ocular palsies with sinusitis · j. neurol. neurosurg. psychiat., 1950, 13, 225. ocular palsies...

J. Neurol. Neurosurg. Psychiat., 1950, 13, 225.

.. OCULAR PALSIES WITH NASAL SINUSITISBY

HELEN DIMSDALE and D. G. PHILLIPS

The diagnosis of nasal sinusitis as a cause ofocular palsy has recently fallen into disfavour,particularly since the importance of congenitalaneurysm as a cause of third nerve palsy has beenrecognized.

It is the purpose of this communication to recorda series of fully investigated cases of ocular palsyobserved over some years, in which the palsies wereassociated with the presence of a chronic infectionof the nasal sinuses. We made a short preliminaryreport of these cases in 1948.* Since then onefurther example has been added to the series.

Historical ReviewThe association of ocular palsies with nasal sinus

infection has been recognized for many years.Trantas (1893) described a patient with left ex-ophthalmos and total left ophthalmoplegia, in whomrecovery from ocular palsy followed drainage of theinfected sinuses, though severe visual loss resulted,with optic atrophy. Trantas mentions the occur-rence of other cases of sinus disease with blindnessand third nerve palsy in the literature. Furtherearly cases in the continental literature are quotedby Onodi (1914) and Rollet (1933). In recent timesthe relatively few recorded cases include thosewith isolated third nerve palsy (Sluder, 1927;Rollet and Parthiot, 1929; Genet, 1929; Rollet,1933 ; Yaskin, 1939), isolated fourth nervepalsy (Sluder, 1927; Redslob and Delbos, 1941),isolated sixth nerve palsy (Caliceti, 1927 ; Sargnonand Parthiot, 1930; Horgan, 1931 ; Diamant,1937), and multiple ocular palsies (Sargnon, 1923;Sluder, 1927; Stieren and McKee, 1932; Yaskin,1939; Kretzschmar and Jacot, 1939). Nearly allthe patients had short histories and rapid andcomplete recoveries following treatment of infectedsinuses. The only fatal case among these was aman who died 40 days after operation of meningitis

* Communication read at the Congress of the United KingdomOphthalmological Society in April, 1948.

(Rollet, 1933). This patient had, in addition toocular nerve palsy, an optic neuritis.

Pathological AnatomyExhaustive studies of the relation of the ocular

nerves to the nasal sinuses have been made bySluder (1913), the Onodis (1914), and Houser (1933).During the course of these nerves from the brainstem through the superior orbital fissure to theorbit, there are two sites where the anatomicalrelationships predispose to palsies as a result ofsinus infection.The third nerve after it emerges from the anterior

end of the cavernous sinus lies in close relation to theupper part of the lateral wall of the sphenoidal andposterior ethmoidal sinuses, especially if pneuma-tization has extended into the attached root of thelesser wing of the sphenoid. It should be noted thatthe optic nerve is also in close relation here.The fourth and sixth nerves are more laterally

placed, but may be involved by extension of theinfective process from the anterior or posteriorgroups of sinuses into the superior orbital fissure.The sixth nerve alone is in relation to the posterior

wall of the sphenoidal sinus in Dorello's canal.This canal is bounded by the posterior clinoidprocess, the apex of the petrous bone, and thepetro-clinoid ligament, and transmits the sixth nerveand the inferior petrosal sinus. There is muchvariation in the extension of the sinus cavity back-wards in the body of the sphenoid bone, and in someskulls there may be as little as two millimetresbetween Dorello's canal and the interior of the sinuscavity (Houser, 1933).

Involvement of the sixth nerve by a spread ofinflammation to theb apex of the petrous bone froman ear infection, as in Gradenigo's syndrome, iswell known. Symonds (1944) suggested that in aproportion of cases this syndrome may result from athrombophlebitis of the inferior petrosal sinus. Insome individuals the sixth nerve reaches the lateral

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HELEN DIMSDALE AND D. G. PHILLIPS

wall of the cavernous sinus by first penetrating theinferior petrosal sinus. In view of the relativefrequency of sixth nerve palsy in association withotitis media and mastoiditis, it is rather surprisingthat it should not be encountered more frequentlyas a result of sphenoiditis.

Case MaterialThe cases are divided into two main groups:

ocular palsies with sphenoiditis; ocular palsieswith inflammation of the superior orbital fissure.

Ocular Palsies with Sploiditis (Four Cases).-These cases form a well-defined group. The patientspresented with headache and double vision. Theywere apyrexial and did not complain of nasalsymptoms, but radiological examination showedopacity of the sphenoidal sinuses and extremerarefaction of bone around the sella turcica.Surgical drainage of the infected sphenoidal sinuseswas performed, with immediate improvement in theocular palsies, progressing to partial or completerecovery. Radiological examination after somemonths showed regeneration of the decalcified boneabout the sella.

Case 1.-Mrs. F. B., aged 60 years, was admitted toChase Farm Hospital on August 8, 1943, from the RoyalLondon Ophthalmic Hospital. Five months previouslyshe had noticed double vision on looking to the left;this lasted for two weeks. Three weeks before admissionthe double vision recurred accompanied by pain in theright side of the forehead and drooping of the righteyelid. About the same time she noticed the sight ofthe left eye was deteriorating. For many years she hada nasal discharge with loss of sense of smell, but aboutfive years ago the discharge had ceased.On examination there was bilateral anosmia. She

was myopic, otherwise the fundi were normal. Thevisual field of the left eye showed a slight superior nasalconstriction and a hemianopic temporal defect withsparing of fixation to 3/1500 white. The visual field ofthe right eye was full. The left visual acuity was 6/36,and the right 6/12 corrected. There was a right partialptosis, with absence of elevation and adduction;depression was weak. The superior oblique muscle wasactive. The right pupil was slightly larger than theleft but reacted normally. The rest of the nervoussystem was normal. The blood pressure was 180/100mm., and there was moderate peripheral arteriosclerosis.The sedimentation rate was 17 mm. in one hour;

the blood count was normal. The blood Wassermannreaction was negative, and the cerebrospinal fluid wasnormal. Radiological examination showed erosion ofthe middle of the dorsum sellk, floor and neighbouringparts of the sphenoid, with generalized opacity of thenasal sinuses.On September 2, 1943, a bilateral Caldwell-Luc

operation was performed by D.G.P. with free drainage ofpus from the antra, ethmoids, and sphenoidal sinuses.

