Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5221_Библиотеки_им_академика_М_И_Перельмана.pdf
Infectious Disease and Neurocognition
Conclusion
Toxocariasis is a cryptic disease and cerebral toxocariasis even more so. However,
on a global scale, exposure to Tox o ca ra species is extensive and intimately linked to
poverty. Most persons seropositive for toxocariasis do not demonstrate overt neurologic signs (Finsterer & Auer, 2007), although improved awareness and diagnosis
suggest increasing numbers of cases are being detected. Evidence is accumulating
from large- scale associational studies in humans providing evidence that exposure
to Tox o ca r a has implications for human cognition. Animal models provide evidence
that To xo c ar a infection is associated with signicant behavioral changes and indicate
that research investigating this association in humans is warranted. Randomized
control trials of treatment of this neurological involvement are worryingly lacking,
and prevention remains the cornerstone of management (Deshayes et al., 2016).
Mouse models of cerebral toxocariasis are clearly useful in dissecting the host
response to infection. At this point in time, there are a number of clear pieces of
evidence. First, among a variety of animal models of toxocariasis, mouse models
demonstrate a greater propensity for brain involvement and evidence of larval accumulation. Second, within mouse models, inbred strains of mice demonstrate
greater brain involvement compared to outbred strains, and within inbred strains,
there is evidence of signicant variation. Furthermore, the diculty in selecting inbred strains refractory to brain involvement suggests it is more fruitful to compare
infected and non- infected susceptible mice. ird, comparative studies have established that T. c an is has a greater anity for the brain than T. ca ti . Fourth, the cerebral immune response is predominantly anti- inammatory, and this is reected in
a variety of inammatory- related signaling molecules— cytokines, chemokines, and
oxylipins.
Despite the above, signicant variation in genetic background, inoculation dose,
duration of infection, and modes of behavioral testing exists between studies undertaken and makes comparisons dicult (Holland & Hamilton, 2013; Strube et al.,
2020). Furthermore, and perhaps most importantly, the link between the observed
behavioral changes in mice and evidence of pathological and immunological
changes has not yet been rmly established.
References
ABO- SHEHADA, M. N. & HERBERT, I. V. 1989. Variations in innate resistance to experimental
Toxocara canis infection in two strains of mice. Vet Parasitol, 33, 297– 307.
BARDÓN, R., CUÉLLAR, C. & GUILLÉN, J. L. 1994. Larval distribution of Toxocara canis in BALB/ c
mice at nine weeks and one year post- inoculation. J Helminthol, 68, 359– 360.
BEAUTYMAN, W., BEAVER, P. C., BUCKLEY, J. J. & WOOLF, A. L. 1966. Review of a case previously
reported as showing an ascarid larva in the brain. J Pathol Bacteriol, 91, 271– 273.
Toxocara 259
BEAUTYMAN, W. & WOOLF, A. L. 1951. An ascaris larva in the brain in association with acute ante-
rior poliomyelitis. J Pathol Bacteriol, 63, 635– 647.
BEAVER, P. C., SNYDER, C. H., CARRERA, G. M., DENT, J. H. & LAFFERTY, J. W. 1952. Chronic eo-
sinophilia due to visceral larva migrans; report of three cases. Pediatrics, 9, 7– 19.
BURREN, C. H. 1971. e distribution of Toxocara larvae in the central nervous system of the mouse.
Trans R Soc Trop Med Hyg, 65, 450– 453.
BURRIGHT, R. G., DONOVICK, P. J., DOLINSKY, Z., HURD, Y. & CYPESS, R. 1982. Behavioral
changes in mice infected with toxocara canis. J Toxicol Environ Health, 10, 621– 626.
CHOU, C. M., LEE, Y. L., LIAO, C. W., HUANG, Y. C. & FAN, C. K. 2017. Enhanced expressions of
neurodegeneration- associated factors, UPS impairment, and excess Abeta accumulation in the hippocampus of mice with persistent cerebral toxocariasis. Parasit Vectors, 10, 620.
CONGDON, P. & LLOYD, P. 2011. Toxocara infection in the United States: the relevance of poverty,
geography and demography as risk factors, and implications for estimating county prevalence. Int J
Public Health, 56, 15– 24.
