Journal of Neuro-Ophthalmology, June 1985, Volume 5, Issue 2

Cysticercosis.

T. Gin. Ncuro-ophtlltllmol. 5: 127-143, 19H5 Cysticercosis MANUEL MARTINEZ-LOPEZ, M.D. FRANCISCO QUIROZ Y FERRARI, M.D. "CystiLerCllsis reveals in the Wllrld ,1S a not,1ble coincidence with tht.' dM" Zl)J1eS lli poverty ,md social unt.'quality ,11t11l)u~h no slKi,ll c1,iss llf ethnic group is free lli slIiierin~ il." C~'sticerci are probably a degenerated form of the lar.ae of Tacnia ~lllilllll. 2 The larvae are ac­quired b~' humans, who act as the intermediate host after ingesting the eggs of the taenia. A brief review of the biologic cycle of T. ~Olilllll is pertinent for the proper understanding of the natural history of cvsticercosis.:1 Taeniasis is-an intestation of humans, who act as a definitive host; it is acquired after the inges­tion of insufficiently cooked pork meat contam­inated with the larvae of Clf~tict'rcll~ celllllo~I1l'. In the human small bowel the larva develops into the adult tapeworm, which may attain a length of 1-8 m. The scolex (or head) of the cestode attaches to the intestinal mucosa and starts to form multiple segments called proglot­tids. Each proglottid, after fecundation, carries thousands of ova that are excreted in the human feces. Swine, acting as an intermediate host, ingest the eggs of the parasite that later develop into the larvae of C. celllllo~l1e, thus completing the cycle. Any individual may acquire cysti­cercosis and act as intermediate hosts by ex­ternal autoinfestation, e.g., ingesting eggs con­tained in contaminated water or food, especially raw vegetables and some fruits. Other ways to get the disease are autoinfestation via anus­hand- mouth contact in persons who harbor the adult parasite and who exercise poor hygiene. A form of internal autoinfestation has been sug­gested in which mature proglottids are regur­gitate into the stomach, liberating the eggs by enzymatic activity; however, this has not yet From the Neuroradiology (M.M.-L.l and Ultrasound and Computed Tomography (F.Q.F.) Sections. Department of Radiology, Instituto Nacional de la Nutricit'm "Salvador Zu­biran," Radiologia, Ultrasonido y Medicin,] NllrieM. S.c.. Mexico. Write for reprilll5 to: M. Martinl·z-ll"pez. M. D.. Nellror,l­diology Section, Vasco de Quiroga No. I'i. Col. rlalp,m. 14000 Mexico, D.F. "OJ 1985 Raven Press, New York been proven. After the ingestion of the eggs, the action of bile and digestive enzymes liber­ates and activates embryos that bear hooks; they are called oncospheres and were protected previously by a thick shell. These embryos in­vade the intestinal wall, enter the circulatory system, and are transported to various tissues where they form the vesicles of cysticerci. 3- 7 Muscle and brain are the main targets because of their high glucose and glycogen contents and the rich vascular net, which also explains the embryos' predominant location in the gray matter, subarachnoid space, and ventricular system. The eye and spine are other important targets. The parasite may be present in two forms. The most frequent, C. celllllosl1e, has a characteristic scolex. The other form is C. rnce­11l0~ e, which lacks a scolex, is larger, and shows a tendency to predominate in the subarachnoid space. I - HIt probably represents a degenerative form of C. celllllo~l1e. Human cysticercosis is the most frequent par­asite- caused disease in the world affecting the central nervous system (CNS). Although it has been found frequently in developing countries, with recent massive immigration, more cases have been found in the southwest United States and other countries ..J.H In Latin America, the disease ,is particularly frequent, especially in MeXICO. _A-b.'! Based on an autopsy series from Mexico, it was concluded that 3 of 100 individuals suffer from the disease and that in 1 of 100 the parasite is the cause of death. III Additional data, mainIv from Mexico, include the following: . 1. The disease is the third most frequent cause of admission (excludinppsychiatric disorders) in neurological wards. I 2. The brain is involved in 60-927r of patients with cysticercosis,12 and 17-25(1c of patients with cerebral cysticercosis had simultaneous in­festation with taeniasis. 1:1 3. In neurological interventions over a period of 5 years, 28.2'7, were motivated by neurolog­ical symptoms secondary to cerebral cysticer­cOSiS. 11I 4. Cysticercosis was found in 25'ic· of crani­otomies performed on the basis of the clinical diagnosis of brain massl.J (before the advent of computed tomography). 127 5. C\'~tin'rl"l)~i~ i~ found in 25'lt. of patients WI.t I1 .Il'lrrl"l~l'li I.ntr,lCr,lnl.,l I prl'SSUIT. II ('. Pl'.lth occur~ in I of l'very 5 patients with eNS l'\'~ticl'rcosi~.I', 7. IIi ~lll1ll' countril's, till' disl"l~l' is consid­l'rl'd till' mo~t fn'quent nonnl'opl,lstic, space-oc­cup\' ing Il'sion intr,lCr,lIli,llly ,1Ild .1 major Cclu~e of di~,lbility. II> ~. In a I:eview of Ll5 'llltopSY cases, !{abiel,l l't aLI' concluded that in I{O'k the finding of cys­ticl'rcosis W,lS incidental, without clinical symp­tlllnS, .1Ild in 20'lt the parasitosis caused symp­toms or death. This conclusion would indicate, in theory, the possibility of some kind of im­munologically mediatl'd relationship between host and parasite that determines the aggres­siveness of the disease. Based un this idea, Estanul 17 proposed several types of cerebral cys­ticercosis in humans, including: (tI) cerebral in­festation without disease; (11) cerebral infestation with benign disease that resolves sponta­neously with calcifications of the parasite; this type could produce sequelae, mainly in the form of an irritative area that causes seizuresH. 