Culture grew haemolytic streptococci. Sulphathiazolewas given post-operatively.On September 6 the ocular movements had improved

and ten days after operation were full, apart from slightptosis. The visual field of the left eye had expandedand the left visual acuity was 6/12 corrected. Radiologicalexamination a month after operation showed somere-formation of the dorsum sellhe.

Five years later the patient was well, and the sellaturcica was normal apart from slight irregularity of thefloor.

Although there were no recent nasal symptoms,a sphenoiditis and pansinusitis produced a rightthird nerve palsy complete except for the pupillaryfibres. There was interference chiefly with the nasalfibres of the left optic nerve. Recovery resultedfrom drainage of the infected sinuses.

Case 2.-Martin W., a man aged 46, was admitted toChase Farm Hospital on October 10, 1946, from theRoyal London Ophthalmic Hospital. He complainedof attacks of shooting pains in the right temple for thepast six months. One month before admission hestarted to see double and the right eyelid drooped.There was no history of nasal discharge.On examination there was no anosmia. The fundi,

fields, and visual acuity were normal. The right pupilreacted sluggishly to light and accommodation. Therewas a right partial ptosis with weakness of elevation,adduction, and depression. Two weeks after admissiona weakness of the right superior oblique muscledeveloped. No clinical evidence of sinus infection wasdetected.The sedimentation rate was 12 mm. in one hour, the

blood count normal. The blood Wassermann reactionwas negative, and the cerebrospinal fluid was normal.Radiological examination showed that the dorsum andfloor of the sella were destroyed, with an opacity of thesphenoidal sinus. Bilateral carotid arteriography andair encephalography demonstrated no abnormalities.On December 17, 1946, at the Brentwood Annexe of

the London Hospital the sphenoidal sinus was exploredby Mr. Keogh. The posterior part of the bony roof ofthe sinus felt soft. The sinus was filled with 4 ml. ofdark brown fluid under pressure containing pus cells,and on culture grew Staphylococcus pyogenes.Three months after operation some weakness of

elevation and depression remained, but the other move-ments were full, and there was no ptosis. Radiologicalexamination a year later showed partial re-formation ofthe floor of the sella.

Paresis of the right third and fourth nerves wasproduced by an infected cyst of the sphenoidalsinus. There were no nasal symptoms. Partialrecovery occurred after drainage of the sphenoidalsinus with re-formation of the bone.

Case 3.-J. S., a man aged 60 years, was admitted tothe London Hospital on November 10, 1947. Ninemonths previously he had noticed double vision for

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OCULAR PALSIES WITH NASAL SINUSITIS

FIG. la (Case 3).-Rarefaction of sella turcica; opacsphenoidal sinus.

three weeks, and a dull aching pain in the left temple.The double vision recurred in May and September, 1947,and lasted three weeks on each occasion. There was ahistory of chronic nasal discharge since a blow on hisnose by a cricket ball in 1912. In 1920 a nasal polyp wasremoved.On examination there was no anosmia. The fundi

and pupils were normal. There was diplopia on lookingup and to the right, suggestive of a left inferior obliqueparesis. There was no clinical evidence of sinusitis.Radiological examination showed destruction of thefloor of the sella turcica, with opacities of very largesphenoidal sinuses and the maxillary sinuses (Fig. Ia).

FiG. lb (Case 3).-Regeneration of sella; clear sphenoidalsinus (two months later).

On October 29, 1947, Mr. Bowen-Daviesperformed operative drainage of the sinuses.Polypoid mucosa was found in the posteriorethmoidal cells. The left sphenoidal sinuscontained some curious material almost ofthe consistency of dark brown plasticine.The histological changes were those of aohronic pyogenic inflammation.On November 5, 1947, there was no

diplopia and the ocular movements were full.On radiological examination two months afteroperation the sella was seen to be re-forming(Fig. lb). Six months later the patient hadremained well.There was a history of catarrh, although

there was no clinical evidence of sinusinfection. The partial left third nerveparesis recovered after drainage of theinfected sphenoidal sinus, and the erodedsella re-formed.

city of Case 4.-Maurice W., a man aged 45, wasadmitted to Chase Farm Hospital on Novem-ber 14, 1942, from the London Hospital. He

complained of generalized headache and double visionfor two months. He had noticed a blood-streaked,post-nasal discharge for ten years. He was a treateddiabetic.!1 rwr~~~~~~~~~~:F''>:..>,.

FIG. 2a (Case 4).-Absorption of bone of sella turcica.

On examination there was a right external rectusparesis; otherwise the nervous system was normal.There was no clinical evidence of nasal sinus infection.The blood Wassermann reaction was negative, andthe cerebrospinal fluid was normal. Radiologicalexamination of the skull and sinuses showed dullnessof the sphenoidal sinuses with erosion of the floor of thesella turcica together with the posterior clinoid processessuggestiveofa neoplasm ofthe sphenoidalsiDuses (Fig. 2a).

