|Year : 2016 | Volume
| Issue : 1 | Page : 24-29
Clinical profile of acute flaccid paralysis: A study from a tertiary care centre in Kashmir, India
Naveed Mohsin1, Ravouf Asimi2
1 Department of General Medicine, Sher-I-Kashmir Institute of Medical Sciences, Srinagar, Jammu and Kashmir, India
2 Department of Neurology, Sher-I-Kashmir Institute of Medical Sciences, Srinagar, Jammu and Kashmir, India
|Date of Web Publication||6-Sep-2016|
Department of General Medicine, Sher-I-Kashmir Institute of Medical Sciences, Married Doctors Hostel G 15, Soura, Srinagar, Jammu and Kashmir
Source of Support: None, Conflict of Interest: None
| Abstract|| |
Background and Aims: As a part of Global Polio Eradication Programme by World Health Organisation, surveillance of acute flaccid paralysis (AFP) was an important public health activity in many countries. With nearing the eradication of poliomyelitis, other causes of AFP are gaining importance in both children and adults. This study was designed to know the clinical characteristics, and differential diagnosis of causes of AFP, including distribution by age, gender, and time. This was a prospective observational study.
Methods: AFP cases were diagnosed on the basis of history and physical examination. The underlying etiology was ascertained by appropriate laboratory investigations such as arterial blood gas analysis, urinary pH, electrolytes, thyroid profile, electrophysiological studies, cerebrospinal fluid analysis, and imaging.
Results: Between July 2010 and September 2012, 106 cases of AFP were enrolled. Out of 106 patients, 58 (54.7%) were suffering from acute inflammatory demyelinating polyneuropathy, a subtype of Guillain-Barré syndrome (GBS), 15 (14.2%) from hypokalemic paralysis, 8 (7.5%) from myasthenia gravis, 8 (7.5%) from thiamine deficiency, 5 (4.7%) from transverse myelitis, and 2 (1.9%) from cord compression. Other diagnoses include; acute motor axonal neuropathy 3 (2.8%), acute disseminated encephalomyelitis 2 (1.9%), meningoencephalitis 2 (1.9%), diabetic polyneuropathy 2 (1.9%), and chemotherapy-induced neuropathy 1 (0.9%). Most cases, 42/106 (39.6%) were admitted during the spring season.
Conclusion: GBS was the most common cause of AFP in all age groups. Most of the AFP cases occurred during spring season. No case of poliomyelitis was found.
Keywords: Acute flaccid paralysis, Guillain-Barré syndrome, hypokalemic paralysis, standard deviation, world health organization
|How to cite this article:|
Mohsin N, Asimi R. Clinical profile of acute flaccid paralysis: A study from a tertiary care centre in Kashmir, India. Ann Nigerian Med 2016;10:24-9
|How to cite this URL:|
Mohsin N, Asimi R. Clinical profile of acute flaccid paralysis: A study from a tertiary care centre in Kashmir, India. Ann Nigerian Med [serial online] 2016 [cited 2021 Jan 24];10:24-9. Available from: https://www.anmjournal.com/text.asp?2016/10/1/24/189805
| Introduction|| |
The World Health Organization (WHO) defines acute flaccid paralysis (AFP) syndrome as “characterized by rapid onset of weakness of an individual's extremities, often including weakness of the muscles of respiration and swallowing, progressing to maximum severity within 1–10 days. The term 'flaccid' indicates the absence of spasticity or other signs of disordered central nervous system motor tracts such as hyperreflexia, clonus, or extensor plantar responses.”
With the Global Polio Eradication Initiative by the WHO in 1988, Surveillance for AFP is an important public health activity in many countries. With the WHO's impressive progress, poliomyelitis is nearing its eradication in the world and other causes of AFP have gained importance.
AFP is a heterogeneous group and the medical conditions that fall under AFP were discussed by Marx et al. as lesions of the anterior horn cell including poliomyelitis, the spinal cord (as in transverse myelitis), the peripheral nerve (as in Guillain-Barré syndrome [GBS]) and toxic neuropathies from various infections including diphtheria, the neuromuscular junction (as in botulism) and muscle disorders, such as metabolic myopathies including hypokalemia and myositis.
The differential diagnosis of AFP varies from region to region. In Malaysia, GBS, central nervous system infection and transverse myelitis were the most common causes of AFP. Apart from GBS and transverse myelitis that was the most common diagnoses, the conditions classified under AFP in Australia included acute disseminated encephalomyelitis, tick-bite paralysis, and infant botulism. In South West Nigeria, the classification of AFP included traumatic sciatic nerve palsy, acute polyneuritis, neuropathy, and acute poliomyelitis.