1H ; (c) cerebral infestatiun with pro­gressive disease, with inflammatory reaction in the form of arachnoiditis, vasculitis, and mul­tiple granulomatous or cystic lesions in anv compartment of the brain.' . The mechanisms of production of cerebral le­sion in cysticercosis include 17 (tI) mechanical, with obstruction of free pathways of cerebro­spinal tluid (CSF) and mass effect; and (Il) in­tlammatory, with arachnoiditis, vasculitis and ischemia, multiple granuloma, and edema. The mechanisms that produce symptoms are cortical irritation, cerebral compression, tissue destruc­tion, and intracranial hypertension. 17 The severity of cerebral lesions is related to the number and location of the cysts or granu­lomas, the degree of mass effect or surrounding edema, extension of the process, time of expo­sure, vascular and inflammatory activity, glial scarring, obstruction within the ventricular system, and basal arachnoiditis with impair­ment of CSF circulation. 1lJ Neurocysticercosis may mimic any neurologic disorder..( 7.1II.1'J-~1 It may present with minimal or a wide variety of symptoms and signs, which may improve or worsen spontaneously and rap­idly. In multiple lesions in the brain paren­chyma or involvement with mixed disease in differt'nt compartments, the clinical expression of the disease may be the combination of the findings in the affected areas. The eye, usually via the ophthalmic artery, is affected in less than 2';' of cysticercosis cases. Cysticerci can be car­ried to any part of the orbit and globe. 19 • 22 . 23 Both eyes are infrequently affected simulta­neouslv, and it is rare that one eye is involved by multiple cysticerci. The most' common im­plantation site is under the retina over the mac­ular area (67.5-90.5'lc), and total retinal detach­ment can occur.~1 The parasite can migrate through the hvaloid membrane to become free in the vitreous. The death of the parasite may be associated with a marked immunologic reac­tion, with acute swelling leading to uveitis and, rarely, atrophy or e\'en sudden blindness.:!] The clinical diagnosis of intraocular cysticer­cosis is not difficult if the parasite is alive, but if the parasite dies its disintegration causes dis­organization of intraocular structures, making the proper diagnosis almost impossible. 22 The laboratory tests used in the diagnosis of suspected neurocysticercosis are several. The b) Figure 1. Acute fucal enn'phalitic phase llf cvsticercllsis in ,1 )-vt'af-llld girl. a: Noncontrast-enhanced CT scan shows a hyplldense area In till' llCOpltill, rt'gillil in relatillil tll l'del1lil, b: Clllltrash'llhanced CT scan shows the cysticercus vesicle as a thick ring llt I'nhann'nlL'1l1 With cl'lltrdl tluid dl'llsit\'. pl·riph!'r.lll\' pldCt'd in the area of edema. 128 Journal of Clinical Neuro-ophthalmology M<1ftim'z-U)~1l'Z, Quiroz y Ferrari lei Figure 2. Acute diffuse encephalitic phase of cysticercosis in a lO-year-old, a: Noncontrast-enhanced CT scan shows diffuse hypodense areas affecting mainly white matter. The lateral ventricles are small. b: Multiple small supratentl)rial ring lesil)ns and diffuse edema. c and d: Scan from same patient 7 months later. Therl' are Iwdrocephalus and <ltwphl'. The edema persists in focal areas, and some vesicles are still seen, with thickening ot till' wall. CSF examination results may be normal or the findings may include pleocytosis with a pre­dominance of lymphocytes, eosinophilia, and an increase in total proteins, mainly gamma­globulins. The glucose content can be normal or low; this finding could be related to a severe process. 4.6,7,111 The Nieto complement fixation test~4,~'i has been used widely, with an accuracy of 80-l)7'!r when performed in the spinal fluid during the active phase of the disease; this test might have a negative result in cases of parenchymal cys­ticercosis when the vesicles are not in contact with the subarachnoid space. There also may be cross-reactions with other cestodes and trepo­nemas. 4 Another, more recent test is an indirect hem- June 1985 agglutination tl'st~h in which serum titers of 1:6-! or more are positive in 87';; of cvsticercosis cases, This test may also show false-positive re­sults due to cross-reactions with Echillococcus and other cestodes. 4 Electroencephalographic recordings may show abnormal, although nonspecific, findings in patients with proven cysticerCl1sis. K,<J A short description of the pathological changes that occur with parasite infestation is necessary bdore the computed tomography (CT) findings are reviewed. Cysticercosis show several stages of evolu­tion. l,~7 The earliest is the vesicular stage, in which the inflammatory reaction and edema predominate, along witli capillary network pro­liferation and the formation of a connective 129 CystiLen:osis tissue capsule around the vesicle with fluid. The overall picture is similar to that of any granu­lomatous reaction. 27 The next is the colloidal stage, in which the inflammatory reaction di­minishes and the fluid is replaced by a jelly-like material secondary to hyaline degeneration. In the granular nodular stage, the cyst reduces in size and mineralization starts. The last stage is the calcified nodule. It is believed that cysticerci live an average of 2-5 years before they reach this last stage] In the meningeal and intraven­tricular localization of the parasite, all the dif­ferent stages can be found, but the inflamma­tory reaction can be worse and persist longer, producing arachnoiditis or ependymitis that can lead to fibrosis and obstruction. These latt'r forms can also produce vasculitis to ,1 v.uiabk degree. ' ·4• 11 CT is the most reliable and sensitive method of evaluating patients who haw this disease. It 130 Figure 3. Acute focal encephalitic phase of cysticer­CLlsi~. a: Contrast-enhanced CT scan shows an 18-mm ring ve~icle with penlesional edema in the parietal regilln. b: One and one-half months later. the ring lesion has decceased in size and is homogeneously enhanced. The edema shDws significant improve­ment. c: :\llncontrast-enhanced CT scan 6 months later Thece i, pactial calcificatilln l)f the cysticercus. has provided much information about the nat­ural history of the disease. 