COX, D. M. & HOLLAND, C. V. 1998. e relationship between numbers of larvae recovered from the
brain of Toxocara canis- infected mice and social behaviour and anxiety in the host. Parasitology,
116, 579– 594.
COX, D. M. & HOLLAND, C. V. 2001a. Inuence of mouse strain, infective dose and larval burden in
the brain on activity in Toxocara- infected mice. J Helminthol, 75, 23– 32.
COX, D. M. & HOLLAND, C. V. 2001b. Relationship between three intensity levels of Toxocara canis
larvae in the brain and eects on exploration, anxiety, learning and memory in the murine host. J
Helminthol, 75, 33– 41.
DESHAYES, S., BONHOMME, J. & DE LA BLANCHARDIERE, A. 2016. Neurotoxocariasis: A sys-
tematic literature review. Infection, 44, 565– 574.
DOLINSKY, Z. S., BURRIGHT, R. G., DONOVICK, P. J., GLICKMAN, L. T., BABISH, J., SUMMERS,
B. & CYPESS, R. H. 1981. Behavioral eects of lead and Toxocara canis in mice. Science, 213,
1142– 1144.
DOLINSKY, Z. S., HARDY, C. A., BURRIGHT, R. G. & DONOVICK, P. J. 1985. e progression of be-
havioral and pathological eects of the parasite Toxocara canis in the mouse. Physiol Behav, 35, 33– 42.
DUBINSKY, P., HAVASIOVA- REITEROVA, K., PETKO, B., HOVORKA, I. & TOMASOVICOVA, O.
1995. Role of small mammals in the epidemiology of toxocariasis. Parasitology, 110 Pt 2, 187– 193.
DUNSMORE, J. D., THOMPSON, R. C. & BATES, I. A. 1983. e accumulation of Toxocara canis
larvae in the brains of mice. Int J Parasitol, 13, 517– 521.
EID, M. M., EL- KOWRANY, S. I., OTHMAN, A. A., EL GENDY, D. I. & SAIED, E. M. 2015.
Immunopathological changes in the brain of immunosuppressed mice experimentally infected with
Toxocara canis. Korean J Parasitol, 53, 51– 58.
EPE, C., SABEL, T., SCHNIEDER, T. & STOYE, M. 1994. e behavior and pathogenicity of Toxocara-
canis larvae in mice of dierent strains. Parasitol Res, 80, 691– 695.
ERICKSON, L. D., GALE, S. D., BERRETT, A., BROWN, B. L. & HEDGES, D. W. 2015. Association
between toxocariasis and cognitive function in young to middle- aged adults. Folia Parasitol (Praha),
62, 2015.048.
ERICKSON, L. D., HEDGES, D., STONE, A., BROWN, B. L., EMBLEY, B. & GALE, S. D. 2022.
Association between toxocariasis seropositivity and serointensity and cognitive function in older
U.S. adults. Folia Parasitol (Praha), 69, 2022.011.
FAKHRI, Y., GASSER, R. B., ROSTAMI, A., FAN, C. K., GHASEMI, S. M., JAVANIAN, M., BAYANI,
M., ARMOON, B. & MORADI, B. 2018. Toxocara eggs in public places worldwide— A systematic
review and meta- analysis. Environ Pollut, 242, 1467– 1475.
FAN, C. K., HOLLAND, C. V., LOXTON, K. & BARGHOUTH, U. 2015. Cerebral toxocariasis: Silent
progression to neurodegenerative disorders? Clin Microbiol Rev, 28, 663– 686.
FINSTERER, J. & AUER, H. 2007. Neurotoxocarosis. Rev Inst Med Trop São Paulo, 49, 279– 287.
GILLESPIE, S. H. 1993. e clinical spectrum of human toxocariasis. In: LEWIS, J. W. & MAIZELS,
R. M. (Eds.), Toxocara and Toxocariasis. London: Institute of Biology and the British Society for
Parasitology, pp. 55– 61.
Infectious Disease and Neurocognition
GOOD, B., HOLLAND, C. V. & STAFFORD, P. 2001. e inuence of inoculum size and time post-
infection on the number and position of Toxocara canis larvae recovered from the brains of outbred
CD1 mice. J Helminthol, 75, 175– 181.