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On March 31, 1943, the ethmoidal and sphenoidalsinuses were explored by D.G.P.; mucous discharge andhypertrophied polypoid mucosa were found. On sectionthis showed granulation tissue infiltrated with poly-morphonuclear and plasma cells. Culture grewCoccobacillus fwtidus ozaene.There was an improvement of abduction of the right

eye three days after operation, and by the twelfthpost-operative day the diplopia had cleared. Occasionaldiplopia recurred over a year, but during the nextfive years recovery was complete. Radiological exami-nation seven months after operation showed re-calcification of the sphenoid (Fig. 2b).

FIG. 2b (Case 4).-Regeneration of sella (seven months

Sphenoiditis with destruction of bone waspresent without nasal symptoms apart fromsome post-nasal catarrh. It must be admitted thatthe diagnosis of the cause of the sixth nerve paresiswas complicated by the' presence of diabetes, butpermanent recovery appeared to be related to thedrainage of the infected sphenoidal sinus.

DiscussionChronic sphenoiditis may be present in the

absence of nasal symptoms, although a past historyof a period of nasal discharge was usually obtainablefrom these patients. Cessation of discharge was

probably due to blockage of the ostium of the sinus.The increase of tension in the sinus finally producederosion of its bony wall with the development ofocular' palsies. The palsies might be intermittentat first due to changes in tension of the contents ofthe sinus. Hermann and Hall (1944) have des-cribed the case of a patient with periodic headacheassociated with a partial third nerve palsy due tomucocele of the sphenoidal sinus.

Relative sparing of the puplUary fibres in thesepatients (Cases 1, 2, and 3) was probably fortuitous.Hermann and Hall found ptosis and an inactivepupil in their patient. Rollet (1933) and Yaskin(1939) also described internal ophthalmoplegia dueto sphenoiditis.

Certain clinical features may assist in the differ-entiation of ocular palsies due to sphenoiditis fromthose due to supraclinoid aneurysms. The uni-lateral frontal pain was aching in character and wasnot intense. The palsy did not develop simul-taneously with the pain. There were no symptoms,

such as stiffness of the neck, suggestive ofa leaking aneurysm. The third nervepalsies were incomplete and other cranialnerves, the second (Case 1) and the fourth(Case 2) were involved. Jefferson (1947) hasstated that it is the completeness of anisolated third nerve palsy that is socharacteristic of an aneurysm of the pos-terior communicating artery.kThe symptomatology of carcinoma of

the naso-pharynx has been studied byGodtfredsen (1947) who found that thesixth nerve was frequently first affected,then the contralateral sixth, and thetrigeminal nerve. Palsies of the third andfourth nerves were infrequent.The appearance of an ocular palsy due

to disseminated sclerosis in a patient withsinus infection may be misleading. Thepatients under consideration were old for

later). the onset of this disease ; other signsof disseminated sclerosis were lacking and

did not develop during the period of observation.Neurosyphilis was excluded by the negative

serology.Radiological appearances of a pansinusitis may

clarify the diagnosis; but if the sphenoidal sinusesonly are opaque, with erosion of the sella, ex-ploration is necessary to determine the nature ofthe lesion.The site of the lesion of the third nerve in these

patients was probably at the medial end of thesuperior orbital fissure, and of the sixth nerve inDorello's canal, associated with erosion of theposterior clinoid processes.

Ocular Palsies with Inflammation of the SuperiorOrbital Fissure (Six Cases).-These cases corres-ponded generally with the syndrome de la fentesphenoidale described by Rollet (1933) and Kretz-schmar and Jacot (1939), and orbital periostitis(Cairns, 1938 ; Collier, 1922). The patients presentedwith unilateral headache, and double vision dueto multiple ocular palsies. Proptosis, generally

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slight, was present in all. Unilateral papillcedema,trigeminal nerve involvement, and intracranialspread of inflammation were seen in a varyingdegree. Nasal symptoms were not prominent,but all showed radiological evidence of sinusitisat some period of their illness.

Case 5.-Mrs. L. S. aged 46 years was admitted to theMaida Vale Hospital for Nervous Diseases, London,on April 9, 1947, from the Moorfields, Westminster andCentral Eye Hospital (Royal London OphthalmicHospital).Nine weeks previously she had noticed protrusion of

the right eye and drooping of the lid. She then startedto have an aching pain on the right side of the forehead.Although she had a past history of catarrh there was norecent nasal discharge.On examination there was no anosmia. The fundi

and visual fields were normal. The right visual acuitywas 6/9, left 6/6 uncorrected. The right eye wasproptosed downwards and forwards. There was partialright ptosis, with weakness of elevation and adduction.The pupils were normal. The rest of the nervous systemwas normal. The blood pressure was 220/120 mm.,and the heart moderately enlarged.The sedimentation rate was 11 mm. in one hour, and

the white count was normal. The blood Wassermannreaction was negative, and the cerebrospinal fluid normalin pressure and constituents.

Radiological examination of the skull showed noabnormality of cranium or orbit. Thickened mucosa orfluid was present in the right antrum, and fluid in theleft antrum.On April 12, 1947, an oval mass about 2 cm.

x 0 5 cm. was detected in the posterior partof the orbit, which was thought to be inflam-matory and related to sinus infection. Someimprovement followed antral puncture andconservative treatment. Subsequently theproptosis increased, and cedema cf the lidsappeared. Although the fundus and visualfield were normal, the right visual acuitydeteriorated to 6/18. Radiological examina-tion now showed a patch of osteitis in theroof of the orbit (Fig. 3). The conditionwas considered to be inflammatory by Mr.Wylie McKissock.A radical frontal sinus operation was

performed by Mr. Howells in July, 1947,at Slough Emergency Hospital; chronicfrontal sinusitis was found with necrosisof the anterior wall of the sinus. The patientmade a satisfactory recovery.

