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Show Joumal of Gilli.. al N" uT( l-( lp" t1IOIIl/( lI".~ 11 11( 21: 122- 124, 1991. Accommodation Failure Following Tetanus Kanwar Mohan, M. S., Birgit Khandalavala, M. S., Amod Gupta, M. S., and Subhadra Jalali, M. S. © 1991 Raven Press, Ltd., New York A patient with tetanus had isolated and progressive failure of accommodation over a period of more than 1 year and did not show any recovery at 51/ 2 years after the onset. Key Words: Tetanus- Accommodation paralysisAccommodation failure. From the Department of Ophthalmology, Postgraduate Institute of Medical Education and Research, Chandigarh, India. Address correspondence and reprint requests to Dr. Kanwar Mohan at Department of Ophthalmology, Postgraduate Institute of Medical Education and Research, Chandigarh- 160 012, •.- 1; Abnormalities of accommodation are usually acquired, although congenital anomalies do occur. Acquired disturbances of accommodation occur most frequently as part of the normal aging process that begins shortly after birth and becomes manifest in emmetropic persons in the fourth decade of life. Insufficiency or paralysis of accommodation in young persons is seen in a number of pathologic conditions, including ocular inflammation and trauma; systemic myopathies such as myasthenia gravis and botulism; neurologic diseases such as encephalitis and multiple sclerosis affecting the third cranial nerve, its nucleus, or supranuclear connections; and systemic diseases such as diphtheria and diabetes mellitus ( 1). Idiopathic deficiency of accommodation in young, healthy individuals is also known ( 2,3). Cephalic tetanus may give rise to accommodation paralysis ( 4). However, whether it occurs in isolation or as a part of total ophthalmoplegia has not been addressed in the literature. To the best of our knowledge, there is no previous report of isolated, progressive, and irreversible paralysis of accommodation caused by tetanus. Here we document one such case. CASE REPORT A B- year- old boy was admitted in October 1984 to the emergency service with trismus, generalized spasms, neck stiffness, and exaggerated tendon reflexes following contusion injury to both lower limbs in a roadside accident a month before. There was no other neurological deficit or history of trauma to the head. A diagnosis of tetanus was made, and he was put on supportive therapy including intravenous diazepam 10 mg every 6 hours, tablet phenobarbitone 60 mg every 8 hours, and tablet chlorpromazine 25 mg twice daily. He responded well to the above treatment, which was continued for 2 weeks upon discharge from the hospital. One week later, he presented to us with 122 ACCOMMODATION FAILURE FOLLOWING TETANUS 123 a history of difficulty in reading. There was no other systemic complaint during this period. He was not diabetic. On ocular examination, his uncorrected distance visual acuity was 6/ 6 in either eye, while his near visual acuity at reading distance was N- 36 in either eye. Amplitude of accommodation measured 3.20 in either eye, approximately 7.30 below the minimal normal for his age. With + 2.00 sphere in front of both eyes, he could read the smallest near test print ( N- 6) with either eye. Cycloplegic refraction did not reveal any significant refractive error. Pupillary reaction to light was brisk, but was markedly sluggish to near stimulus. The rest of the eye examination, including fundus and near point of convergence, was normal. Slit lamp biomicroscopy did not show any abnormality of the lens and zonules. Somatic and neurologic examinations were normal. Two months later, his distance visual acuity decreased to 6/ 12 in either eye and the amplitude of accommodation further receded to 2.00 in either eye. Now he required + 0.750 sphere in front of either eye for distance visual acuity of 6/ 6 and an additional + 2.50 sphere for near visual acuity of N- 6. Bifocal glasses were prescribed. Seven months later, he had further deterioration of his distance and near visual acuity. The uncorrected distance visual acuity at this time was 6/ 60 in either eye, and he required + 1.50 sphere bilaterally for visual acuity of 6/ 6 and an additional + 2.50 