Various data analysis of AFP cases over the last two decades have consistently reported GBS as the most common cause of nonpolio AFP worldwide,, with a frequency ranging from 21.09% in Pakistan  to 72.2% in Central America.
With this aim, a prospective observational study was conducted to know the clinical characteristics and differential diagnosis of individual cases of AFP, including distribution by age, gender and time.
| Methods|| |
This study was a prospective observational descriptive study. Cases admitted to the Neurology Department from July 2010 to September 2012 with provisional diagnosis of AFP were enrolled. All cases with AFP, irrespective of age, gender and time were selected. All cases of traumatic, spastic, chronic flaccid paralysis or sudden onset of weakness as in cerebrovascular accident were excluded from this study.
The clinical evaluation of AFP is often limited by meager resources and health infrastructure. The cases were selected on the clinical grounds. In addition to routine baseline investigations, lactate dehydrogenase, creatine kinase, arterial blood gas analysis, urinary pH, electrolytes, thyroid profile, electrophysiologic studies (nerve conduction studies, electromyography etc.), cerebrospinal fluid (CSF) examination, imaging of the spine and brain (radiography, computed tomography, or magnetic resonance imaging), stool examination were carried out in relevant cases.
| Results|| |
The results are shown in [Table 1],[Table 2],[Table 3],[Table 4],[Table 5]. A total of 106 cases of AFP were enrolled from July 2010 to September 2012. Out of 106 patients, the majority of cases, 58 (54.7%) were suffering from acute inflammatory demyelinating polyneuropathy (AIDP), a subtype of GBS. The mean age in males was 40.2 years (standard deviation [SD] 17.1) and the mean age in females was 33.4 years (SD 14.1) and 61/106 (57.5%) were males and 45/106 (42.5%) were females. Age and gender distribution of AFP cases are shown in [Table 3]. Out of 106 cases of AFP, most of the cases, 42/106 (39.6%) were admitted during the spring season, as shown in [Figure 1].
|Table 1: Frequency distribution of cases of acute flaccid paralysis (n=106)|
Click here to view
|Table 3: Age and gender distribution of the acute flaccid paralysis patients|
Click here to view
Out of the 58 patients with AIDP, a subtype of Guillain–Barré syndrome, 37/58 (63.8%) were males and 21/58 (36.2%) were females. The mean age was 35.38 years (SD 16.72) with a range from 13 years to 70 years. Most of the patients, 40/58 (69%) were <40 years of age. Out of 58 cases of GBS, most cases, 25/58 (43.1%) occurred during the spring season.
The clinical characteristics of AIDP, a subtype of GBS are shown in [Table 4]. Ascending lower limb weakness, 58/58 (100%) was the presenting symptom followed by upper limb weakness, 36/58 (62.1%). Cranial nerve (CN) VII was most often involved 6/58 (10.3%).
Albumino-cytological dissociation in CSF with average CSF protein level of 118 mg/dl (SD ± 40) was present in 42/58 (72.4%) patients during the 2nd week and reduced motor conduction velocities slowed F-wave responses and prolonged distal latencies were evident in all on electrophysiologic studies. Clinically six patients were objectively found to have respiratory weakness and received intravenous immunoglobulins, out of which, 2/58 (3.4%) patients needed ventilatory support. All cases survived and there was no mortality.
Fifteen patients with hypokalemic paralysis (HP) were enrolled. The etiological causes of HP were renal tubular acidosis Type I (8 patients), HP secondary to diuretics (5 patients) and hypokalemic periodic paralysis (2 patients). Lower limb weakness, both proximal and distal, was the predominant symptom in all and upper limb weakness was present in 14/15 (93.3%). Two patients had familial history of lower limb weakness.
Myasthenia gravis (MG) constituted, 8/106 (7.5%) cases of AFP. Females were 5/8 (62.5%) and males were 3/8 (37.5%). The mean age was 37.8 years (SD 11.88) with a range from 23 years to 50 years.
The clinical characteristics of MG are depicted in [Table 5]. Electrophysiological studies were showing decremental nerve conduction in all and computed tomography scan chest was showing thymus gland enlargement in 3/8 (37.5%) patients. Tensilon test was positive in all patients. Two, 2/8 (25%) of patients had respiratory distress with single breath count <20 and respiratory expansion <5 cm. Ventilatory support was need in, 2/8 (12.5%) and one patient had recurrence of symptoms.