Maxillary and frontal sinusitis withoutrecent nasal symptoms was diagnosed.There was proptosis, partial right thirdnerve palsy, and deterioration of rightvisual acuity due to an inflammatorylesion in the posterior part of the orbit.Recovery took place with drainage of the FIG. 3frontal sinus.

Case 6.-C. C., a boy aged 12, was admitted to theLondon Hospital on August 26, 1946.He had complained of headaches for some months.

Three weeks before admission he became drowsy, andvomited several times. It was noticed that his right eyewas prominent, and he began to see double.On examination there was a tender swelling in the

right temporal fossa extending over the zygoma anteriorto the pinna. The right side of the face was warm andflushed. There was papilloedema of the right optic disc,the left disc was normal, and the visual fields were full.There was proptosis of the right eye with incompleteptosis, weakness of elevation and adduction, and absenceof abduction. The rest of the nervous system wasnormal.The sedimentation rate was 36 mm. in one hour.

The white count was normal. The cerebrospinal fluidpressure was normal in pressure and contained protein50 mg. per 100 c.cm., no pleocytosis; Lange curve12322100. Radiological examination of the skullshowed translucency of the lateral wall of the orbiton the right side (Fig. 4a), suggesting infection.There was extensive loss of bone in the posterior andlateral walls of the orbit and destruction of the floor.Both maxillary sinuses showed opacities, suggestingthickened mucosa. There was a roughly sphericalopacity in the upper part of the right antrum adjacentto the localized area of erosion in the lower andoutermost part of the greater wing of the sphenoid(Fig. 5a).The patient recovered spontaneously during the next

two months and a year later passed the eye examinationfor a navigation school. Radiological examination 12and 17 months later showed progressive regeneration

b(Case 5).-Patch of osteitis in the posterior part of theroof of the right orbit.

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FIG. 4a (Case 6).-Absorption of greater wing ofsphenoidin right orbit.

of the orbital wall (Fig. 4b), but the appearances ofmucosal thickening in the antra persisted (Fig. 5b).

This patient developed a subacute inflammationof the soft tissues and bony wall of the orbit,including the outer wall common with the temporalfossa, and the lateral extremity of the superiororbital fissure. The second, third, and sixth cranialnerves were involved, probably at the apex ofthe orbit. Apart from an increase of protein inthe cerebrospinal fluid, there was no evidence of

FIG. 5a (Case 6).-Patch of osteitis lower and outer part ofright orbit, with spherical opacity in upper part ofrightantrum.

FIG. 4b (Case 6).-Regeneration of greater wing ofsphenoid (17 months later).

intracranial extension. Although there were nosymptoms of nasal infection, the peculiar radio-logical appearance of the right antrum was verysuggestive of a connexion between the conditionof the antrum and the osteitis of the orbit. Thesinusitis may, however, have been contemporaneousrather than causative.

Case 7.-A. L., a man aged 49, was admitted toChase Farm Hospital on March 7, 1946. Threemonths previously he had had a bad cold, with

FIG. 5b (Case 6).-Recovery of osteitis (12 monthslater).

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pain in the left forehead and behind the eye, radiatingover the left side of the head. Two days after the onsetof pain he began to see double. The nasal dischargesuddenly ceased but the pain and double visionpersisted. Chronic catarrh had been present sincechildhood, and four years before he had undergonean operation for deflected nasal septum. Radiologicalexamination shortly before admission showed a faintopacity of the left maxillary sinus.On examination there was no anosmia. The fundi and

pupils were normal. There was slight proptosis ofthe left eye, with partial ptosis, weakness of elevationand absent abduction. Appreciation of pinprick wasimpaired over the distribution of the first andsecond divisions of the left trigeminal nerve. Therewas a right lower facial weakness, with increasedreflexes in the right arm and leg, and the rightplantar response was equivocal.The sedimentation rate was 22 mm. in one hour.

The cerebrospinal fluid was normal in pressure andcontained red blood cells. Ventriculography showedsome increase in the subarachnoid space but no otherabnormality. The ventricular fluids were also slightlybloodstained.

Radiological examination on March 30, 1946,showed the right maxillary antrum to be semi-opaque,and an appearance of the right frontal sinussuggestive of infection. He had complained ofextension of pain to the right orbit and eyeball.The patient improved spontaneously, but in June,

1946, he had a recurrence of left-sided pain andnasal discharge. There was still slight left-sided proptosis,but the ocular movements were full. The reflexes werebrisk and equal. When the patient was seen 15 monthslater there was no proptosis.

The onset of symptoms was associated with anexacerbation of chronic nasal discharge, which thendried up. The left antrum showed radiologicalevidence of infection. There was a partial lesionof the left third nerve, involvement of the sensoryfibres of the trigeminal, and a complete sixth nervepalsy. The cause of the contralateral pyramidalsigns was obscure. The presence of blood incerebrospinal fluid in the lumbar sac and in theventricles may have been due to an insidious intra-cranial venous thrombosis. The course of theillness was unlike a subarachnoid hmmorrhage dueto aneurysm. The patient was considered to besuffering from a low-grade infection of the tissuesaround the left superior orbital fissure, and possiblyleptomeningitis.

Case 8.-S. F., a man aged 18, was admitted to ChaseFarm Hospital from the London Hospital on February25, 1942.