sphere for near vision of N- 6. After 11/ 2 years, his distance visual acuity of 6/ 6 was still corrected with + 1.50 sphere, but now he needed an additional + 3.000 sphere for near vision of N- 6. After 4112 years, the amplitude of accommodation was still 2.00 in either eye. The visual acuity and refraction were unchanged, and he still required + 1.50 sphere bilaterally for distance visual acuity of 6/ 6 and an additional + 3.000 sphere for near vision of N- 6. After 51/ 2 years, his amplitude of accommodation, pupillary reactions, visual acuity, and refraction remained unchanged and he still needed the same refractive correction for normal distance and near vision. On instillation of pilocarpine 0.5%, the amplitude of accommodation measured 7.10 in either eye. Though the corrected distance and near vision were normal, the patient had asthenopic symptoms which made reading and near work considerably difficult. DISCUSSION Paralysis of accommodation in this patient can certainly be attributed to tetanus because ( a) the paralysis followed soon after the onset of the dis-ease and ( b) the other causes of accommodation failure such as head trauma, botulism, diphtheria, encephalitis, myasthenia gravis, multiple sclerosis, diabetes, and ocular inflammations could be ruled out at the outset, in view of the case history. Also the drugs such as phenobarbitone, diazepam, and chlorpromazine which this patient received for control of spasms are not known to cause accommodation failure. The condition is also unlikely to be functional, because the pupillary reaction to near stimulus was impaired. Tetanus, often called ' lock- jaw,' is an acute neuromuscular disease that results from the exotoxin produced by the anaerobic spore- forming bacteria, Clostridium tetani, and is characterized by uncontrolled spasms of voluntary muscles. Cephalic tetanus is a rare variety of tetanus associated with paresis or palsies of one or more cranial nerves as a prominent symptom, together with more or less well- marked symptoms of tetanus. It is generally confined to the region of the head and neck, though at times it can involve the entire body ( 5). It generally follows injuries of the head or face, but can occur in cases with injuries to other areas and also without any apparent wound ( 6,7). Paralysis usually follows trismus, but rarely they may come together or paralysis may even precede trismus ( 6). The facial nerve is involved in about 95- 100% of the cases, and the palsy is usually of lower motor neuron type ( 6,8). Next to facial involvement comes oculomotor, abducent, trochlear, and hypoglossal nerves, in order of frequency ( 5). In most of the cephalic tetanus patients, paralysis of ocular muscles is associated with facial palsy, but isolated ocular involvement can also occur ( 6,9,10). Ptosis is the commonest and may be the only ocular manifestation of cephalic tetanus ( 6). Other manifestations are external or total ophthalmoplegia, mydriasis of pupil, nystagmus, exophthalmos, and diplopia ( 6,7,9). Cephalic tetanus is known to cause accommodation paralysis ( 4), but whether it occurs in isolation or as a part of total ophthalmoplegia has not been addressed in the literature. In an extensive review of the literature on cephalic tetanus by Jayme- Goyaz ( 7) and Wetzel ( 9), there was not a single case of isolated accommodation paralysis. We feel that our patient had a variant of cephalic tetanus occurring after contusion injuries to the lower limbs and his condition was not associated with any other ocular palsy. The pathogenesis of cephalic tetanus is still obscure. The exotoxin tetanospasmin attacks synaptic functions to produce disinhibition of ( X and ' Y motor systems. Peripherally, it produces neuromuscular blockade. There is evidence that tetanus 1 Clin Neuro- ophthalmol. Vol. 11. No. 2. 