Out of the eight patients with thiamine deficiency, 6/8 (75%) were females and 2/8 (25%) were males. Most patients, 6/8 (75%) were of <40 years age.
Lower limb weakness (distal > proximal) was present in all cases followed by upper limb weakness. Two, 2/8 (25%) had features of wernicke's disease with extraocular movement paresis, nystagmus, and confusion with mini mental state examination <22. Three, 3/8 (37.5%) had features of wet beriberi with cardiomegaly, swelling of feet and tachycardia. CN VI was bilaterally involved in, 2/8 (25%) and magnetic resonance imaging (MRI) brain was abnormal in 2/8 (25%).
Out of the five patients with transverse myelitis, 3/5 (60%) were females and 2/5 (40%) were males. All patients were <40 years of age. Two, 2/5 (40%) had transverse myelitis secondary to multiple sclerosis with objective evidence of pyramidal tract involvement, with T2-weighted (T2W) MRI images of the brain showing multiple periventricular hyperintensities, abnormal brain stem evoked response audiometry and oligoclonal bands in CSF. T2W images of spinal cord were showing hyperintensities with swollen cord over variable segments in 3/5 (60%) patients.
Two patients with the diagnosis of cord compression were admitted. Both patients were males, one with age of 32 years and other with age of 60 years. One had cord compression secondary to cervical tuberculosis and other secondary to multiple cervical disc prolapses.
Acute motor axonal neuropathy (AMAN), a variant of GBS constituted 3/106 (2.8%) cases. Two were males and one was female. Albuminocytological dissociation of CSF was found in all and nerve conduction studies were of motor axonal neuropathic type in all. Two patients had respiratory distress with single breath count <20, respiratory expansion of <5 cm, and were in need of ventilatory support. All have survived.
Acute disseminated encephalomyelitis was present in 2/106 (1.9%) patients. One patient was male with 16 years of age, and other was female with 15 years of age. Both upper and lower limb weakness was present in all, bulbar weakness in 1/2, nonspecific respiratory infection preceded in one patient. One of the patients had signs of meningismus and was confused. One patient had bilateral cranial nerve VII weakness, with high protein in CSF in both patients. T2W MRI images of the brain were showing widespread hyperintensities in periventricular and subcortical areas.
| Discussion|| |
With poliomyelitis nearing its elimination in the world, the other causes of AFP in children and adults have become significant. Unlike other studies which are important from epidemiological point of view, because the WHO is running polio eradication campaign, this study was mainly conducted to know the clinical characteristics and differential diagnosis of individual causes of AFP, including distribution by age, gender, and time.
Various data analysis of AFP cases over the last two decades have consistently reported GBS as the most common cause of nonpolio AFP all over the world, with a frequency ranging from 20% in Oman  to 72.2% in Central America. Mostly the frequency of GBS lies between 32.3% to 47.29%. Although the results of this study confirm to the rest of the national and international literature in having GBS as the most frequent cause of nonpolio AFP, the frequency stands on higher side at 54.7%, which may be because of cumulative frequency of GBS across all age ranges, unlike to most other studies carried out in children <15 years.
In this study, the frequency of HP was 14.2%, which is consistent with other studies., Most of the AFP studies conducted in children <15 years of age, don't mention MG to occur with significant frequency, as in a study by Morris et al. with the frequency of 2/143 (1.4%). In this study, MG was present with frequency of 7.5%, which may be due to more aged profile of our patients, a single referral institute in our place and needs further studies. The frequency of transverse myelitis in this study, 4.7% was consistent with other studies., AMAN, subtype of GBS, was present with a frequency of 2.8% of AFP cases and 4.9% of GBS cases that was consistent with 3.2% of GBS cases in a study by Koul et al. but lower than in a study in China. The frequency of ADEM in our study of 1.9% lies between 3.5% to 26.6% in other studies., Viral meningoencephalitis varies in frequency from 6.75% to 12.5% in other studies , which in contrast to our study stands at 1.9%.
The males outnumbered (57.5%) females (42.5%), which was in accordance with a study by Shah et al. Most cases of AFP, (39.6%) occurred during spring season (March to May) which was in contrast to summer season (June to August) in a study by Lam et al.
There was a preponderance of males (63.8%) over females (36.2%) in Guillain–Barré syndrome, which was consistent with most of the earlier studies.,,, However, in a study by Prevots and Sutter  the relative risk for GBS according to sex varied with age. This could be due to small sample size of our study and regional variation in the occurrence of GBS.
