help of newer diagnostic facilities, the probability of finding an etiology of pediatric stroke is increased in both non-infectious and infectious etiologies, which can greatly facilitate to adopt early and appropriate measures to decrease the chances of recurrences of such events and provide immediate care for better neurological outcomes.

Key Messages:

Acute hemiplegia in infancy has myriad of etiologies but in this part of the world acute CNS infections and the stroke are the most common infective and non-infective causes. CNS infection related infantile hemiplegia should be differentiated and managed aptly for better outcome.

Financial support and sponsorship: Nil

Conflict of Interests: None to disclose

References:

Dooling EC. Acute hemiplegia in infancy. Indian J Pediatr. 1990;57(3):325-335. doi:10.1007/BF02727908
Chung B, Wong V. Pediatric stroke among Hong Kong Chinese subjects. Pediatrics. 2004;114(2):e206-e212. doi:10.1542/peds.114.2.e206
De Schryver EL, Kappelle LJ, Jennekens-Schinkel A, Boudewyn Peters AC. Prognosis of ischemic stroke in childhood: a long-term follow-up study. Dev Med Child Neurol. 2000;42(5):313-318. doi:10.1017/s0012162200000554.
Schoenberg BS, Mellinger JF, Schoenberg DG. Cerebrovascular disease in infants and children: a study of incidence, clinical features, and survival. Neurology. 1978;28(8):763-768. doi:10.1212/wnl.28.8.763
Chinnabhandar V, Singh A, Mandal A, Parmar BJ. Acute Hemiplegia in Children: A Prospective Study of Etiology, Clinical Presentation, and Outcome from Western India. J Neurosci Rural Pract. 2018;9(4):504-509. doi:10.4103/jnrp.jnrp_574_17
Giroud M, Lemesle M, Gouyon JB, Nivelon JL, Milan C, Dumas R. Cerebrovascular disease in children under 16 years of age in the city of Dijon, France: a study of incidence and clinical features from 1985 to 1993. J Clin Epidemiol. 1995;48(11):1343-1348. doi:10.1016/0895-4356(95)00039-9
Nagaraja D, Verma A, Taly AB, Kumar MV, Jayakumar PN. Cerebrovascular disease in children. Acta Neurol Scand. 1994;90(4):251-255. doi:10.1111/j.1600-0404.1994.tb02716.x
Obama MTA, Dongmo L, Nkemayim C, Mbede J, Hagbe P. (). Stroke in children in Yaounde, Cameroon. Indian Pediatrics. 1994;31:791-791.
Awada A, al Rajeh S, Ammar A, Adeyokunnu A. Stroke in children: a study of 21 cases from Saudi Arabia. Ann Trop Paediatr. 1994;14(2):131-135. doi:10.1080/02724936.1994.11747705
Shivalli P, Kumar KK, Santosh S, Nagendra K. Clinical analysis of pediatric hemiplegia at tertiary care hospital in Bangalore. Int J Basic Appl Med Sci. 2014;4:246-57.
Patra C, Sarkar S, Guha D, Dasgupta MK. Clinico-etiological profile of childhood stroke in a Tertiary Care Hospital in Eastern India. J Neurosci Rural Pract. 2015;6(4):515-519. doi:10.4103/0976-3147.165414
Rivers RP, Hathaway WE, Weston WL. The endotoxin-induced coagulant activity of human monocytes. Br J Haematol. 1975;30(3):311-316. doi:10.1111/j.1365-2141.1975.tb00547.x
Esmon CT, Taylor FB Jr, Snow TR. Inflammation and coagulation: linked processes potentially regulated through a common pathway mediated by protein C. Thromb Haemost. 1991;66(1):160-165.
Woodhouse PR, Khaw KT, Plummer M, Foley A, Meade TW. Seasonal variations of plasma fibrinogen and factor VII activity in the elderly: winter infections and death from cardiovascular disease. Lancet. 1994;343(8895):435-439. doi:10.1016/s0140-6736(94)92689-1
Ameriso SF, Wong VL, Quismorio FP Jr, Fisher M. Immunohematologic characteristics of infection-associated cerebral infarction. Stroke. 1991;22(8):1004-1009. doi:10.1161/01.str.22.8.1004
Lanthier S, Carmant L, David M, Larbrisseau A, de Veber G. Stroke in children: the coexistence of multiple risk factors predicts poor outcome. Neurology. 2000;54(2):371-378. doi:10.1212/wnl.54.2.371
Lee YY, Lin KL, Wang HS, et al. Risk factors and outcomes of childhood ischemic stroke in Taiwan. Brain Dev. 2008;30(1):14-19. doi:10.1016/j.braindev.2007.05.002
Siddiqui TS, Rehman Au, Ahmed B. Etiology of strokes and hemiplegia in children presenting at Ayub Teaching Hospital, Abbottabad. J Ayub Med Coll Abbottabad. 2006;18(2):60-63.
Takeoka M, Takahashi T. Infectious and inflammatory disorders of the circulatory system and stroke in childhood. Curr Opin Neurol. 2002;15(2):159-164. doi:10.1097/00019052-200204000-00006
Shah SS, Zimmerman RA, Rorke LB, Vezina LG. Cerebrovascular complications of HIV in children. AJNR Am J Neuroradiol. 1996;17(10):1913-1917.
Malik GK, Chhabra DK, Sharma B, Sharma NL. Radiological studies in acute infantile hemiplegia syndrome. Indian Pediatr. 1979;16(8):689-692.
Phornphutkul C, Rosenthal A, Nadas AS, Berenberg W. Cerebrovascular accidents in infants and children with cyanotic congenital heart disease. Am J Cardiol. 1973;32(3):329-334. doi:10.1016/s0002-9149(73)80142-0
De Veber GA, MacGregor D, Curtis R, Mayank S. Neurologic outcome in survivors of childhood arterial ischemic stroke and sinovenous thrombosis. J Child Neurol. 2000;15(5):316-324. doi:10.1177/088307380001500508
Chou YH, Wang PJ, Lin MY, Shen YZ, Lee CY. Acute hemiplegia in infancy and childhood. Zhonghua Min Guo Xiao Er Ke Yi Xue Hui Za Zhi. 1994;35(1):45-56.
Goraya JS, Berry S, Saggar K, Ahluwalia A. Stroke After Minor Head Trauma in Infants and Young Children With Basal Ganglia Calcification: A Lenticulostriate Vasculopathy. J Child Neurol. 2018;33(2):146-152. doi:10.1177/0883073817750501
Medical Reserarch Council (MRC) mannual muscle testing grading, 2005 system. (Medical Research Council, 1943; Dyck et al., 2005)