2S The diagnostic ac­curacy of the method has been reported to be as high as 97,:(.25.24 In a review of 10,000 CT scans done over a period of 5 years, some form of cvsticercosis was found in 20A'!,. III In another series l)f 10,895 CT examinations done over a similar peril)d, 1,107 cases demonstrated find­ings Cl)mpatible with intracranial cysticercosis. 28 This entitv has been classified by CT results ac­cording tl) the areas of involvement, i.e., paren­chyma!, meningeal, intraventricular, and mixed forms.~·ll1 PllrCllc!rYIIIIlI FOr/II The parenchvmal type is the most fre­quent. 1S25.24 It is'widely 'divided into two forms: an acute encephalitic phase and a nonenceph­alilic phase, which can be either acute or chronic.; jlmmal of Clinical Neuro-ophthalmology Marlinl'z-L()pl'Z, Quiroz y Ferrari Ie) fb) Figure 4. Nonencephalitic phase of cysticercosis. a: Con­trast- enhanced CT scan shows a small vesicle in the left frontal region. The round density within the cyst rep­resents the scolex. No edema is present. b: Contrast­enhanced CT scan shows several cystic lesions. two of them with a thin wall. The sulci are obliterated in the affected area. c: C<mtrast-enhanced CT scan shows mul­tiple cystic lesions without a discernible wall. The earliest and most frequent presentation found in children and young adults is the acute encephalitic phaseY-29 The unenhanced CT scan shows a single area of low parenchymal density in relation to focal edema, usually in the subcortical white matter, without ventricular compressionl8 (Fig. la). Clinically, the patient presents without intracranial hypertension. In the same phase, other presentations include dif­fuse or multiple areas of irregular low density, representing edema, that accentuate the ap­pearance of white matter mainly at the region of the centrum ovale (Fig. 2a). There is a sym­metrical decrease in the size of the ventricles and, clinically, intracranial hypertension may be found. The contrast-enhanced scan shows a single 5-15 mm, well-defined, ring-like lesion adjacent to the area of edema, or multiple, dif­fusely distributed annular lesions with similar characteristics18.31 (Figs. Ib and 2b-d). The ring June 1985 of enhancement is explained by an increase in vascularity, with capillary proliferation adjacent to the vesicles.·1 A single focal lesion is seen in approximately 15'7,. of cases and multiple ones in 85'7,.27 TI;is acute phase usualh' lasts 2-6 months and varies in intensity and duration with each individual. The ring tlf enhancement persists through the acute phase, and edema subsides more rapidly in single lesions and lasts longer in the multiple form (Fig. 3a-3r). It ma~' persist after tlw vesicles have become isodense with the brain parl'IKhyma. The ventricles re­turn to normal size ,1S soon as the edema starts to subside. If the disl'asl' does not WtlfSen, there is a good correlation betwL'en clinical improvement and the progrl'ssive disappearanct' of the lesions. There seems to lw a mortality of about 10% in the acute phase, despite a'ppropriate treat­ment. 27 Follow-up examination may show a 131 CystiCt'rcosis normal appearance of the brain or a wide spec­trum of findings, ranging from parenchvmal focal abnormalities and/or hydrocephalus to re­sidual small, single or multiple calcifications (Fig. 2c and 2d). These multiple parenchymal calcifications have been called the miliarv form IS (Fig. 16c). This type of calcification is -seen in only 30';{, of skull radiographs. An unusual pre­sentation of the acute encephalitic phase is normal-appearing brain parenchyma with small ventricles and no ring-like lesions present, an image similar to findings of pseudotumor Ct'r­ebri. 32 The nonence~halitic phase of parenchv­mal cysticercosis .111.2'1 may show well-define~i. regular cystic lesions, varying in size from a few millimeters to several centimeters (Fig . .tIl 'lI1d 4c). Some of the small cystic lesions show ,1 small, eccentric density within the IUI11l'n that represents the invaginatl'd scolex of the cvsti­cerci (Fig. 4a). The contrast-enhanced scan dl'm­onstrates better definition of the lesil\J1S due to 132 Figure 5. Parenchvmal cysticercosis with different stage~ of evolution in the same examination of a -l8-vear-old woman. a: Noncnntra~t-enhancedCT scan shows sev­eral ~mall calcified cv~ticerci in the left hemi~phere. b: Contra~t-enhanced CT scan ~how~ two ring le~lOns with minimal peri­lesional edema located in the right tem­poral region. Two cvstic lesions without peripheral enhancement or edema are seen in the left hemisphere. c: A mi'\ture of cal­cifications, vesicles, and nodules are seen in the la~t Image ~can. Figun' b. I'.H,'ncl1\' 111.11 cysticercosis, calcified stage. Non­contr. l~t-,'nh.1l1ced CT SC.1I1 shows multipk small calcifica­tions in both c"H'br.11 1ll'l11isplll'res. Not,' the tendency of 111.1n\· It'si,'ns to b,' I,'cat,'d close t" the sub.lI'achnoid space. The I.,rg,'st c.lkific.1ti'lll in the l11idlilll' is plwsiologic and rel.lted to till' t.ll,\. lournal of C1inic,l) Nl'ul'll-ophthaIll1o!ogy Figure 7. ~Ieningeal form of c\'sticercosis. a: Noncontrast­enhanced CT scan ,hows multiple c\'stic le,ion' at the base of the brain In the subarachnoid space, with ,,'me calcifi­cations at the right S\'lvian fi"ure. Thl' temporal horns are prominent. b: Another patil'nl with similar findll1gs In thl' contrast-enhanced CT scan no ring l'nhancl'ml'nl is l'\',dl'nt A small c\'sl ,s seen adjacl'nl to Ihl' left middle c"r"br,,1 arter\'. There is curvilinear calcificalion bl'twl'l'n the Iwo c\'sls in Ihl' right Svil'ian fi"url'. discrete enhancement of the thin, regular wall surrounding the cyst (Fig, 4b), Larger Il'sions might not show any enhancement of the wall with contrast medium administration, Large