In this study, acute gastroenteritis preceded in 20.7% of cases and mild upper respiratory infection preceded in 13.8% of cases, which was in contrast to airway infections dominating over gastrointestinal infections, in other studies.,
All of the patients of GBS had progressive muscle weakness in a roughly symmetrical distribution, with areflexia of lower limbs in 100% of the cases and hyporeflexia of upper limbs in 12.1%, which was consistent with data from a study by Olivé et al. CN involvement was present in 37.9% of cases with CN VII involved in most cases, (10.3%) as against 50% in a study by Morris et al. to 21% in a study by Olivé et al., with CN VII most often affected. Respiratory depression was present in 10.3% of cases in comparison to 16% in a study by Olivé et al.
Clinically six patients were objectively found to have respiratory depression, out of which, 2 (3.4%) needed ventilatory support against 16%, in need of artificial ventilation in a study by Korinthenberg and Mönting.
HP was present in 14.2% of patients, lower than when compared to a study by Shah et al. This discrepancy may be due to under-reporting of cases, transient nature of paralysis and variable sample size of the study.
Female predominance, 5/8 (62.5%) of MG in this study was consistent with other studies., Two, 2/8 (25%) patients had respiratory depression and were in need of ventilatory support, against 12/50 (24%) requiring ventilatory support in a study by Jacob et al.
There was female predominance and younger age of presentation of thiamine deficiency in our patients, in contrast to a study by Koike et al. This could be the geographic variation in the occurrence of thiamine deficiency. Recurrent vomiting preceded in 5/8 patients, who were suffering from acid peptic disease (APD) and were females. As against, no patient in a study by Koike et al. had vomiting, who were operated for gastric problems; APD/neoplasm. In comparison to a study by Koike et al., the initial symptom was weakness of the limbs in 11/17 patients and a burning sensation in the feet in 6/17 patients. In our study, 2/8 had features of Wernicke's disease, and 3/8 had features of wet beriberi. In comparison to a study by Koike et al., four patients manifested Wernicke-Korsakoff Syndrome More Details, and 10 patients manifested signs of heart failure.
Female predominance, 3/5 (60%) of transverse myelitis was evident in this study as seen in a study by Morris et al. but against the male predominance in other studies (al Deeb et al. and Jeffery et al.). With respect to the clinical presentation, our findings agree with a study by al Deeb et al. In this study, 2/5 (40%) had transverse myelitis secondary to multiple sclerosis compared with 21% of multiple sclerosis in a study by Jeffery et al. All patients received methylprednisolone and 4/5 had good outcome, which was consistent with a study by Dowling et al.
AMAN constituted, 3 (2.8%) cases of AFP and 3/61 (4.9%) of GBS cases, comparable with 3.2% cases of GBS in a study by Koul et al., but lower than, 14.7% in a study by Dourado et al. and 47% in a study by McKhann et al. Two of our patients had respiratory distress compared to 22% in a study by Dourado et al., who needed ventilatory support with IV immunoglobulins. All patients improved.
Two cases (1.9%) of AFP had viral meningoencephalitis compared with 6.75% in a study by Anis-ur-Rehman et al. to 12.5% in a study by Saraswathy et al. and 16.2% in a study by Hussain et al. 1.9% AFP cases had diabetic polyneuropathy and 0.9% had chemotherapy-induced neuropathy as against 3% cases of diabetic neuropathy and 8% cases of chemotherapy-induced neuropathy in a study by Lee et al.
| Conclusion|| |
AIDP, a subtype of GBS was the most common cause of AFP in all age groups. Most AFP cases occurred during the spring season. No case of poliomyelitis was found.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
World Health Organization. Acute onset flaccid paralysis. WHO/MNH/EPI/93.3. Geneva: World Health Organization; 1993.
Alcalá H. The differential diagnosis of poliomyelitis and other acute flaccid paralyses. Bol Med Hosp Infant Mex 1993;50:136-44.
Marx A, Glass JD, Sutter RW. Differential diagnosis of acute flaccid paralysis and its role in poliomyelitis surveillance. Epidemiol Rev 2000;22:298-316.
Hussain IH, Ali S, Sinniah M, Kurup D, Khoo TB, Thomas TG, et al.
Five-year surveillance of acute flaccid paralysis in Malaysia. J Paediatr Child Health 2004;40:127-30.
Morris AM, Elliott EJ, D'Souza RM, Antony J, Kennett M, Longbottom H. Acute flaccid paralysis in Australian children. J Paediatr Child Health 2003;39:22-6.