HAMILTON, C. M., BRANDES, S., HOLLAND, C. V. & PINELLI, E. 2008. Cytokine expression in the
brains of Toxocara canis- infected mice. Parasite Immunol, 30, 181– 185.
HAMILTON, C. M., STAFFORD, P., PINELLI, E. & HOLLAND, C. V. 2006. A murine model for cere-
bral toxocariasis: Characterization of host susceptibility and behaviour. Parasitology, 132, 791– 801.
HAVASIOVAREITEROVA, K., TOMASOVICOVA, O. & DUBINSKY, P. 1995. Eect of various doses
of infective Toxocara- canis and Toxocara- cati eggs on the humoral response and distribution of
larvae in mice. Parasitol Res, 81, 13– 17.
HAY, J. & AITKEN, P. P. 1984. Experimental toxocariasis in mice and its eect on their behavior. Ann
Trop Med Parasitol, 78, 145– 155.
HAY, J., AITKEN, P. P. & ARNOTT, M. A. 1985. e eect of Toxocara canis on the spontaneous run-
ning activity of mice. Ann Trop Med Parasitol, 79, 221– 222.
HAY, J., KENDALL, A. T., AITKEN, P. P. & ARNOTT, M. A. 1986. Toxocara- canis infection and hyper-
activity. Ann Trop Med Parasitol, 80, 531– 533.
HOLLAND, C. V. 2017. Knowledge gaps in the epidemiology of Toxocara: the enigma remains.
Parasitology, 144, 81– 94.
HOLLAND, C. V. & HAMILTON, C. 2006. e signicance of cerebral toxocariasis. In HOLLAND, C. V.
& SMITH, H. V. (Eds.), Toxocara: e Enigmatic Parasite. Wallingford: CABI International, pp. 58– 73.
HOLLAND, C. V. & HAMILTON, C. M. 2013. e signicance of cerebral toxocariasis: a model system
for exploring the link between brain involvement, behaviour and the immune response. J Exp Biol,
216, 78– 83.
HOTEZ, P. J. 2008. Neglected infections of poverty in the United States of America. PLoS Negl Trop Dis,
2, e256.
HOTEZ, P. J. 2014. Neglected infections of poverty in the United States and their eects on the brain.
JAMA Psychiatry, 71, 1099– 1100.
HOTEZ, P. J. & WILKINS, P. P. 2009. Toxocariasis: America’s most common neglected infection of pov-
erty and a helminthiasis of global importance? PLoS Negl Trop Dis, 3, e400.
JANECEK, E., BEINEKE, A., SCHNIEDER, T. & STRUBE, C. 2014. Neurotoxocarosis: Marked pref-
erence of Toxocara canis for the cerebrum and T. cati for the cerebellum in the paratenic model host
mouse. Parasit Vectors, 7, 194.
JANECEK, E., WAINDOK, P., BANKSTAHL, M. & STRUBE, C. 2017. Abnormal neurobehaviour and
impaired memory function as a consequence of Toxocara canis— As well as Toxocara cati- induced
neurotoxocarosis. PLoS Negl Trop Dis, 11, e0005594.
KEEGAN, J. D. & HOLLAND, C. V. 2010. Contamination of the hair of owned dogs with the eggs of
Toxocara spp. Vet Parasitol, 173, 161– 164.
KVALSVIG, J. & ALBONICO, M. 2013. Eects of geohelminth infections on neurological develop-
ment. Handb Clin Neurol, 114, 369– 379.
LIAO, C. W., FAN, C. K., KAO, T. C., JI, D. D., SU, K. E., LIN, Y. H. & CHO, W. L. 2008. Brain injury-
associated biomarkers of TGF- beta1, S100B, GFAP, NF- L, tTG, AbetaPP, and tau were concomitantly enhanced and the UPS was impaired during acute brain injury caused by Toxocara canis in
mice. BMC Infect Dis, 8, 84.
MACIAG, L., MORGAN, E. R. & HOLLAND, C. 2022. Toxocara: Time to let cati “out of the bag.”
Trends Parasitol, 38, 280– 289.
MAGNAVAL, J. F., GALINDO, V., GLICKMAN, L. T. & CLANET, M. 1997. Human Toxocara infection
of the central nervous system and neurological disorders: A case- control study. Parasitology, 115,
537– 543.