Six weeks earlier he had developed right frontalheadache, with swelling of the right eyelids, right ptosisand double vision. He had a cough, felt shivery, sleptpoorly, and sweated at night. Pyrexia was absent, buthe had been treated with sulphonamides. Radiological

examination on February 11 showed opacity of the rightmaxillary antrum and sphenoidal sinus.On examination there was no anosmia. The right

optic disc was congested; the right visual acuity was J2,the left visual acuity Jl. There was irreducible proptosisof the right eye, with partial ptosis, absence of elevationand abduction, and impaired depression. The rightpupil was smaller than the left but reacted normally.The rest of the nervous system was normal. The rightnasal cavity was congested, but no pus was obtained onpuncture of the right maxillary antrum. Radiologicalexamination of the skull showed no abnormality.On March 2 the patient developed severe pain and

relative hypalgesia with diminished corneal response inthe right trigeminal area. The right pupil becamesluggish. He had a series of fits of an uncinate typewith hallucinations of taste and smacking of the lips.At repeated examinations, the cerebrospinal fluid was

normal in pressure and showed an increase of cells from30 to 230 per c.mm. (40% polymorphonuclears and 60%lymphocytes), protein 40-60 mg. per 100 c.cm. It wassterile on culture. A ventriculogram was normal.The white blood count increased from 5,000 perc.mm.

(polymorphonuclears 40%) to 13,800 per c.mm. (poly-morphs 68%). On March 6 several more uncinateattacks occurred, and on March 7 a right frontalcraniotomy and decompression was performed by Mr.Northfield. In the region of the superior orbital fissurethe dura mater was grossly indurated, and had a granularexternal surface. Biopsy showed fibrous granulationtissue, and the culture grew a small clump of Staphylo-coccus albus only. No abscess was found.On March 17 the right fundus showed a secondary

optic atrophy and there was no perception of light.There was a complete right external and internalophthalmoplegia.On May 30 the patient suddenly developed a spastic

left hemiplegia associated with pyrexia. Ventriculo-graphy showed displacement of the ventricles to theleft. The craniotomy was reopened but only muchthickened dura was found in the anterior and middlecranial fossae. He became aggressive with highlyorganized delusions and was admitted to NapsburyMental Hospital for five months.

In the following year he returned to heavy work. Hehad some left-sided fits preceded by an olfactory aura,but these were controlled by phenobarbitone.

In October, 1943, the right visual acuity was percer-tion of light only, there was a right secondary opticatrophy, the ocular movements were almost full, and theleft hemiplegia had recovered. During the next fivemonths the visual acuity of the left eye deteriorated from6/9 to 6/18. On examination there was left anosmia,left primary optic atrophy with a paracentral scotoma,and an upper left temporal defect. On April 13, 1944,the chiasmal region was explored through a left frontalcraniotomy by Mr. Northfield. Where the left opticnerve entered the optic canal dense, fleshy adhesionswere found, binding down the region of the gyri recti,the olfactory tract and the optic nerve to the surface ofthe dura mater. The adhesions round the optic nervewere divided and the optic canal was decompressed.

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FIG. 6a (Case 8).-Eroded right optic foramen. FIG. 6b (Case 8).-Contracted right optic foramen (fouryears later).

Radiological examination in March, 1944, showedresidual destructive changes on the right side, witherosion of the lesser wing of the sphenoid (Fig. 7a),upper border of the optic foramen (Fig. 6a), andenlargement of the superior orbital fissure (Fig. 7a).

In 1948 the patient was working as a packer. He stillhad olfactory hallucinations but no fits. The left opticdisc was pale and the left visual acuity was 6/12 corrected.There was a right secondary optic atrophy with P.L.only. The ocular movements were full without prop-

tosis. Radiological examination showed some enlarge-ment of the right superior orbital fissure but the definitionof its outer border had improved (Fig. 7b). There wasno deficiency in the outline of the optic foramina but theright (Fig. 6b) was smaller than the left (Fig. 6c).

Radiological evidence of infection of the rightmaxillary and frontal sinuses was present at theonset of the illness, though clinical effects wereprobably masked by sulphonamides.

FIG. 7a (Case 8).-Destruction of right lesser sphenoidalwing, and erosion of superior orbital fissure.

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FiG. 6c (Case 8).-Left optic foramen (for comparison).



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The right second, third, fourth, and sixth cranialnerves, the fifth to a less extent, and possibly theocular sympathetic were involved in the inflam-matory process at the apex of the orbit. Intracranialcomplications consisted of uncinate attacks andlater mental changes due to the thickened adherentdura in the middle and anterior cranial fossee. Thesudden onset of a contralateral hemiplegia suggesteda vascular element in the spread of the disease.

FIG. 7b (Case 8).-Partial regeneration of bone aroundright superior orbital fissure (four years later).

Extension of the pachymeningitis to the oppositeside resulted in involvement of the left optic nerve,relieved by decompression of the optic canal. Theeroded bone round the right superior orbital fissureand optic foramen re-formed, with contraction ofthe optic foramen. The condition was subacute orchronic with extension over two years.

Case 9.-Mrs. M. T. was admitted to Chase FarmHospital on May 4, 1946.

Fourteen months earlier her left eye had becomeprominent, and about this time she began to see double.She complained of a dull pain in her temple and afeeling of "something pushing" behind the left eye.She had no nasal symptoms. She suffered fromrecurrent polyarthritis affecting the small joints of thehands and the knees. Radiographs taken four monthsafter the onset of symptoms showed well-markedchanges of maxillary sinusitis, more on the left side,and left ethmoidal sinusitis.On examination there was no anosmia. The fundi

and pupils were normal. The left upper lid wascedematous ; the left eye was proptosed downwardsand forwards. There was weakness of abduction andelevation. The rest of the nervous system was normal.