Fawole OI. Acute Flaccid Paralysis. A Proceeding of Oluwaseun Physiotherapy Forum, Ibadan, Nigeria; 2003.
Lam RM, Tsang TH, Chan KY, Lau YL, Lim WL, Lam TH, et al.
Surveillance of acute flaccid paralysis in Hong Kong: 1997 to 2002. Hong Kong Med J 2005;11:164-73.
Iqbal AM, Ammarah J, Fehmina A, Ghulam M. Causes of non-polio acute flaccid paralysis in children residing in the province of Sindh. Med Channel 2010;16:357-61.
Molinero MR, Varon D, Holden KR, Sladky JT, Molina IB, Cleaves F. Epidemiology of childhood Guillain-Barré syndrome as a cause of acute flaccid paralysis in Honduras: 1989-1999. J Child Neurol 2003;18:741-7.
Koul R, Al-Futaisi A, Chacko A, Fazalullah M, Al-Nabhani S, Al-Awaidy S, et al
. Clinical characteristics of childhood Guillain-Barré syndrome. Oman Med J 2008;23:158-61.
Saraswathy TS, Zahrin HN, Apandi MY, Kurup D, Rohani J, Zainah S, et al.
Acute flaccid paralysis surveillance: Looking beyond the global poliomyelitis eradication initiative. Southeast Asian J Trop Med Public Health 2008;39:1033-9.
Anis-ur-Rehman, Idris M, Elahi M, Jamshed, Arif A. Guillain Barre syndrome: The leading cause of acute flaccid paralysis in Hazara division. J Ayub Med Coll Abbottabad 2007;19:26-8.
Shah FU, Salih M, Malik IA. Clinical evaluation of patients with acute flaccid motor weakness. Pak J Med Res 2002;41:58-63.
McKhann GM, Cornblath DR, Griffin JW, Ho TW, Li CY, Jiang Z, et al.
Acute motor axonal neuropathy: A frequent cause of acute flaccid paralysis in China. Ann Neurol 1993;33:333-42.
Rasul CH, Das PL, Alam S, Ahmed S, Ahmed M. Clinical profile of acute flaccid paralysis. Med J Malaysia 2002;57:61-5.
Prevots DR, Sutter RW. Assessment of Guillain-Barre syndrome mortality and morbidity in the United States: Implications for acute flaccid paralysis surveillance. J Infect Dis 1997;175:SI51-5.
Olivé JM, Castillo C, Castro RG, de Quadros CA. Epidemiologic study of Guillain-Barré syndrome in children <15 years of age in Latin America. J Infect Dis 1997;175 Suppl 1:S160-4.
Korinthenberg R, Mönting JS. Natural history and treatment effects in Guillain-Barré syndrome: A multicentre study. Arch Dis Child 1996;74:281-7.
Rastenytė D, Vaitkus A, Neverauskas R, Pauza V. Demographic-clinical profile of the patients with myasthenia gravis. Medicina 2002;38:611-6.
Jacob PC, Tharakan JT, Chand PR, Koul RL, Chacko AP. Clinical profile of myasthenia gravis in the Sultanate of Oman. Saudi Med J 2003;24:774-5.
Koike H, Misu K, Hattori N, Ito S, Ichimura M, Ito H, et al.
Postgastrectomy polyneuropathy with thiamine deficiency. J Neurol Neurosurg Psychiatry 2001;71:357-62.
al Deeb SM, Yaqub BA, Bruyn GW, Biary NM. Acute transverse myelitis. A localized form of postinfectious encephalomyelitis. Brain 1997;120(Pt 7):1115-22.
Jeffery DR, Mandler RN, Davis LE. Transverse myelitis. Retrospective analysis of 33 cases, with differentiation of cases associated with multiple sclerosis and parainfectious events. Arch Neurol 1993;50:532-5.
Dowling PC, Bosch VV, Cook SD. Possible beneficial effect of high-dose intravenous steroid therapy in acute demyelinating disease and transverse myelitis. Neurology 1980;30(7 Pt 2):33-6.
Dourado ME, Félix RH, da Silva WK, Queiroz JW, Jeronimo SM. Clinical characteristics of Guillain-Barré syndrome in a tropical country: A Brazilian experience. Acta Neurol Scand 2012;125:47-53.
Lee HS, Park WS, Ko CW, Sohn YK, Kwon SH. A clinical profile of peripheral neuropathy in Korean children. J Korean Child Neurol Soc2003;11:128-34.
[Table 1], [Table 2], [Table 3], [Table 4], [Table 5]