1991 124 K. MOHAN ET AL. toxin has a selective action on certain cell groups in the medulla ( 11). The paralytic phenomenon in cephalic tetanus may be due to selective action of toxin on the cranial nerve nuclei ( 5), to high local concentration of toxin in the brain system ( 12), or to centripetal spread of the toxin to the cranial nerve nuclei ( 13). Chromatolysis and neuronophagia have been found in the brain stem nuclei ( 14). In our patient, the accommodation paralysis associated with impairment of the pupillary near reflex and a positive accommodative response to pilocarpine ( which is a directly muscle- acting substance) suggests a central rather than peripheral lesion. There is experimental evidence in the macaque monkey that a discrete cell mass within the Edinger- Westphal nucleus subserves accommodation, whereas a separate discrete cell mass in the same nucleus subserves pupillary constriction ( 15). Since these areas are believed to be contiguous or overlapping in an intermediate zone, it is probable that a causative factor would influence both, hence impairing accommodation as well as the pupillary near reflex. The third nerve nucleus is a big nucleus divided into many islands of nerve cells, and it is possible that tetanus toxin has a selective action on the Edinger- Westphal nucleus. The associated hypermetropia in this patient appears to be the latent hypermetropia which became obvious when the accommodation failed. All the effects of tetanus toxin manifest shortly following a soil- contaminated wound, and are selflimiting and completely reversible in about four weeks in most of the survivors ( 16). Cranial nerve paralysis usually improves simultaneously with the disease. However, rarely residual palsies may persist for several weeks to several months, even after other features of tetanus have cleared ( 5). The exact time of onset of accommodation paralysis in this patient is not known, because we first examined him 3 weeks after the diagnosis of tetanus. A progressive failure of accommodation for about 1V2 years and no sign of recovery even 5V2 years after the onset of tetanus is rather unusual. However, Roberts and Williamson ( 17) have reported a case JClin Neuro- ophliullmol, Vol. iI. No, 2, 1991 of progressive ophthalmoplegia caused by tetanus. It may be assumed that tetanus toxin caused progressive and irreversible pathologic changes in the Edinger- Westphal nucleus. Most of the patients with accommodation deficiency do well with reading glasses or bifocal lenses. This patient, however, had asthenopic symptoms despite the best visual correction. We suggest that if a patient who had tetanus complains of difficulty in seeing near work, the possibility of accommodation paralysis must be considered. REFERENCES 1. Walsh FB, Hoyt W. Paresis of accommodation. In: Clinical neuro- ophthalmology. 3rd ed., William & Wilkins, Baltimore, 1969: 546- 50. 2. Chrousos GA, O'Neill JF, Lueth BD, Parks MM. Accommodation deficiency in healthy young individuals. J Pediatr Ophthalmol Strab 1988; 25: 176- 9. 3. Tornqvist G. Paralysis of accommodation. Acta Ophthalmol 1971; 49: 702~. 4. Duke- Elder S. Paresis of accommodation. System of ophthalmology. Vol. 12. London: Henry Kimpton, 1971: 698- 706. 5. Brown AJ. Cephalic tetanus. Ann Surg 1912; 55: 473-- 84. 6. Vakil BJ, Tulpule A, lyer SN, Tulpule TH. Cephalic tetanus. J Indian Med Assoc 1964; 42: 212- 9. 7. Jayme- Goyaz GG. Cephalic tetanus follOWing injury to the eyeball. Am J OphthalmoI1941; 24: 1281- 99. 8. Chopra K, Kumar P. Cephalic tetanus. Indian J Pediatr 1987; 24: 172- 4. 9. Wetzel JO. Tetanus following eye injury. Am JOphthalmol 1942; 25: 933- 44. 10. Wilson SAK. Neurology. 1st ed. London: Arnold, 1940: 630. 11. Vakil BJ, Tulpule A, Iyer SN, Tulpule TH. Cephalic tetanus. J Indian Med Assoc 1964; 42: 212- 9. 12. Dastur FD, Shahani MI, Dastoor DH, et al. Cephalic tetanus: demonstration of a dual lesion. JNeurol Neurosurg Psychiatry 1977; 40: 782- 6. 13. Abde VW, Dekate MP. Cephalic tetanus ( clinical analysis of 9 cases). J Indian Med Assoc 1980; 74: 111- 3. 14. Harriman DGF. Symposium on tetanus in Great Britain. Leeds: National Lending Library, 1967. 15. Jampel RS, Mindel J. The nucleus of accommodation in the midbrain of the macaque. Invest Ophthalmol Vis Sci 1967; 6: 40- 50. 16. Thorn GW, Adams RD, Braunwald E, Isselbacher KJ, Petersdorf RG, eds. Harrison's principles of internal medicine. 8th ed. Blackiston: Kogakusha, 1977: 886- 90. 17. Jayme- Goyaz GG. Cephalic tetanus following injury to the eyeball. Am J OphthalmoI1941; 24: 1281- 98. |
