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Show -'. 1'1111> Raven Pre''', New York Trochlear Nerve Pareses with Brainstem Lesions James R. Keane, M.D. Thr~'l' (,lS~'S llf radillgraphi( IO(,llizollion of fourlh nerve Il'sillnS ar~' r~'porled: (,be 1-bilatL'ral parese~ due lu Ir,lUlllalk (ontusion; (,lSl' 2-1l'f1 paresis from ,1 (ulli(ular gUllSI1ll1 wound; alld (ase 3-bilalerill pclfl'Sl'S due III a (vsli(l'r(ill) (ySI in the (iludal (erebroll aLJuedud. From thL' D~'pMtment of Neuf(ll,,~v, LIIS An~"Il's CountyUnivL'rsity of Southl'rn Californi,' Ml'dlc,ll Cl'nter, L,ls An~l'lt;s, California. Addr~'ss corrl'spondl'ncl' dnd feprint fl''1Ul'sls to J. R. K",lIll', M.D.,1200 orth Stolt.' Stfl'd, Los An~.'Il·s. CA 90m3. 242 Fourth nerve palsy is a clinical diagnosis rarely supported by radiographic or pathological confirmation. As the following three cases illustrate, modern imaging techniques now allow sufficient brainstem resolution to demonstrate some of the lesions causing proximal trochlear nerve damage. CASE HISTORIES Case 1 A -!3-year-old man was rendered briefly unconscious in an automobile accident. He was discharged from the neurosurgical service the following day after normal neurological and computed tomography (eT) scan examinations. Five days later, reexamination for complaints of double vision and right upper extremity numbness revealed bilateral trochlear pareses, greater on the right (Fig. 1), mildly decreased hearing in the right ear, moderate right hemihypesthesia, and mild truncal ataxia. A discrete left collicular hemorrhage was evident on CT scan (Fig. 2). ell/lllllell t The precise location of traumatic fourth nerve damage rarel~' is determined. The trochlear decussation at the exit of the nef\'es behind the inferior colliculis has been held to be the probable site of maximal traumatic stress, and limited pathological studies support that localization (1). Our patient exhibited a delay both in symptoms of bilateral trochlear nerve pareses and in the CT appearance of a hemorrhagic contusion in the left inferior colliculus. In a similar case of delayed diplopia following head trauma, a left fourth nerve palsy was associated with a pericollicular hemorrhage (2). Case 2 A 3D-year-old man was dragged from his car and shot in the head. He did not lose consciousness, but immediately experienced numbness of TROCHLEAl? NU?VE Pl\l?ESES 243 FIG. 2. Case 1. CT scan (EM I 1010) shows hemorrhagic contusion of the left collicular plate. ~.. FIG. 1. Case 1. Bilateral superior oblique muscle limitation. the entire right side of his body, vertical diplopia, and unsteadiness when walking. On arrival at the hospitaL he was lethargic but oriented and able to converse. He showed right hemianesthesia to pinprick, as well as a moderate reduction in vibration sensitivity and a slight decrease in position sensation. Moderate gait and left extremity ataxia were present, but his strength was normal. A left trochlear nerve palsy, confirmed by Lancaster diplopia fields, was the cause of double vision (Fig. 3). A CT scan showed that the bullet had travelled through the left paramedian cerebellum to lodge immediately behind the left side of the midbrain (Fig. 4). Angiography revealed no arterial or venous damage and helped localize the intracranial bullet fragment as lying at the surface of the left inferior colliculus (Fig. 5). The bullet was left in place. Five months later, the patient's trochlear palsy and other neurological signs remained unchanged. Comment The radiographs in the case illustrate a large bullet fragment at the left inferior colliculus, adjacent to the impaired fourth