cysts can produce compression and displace­ment of brain tissue, the ventricular system, and the subarachnoid space (Fig, 19), Multiple, small bilateral lesions usually will not produce any mass effect. Although most of the cysts will show perilesional edema in the scans, histolog­ically, inflammatory infiltrates may be tound, June 1985 Martinez-Lopez, Quiroz y Ferrari Figure 8, Cysticercosis, meningeal form, racemose variet\' a: Conglomerate of c\'stic lesions in the left lempl1wparietal region without ring l'nhllI1Ct' llll'nt, Llnd Cl)1l1pressil111 llf brain parl'nch\'I1l'l ,md left \'l'ntricll'. Sm,lll c,llcdic,ltillns bl't\\'l'en c\,sts arl' l'\'idl'nL b: Anotlll'r p,ltil'nt with multi!Llccul,'tl'd cvstic lesions ,lt thl' Idt Il'mpor"l !L,bt'. dl'tllf'llling till' sub­ardchnoid Sp,Kl' ,md S\'lvi,m tissurl', Not infrequentlv, the e\.amination shows CYsts of different sizes th,lt h,lVe yariable responses to contrast Ill,lteri,ll, in ,lddition to isolated focal edema and sonll' l"llcific,ltions, which indicate diffl'rent st'lges in the evolutil1l1 of the par,lsite2S (Fig. 5), Solitary cystic lesions are unusu,ll and must be differenti'lll'd frolll otl1l'r cyst-like lesions and 11l'opl,lSIllS such as hvd'ltil1 cyst, tubercu­loma, abscess, ,llld cystic ,lstrocvtoma, The cystic nOIll'nl'l'phalitic torlll of parenchymal dis- 133 Figure 9. Meningeal form of cysticercosis with basal arachnoiditis. a: Noncontrast-enhanced CT scan shows obliteration of the basal cisterns and Sylvian fissures, with an image isodense tl) the brain parenchyma. b: Cllntrast-enhanced CT scan shows diffuse leptomeningeal enhancement at the basal cisterns and Svlvian fissures. c: \:oncontrast-enhanced CT scan in a different patient shows the way of the Sylvian fissure slightl\' denser than the nl)rmal brain parench\'ma with a calcification (curved arrow). d: Contrast-enhanced CT scan shows thickening ,111d enhancement ot the leit middle cerebral artery related to arachnoiditis and vasculitis (arrow). ease predominates in the supratentorial com­partment and shows some predilection to be lo­cated near the cisterns, fissures, sulci, and ven­tricles. In comparison with cysticerci involving skel­etal muscle, which calcify almost invariably within 5 years, the cerebral cysts show incom­plete and less frequent calcification in from 1 to 5 years.OJ The size of the calcification is about one-quarter of that of the original lesion; calci­fication occurs in approximately 64.7% of cases.1' It is the most common finding and results from calcium deposition in dead larvile14 (Fig. 6). Other, less common presentations of the pa- 134 renchymal form are single or multiple homo­geneous nodules observed in the contrast-en­hanced scan, II' without the characteristic cystic component and with or without surrounding edema. The most unusual parenchymal lesions show as an isodense, single mass lesion that enhances homogeneously with contrast admin­istration. 1l These uncommon forms may mimic primary brain tumor or metastatic disease. s Brain infarctions are secondary or indirect forms of presentation of meningeal cysticercosis, man­ifested in the scans in a fashion similar to in­farcts of other origin. 10,29 Brain atrophy may be another secondary manifestation in cases of Journal of Clinical Neuro-ophthalmology rjJfJ MMlim'z-Lt'lpl'Z, Quiroz y Ferrari Figure 10. Sequelae of basal arachnoid­itis and parenchvmal cI'sticercosis. a and b: Communicating Iwdrocephalus. Note associatl'd multiple parenchymal calcifications. c: Scan from a different patient showing cortical and subcortical atrophy, parenchvmal calcifications, and e' I'acuo Iwdrocephalus. Figure 11. Intracranial cysticercosis, intraventricular form. a: Noncontrast-enhanced CT SC.1I1 slwws dl'tormitv .1I1d dilat.ltion of the fourth ventricle. b: contrast-enhanced CT scan shows ,mnul<1r, penphl'r,ll l'nhancenll'nt of till' cysticercus cvsl. A lesser degree of dilatation is seen in the supratentorial ventricles, A right tempor.ll calcification is l'l'idenl. . June 1985 135 Cvslil'l'n:~lsis Figure 12. InlraVt'ntriculM cysticercosis. Magnified con­tr, 1st-enhanced CT scan shows multiplt' nOnllbstrucli\'e in­tr,)\" entricular lesi~1ns (arruws) attached tll the choroid ple:\us. Additional parenchymal lesiuns are seen. proven cysticercosis; cases of focal atrophy may be explained by previous infarcts, and general­ized atrophy could be incidental. T~ere has been no ftroof of a direct cause and ettect rela­tionship. 1I Me1lillgeal Form The meningeal type of cysticercosis shows up on CT scans as single or multiple cystic lesions firmly or loosely attached to the leptomeninges, usually at the base of the brain (Fig. 70 and IJ). When they are present over the convexity they can excavate into the cortical gray matter J The racemose variety of the parasite shows predom­inance in the subarachnoid space, where it en­counters less pressure and resistance and is thus allowed more expansion. Therefore, the ra­cemose variety may grow as a large cyst, up to 10 em in diameter. It presents, sometimes, as a conglomerate or as multilocculated cystic le­sions, usually found at the base of the brain or Sylvian fissureH (Fig. 8a and b). These lesions also mimic congenital cysts or cystic tumors af­fecting any cistern or fissure. The mass effect that these lesions produce is variable and, de­pending on their size, may produce intracranial hypertension, compress vascular structures and ventricles, and even produce herniations. The subarachnoid space is usually distorted, even with small cystic lesions. As in the parenchymal form of the disease, the cysts may also calcifylll (Fig. 7a and 7/1). When there is compression of vessels by the 136 cystic mass, brain infarction may develop; how­ever, ischemic lesions may also result from vas­culitis. 