The cerebrospinal fluid was normal in pressure andconstituents. Radiographs of the skull and an airencephalogram showed no abnormality, but on leftcarotid arteriography there was delay in the passageof the opaque medium above the carotid syphon.Exploration was undertaken to exclude the presence of asphenoidal ridge meningioma.On June 5, 1946, a left frontal craniotomy was per-

formed by Mr. Northfield. No abnormality of thebrain was found. The dura mater was thickened andreddened at the medial part of the sphenoidal ridge,and there were some fine adhesions between the duraand arachnoid. The day following operation thepatient had a number of right-sided fits and becameunrousable with a pyrexia of 1010 F. Re-explorationrevealed some hxmorrhagic swelling of the brain. Thefits continued, and two days later she was still deeplyunconscious with a right flaccid hemiplegia. Onrecovery of consciousness she was aphasic.A month later she had slight dysphasia with increased

reflexes in the right upper limb. The ocular signs wereunchanged. Radiological examination now showedclearing of the left ethmoidal sinuses.

Gradual improvement occurred and by November,1947, though she complained of diplopia, the left ocularmovements appzared full. There was slight proptosis.The right-sided pyramidal signs had recovered.

In the absence of clinical evidence of sinusinfection, the significance of the radiologicalfindings was uncertain. There appeared to havebeen sinusitis present shortly after the onset ofsymptoms, which was more marked on the side ofthe affected eye. Oedema of the lids, left proptosis,and a partial third and sixth nerve paresis developedslowly. Exploration revealed the presence ofinflammatory changes on the meninges adjacent tothe left superior orbital fissure. The post-operativecomplication of a sudden right hemiplegia precededby right-sided fits was thought to be due to a leftvenous thrombosis, though the exposed corticalveins appeared normal.

Case 10.-S. H., a man aged 41, was admitted to ChaseFarm Hospital on October 15, 1942. Fifteen monthspreviously he developed pain in the right cheek radiatingto the forehead and the back of the neck, also droopingof the right eyelid and watering of the eye. Radiologicalexamination of the sinuses four months after the onsetof the pain had shown thickening of the mucosa of themaxillary antra. For some months he had vomiteddaily, and two weeks before admission he first noticeddouble vision.On examination there was no anosmia. The right

optic disc was pinker than the left. The right pupilreacted sluggishly to light and accommodation. Therewas slight proptosis of the right eye with chemosis of theconjunctiva, and weakness of adduction. Power wasdiminished in the left upper limb, with exaggeration ofthe tendon jerks. The blood Wassermann reaction wasnegative. The cerebrospinal fluid was normal in

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pressure and constituents. Radiological examination ofthe skull and sinuses at this time showed no abnormalityapart from some absorption of the dental alveoli.On November 5 and 9, the patient had a series of

dental extractions, and after the second operationdeveloped an external rectus palsy of the right eye.

A right carotid arteriogram showed no abnormality.Right frontal craniotomy was performed on November21 by D.G.P. to exclude the presence of neoplasm inthe middle cranial fossa. A free exposure of the middleand anterior cranial fossm showed no abnormality of thebrain or adjacent structures except for a definite bulgingof the lateral wall of the cavernous sinus, suggestinglocalized thickening of the dura.By March, 1943, the ocular movements had improved,

but the right eye was still displaced downwards. Thepatient complained of persistent pain in the right cheekand in June, 1943, was readmitted to Chase FarmHospital.

Examination on June 30 showed papilloedema of theright optic disc. The eye was displaced downwards,and there was diffuse swelling of the right upper lidand of the outer two-thirds of the superior orbitalmargin. The ocular movements were full apart fromright ptosis. On July 22, 1943, the right gasserianganglion was injected with alcohol. Unusually toughresistance was detected on passage of the needle throughthe foramen ovale. There was considerable relief ofpain. Radiological examination in July, 1944, showed a

slight haziness of the right maxillary antrum.In May, 1945, the vision of the right eye became misty.

There was slight papilleedema with reduction of visualacuity to 6/36. The visual field showed a generalizedperipheral constriction with a central scotoma to 5/2000white. The vision continued to deteriorate in this eye

and during the next year was reduced to 6/60. The rightoptic disc showed a secondary atrophy. In 1947 thepatient's condition was unchanged.

At the time of onset of the right-sided facial painthe patient had radiological evidence of maxillarysinusitis which was seen later on the right side only.A year later he developed right proptosis andpapilloedema, a partial right third nerve paresis, a

sixth nerve palsy, and pyramidal signs in the leftupper limb. The sixth nerve palsy may have resultedfrom dental extraction. At craniotomy the appear-ances were suggestive of thickening of the lateralwall of the right cavernous sinus. Right papill-cedema proceeded slowly to secondary optic atrophy.Persistent pain in the distribution of the righttrigeminal nerve was relieved by injection of thegasserian ganglion. The dura was abnormallyresistant to the passage of the needle.

DiscussionThe course of the infection in all these patients

was subacute or chronic. There appeared to be a

high resistance to the infecting organisms, and as

the inflammatory process subsided, complete or

partial recovery occurred in every patient. Taylor(1949) has commented on the high natural resistanceto intracranial infection developing from the sinusesor middle ear.tl erl r jW eo os

were present for weeks or months with frontalheadache, pain behind the eye, and double vision.Paralysis of the external ocular muscles on theaffected side, especially of the elevators and abduc-tors, developed, sometimes with papilloedema pro-ceeding to optic atrophy, and slight hypalgesia inthe distribution of the first and second divisions ofthe trigeminal nerve. The condition might recoverspontaneously (Case 6), or after drainage of thenasal sinuses (Case 5). Intracranial extensionoccurred in four patients (Cases 7, 8, 9, 10) withsevere trigeminal pain in three (Cases 7, 8 10),contralateral pyramidal signs, and in one patient(Case 8), uncinate attacks.The portal ofentry of the infection was speculative

in five patients (Cases 6, 7, 8, 9, 10). There were nosymptoms or signs of acute nasal infection, but theonset of double vision in one patient (Case 7) wasassociated with sudden suppression of a chronicnasal discharge. Radiological evidence of antralinfection was difficult to assess when it consisted ofopacity without a fluid level. All that can be saidis that sinusitis had been present in every patientat the time of the illness or earlier, and that itappeared worse on the affected side. Exacerbationof ophthalmoplegia followed dental extraction inone patient.