MARMOR, M., GLICKMAN, L., SHOFER, F., FAICH, L. A., ROSENBERG, C., CORNBLATT, B. &
FRIEDMAN, S. 1987. Toxocara canis infection of children: Epidemiologic and neuropsychologic
ndings. Am J Public Health, 77, 554– 559.
MIYAZAKI, I. 1991. An Illustrated Book of Helminthic Zoonoses. Tokyo: International Medical
Foundation of Japan.
Toxocara 261
MIZGAJSKA- WIKTOR, H. & UGA, S. 2006. Exposure and Environmental Contamination. Wallingford: CABI
International.
NELSON, S., GREENE, T. & ERNHART, C. B. 1996. Toxocara canis infection in preschool age children: Risk
factors and the cognitive development of preschool children. Neurotoxicol Teratol, 18, 167– 174.
NICHOLS, R. L. 1956. e etiology of visceral larva migrans. I. Diagnostic morphology of infective
second- stage Toxocara larvae. J Parasitol, 42, 349– 362.
O’LORCAIN, P. 1994. Epidemiology of Toxocara spp. in stray dogs and cats in Dublin, Ireland. J
Helminthol, 68, 331– 336.
OTHMAN, A. A., ABDEL- ALEEM, G. A., SAIED, E. M., MAYAH, W. W. & ELATRASH, A. M. 2010.
Biochemical and immunopathological changes in experimental neurotoxocariasis. Mol Biochem
Parasitol, 172, 1– 8.
RESENDE, N. M., GAZZINELLI- GUIMARAES, P. H., BARBOSA, F. S., OLIVEIRA, L. M.,
NOGUEIRA, D. S., GAZZINELLI- GUIMARAES, A. C., GONCALVES, M. T. P., AMORIM, C.
C. O., OLIVEIRA, F. M. S., CALIARI, M. V., RACHID, M. A., VOLPATO, G. T., BUENO, L. L.,
GEIGER, S. M. & FUJIWARA, R. T. 2015. New insights into the immunopathology of early Toxocara
canis infection in mice. Parasit Vectors, 8, 354.
RODDIE, G., HOLLAND, C., STAFFORD, P. & WOLFE, A. 2008. Contamination of fox hair with eggs
of Toxocara canis. J Helminthol, 82, 293– 296.
ROSTAMI, A., RIAHI, S. M., HOLLAND, C. V., TAGHIPOUR, A., KHALILI- FOMESHI, M., FAKHRI,
Y., OMRANI, V. F., HOTEZ, P. J. & GASSER, R. B. 2019. Seroprevalence estimates for toxocariasis in
people worldwide: A systematic review and meta- analysis. PLoS Negl Trop Dis, 13, e0007809.
SANCHEZ, S. S., GARCIA, H. H. & NICOLETTI, A. 2018. Clinical and magnetic resonance imaging
ndings of neurotoxocariasis. Front Neurol, 9, 53.
SEGOVIA, J. M., TORRES, J., MIQUEL, J., LLANEZA, L. & FELIU, C. 2001. Helminths in the wolf,
Canis lupus, from north- western Spain. J Helminthol, 75, 183– 192.
SHARGHI, N., SCHANTZ, P. M., CARAMICO, L., BALLAS, K., TEAGUE, B. A. & HOTEZ, P. J. 2001.
Environmental exposure to Toxocara as a possible risk factor for asthma: A clinic- based case- control
study. Clin Infect Dis, 32, E111– E116.
SHIELDS, J. A. 1984. Ocular toxocariasis. A review. Surv Ophthalmol, 28, 361– 381.
SKERRETT, H. & HOLLAND, C. V. 1997. Variation in the larval recovery of Toxocara canis from the
murine brain: implications for behavioural studies. J Helminthol, 71, 253– 255.
SMITH, H., HOLLAND, C., TAYLOR, M., MAGNAVAL, J. F., SCHANTZ, P. & MAIZELS, R. 2009.
How common is human toxocariasis? Towards standardizing our knowledge. Trends Parasitol, 25,
182– 188.
SPRENT, J. F. A. 1955. On the invasion of the central nervous system by nematodes: II. Invasion of the
nervous system in ascariasis. Parasitology, 45, 41– 55.