5,H,2H,2'1 In cases of subarachnoid vascu­litis the contrast-enhanced CT scan most often is n'ormal, but occasionally asymmetric thick­ening of some vessels, such as the middle ce-rebral artery, may be seen. . . Cysticercus at the base of the bral~ offer dIs­tinctive features explained on the basIs of patho­logic findings. 3 The contents of degenerated or ruptured ves­icles are mixed with CSF, which may explain the severe inflammatory reaction in the sub­arachnoid space that may persist for a long pe­riod after the death of the parasite. 4 This inflam­matory process causes considerable thickening of the leptomeninges, with s~bseque~t ad~e­sive arachnoiditis and ventncular dtiatatlOn this secondary to blockage of the absorption pathways of CSF, ~hich l~ads to communi­cating hydrocephalus",6,10 (FIgs. lOa and lOe), or to obliteration of the Sylvian aqueduct by the extrinsic process. Sometimes the distinctive CT features of this arachnoiditis include an iso­dense configuration of the Sylvian fissure and basal cisterns in the noncontrast-enhanced scan. When contrast medium is administered, a diffuse leptomeningeal enhancement in the pre­viously isodense subarachnoid space can be seen, mimicking extravasation of the contrast agent4.10.12.2'1 (Figs. 9a-9d). This appearance does not occur frequently, and, if present, it will persist to a lesser degree in follow-up scans for several months. Most of the time, basal arach­noiditis will be recognized only by the sequelae of the process manifested by hydrocephalus on the CT scan (Fig. 100 and 10/1). Illtral'e1ltriCl/lar Form In most cases, the intraventricular type of in­volvement is detected only by the presence of hydrocephalus. This is produced by single or multiple cysts large enough to obliterate the Syl­vian aqueduct, outlet foramina of Luschka, Ma­gendie, or Monro, or by complete obliteration of the fourth, third, or lateral ventricles. 10.30 The most common presentation is a single parasite lodged in the fourth ventricle30,35 (Figs, 11a and 11/), and 13b). The cysts may float freely or be attached to a pedicle that allows a ball-valve effect. They can also be firmly attached to the walls of the ventricle or to the choroid plexus. 4,12,36 The cysts show the same density in noncontrast- or contrast-enhanced scans and will not be seen most of the time. Their presence may be suspected if there is disproportionate dilatation of the affected area, although occa- Journal of Clinical Neuro-ophthalmology Milrlinez-Ulpez, Quiroz y Ferrari (.-I Figure 13, Intraventricular and ,ubarachn"idal c\',tic,'rc,'Si" <In metrizamide H'ntricul,)~r.lpl1\' a: The c",tict'rcu" \"'''Iclt' shows up a., a h\l'<ldense filling defect with fluid dl'n"itv within tht' ri~ht lateral wntricl,', Thi" Il'"i,'n i" Lit'IiIlt'.llt'd b\' tht' metrizamide Occup\'ing the rt"t of the \'entrid,''', b: An<lthl'r p.lti,'nt with .1 lar~l' cv"ticercu" l<ld~L'd in thL' fourth H'ntricle, which appears dilated rclo"l'd arww,,), Th,' tl'mpllr.ll h<lrn" ,H" <lp.lCiIiL'd with I1lL'tri/.lmid,' (,'p,'n .Hr<'W') .1Ild .H,' dil.lted, :\:0 contrast IS .,e"n In the fourth \'L'ntrlck b'·C.1U'L· <It till' lar~L' n'''1. c: ~,'"n twm " difkr,'nt p.,tiL'nl. [)l'!.lH'd .1\ i., I tr.lI1"H'r"t' scan shows multipl" cv.,tic Il'"ion" occupvin~ thL' pw\im.ll righl ~vh'i.lIl ti"urL' .lI1d L'i ... t,'rn bL'hind 11lL' LII'r"'llll1 "'L,II.ll' (arrows), d: Corondl ...can in the ...am,' polti"nl (, ) ...11\Iw,l1g til<' lIonlilkd L'i ... lL'rn ... dllL' (0 til<' Lv l'L' IL·... '(llh (MI'II\\ ,), I~'."L" (a) and (b) bv courtl'W <It Daniel \'.' ...conc,·I, ..... 7I.I.D,. ,\;.,tlon.,I,\h-d'L'.,ll ,·nll'l'. I r<1.~~,. r-.1,·\ICll, 11.1 I sionally an annular, peri pheral en ha ncemen t may be seen in large lesions l2 (Fig, 11/1). Smaller, nonobstructing intraventricular cysts or vesicles may be recognized also by d ring of enhancement, probably related to the inilam­matory reaction of the adjacent ependyma or choroid plexus on which these vesicles can be attached and the concomitant capillary prolif­eration mentioned before l2 (Fig, 12), In some cases, the parasite is not the primary cause of obstruction but may produce ependymitis thilt can obstruct the free pathway of CSF ilt any June 1985 level within the ventricular svsk'm ,1I1d alsll pro-duce hydroc,'phalus, 1,1 ' In C,lSl'S ~lf suspected intr,l\'t'ntrinl!,u cvsts, the di,lgnosis can be cl1l1firnwd bv bllth CT and convention,ll llll'triz,llllide vl'ntricuillgra­phyH, 11I,12,2~,2",1, (Figs, !JtI and !JII) , This is a rel-atively nllllinv,lsivl' pl'llcedur,' perf~lrJl1ed in pa­til'nts wh~l h.we vl'ntriculopel'itone,ll lll' ventric­uloatri, ll shunts, The pl'llcedure is now widelv performed beca use of the low tllxicity of thiS water-solublt:' contrast Illediulll, which is used routinely in myeillgrams, The contrast medium 137 I"l is injected into the lateral ventricles by a trans­valvular percutaneous puncture, by a fine needle, in the antichamber of the shunting system. The administration of 3-5 ml metriz­amide at a concentration of 200-250 mg/ml will be enough to allow recognition of the lesions, their location, number, size, shape, relation to adjacent structures, motility, and the exact site of obstruction.5~ The entrance of contrast ma­terial to the interior of some Cystic lesions has recently been describedY The ~entricular injec­tion and delayed CT images, or the contrast me­dium given by a lumbar puncture in patients without hydrocephalus, can be useful proCt'­dures in cases of suspected cysts in the sub­arachnoidal locationX (Figs. Dc and 13d). Mixed Form A variety of combinations of forms of presen­tation may be found in tht' mixed form llf this disease. Parenchymal cysts can be associated 138 Figure 14. Intracranial parenchl'mal c'"~ticercosis as­~ llciated I\"th extracranial di""asl' in the same patient. a: Multiple ,mall nng lesions In both cerebral hemi­sphere' withllut perilesillnal edema, A small calciiied C,"stiCl'rcus is nL,ted adjacent tll the right irontal horn. b: Intraocular c,"stlcercus in the nght el'e shows up as a small \'esicl~ With a thin \\'all in the medial upper t.1uadrant oi the gll'be (arww). c: L1trasl'und exami­nation ot the same eve ~hl1\\'s the cysticercus as a small. echogenic cUfl·ihnear structure ~ttached to the wall (am)w), leDurte,,' l,i Daniel \'elez. \1.0.. :\a­tiona! Institute l'l \lenta! Health. \lexiw, D.F.] with intra\'entricular or arachnoidal le­sions. ~,lll,2s Intracranial L\'sticercosis can also be associ­ated with spinaL orbitaL muscular, subcuta­neous. and e\'en pulmonary in\·ol\,ementI.19 (Figs. l-l and 15). t\IYelography is the procedure of dwice in suspected spinal cysticercosis. 