Pathological evidence of infection as shown by anincreased sedimentation rate, leucocytosis or changesin the cerebrospinal fluid, was infrequently present.The inflammatory nature of the lesion was

detected by radiological examination or at operationin four cases. In one patient (Case 7) diagnosisdepended on relationship of symptoms to nasaldischarge, the presenice of a raised sedimentationrate and the spontaneous recovery. In one (Case10) diagnosis rested on the findings at operation inconjunction with the clinical course of the diseaseobserved over several years.

Radiological changes consisted of erosion of bonein the orbital roof (Case 5), destruction of the wallsof the orbit (Case 6), and of the lesser wing of thesphenoid and optic foramen (Case 8). Recoverywas associated with regeneration of bone, and inone case with reduction in size of the optic foramen(Case 8).Craniotomy was performed on three patients.

In two (Cases 8, 9) pachymeningitis was found inthe region of the sphenoidal ridge and middlecranial fossa. When the infection was prolongedover years (Case 8) extension to the opposite side

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occurred. Distortion of the wall of the cavernoussinus and toughness of the dura mater at theforamen ovale suggested the presence of thickeningof the dura in a third patient (Case 10).The diagnosis of a chronic infection in the region

ofthe superior orbital fissure is not easy; air studies,arteriography and exploration may be necessary toexclude the presence of other lesions. The idio-pathic or " rheumatic" form of orbital periostitisas described by Collier (1922) was characterized bythe rapid onset of the ocular palsies, with pain andproptosis. Recovery was usually complete in a fewmonths and intracranial complications did not occur.

The production of proptosis and ophthalmo-plegia by a non-fistulous carotid aneurysm in theanterior part of the cavernous sinus has been dis-cussed by Jefferson (1938). Pain was sudden inonset. The ophthalmoplegia tended to be completeand there was dense anmsthesia of the first andsecond division of the trigeminal nerve. Godtfred-sen (1947) considered that exophthalmos andophthalmoplegia due to penetration of the orbitby a nasopharyngeal growth occurred late and was

associated with a poor general state. A meningiomaarising from the medial third of the sphenoidalridge may produce proptosis and ophthalmo-plegia, but pressure on the optic nerve usuallyresults in primary optic atrophy with a nasalhemianopia. Hyperostosis of the sphenoidal ridgemay be detected on radiological examination.Eosinophilic granuloma of bone is a rare lesionoccurring mainly in children and adolescents. Itis considered to be related to Hand-Schuiller-Christian disease (lipogranulomatosis), " apparentlyrepresents a peculiar inflammatory reaction to some

as yet unknown agent of infection" (Jaffe andLichtenstein, 1944), and may recover spontaneously.In the calvarium the lesion presents radiologicallyas a translucent " punched-out " area. Hill (1949)states that periosteal new bone formation in thiscondition is usually slight and appears to be con-

fined to the shafts of the long bones. This is incontradistinction to the well-marked radiologicalappearances of periosteal new bone formationduring the stage of recovery in two of our patients(Cases 6, 8). Benign giant cell tumour, reviewed byMcNerney (1949) is another rare lesion which may

affect the base of the skull; as with other neoplasmsthis is, untreated, a progressive condition, and theradiological appearance is purely that of bonedestruction, with a clear-cut edge. In unilateralexophthalmic ophthalmoplegia and pseudo-tumourof the orbit pain is absent. Insidious thrombosisof the cavernous sinus is usually associated withcongestion of the orbital and angular veins andsigns of extension to the opposite sinus.

Whether any degree of sinus or venous thrombosiswas present in these patients requires consideration.The occurrence of multiple cranial nerve palsies inthe posterior fossa due to inferior petrosal sinusthrombophlebitis complicating otitis media hasbeen described by Symonds (l944l, though in anearlier discussion of these cases (1927) extraduralinflammation *was postulated. Extensive post-mortem studies recorded by Byers and Hass (1933)and Courville and Neilsen (1934, 1935, and 1937)supported the hypothesis of a thrombophlebitis.The multiple cranial nerve palsies in our patientscan be accounted for by the presence of localinflammation in the superior orbital fissure, some-times with osteitis and pachymeningitis. It appearsthat this fissure may act as a channel for the spreadof inflammation into the cranial cavity. In thesepatients the nasal sinuses provided a possible sitefor the origin of the infection. The development ofan external rectus palsy after dental extraction in apatient with a partial third nerve palsy may havebeen due to an extension of the local inflammatorylesion or to a spreading thrombophlebitis from thetooth socket. Brain (1947) has described theoccurrence of ocular palsies with trigeminal involve-ment following extraction of a tooth from the upperjaw.

The nature of the lesion causing contralateralpyramidal signs in the last four patients was notclear. In Case 8 there was evidence at craniotomyof the direct spread of infection in continuity to thebrain, but the sudden onset of hemiplegia suggesteda vascular lesion.

