3.5 direct traumatic third nerve palsy

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19 July 1980 SA MED ICAL JOURNAL 109

avoid caval compression; (iii) avoid adrenaline in thelocal anaesthetic; (iv) because epidural analgesia may augment the response of antihypertensive therapy, modify thedosage of antihypertensive drugs before an epidural needleis inserted; (v) avo id epidura l analgesia in the presenceof coagulation defect; and (vi) avoid an epidural blockfor caesarean sect ion if t he degree of hypertension is

moderate to severe - the block must extend up to T6 inorder to provide pain rel ief dur ing the operation, and thisreduces the capacity of the patient's system to reactpromptly and appropriately to an episode of sudden haemorrhage such as is frequently encountered at caesareansection.

CONCLUSION

The management outlined is of intensive antepartum andpostpartum care of hypertensive pregnant patients. Thisinvolves prolonged hospitalization, and the financial costsare high. Significant savings are evident, however, whenthe cost of hospital izat ion is compared with the cost of astay in a neonatal intensive care unit for a grossly pre-

mature or severely ill neonate - intensive neonatal careis much more expensive than the cost per day for amother. I t is apparent that in most circumstances themuther is not only the best incubator for the infant but

the most cost-effective one as well!

REFERENCES

I. Gant, N. F. , Chand , S .,Wo rl ey , R . J. eI al. (1974): Ame r. J . Obst et .Gynec., 120, I.

2. Menon , M . K . K. (1961): J. Obstet. Gynaec. Brit. Cwlth, 68, 417.3. Lopez-Llera, M. (1967): Ibid., 74, 379.4. Crichton, D. , Notelvitz. M. and Hel ie r, I. (1968): Ibid., 75, 379.5. Ruoss, C. (1974) S. A fr. med J. , 48, 1459.6. Lopez-L1era , M. in lindheimer, M. D., Katz, A. r. and S u s p ~ n ,

P. F. eds (1976): Hypertension in Pregnancy, pp. 34 - 35. 'ew York:John Wiley & Sons.

7. Pritchard, J. A. (1975): Amer. J. Obstet. Gynec., 123, 543 .8. Vink, G. , Moodley, J. and Phi lp ot t, H. (1979): Ob stet. and Gy

naec. (in press).9. Campb el l, D . M . and MacGillivray, 1. (1975): Brit. J. Obstet. Gynaec. ,

82, 572.10. Liebermann, B. A. , Stirrat, G. , Cohen, S. et al. (1978): Ibid., 85, 893.11. Joelso", !. and Buton, M. D. (1969): Acta obs te t. gynec. scand., 48,

supp!. 3, p. 75.12. Bon na r. J . (1976): J. clin. Path., 2a, supp!. 10, p. 35.13. Redman, c. W. G. , Beilen, L. J. , Bonna r, J . et al. (1976): Lancet 1.

1370.14. Crawford, J. S. (1977): Clin. Obs te t. Gynec., 4, 735.

Direct Traumatic Third N'erve Palsy

N. B. SOLOMONS, D. J. SOLOMON, J. C. DE VILLIERS

SUMMARY

Traumatic third nerve palsy is an u nu sua l co nd i ti o n. It is

a se ri o us p r o gn o sti c fe atu re , no t fo r life bu t fo r permanent,

serious neuf.ological deficit. It can only be diagnosed with

confidence if it is known to have been present from th e

moment of impact and if a d eq u ate i n ve sti g ati on e xcl u de s

a compressing haematoma.

S. A fr . med. J., 58, 109 (1980).

Oculomotor palsy frequently follows head in jury whenspace-demanding intracranial lesions such as intracerebral,

subdural and extradural haematomas cause transtentorialherniation. Less frequently, direct injury to the third

Department of Neurosurgery, Groot e Schuur Hospi ta l andUniversity of Cape Town

N. B. SOLOMONS, Final-Yea'r Medical StudentD. J. SOLOMON. Filla!-Year Med-iclll Student

J. C. DE VILLIERS, M.D. , F .R .C.S. , Professor

D ~ t e received: 4 December 1979.

nerve anywhere along its course may occur. Traumatic

mydriasis and intra-orbital injury to ocular muscles maysimulate partial third nerve palsy and give rise to diagnosticconfusion.

The mechanism by which indirect or compressive thirdnerve palsy is produced is now universally accepted ascompression, displacement and deformity of the thirdnerve and brainstem by transtentor ia l herniat ion causedby a supratentorial expanding lesion.'·3 Little has beenwritten about the incidence and mechanism of direct third

nerve palsy : The present study, therefore, has been carried out to determine the incidence of primary traumaticthird nerve palsy, its frequency in craniocerebral trauma,

and the significance of the associated neurological statein the eventual outcome.

MATERIAL AND METHODS

The case summaries of all patients treated for head injuryin the Depar tment of Neurosurgery, Groote Schuur Hos

pital, Cape Town, from 1966 to 1977 were examined.



19 July 1980 SA MED ICAL Jo R TAL I I Icharacterized by a moderately but not maximally dilated,eccentric pupil , sometimes with absent but usually withdiminished reactions to light and accommodation. Themechanism of these react ions is disputed and is probably

varied.s -Io The frequent absence of pathological change inthe eye suggests that the effect may be due to damage tothe nerves in their passage through the ocu la r tissues bythe pressure wave which traverses the eye. In other cases

tears in the iris are visible or transillumination revealsruptures in the sphincter ic muscle . In 1947 KilgoreS experimentally demonstrated in the monkey that after relatively slight injury cyclitic changes, followed by replacement fibrosis of the muscle and subsequent atrophy, are

frequent sequelae.