28.29 Ultrasound can demonstrate easil\' the intra­ocular location of the parasite as a smalL mov­able Cystic collection or as a smalL echogenic image surrounded b\' the \'itreous space (Fig. l-lc). On CT examination, the lesion is demon­strated if it is calcified or if there is a ring of enhancement in the contrast-enhanced scan, usually in lesions attached to the inner wall. Other\\'ise, the \'t'sicle Olav be isodense with the fluid of the chamber ,md \~'ill not be distinguish­able (Fig. l-ll,). The findings of intracranial cysticercosis in conventional radiographs are limited. Skull films can demonstrate smalL oval or round cal­cifications, 3-12 mOl in size, with an additional Journal of Clinical Neuro-ophthalmology Martinez-Lopez, Quiroz y Ferrari bll Figure 15. Extra- and intracranial cv~tlLerCll~i~ in thl' same patient. a: Cnntrast-enhancl'd SC.ln sl1l'\\'~ multipil'. sm.lll, an· nular. hvpodense lesions with a faint ring of enhanCl'ment. b: Chl'st x-r.w film ShllWS multiple puln1llnar\' n"dult's in till' right lung base related to cv~ticerci. c: CT ,,-an ot th., che~t sh"ws multipl., s"lid n"dult's with'lut c.lkific.1ti"n. small density situated eccentrically within the calcification that represents the scolex. J~ When the disease is manifested by chronic intracranial hypertension, widening of sutures, erosive changes at the sella turcica or tip of the petrous ridges, and prominence of convolutional mark­ings in the inner table may be present. 2H,2" Air ventriculography and cerebral angiography are less frequently used in the diagnosis of thl' dis­ease because of their invasive nature and lesser accuracy, compared with CT.~,JII,2H,2'1 Nuclear medicine brain scans are usually neg­ative,~, 1O,18 although recently cysticercus anti­bodies labeled with indium have been used. June 1985 These show preferential uptake in intracranial lesions. An accuracy close to lOO'/( has been re­ported for this metl10d. Further investigation of this proced urI' is needed for conclusive data; however, it may be valuable as a less expensive screening test in the presence of suspicious but nonconclusivt' CT scans. It may also bl' useful in determining activity llf the disease or re­sponse tll trl'atment.'s The treatn1l'nt llf intracranial cysticercosis varies according to the location of "the disease, symptomatology, and complications. [n cases of a single cyst or vl'sid,' with or without focal edema, no treatment is USlltllly required unless 139 Figure 16. Parenchymal cysticercosis. Evolution after treatment with Prazi'1uantel. a: :\oncontrast-enhanced CT scan showing multiple areas of edema. b: Contrast-enhanced CT scan sl1llwing multiple ring les\l1ns. c: :\l1ncontrast-enhanced CT scan 6 months later, after treatment with Praziquantel. sl1llwS that the edema has resl)l\·t'd. There are two parenchvmal calcifications not seen in the first scan. d: Contrast-enhancl'd CT sC,1n shllws rt'sl)lutll)n l)t Sl'me C\'stlc lesions. Others ha\'e decreased in size. Figure 17. Parl'nchymal cvsticl'rcosis treated with Praziquantel. a: Multiple cystic lesions in both cerebral hemispheres Without edem,l. Sever,,1 ot the It'slons show the scolt" in tlw lunll'n. b: Twolllonths later, after treatment with Praziquantel. there IS consllkr,lbk Improvenwnt. Most ot till' It'Sllllls h'l\'L' dis,lppl'dred, The residual cystic lesions do not show images of the scolex. • Figure 18. Parench\'mal cysticercosis. Earl\' changes aflt'r treatment with Praziquantel. a: Pretreatment scan shows two c\'sticercu., \'esicles with a thin ring of l'nhancL'ml'nl. b: One and onl'-half months lalt'r, thl' nght parietal Il'sion IS smaller. The left hemispherl' Il'sion shows SomL' pL'niL'slllll'll edema and the nng of enhancl'ment is thickL'r 'lI1d bettL'r defined. These changl''' are probabl\' rL'latL'd to thL' lI1t1dm­matory reaction observed after the death of thL' paraSltl'. the lesion acts as an irritative area causing sei­zures. Then, anticonvulsant drugs and close follow-up with serial examinations will deter­mine the evolution of the process and the need for further treatment. In the generalized en­cephalitic stage with multiple vesicles, diffuse edema, and intracranial hypertension, specific medications to treat mainly the hypertension and symptomatic drugs as needed. 4,111,17.27.1Y The medical treatments directed specifically to the parasite include several types of antipar­asitic drugs that destroy the cysticercus cyst and June 1985 M<lrtinl'z-LlJpl'Z, Quiroz y Ferrari larva without secondary damage to adjacent normal tissues and without triggering allergic or anaphylactic reactions. These drugs include fluobendazole lll and mctrifonate. 41 Although they haw been provl'n to be relatively effective ,1gainst cysticerci, their use has been limited, de­spite till' favorable results reported especially for the latter. The association of metrifonate and atropine sulfate has decreased considerably the undesirable cholinergic effect of metrifonate. 