SPRINGER, A., HEUER, L., JANECEK- ERFURTH, E., BEINEKE, A. & STRUBE, C. 2019.
Histopathological characterization of Toxocara canis- and T. cati- induced neurotoxocarosis in the
mouse model. Parasitol Res, 118, 2591– 2600.
STRUBE, C., WAINDOK, P., RAULF, M. K. & SPRINGER, A. 2020. Toxocara- induced neural larva
migrans (neurotoxocarosis) in rodent model hosts. Adv Parasitol, 109, 189– 218.
TAIRA, K., SAITOH, Y. & KAPEL, C. M. 2011. Toxocara cati larvae persist and retain high infectivity
in muscles of experimentally infected chickens. Vet Parasitol, 180, 287– 291.
TAIRA, K., SAITOH, Y., OKADA, N., SUGIYAMA, H. & KAPEL, C. M. 2012. Tolerance to low temper-
atures of Toxocara cati larvae in chicken muscle tissue. Vet Parasitol, 189, 383– 386.
TAYLOR, M. R., KEANE, C. T., O’CONNOR, P., MULVIHILL, E. & HOLLAND, C. 1988. e ex-
panded spectrum of toxocaral disease. Lancet, 1, 692– 695.
VIDAL, J. E., SZTANJNBOK, J. & SEGURO, A. C. 2003. Eosinophilic meningoencephalitis due to
Toxocara canis: Case report and review of the literature. Am J Trop Med Hyg, 69, 341– 343.
WAINDOK, P., JANECEK- ERFURTH, E., LINDENWALD, D., WILK, E., SCHUGHART, K.,
GEFFERS, R., BALAS, L., DURAND, T., RUND, K. M., SCHEBB, N. H. & STRUBE, C. 2019.
Multiplex proling of inammation- related bioactive lipid mediators in Toxocara canis- and
Toxocara cati- induced neurotoxocarosis. PLoS Negl Trop Dis, 13, e0007706.
Infectious Disease and Neurocognition
WAINDOK, P. & STRUBE, C. 2019. Neuroinvasion of Toxocara canis- and T. cati- larvae mediates dy-
namic changes in brain cytokine and chemokine prole. J Neuroinamm, 16, 147.
WALSH, M. G. & HASEEB, M. A. 2012. Reduced cognitive function in children with toxocariasis in a
nationally representative sample of the United States. Int J Parasitol, 42, 1159– 1163.
WAPENAAR, W., BARKEMA, H. W. & O’HANDLEY, R. 2013. Fecal shedding of Toxocara canis and
other parasites in foxes and coyotes on Prince Edward Island, Canada. J Wildl Dis, 49, 394– 397.
WORLEY, G., GREEN, J. A., FROTHINGHAM, T. E., STURNER, R. A., WALLS, K. W., PAKALNIS, V.
A. & ELLIS, G. S., JR. 1984. Toxocara canis infection: Clinical and epidemiological associations with
seropositivity in kindergarten children. J Infect Dis, 149, 591– 597.
YOSHIKAWA, M., NISHIOFUKU, M., MORIYA, K., OUJI, Y., ISHIZAKA, S., KASAHARA, K.,
MIKASA, K. I., HIRAI, T., MIZUNO, Y., OGAWA, S., NAKAMURA, T., MARUYAMA, H. &
AKAO, N. 2008. A familial case of visceral toxocariasis due to consumption of raw bovine liver.
Parasitol Int, 57, 525– 529.
17
Eects of Neurocysticercosis on Cognitive
and Neuropsychiatric Function
Shawn D. Gale and Dawson W. Hedges
Introduction
Characterized by a widespread distribution (Budke et al., 2009), neurocysticercosis
is caused by the cestode Taenia solium, the pork tapeworm (Butala et al., 2021).
Endemic regions include South America, Africa, Central Europe (De Almeida &
Gurjao, 2010), and parts of Asia (Carpio & Romo, 2014) including China, India,
and Nepal (Gripper & Welburn, 2017). In regions where T. solium is endemic, its
seroprevalence can be high. In the Mocuba district of Zambézia province in central
Mozambique, for example, the seroprevalence of T. solium was 10.3 percent (Langa
et al., 2022). e most common cause of neuroparasitosis, T. solium infects an estimated 50 million people worldwide (El- Kady et al., 2021), although good epidemiologic data are oen not available (Gripper & Welburn, 2017). Increasingly, cases of
T. solium are identied in high- income nations in immigrants from endemic regions
(Carpio & Romo, 2014), although neurocysticercosis tends to be more prevalent in
socioeconomically disadvantaged regions (Budke et al., 2009).