Site of Injury

There is surprisingly little information as to the sitewhere direct third nerve injury usually occurs. ' Walsh

and Hoyt' believe that this happens at the point wherethe th ir d nerve pierces the dura to enter the cavernoussinus. They also state that fractures with momentary dis

placement of bone fragments may lacerate the nerve.The nerve, however , bears a close bony relationship onlyto the margins of the orbital fissure and the posteriorclinoid process, bu t the latter is hardly ever involvedin a fracture. Stretching and distortion of the thi rd nerveat the time of impac t a re probably the main causes ofthe nerve injury. The two oculomotor nerves project for

wards, laterally and sl ight ly downwards in an open Vformation that extends from the interpeduncular fossa

to the two posterior clinoid processes. This configurationwould predispose the t hir d nerve to shear and stretch by

a frontal blow, causing a line of force along its course.This is probab ly why bi later al direct thi rd nerve injury

is rarely observed clinically.

Variations in siZe of the tentorial incisura may play arole in the pathogenesis of t raumat ic thi rd nerve palsy.A large tentorial opening may allow free movement of

the midbrain and adjacent structures attached to it at thetime of impact.' During transient downward displacement,the third nerve may impinge on the posterior clinoid

process.As regards the mechanism and the site of production

of the third nerve palsy, there is little that our study canadd. Only 3 of the patients had injury to the oppositeside of the head and the rest had ipsilateral or diffusehead injury. The virtually constant presence of a frontalinjury, as noted by Hooper: was not found in this series.

It is of some inter est to consider the importance of

orbital fractures. Seven of our 21 patients had local orbital in jury, but no other nerves passing through thesuperior orbital fissure, except the third nerve, were involved. This suggests that localized involvement of thethird nerve at this level is not very likely. The forcefrom a blow to the orbit would be virtually directlytransmi tted backwards in line with the long axis of theorbit and the intracranial course of the ipsilateral thirdnerve, so that stretching of this nerve behind the cavernous sinus is very likely. Cross ' and Hooper· found tha t

orbital injury was frequently responsible for oculomotor

7

damage and that the resultant paralysi may be partialand often associated with other orbital nerve injuries.The fact that there were 6 cases of hemiplegia, of

which only 2 were cont ra lateral, makes it rather unlikelythat one is dealing with a traumatic Weber syndrome'

with damage to the third nerve fa cicles in the brainstem. I t is more likely that there i diffu e injury withassociated stretching or distortion of the third nerve in

these patients. Only in the 2 patient with cros ed palsycould one reasonably suggest that the damage occurredin the upper brainstem, but this could not be proved.The possibility remains that the in jury may occur at

the ite where the nerve passes through the dura, andthat during the time of impac t the tension on the duralfold, through which it pa se , may be such that the nerveis injured.' I t has been shown experimental lyll that thecommon, lateral crush injury, which produces longitudinalfractures of the petrous bone and is frequently associatedwith seventh nerve palsy, may cause such tension. Distortion of and tension on the nerve during its passagethrough the dura may be a more common cau e of injurythan has been thought previously, and would explain the

association with diffuse head injury causing transient deformity of the kull at t he t ime of impact. Dural tensionmay, of course, in particular instances be associated with

the other' mechanisms of nerve stretching, rotation and

downward displacement of the brainstem.

It is l ikely that, at the time of impact, many factorare at work and the injury to the third nerve could occur'either by stretching at the time of the initial impact, orby downward movement of the brainstem or rotationalstrain exerted on the brainstem. Such mechanisms alsomay involve the nerve or its branches in the orbitalfissure or in the orbit .The practical implications of this survey are clear-cut .

I t would be highly dangerous to diagnose primary third

nerve injury on purely clinical grounds. A history ofpalsy from the moment o f impact and of an improvingclinical s ta te would indicate that this may be the case,but such an accurate, reliable history is often lacking.

Fo r the pa tient 's sa fety i t would be better to perform an

investigative procedure, p re fe rably a non-invasive onelike computed tomography, to exclude the presence of a

compressive lesion. I t is important to recognize a primarythird nerve injury, because prognostically it indicate aserious injury wi th pro longed unconsciousness and permanent brain damage in more than 5 0 o ~ of ins tance.

However, in a significant number of patients it is not followed by a fatal outcome.

REFERENCES

1. Sunderland, S. (19 52 ): Brit. J . Oph thal .. 36, 638.2. Wat sh , F. B. and Hoyt, W. F. (1969): Clinical Neuro-OpJllhalmology,

3rd ed., p. 23 . Baltimore: Williams & Wilkins.3. Sunderland, S. (195): Brit. J. Sur g., 193. 422.4. Memon, M. Y. and Paine, K. W. E. (l97/): J. eurosurg., 35, 461.5. Turne r, J . W A. (1943): Brain, 66 , 140.6. Hooper, R. S. ( 1951 ): Brit. J. Surg., 39, 126. .7. Chusid, J. G. (1976): Correlative Neuroanatomy and Functlonal eu-

rology, 16th ed., p. 89. Los Altos , CaIif.: Lan.e Medical Publicarions.8. Ki lgor e, G . L. ill Duke-Elder, S. and MacFaul, P., eds ,.<1972):

System of Ophthalmology, vol. XIV, p. 90. London: Henry Klmpton.9. Cross, A. G. (1948): Ann. TOy. CoIl. Surg. Eng l. , 2, 233.10. Rowbotham, G. F. (1964): Acute Injuries to the Head, 4 th ed. , p. 419.

Edinburgh: Livingstone.11. De Villiers, J. C. (1971): J. 'eurol. Neurosurg. Psychiat ., 34 , 104.

3.5 direct traumatic third nerve palsy

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