nerve. Other clinical signs indicate damage to the nearby left superior cerebellar peduncle and the left lateral lemniscus, with sparing of the remainder of the pontomesencephalic tegmentum, as well as of the basis pontis. Minimally higher muzzle velocity undoubtedly would have been fatal. Case 3 A 22-year-old man, born and raised in Mexico, was admitted with a history of intermittent headache of 1 year's duration and diplopia for 1 week. On examination, his pupils were each 6 mm in diameter and exhibited slightly limited light reactions, but normal responses to near fixation. His eye movements revealed a "V" pattern esotropia, with gross impairment of the movement of each eye when directed down and inward (Fig. 6). Lancaster diplopia fields confirmed the presence of bilateral trochlear nerve pareses. Metrizamide ventriculography revealed hydrocephalus of the third and lateral ventricles caused by a (presumed cysticercal) cyst lodged in the caudal aqueduct and rostral fourth ventricle (Fig. 7). Because of its location partly within the aqueduct, surgical removal was deemed inadvisable, and the cerebrospinal fluid I CIIII NCllril-Ill'lIthalmill. Vol. 6. No.4. 1986 I. 1\. KEANE FIG. 3. Case 2. Left trochlear nerve paresis. (CSF) was diverted by means of a ventriculoperitoneal shunt. Follow-up examination 1 month later revealed no change in the physical or radiological findings. Comment Cysticercosis, the infestation by the larval form of the pork tapeworm, is primarily a central nervous system disease, involving both brain ~arenchyma and CSF pathways. Cysticercal menmgitis is relatively indolent and only rarely produces clinical signs of secondary arteritis or (aside from abducens pressure palsies) cranial neuropathy. However, vertical diplopia is a common symptom of cysticercosis, usually occurring with pretectal signs in association with hydrocephalic dilatation of the third ventricle (3). Skew deviation is the probable mechanism of such vertical diplopia (4), but involvement of third or fourth nerve nuclei or fascicles may be difficult to exclude. In the present case, obstructive hydrocephalus was minimal, and pretectal signs were limited to minor pupillary abnormalities. The precise lodgement of the Cyst in the caudal aqueduct undoubtedly produc~d bilateral trochlear pareses by stretching the nerves at their decussation. DISCUSSION These three patients were unusual in having CT scan evidence of proximal damage to the fourth nerves. Trauma resulting in bilateral trochlear palsies probably acts at the trochlear decussation, whereas individual nerves are susceptible to trauma as thev cross the tentorium or enter the dura (5), as well as at their exit from the brainstem (1). Rostral brainstem contusions tend to occur at the superior-lateral aspect of the midbrain (6), and that location may prove to be a common site of trauma to the fourth nerve, as in our first patient and that of Lavin and Troost (2). Bilateral trochlear palsies are usually the result of severe head FIG. 4. Case 2. CT scan views show bullet fragments at site of entry (right) and final position (left) of bullet at the level of the left inferior colliculus. T/\OCfIlJA/\ NU,VL flAf\LSES 245 FIG. 5. Case 2. Angiogram assists in localizing large intracranial bullet fragment (arrows). trauma (5,7)-in 82'i( (18/22) of patients at our hospitals (Table I)-but CT increasingly is documenting other causes (8-10). as in our third patient. The fourth nerve's unique exit from the dorsal brainstem partly explains why it rarely is involved in intrinsic stem lesions. In only one of 33 patients (3ci() in the series of Burger and associates (5), seven of 43 patients (16%) of Coppeto and Lessell (11), and 3 of 154 (2%) at our hospitals, did trochlear nerve injury result from documented intrinsic stem lesions. Proximity of the fourth nerve nucleus to that of the third nerve and to the medial longitudinal fasciculus undoubtedly helps obscure trochlear nerve damage. Despite the relative frequency of demyelinating plaques adjacent to the FIG. 6. Case 3. Bilateral fourth nerve palsies. 