Humans are the denitive host for T. solium, where adult worms live in the human
intestinal tract. Pigs are intermediate hosts, although humans also can be intermediate hosts (El- Kady et al., 2021). Pigs become infected aer eating eggs or proglottids from adult tapeworms in the human small intestine (Gripper & Welburn, 2017),
shed from humans in feces (Garcia et al., 2020). In pigs, larval cysts form in muscle.
When humans eat undercooked pork infected with larval cysts, larvae from cysts
mature into adult tapeworms in the human small intestine, which then shed eggs
into the environment. Once mature, a tapeworm can release 100,000 eggs per day
(Gripper & Welburn, 2017). When humans ingest eggs shed in human feces, larvae
penetrate the intestinal wall and can migrate to various regions, including the brain,
muscle, eyes, skin (Gripper & Welburn, 2017) and cardiac muscle, where they form
metacestodes (Bustos et al., 2005; Butala et al., 2021; Gripper & Welburn, 2017).
In the brain, metacestodes go through a vesicular phase, then to a colloidal stage,
and next to a granular stage (Gripper & Welburn, 2017), where cyst viability is lost
(El- Kady et al., 2021). With time, cysts can degenerate and become no longer visible
on brain imaging or remain as calcied nodules (Carpio & Romo, 2014). Further,
Shawn D. Gale and Dawson W. Hedges,
Neurocognitive and Neuropsychiatric Medicine
© Oxford University Press 2024. DOI: 10.1093/ oso/ 9780192870414.003.0018
Infectious Disease and Neurocognition
cysts can be classied by stage of viability— alive, transitional, and degenerative—
and by location (Carpio & Romo, 2014).
While neurocysticercosis can be asymptomatic (Carpio & Romo, 2014;
Millogo et al., 2019), it is oen associated with neurological, neuropsychiatric,
and neurocognitive decits (Ahmed et al., 2022; Del Brutto, 2022; El- Kady et al.,
2021). Cyst stage (Gripper & Welburn, 2017) and location in the brain are associated with the type of neurological or cognitive dysfunction (Ahmed et al., 2022; Del
Brutto, 2022), as is the host immune response to the parasite (El- Kady et al., 2021).
Moreover, symptoms from neurocysticercosis might not occur for several years aer
brain invasion by cysts (El- Kady et al., 2021).
Depending on where the cysts are in the brain, several types of neurocysticercosis
can occur. e parenchymatous type of neurocysticercosis, where cysts form in
the brain parenchyma, can be associated with epilepsy. e cysts also can be in
the meninges, a form of neurocysticercosis that is associated with hydrocephalus,
headaches, and elevated intracranial pressure. ere are also intraventricular and
subarachnoid types of neurocysticercosis, which in addition to hydrocephalus
can cause an acute increase in ventricular volume, which has been associated with
sudden death. ere are also spinal forms of neurocysticercosis (Andino et al., 2022;
El- Kady et al., 2021).
e diagnosis of neurocysticercosis is based on brain imaging— computed tomography and magnetic resonance imaging (MRI)— and antigen and antibody
detection in blood and cerebrospinal uid (CSF), diagnostic techniques that unfortunately are of oen limited availability in regions endemic for neurocysticercosis
(Takayanagui & Haes, 2022). Two broad types of treatment are available for
neurocysticercosis: symptomatic and antiparasitic treatment. Symptomatic treatment is used to control symptoms that arise from neurocysticercosis, such as
antiepileptic drugs for control of neurocysticercosis- related seizures and steroids
to reduce inammation. Antiparasitic treatment seeks to destroy the parasite itself and consists of drugs such as praziquantel and albendazole (Ahmed et al.,
2022; Garcia et al., 2020). In addition, there is evidence that anthelmintic treatment may reduce seizure frequency (World Health Organization, 2021). In some
cases, antiparasitic treatment results in severe cerebral inammation, and so it is
oen necessary to give steroids concomitantly with the antiparasitic drug used to
minimize perilesional inammation. In fact, controversy continues as to the appropriate use, safety, and eectiveness of praziquantel and albendazole in the
treatment of neurocysticercosis (Takayanagui & Haes, 2022), particularly as brain
cysts may resolve with time (Gripper & Welburn, 2017). Although used less now
since the availability of antiretroviral treatment, surgery may be an option in some
cases of neurocysticercosis, although it is mainly used for removal of viable cysts
(Hamamoto Filho et al., 2019) and shunt placement in some cases of hydrocephalus
(Takayanagui & Haes, 2022).