In Case 9 the patient developed a hemiplegia withfits as a post-operative complication. There wassome hemorrhagic swelling of the brain but thesurface vessels appeared normal. In two patients(Cases 7 and 10) contralateral pyramidal signswere detected on clinical examination. In onepatient (Case 7) blood was present in the lumbarand ventricular cerebrospinal fluids due perhapsto the presence of vascular congestion from aninsidious cerebral venous thrombosis. In all thesepatients the pyramidal signs disappeared over afew months.Symonds (1937) described the occurrence of focal

epilepsy, and hemiplegia (with recovery, andwithout brain abscess formation) in cases of otitismedia, and brought clinical evidence for regardingthis as due to thrombophlebitis involving the super-ficial cerebral veins. The last four cases describedhere may be comparable, though craniotomy inthree of them failed to provide visible evidence ofvenous thrombosis.No definite recommendations can be made on the

treatment of chronic infections in the region of the

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superior orbital fissure. Sulphonamides and anti-biotics may have an application in the earlier stagesof the infection. Drainage or any other localtreatment of the sinuses is indicated only if an activeinfection persists there. Intracranial explorationmay be necessary for diagnosis, but vascularcomplications may result. Decompression of theoptic canal and freeing of meningeal adhesions ofthe optic nerve may be necessary to arrest thedevelopment of optic atrophy and visual failure.

SummaryTen cases of ocular palsy associated with nasal

sinusitis, which fall into two clinical groups, aredescribed.The first group is composed of four patients with

palsies of one or two ocular nerves associated withchronic sphenoiditis, and destruction of bone in theregion of the sella turcica. Recovery and regenera-tion of bone followed drainage of the infectedsinuses.The second group consists of six patients with

ocular palsies and signs of a subacute or chronicinflammatory lesion in the region of the superiororbital fissure. All showed radiological evidence ofsinusitis on the affected side at some time duringtheir illness. Destruction of bone in the region ofthe superior orbital fissure with later recovery ofbone density was demonstrated radiologically inthree cases. Involvement of the second and fifthcranial nerves, meninges and cerebrum might occurin the course of the disease.

Resistance ofthe tissues to the invading organismsappeared high. No deaths occurred. All thepatients recovered wholly or in part with subsidenceof activity over a long follow-up.The diagnosis and treatment are discussed.

Our grateful thanks are due to Mr. D. W. C.Northfield for his helpful advice in the preparation ofthis paper, and for permission to publish the records ofthese patients, all of which with the exception of Case 5,were under his care.We should also like to express our indebtedness to

Dr. Russell Brain for permission to record cases admittedto Chase Farm Hospital E.M.S. Neurological Unit,to Dr. S. P. Meadows for cases seen at the Royal LondonOphthalmic Hospital, to Mr. Wylie McKissock for

Case 5; to Dr. M. H. Jupe for his reports and reviewof the radiographs, to Dr. J. W. D. Bull for radiographsof Case 5 ; and to Mr. A. Bowen-Davies, Mr G. H.Howells, and Mr. C. A. Keogh who performed operationson the nasal sinuses, for their operative findings.

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System ", 3rd ed. London. P. 156.Byers, R. K., and Hass, G. M. (1933) Amer. J. Dis.

Child., 45, 1161.Cairns, H. (1938). Trans. Ophthal. Soc. U.K., 58, 464.Caliceti, P. (1927). Riv. Oto-neuro-oftaim., 4, 419.Collier, J. (1922). In " A Textbook of the Practice of

Medicine ", ed. by F. W. Price. 1st ed. London.P. 1284.

Courville, C. B., and Nielsen, J. M. (1934). Arch.Otolaryng., Chicago, 19, 451.

, (1935). Amer. J. Dis. Child., 49, 1.Diamant, M. (1937). Acta oto-laryng., Stockh., 25, 550.Genet, L. (1929). Lyon mid., 143, 738.Godtfredsen, E. (1946-7). Proc. R. Soc. Med., 40,131.Hermann, K., and Hall, I. S. (1944). Trans. Ophthal.

Soc. U.K., 64, 154.Hill, R. M. (1949). Brit. J. Surg., 37, 69.Horgan, J. B. (1931). J. Laryng., 46, 542.Houser, K. M. (1933). Penn. med. J., 36, 411.Jaffe, H. L., and Lichtenstein, L. (1944). Arch. Path.,

37, 99.Jefferson, G. (1938). Brit. J. Surg., 26, 267.

(1946-7). Proc. R. Soc. Med., 40, 419.Kretzschmar, S., and Jacot, P. (1939). Schweiz. med.

Wschr., 20, 1103.McNerney, J. C. (1949). J. Neurosurg., 6, 169.Nielsen, J. M., and Courville, C. B. (1937). Annt. Otol.,

etc., St. Louis, 46, 13.Onodi, A. (1914). Z. Augenheilk., 31, 324.Onodi, L. (1914). J. Laryng., 29, 304.Redslob, E., and Delbos, R. (1941). Ann. Oculist.,

Paris, 177, 371.Rollet, E. (1933). J. Med. Lyon, 14, 165.Rollet, J., and Parthiot (1929). Lyon med., 143, 825.Sargnon, (1923). Arch. franco-belges Chir., 26, 944.--, and Parthiot, (1930). Arch. int. Laryng., N.S., 9,

703.Sluder, G. (1913). Arch. Laryng. Rhin., 27, 369.

(1927). " Nasal Neurology, Headaches and EyeDisorders." London. P. 318.

Stieren, E., and McKee, G. J. (1932). Penn. med. J.,36, 84.

Symonds, C. P. (1927). J. Laryng., 42, 656.- (1937). Brain, 60, 531.

(1943-4). Proc. R. Soc. Med., 37, 386.Taylor, J. (1950). Ibid., 43, 129.Trantas, A. (1893). Arch. Opthal., Paris, 13, 358.Yaskin, J. C. (1939). Arch. Opthal., Chicago, 21,

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ocular palsies with sinusitis · j. neurol. neurosurg. psychiat., 1950, 13, 225. ocular palsies...

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