41 More recently, another drug, PraziquanteI, III, 17,N,4217 which is an antihelmintic with activity against all known species of Sclzis!o:oll1i7, has been proven efficacious in treating selected pa­tients with parenchymal or subarachnoid, well­defin~ d cysticercus cysts without hydroceph­alus. 4 ' Serial CT scans have demonstrated the disappearance of some cysts during and after treatment with this drug (Figs. 16 and 17). Most of the cysts show a decrease in size or some signs of involution, with more thickness of the ring of enhancement or even diffuse enhance­ment in a smaller lesion. Sometimes, during treatment, a small, perilesional, low-density area in relation to focal edema mav be seen, which is probably related to the granulomatous reaction of cerebral tissue occurring at the death of the pa.ra si te, wi th spillage of foreign proteins4,.4, (Fig. 18). The overall improvement in the parenchymal nonencephalitic form of the disease with Praziquantel has been up to 95'; 47 Some selected cases of cvsticercosis in the en­cephalitic phase, without clinical intracranial hypertension, have also shown an impressive response, with disappearance of most of the vesicles and edema, and apparent acceleration of the mineralization of some lesions, which can be calcified in less than a 6-month period4h (Figs. 16 and 17). There is no proof of Praziquantel's effectiveness in cases of intraventricular or in­traocular cysticercosis, but, in theon', it might be extreml:ly limited. Praziquanll'l is' also dft'c­tive against the adult Tl1l'11il1 Sll!i1l1l1 47 The surgical treatment of intr,Krani,ll CYsti­cercosis is limited to the removal or drainage of cysts, mainly the racemose variety that prodUCt' significant compression l)r herniation, or the single, localized and surgically accessible lesil)J1 that produces intract,lbll' seizures 1s (Fig. 19). Perhaps the most common surgic,ll procedures used at present in intracr,mi,ll c~'sticercosis are ventriculoatri,llor peritoneal shunts for cases of arachnoiditis ,md communicating Iwdroceph­alus, and also in obstructing hydrocephalus caused by either ependymitis or intraventricular cysts.H,'l,'IH The surgical removal of ventricu­lar cysts may be performed on rapidly enlarg­ing, unattached, and accessible lesions,H.1h CT is useful not only in the diagnosis of cys- 141 III Figure 19. Cysticl'rcosis, r,Kl'mOSl' \·.HiL'll'. a: Nonconlrilst-l'nh,lncl'd cr scan with multiple n'shc le~iuns. The largest o,ne lllmprl'SSt'S lhl' ,1dj,Kl'nt I'l'nlridl'. b: Contr,l.,t-l'nhancl'd CT ,can ,how, thll1 nng 01 l'nhanct'ment ot the leSIOn, whICh "as treated sur~icaill'. ticercosis but also in the evaluation of the nat­ural behavior of the disease in response to med­ical or surgical treatment. The problem of human cysticercosis is como. plex, and, without question, th~ best torm ot therapy is preventive medicine.~' Improvement of personal hygiene, better public sanitation, and careful pork meat inspection are important measures because the prevention of cvsticer­cosis depends ultimately on reducing the inci­dence of human taeniasis.~ References 1. Damonte Vicelln, L. J.' Descol1l1cimiento de 1,1 epidemiologia de la cisticercnsis en Me,icll. Sailid Publica Mex. 25: 301-305, 19~3. 2. Flisser, A., Woodhouse, E., 'lnd Luraldl', c.: The epidemiology n( human cvsticl'rcosis in tvk'icn. In Cl/sliceYt"(lsis L1f Ihe Cmlml Nerl'olls SI/Stelll (1st ed), Palacios, E., Rodriguez-Carb'lj,lLI .. Tan>ras, M. J., Eds. Springiield, III., Charles C ThLllll,lS, 1983, pp. 7-17 3. Escobar, A.: The pathlllngY ni nl'uron·sticl'rcllsis. In C\fsliccrcosis 0' II,e Cmlml Nerl,,'lIs 51/Stel/l (I sl ed.): Palacios, E., Rodriglll'z-CHbaj,li. I.. f.1\'­eras, M. L Eds. Charles C ThLllll,lS. Springfil'ld, III., 1983, pp. 27-54 4. Grisolia, J. 5., ,llld Wiederholt, W. c.: CNS c\'s-ticercosis. /\,.(//. Nl'I/,.ol. 39: 540-544, Jll82. . 5. Rodriguez, J., Palacios, E., Azar-Ki'l, 13., ,1Ild Churchill, R.: R'ldiologv oi cvsticL'rCl1sis of 11ll' cenlral nervous syslL'm' including cOlllpulL'd tLl­mography. l~adi(l/(lSIf 125: 127 -1.11. Ill7i. 6. Shanley, J. D., ,llld Jord'lIl, C.: CliniL',ll ,1SpL'ctS Ll( CNS cysticercosis. A,.ch. II/tel'll. A1ed. 140: I.1IN­131.1, 11)80. 7. I3L'1tr,ln, C. 1'.' Cvstil'L'rL'(),is of lllL' Ilel'\'ous 142 Sy"tl'm. III. Clinical iindings and treatment. f. :\tell/('~I/r..;. 19: h4I -643, 1962. H. McCLlrm'ick, G. F., Zt't', C S.. and Heiden, J.: CYstict'rcLlsis cerebri: revie\\' of 127 cases. Arch. .\';'1//(1/.39: 534-531), 1982. 9. Oli\'(', J. I., and Angulo-Ri\'ero, P.: CYsticercosis oi the nen'DUS s\·slt'm. I. Introduction and clin­ical aspects. I. .\';'II/(lSl/r,"; 19: 6-11-6-13, 1962. Ill. LLlmb.udll. L.. \I,ltl'L1S, .1. H., and EstailOl, B.: La cisticerwsis cerebral t'n :o..le'ico. Gae. ,'vlt'd. Mn. 118: 1-16,11)81. 11. VelazCL1-Suarez. \1.: C\·sticercosis. Pt'rsonal im­pact and sociLlecLlIlllmic signiiicance. In CyslicCT­ «'''i~ "f Ihe Ce/lfral .\'a""lIs Sll~tcl/l (lst ed.), Pala­cios, E. RL1drigllez-Carbajai. J., Ta\'t'ras, M. J., Eds. Ch.uit's C Thtlmas. Springfield, Ill., 1983, pp 3-b. 12. Zl'l'. C. S. Segall. H D., 1\liller. C, et al.: Un­lIsu, ll nl'1I£llr,ldiL11t1gical ie<ltllres o( intracraneal C\·sticl'rCLlsis. 1~,'d/(I/:''';1I 137: 3tj7 --107, 1980. 13. ('>br,ldllr. S.: C\'stiCl'~(L)sis cert'Qri. Acla NI'I/roc/lir. 10: 320-3b4. 14b2. 14. RLlbit's. c.: CLlnsider,lCil'Iles acerca de 100 casos dl' lunlLlr ct'rehal Llperados. GIl'. !\lll'd. Mt'x. 70: 3-7. 1ll40. 15. R'lbid,l, 1\1. T. Ri\',15, H. A., and Rodriguez, 1.1.' CL1llsidl'r,lCiLlnes anatomopatologicas sobre 1.1 cisticercLlsis cert:'l>ral como-causa de muerte. I'fll""'Slil (,\lex.) 17: 119- D6, 1979. lb. L.Dllll>,HdLl, L.. ,1Ild Mateos, J. H.: Cerebral cys­ticl'rcllsis in I\te'ico. ,\}cl//'(llogy (N. Y.) 11: 824­82S, llJb I. Ii. Eslal)Ll!. B.: CllJlt£ll\'t~rsias en cisticercosis cere­br< ll. GIC. ,\11'£1. ,\lex. 119: -161-466, 1983. It:. l3\Td, S E.. I.L1C\..t', G. E., Biggers, S., and Percy, A. K.: nw CL1lllplltl'd tomographic appearance of cel'ebl',ll c\'sticl'rcL)sis in adults and children. Ra­,1/('''''''; 1/1-14: Slll-S23, 1982. 