An important intervention to control neurocysticercosis is prevention. Public
health measures such as vaccination against T. solium in pigs, improved sanitation,
Neurocysticercosis 265
and keeping pigs away from human sewage are critical approaches in preventing
neurocysticercosis (Garcia et al., 2020).
Associations between neurocysticercosis
and neurological, neuropsychiatric, and
neurocognitive function
Cysticercosis can aect a variety of tissues in addition to the brain, such as the heart
in approximately 25 percent of cysticercosis cases, where it can be associated with
cardiac conduction abnormalities and ventricular arrythmias (Garcia- Martinez
et al., 2022). However, a large part of the disease burden associated with cysticercosis
involves the brain. Because symptoms of neurocysticercosis depend in part on the
location of the cysts in the brain and ventricles, there is no typical neurocysticercosis
presentation (Takayanagui & Haes, 2022). Rather, a range of signs and symptoms
from neurological ndings, neuropsychiatric dysfunction, and neurocognitive
decits can be associated with neurocysticercosis.
Associations between neurocysticercosis and
neurological function
Epilepsy
e most common manifestation of neurocysticercosis is epilepsy (El- Kady
et al., 2021), and T. solium is a common cause of epilepsy worldwide (Carpio &
Romo, 2014; Debacq et al., 2017; Del Brutto, 2022; Millogo et al., 2019) and is
the leading cause of late- onset seizures in low- income and middle- income nations (Debacq et al., 2017). Neurocysticercosis has been associated with both
focal and generalized seizures (Ahmed et al., 2022). e results of a systematic review found that among patients with neurocysticercosis presenting to neurology
clinics, seizures and epilepsy were the most common associated clinical ndings,
occurring in 78.8 percent of neurocysticercosis cases. e authors cautioned that
because these samples were from neurology clinics, the 78.8 percent gure likely
overestimated the actual prevalence of seizures/ epilepsy in neurocysticercosis
(Carabin et al., 2011). Others have estimated the prevalence of seizures in cases of
neurocysticercosis to be lower, at approximately 33 percent (Garcia et al., 2020),
and some cite studies reporting prevalence of neurocysticercosis- related epilepsy
to be closer to 8 percent (Carpio & Romo, 2014). Nonetheless, a systematic review
and meta- analysis of 37 studies carried out in 23 low- income and middle- income
countries in Africa, Asia, and Latin America found that while only 19 of the 37
studies had a signicant association between neurocysticercosis and epilepsy, the
estimated overall odds ratio of epilepsy with neurocysticercosis was 2.7 (95 percent
Infectious Disease and Neurocognition
condence interval: 2.1– 3.6) (Debacq et al., 2017). A small study of 25 pediatric
cases of neurocysticercosis (age range 1– 11 years) found seizures in 25 percent of
the patients (Morales et al., 2000). Not all studies, however, have found an association between T. solium and seizure or epilepsy. In their investigation of associations between T. solium seropositivity and epilepsy and seizures in the Mocuba
district, Zambézia province, Mozambique, Langa et al. (2022) found no association between seropositivity and seizures, although the overall prevalence of epilepsy in this region was very high regardless of T. solium seropositivity status, with
27 percent having generalized epilepsy and 18 percent having focal epilepsy. While
cognitive function and quality of life in those with neurocysticercosis- related epilepsy may be negatively impacted, functioning may not dier from what would be
expected in epilepsy related to other etiologies (Nau et al., 2018). Similarly, because
epilepsy can change over time (Scharfman, 2007), because on its own epilepsy can
aect cognition, mood, and quality of life (Carreno et al., 2008; Leidy et al., 1999),
and because neurocysticercosis may present with cognitive or mood- related
symptoms similar to that found in epilepsy, it may be dicult to distinguish the
eects of one condition from the other. Although treatment with albendazole can
eliminate neurocysticercosis cysts in some patients, placebo- controlled trials with
albendazole do not necessarily appear to decrease the frequency of seizure recurrence (Carpio & Romo, 2014). Finally, in one retrospective study comparing patients with neurocysticercosis- related epilepsy (e.g., calcied parenchymal lesions
from past infection) to those with epilepsy with either no lesions on neuroimaging
and no history of neurocysticercosis or with epilepsy attributed to identiable lesions on neuroimaging and no history of neurocysticercosis, found no group differences in seizure frequency or freedom from seizures (Leon et al., 2015).
