VOLUME 16 NUMBER 4 July/August
traumatic neuritis from poliomyelitis
I read with interest the recent article by H. V. Wyatt.1 He has discussed an
important issue of traumatic neuritis (TN) due to intramuscular injections
and the need to differentiate this entity from cases of poliomyelitis. I would
like to make certain observations.
TN following an intramuscular injection in the gluteal region is well known.2 The duration between the administration of injection and onset of paralysis
varies from one hour to five days.3 The common peroneal division of the sciatic
nerve is more commonly involved as compared to the tibial nerve. Patients usually
present with a foot drop due to weakness of the ankle dorsiflexors. Ankle evertors
are also weak. The distal groups of muscles are thus predominantly affected.
In addition, patients also have sensory impairment in the distribution of the
peroneal nerve, namely, the lateral aspect of the leg and foot and the dorsal
aspect of the foot.
In contrast, poliomyelitis is a pure motor disorder and sensations are not
affected. The pattern of the muscles involved also differs from that of TN.
In poliomyelitis, the quadriceps, hip adductors and tibialis anterior are more
commonly affected.4 Therefore, the presence of proximal weakness and absence
of sensory involvement in a child would favour poliomyelitis as against TN.
The postulated mechanisms of
traumatic nerve injury include direct needle trauma, secondary
constriction by a scar, ischaemia to the nerve, and direct nerve
fibre damage by neurotoxic chemicals in the injected agent.5,6 Introduction of infection or abscess formation due to the use
of unsterile injections could be contributory mechanisms.
Intramuscular injection as a risk factor for paralytic poliomyelitis is well
known.7,8 This is referred to as provocation paralysis.9 The postulated mechanism
is that skeletal muscle injury induces retrograde axonal transport of the poliovirus,
thereby facilitating viral invasion of the central nervous system and the progression
of spinal cord damage.9 Intramuscular injections also increase the risk of
oral polio vaccine-associated paralytic poliomyelitis.10
Unnecessary intramuscular injections should be avoided. Oral drug therapy should
be promoted. If an injection is a must, the site should be the lateral aspect
of the thigh rather than the gluteal region. A detailed neurological examination
is helpful in differentiating TN from poliomyelitis.
5 August 2003
Department of Neurological Sciences
Christian Medical College Hospital
- Wyatt HV. Diagnosis of acute flaccid
paralaysis: Injection injury or polio? Natl Med
J India 2003;16:156–8.
- Combes MA, Clark WK, Gregar CF.
Sciatic nerve injury in infants. JAMA 1960;173:1336–9.
- Anonymous. Surveillance of
acute flaccid paralysis. Field guide. New Delhi:MCH division,
Department of Family Welfare, Ministry of Health
and Family Welfare, India.
- Sharma SC, Sangwam SS, Siwach
RC, Aggarwal R, Khatri CR, Govila VK, et al. The
pattern of residual muscle paralysis in poliomyelitis.
Int Orthop 1994;18:122–5.
- Villarejo FJ, Pascual AM. Injection
injury of the sciatic nerve (370 cases). Childs Nerv
- Ahuja B. Post injection sciatic
nerve injuy. Indian Pediatr 2003;40:368–9.
- Kohler KA, Hlady WG, Banerjee
K, Sutter RW. Outbreak of poliomyelitis due to type
3 poliovirus, northern India, 1999–2000: Injections
a major contributing factor. Int J Epidemiol 2003;32:272–7.
- Wyatt HV, Mahadeven S, Srinivasan
S. Unnecessary injections and paralytic poliomyelitis
in India. Trans R Soc Trop Med Hyg 1992;86:546–9.
- Gromeier M, Wimmer E. Mechanism
of injury-provoked poliomyelitis. J Virol 1998;72:5056–60.
- Strebel PM, Ion-Nedelcu N, Baughman
AL, Sutter RW, Cochi SL. Intramuscular injections
within 30 days of immunizaton with oral poliovirus
vaccine—A risk factor for vaccine-associated
paralytic poliomyelitis. N Engl J Med 1995;332:500–6.