1(/11' NCII",·"!,hth"l,,,ol. Vol. 6, No.4, 1986 I. R. KEANE FIG. 7. Case 3. CT scans with metrizamide instillation: (cysticercal) cyst lodged in the superior fourth ventricle (right) and caudal aqueduct (left). TABLE 1. Etiology of fourth nerve palsy at Los Angeles County-University of Southern California Medical Center and Rancho Los Amigos Hospital during a 16-year period rostral fourth ventricle and aqueduct, trochlear nerve palsy rarely is diagnosed in multiple sclerosis. There are a few reports of damage to the trochlear nucleus by paramedian infarcts of the type that commonly involve the similarly-sited medial longitudinal fasciculus (MLF). Perhaps this is because lacunar infarcts that otherwise might produce an isolated fourth nerve palsy scarcely could spare the adjacent MLF. Possibly, some instances of internuclear ophthalmoplegia with ipsilateral hypotropia (uncommon) may represent concomitant involvement of the MLF and trochlear nucleus. However, MLF involvement in monkeys at the level of the trochlear nucleus apparently does not result in internuclear ophthalmoplegia (12). Number of cases Cause Trauma Surgery Meningitis Congenital Microvascular Tumor Degenerations Vascular malformation Other Total Unilateral 81 14 12 75 4 2 1 6 132 Bilateral 18 1 2 22 Improved imaging by using magnetic resonance techniques will improve further the localization of small brainstem lesions, and may provide some explanation of the apparent eccentricities of intramedullan' trochlear nen'e involvement. Acknowledgment: Drs. Hervey Segall and Chi-Shing Zee assisted with radiographic interpretations. REFERENCES Ht'inzt' .1. Cranial nt'n't' a\'ubi,'n and ,'tht'r nt'ural injurit's in r,'ad accldt'nls . .\led I AII<I Il.)bQ ;2:12"b-9 , La\'in PJM. Troost BT. Traumatic iourth nerve palsy; (hOlCO-anatomic corrt'lations \\'ith c,'mputt'd tomographic scan. Arch XCllr,ll 19&-+:-+l:b7Q-80. 3. Kt'anl' JR :'-:euw-,'phthalm,'l,'gk si~ns and sYmptoms oi c\·sticercosis . .·",·h l),'hth,I/'II,,/ 10 82; 1l10: I....:; - 8. ... Kt'ane JR. Alternatin~ ske\\' de\'iati"n: ..7 patients. :VCIIrt l/{h-:1I ]483;3=':;"23-8. :;. Bur~'er L). Kal\in :'-:H. SmithlL. Ac<]uired lesions oi the ll'urth cranial nt'n·e. Br,1111 11.)7l);1.)3::;b7-7... b. Rl1senblum \\'1. Cret'nbt'r~ Rr. St't'li~ J\L Beckt'r DP. Midbrain It'sillOS: tce<]uent and si~niiicant pw~nostic it'ature in c111sed Iwad iniury. XCIIf",lIr>:a\f 1981;Q:bl3-20. I. Lt·t'.1. Fh'nn JT. B'ilatt'ral sup~ri~'r \lbliqut' palsit's. Br I 01'"tll"/ III,'1 1'~$:;;b9::;08- 13. 8. I\lurr,l\' RS. Aj,n ET. Bilalt'raltfllchlt'ar nt'rw palsies. I Clil! ,\J"/lft·-,'/'"t""/III,'l 11.)8:;;:;::;7-8. 9. Wist'). Comlliin ). Coldbt'r~ LL. Bilalt'ral supt'rior oblique p,llsv: dla~n<lsls and trt'atmt'nt. C"I! I Oplltlla/mol 11.)$3;18:28-31. 1l1. Cl1Ppt'to JR. 5upt'rior oblique paresis and contralateral Hl1rnt'r's syndromt'. Alii, Optllal'1!11/1983;15;681-3. 11. C11Ppt'to JM. Lesst'll 5. Cryptl1genic unilateral paralysis of tht' supt'nor obhqut' muscle. Arch Ophthalmol 1978'95: 2~-~ , 12. Carpentt'r MB, McMasters RE. Disturbances of conjugate hl1nzontal eyt' movements in the monkey. Arch Neurol 1963;$;3-17-68. I Cli" NClIfll-0I'I,tI""l/Iol. Vol. b. No.4. 19K" |