19. Zl'ntl'nll-AI,lIlis, G. H.: A classification of human c\'slicl'rcosis. In CI/slil'crwsis. Prt'st'llt State of .Iourn<ll o( Clinical Neuro-ophthalmology K/lOwll'dge tllld Pcrspectil'e. Flisst'r A, Ed. Aca­dt'mic Prt'ss, Nt'w York: 1982, pp. 107-120. 20. Garcia-Ramos, G., and Rubio Donnadieu, F.: Neurocvsticercosis in till' .1dult. In CI/sticCl'cosis of tile eelliral Neri'(ll/S SI/St,'/II (1st I'd.), ·P.11.lCilIS, f'... Rodriguez-C.Hb.lj,l·1. I .. T.l\·l'r.ls. M. ] .. Eds. Charlt's C Thllm,ls. Springfidd. III.. Il/K'!, pp. h:'l­68. 21. Naya, S..1.: La cisticl'rCllsis dd sis!l'm.l neryiOSll central. Stl/l/d PI//>/ictl Alex. 25: 247 -:'lOll. IWO. .,., Puig, S. M.: Algul1lls aspl'l'tos an.ltllmllCliniclls dt'l cisticerco intr.lllcul.u. S.'/I/d PI/I,/icll Me.\. 24: 649-050. 1482. 23. Lllz,lIlll. E. D.: Uphth.llmk Cysticl'rl'osis. From cysticercosis llf the centr,ll nl'f\'OllS sys!l'm. In LI/SticcrC,'S/S ,11 till' L'<'Iltrlll Neri'olls SI/StCl/I (1st I'd.), P;llacil)s. E.. Rl1drigut'z-C.Hbajal, ]., Taveras. 1\1. J.. Eds. Charles C Thllmas. Springfidd. 111., 1483. pp. 801- 1ll0. 201. :'cJit'tl), D.: CYstict'rCllsis llf the nervous systt'm: diagnosis by' mt'.1I1s llf the spinal tluid comple­ment fixatil)J1 tt'st. Nellr<lh':\1f (Alilllletlp.) 6: 725­738. 1456. 25. \:ieto. D.: C\'stict'rcllsis of the nt'f\'OUS system. Diagnosis b\: mt'ans l)f tht' spinal tluid comple­ment fi'\ation test. In Clisticer,'osis 0/ the Cmtral .\'erl'llIlS SlIsfl'1Il (I st I'd.), ·Palacios. E., Rlldriguez­Carbalal: I .. Taveras. 1\1. ]., Eds. Charles C Thomas. Springfield. 111.. 1483. pp. 55-02. 26. Rvdzewsh. A., Chisholm, E. S.. and Kagan, I.' G.: Comparison of serologic test for human C\'sticercosis by indirect hemmaglutination, in­direct immunotluorescent antibody and agar gt'l precipitate test. ,. Parasito/. 28: 832-842, 1978. 27. Rodriguez-Carbajal. J.• Salgado, 1'., Gutierrez, R.. Escobar, A.. Aruiio. c., and Palacios. E.: The acute encephalitic phast' of neurocysticerosis: computed tomographY manifestations. A.f.N.R. 4: 51-55, 1983. 28. Rodriguez-Carbajal. J.• Palacios, E., and Zee, C. S.: :\'euroradiology of cysticercosis of the cen­tral nervous system. In Cl/sticcrcosis of tile Celltral .':crpous Sl/stl'/;/ (1st ed.), Palacios, E., Rodriguez­Carbajal: J., Tayeras. M. J., Eds. Charles C Thomas, Springfield. 111., 191\3, pp. lUl-143 29. Rodriguez-Carbajal, J., and Boleaga-Duran, B.: Neuroradiology of human cystict'rcosis. In Clfs­ticercosis. Presl'llt Statl' of KllVwledge tllld Paspedi!'e, Flisser A, Ed. Academic Press, New York, 1982, pp. 139-160. 30. Dorfsman, J.: The radiologic aspects of cerebral cysticercosis. Acta Radial. 1: 836-842, 1963. 31. Bentson, J., Wilson, G. H., Helmer, E., and Winter, J.: Computed tomography in intracraneal cysticercosis. f. Computed. Assist. TOlllogr. 1: 464­471, 1977. 32. Lopez-Hernandez, A., and Garaizar, c.: Mani­festations of infantile cerebral cysticercosis. In Cysticercosis of the Cl'n/ral Nauolls Systcl/I (lsll'd.), Palacios, E., Rodriguez-Carbajal, J., TaVl'r,lS, M. J., Eds. Charles C Thomas, Springfil'ld, III., 1983, pp. 69-83. June 1985 Martinez-Lopez, Quiroz y Ferrari 33. Dixon, H., and Lipscomb, F.: Cysticercosis. An ,1nalysis and follow up of 450 cases. Med. Res. C(llIlIcil Spec. J~.'I'- 229: 1-5R, 1961. 34. Santin, G., and Vargas, J.: Roentgen study of cys­tiCl'rcosis uf the central nervous system. Radiology 86: 520-528, 1%6. 35. Madrazo, I., Garcia, J. A., Paredes, G., et al.: Di­agnosis of intraventricular cysticercosis by com­pll! l'rized tomography with positive intraventric­ular contrdst ml'dium. f. NCIlr<lsllrg. 55: 947-951, 1981. 36. Loyo. M., Kleriga, E., and Estanol, B.: Fourth wntricular cysticercosis. NellroslIrgery 7: 456­458, 1980. 37 Zee, C. S., Tsai, F. Y., Segall, H D., Teal, J. S., and Ahmadi, J.: Entrance of metrizamide into an intravt'ntricular cysticercosis cyst. A.'.N.R. 2: 189-191, 1981. 38. Skwmnt'-Kadlubick, G., Celis, c., and Ferez, A.: Cysticercosis of the nervous system. Diagnosis by means of specific radioimmunoscan. AIIIl. NClIrol. 2: 343-344, 1977. 39. Velasco-Suarez, M.: Medical treatment of neu­rocysticercosis. In Cl/stiecreosis of the Celltral Ner­1> 01,'S Sl{stl'm (1st ed.): Palacios, E., Rodriguez-Car­bajal,' J., Taveras, M. J., Charles C Thomas, Springfield, Ill., 1983, pp. 149-154 40. Velasco-Suarez, M., Quirazco, F., and Bravo-Be­cherele, A.: Fluobendazole. Investigacion clinica en el tratamiento medico de la neurocisticercosis. INNN. Mexico, 1980-1981. 41. Trujillo, V. W.. Gonzalez-Barranco, D., Orozco, R., Villanueva, G., and Sandoval, M. E.: Trata­miento experimental con metrifonato en la cisti­cercosis. Arelz. IIIl'cst. Med. (Mex.) 12: 15-28, 1981. 42. Robles. c., and Chavarria. M.: Un caso de cisti­cercosis cerebral curado medicamentI'. Gae. Med. Mex. 116: 65-71, 1980. 43. Robles, c.: Tratamiento medico de la cisticercosis cerebral. Salud Publica MJx. 23: 343-350. 1981. 44. Frohberg, H.: Propiedades iarmacocineticas, iar­macologicas y toxicologicas del praziquantel. Sailld PU/Illea M{t. 24: 005-623, 1982. 45. Dorfsman, I.: Computerized tllmographv of the brain used in ct'rebr.l1 cvstict'rcosi:; pre and post treatml'nt with praziqu;1I1ll'1. StlJud Pul>li(tl Akx. 24: 637-641, 1482. 46. Lombardo, L., VaSCl1l1Ce!os, D., and Cruz-Se­gura. H.: Tratamiento de 1.1 cistict'rcosis con pra­ziquantel: informe preliminar de diez casos. Gae. Ml'd. Mh. 119: 17-22, 1983. 47. Sotelo, J., ESCllbedo. F.. Rllliriguez-Carbajal, J.. Torrl's. B., and RlIbiu-Dll(1I1,ldil'1I, F.: Therapy of p'lfl'nchym'll brain cvstic('rcosis with prazi­qllanll' 1. N. £11,'\1. '. Med. 310: IllOI-IO07, 1484. 48. Escobl'do, F.: Surgic.ll tr(,c1tml'nt llf cysticercosis. In CI/s/iccr(,'s;S ,,, tlz,' CClltmJ Nl'I'l'(lUS System (1st ('d.): Palacios, E., Rodrigut'z-Cubajal, J., Td­veras, M. J., Eds. Charles C Thllmas, Springfield. III., 1483, pp. 144-148. 143