Headache
Headache is a common association of neurocysticercosis (Millogo et al., 2019).
Langa et al. (2022) found in their study of neurological disorders associated with
T. solium in a district in Mozambique an association with chronic headache, with
49.5 percent of people seropositive for T. solium reporting having chronic head-
ache. In the systematic review referred to above in the epilepsy subsection, the
authors found that headaches were the second most common, aer seizures/ epilepsy, clinical nding in patients with neurocysticercosis presenting to a neurology
clinic. In this systematic review, headaches were present in 37.9 percent of the
neurocysticercosis patients, and the gure was even higher among patients with
neurocysticercosis presenting to an imaging clinic (Carabin et al., 2011). In children
with neurocysticercosis, headaches also occur (Veeravigrom & ampratankul,
2022). In one small study, 60 percent of children with neurocysticercosis had
headaches, second only to the percentage of the children with seizures (Morales
et al., 2000).
Neurocysticercosis 267
Focal neurological deficits
Focal neurological decits also have been associated with neurocysticercosis. e
2011 systematic review by Carabin et al. (2011) found that 16 percent of patients
with neurocysticercosis had focal neurological decits. Stroke can occur when
neurocysticercosis elicits an inammatory response that blocks blood vessels in
the circle of Willis (El- Kady et al., 2021), a mechanism by which neurocysticercosis
could produce focal neurological decits.
Movement disorders and parkinsonism
Neurocysticercosis also has been associated with movement disorders. From a registry of 590 patients in Ecuador with neurocysticercosis, Alarcón et al. (2017) found
that 23 (3.8 percent) had demonstrable motor dysfunction on neurologic exam: one
patient had chorea, two had dystonia, ve had tremor, and 15 had signs of parkinsonism (e.g., tremor, rigidity, bradykinesia). e authors reported that most responded to treatment, in contrast to the progressive nature of Parkinson’s disease.
Further, the authors found that while patients with chorea or dystonia tended to
have basal ganglia lesions, the lesion in those with parkinsonism tended be more diffuse and had a worse prognosis (Alarcón et al., 2017). A recent case study (Puig et al.,
2023) of a 49- year- old man presenting with recent onset of dystonic head tremor
suggested neurocysticercosis as the cause. It has been suggested that additional factors such as immune response and the role of genes should be investigated in relation
to movement disorders associated with neurocysticercosis (Bhattacharjee, 2018).
Hydrocephalus
One potential complication of neurocysticercosis is the development of hydrocephalus (Butala et al., 2021). In addition to being located in the parenchyma, cysts
also can develop in the ventricular system, including the subarachnoid space, resulting in obstruction of cerebrospinal uid leading to increased intracranial pressure, hydrocephalus, arachnoiditis, and even vasculitis (Garcia et al., 2020). In a
series of 121 patients with neurocysticercosis, 19 percent had ventricular cysts and
of those 23 patients, 17 (73.9 percent) presented with hydrocephalus (Nash et al.,
2018). Estimates of the prevalence of hydrocephalus in neurocysticercosis vary
widely from 16 percent to 51 percent at disease onset (Hamamoto Filho et al., 2019).
Hydrocephalus can result from cysticercosis- related meningitis, which has a high
mortality rate, and invasion of neurocysticercosis into ventricular and/ or basal cisterns has been described as “malignant” (Takayanagui & Haes, 2022). In a review of
neurosurgical cases, the fourth ventricle was the most common location of cysts in
neurocysticercosis- related hydrocephalus (Yamaki et al., 2023). Endoscopic removal