Brain Circulation

: 2020  |  Volume : 6  |  Issue : 4  |  Page : 225--241

Neurocysticercosis and movement disorders: A literature review

Jamir Pitton Rissardo1, Ana Letícia Fornari Caprara1, ═caro Durante2,  
1 Department of Medicine, Federal University of Santa Maria, Santa Maria, Brazil
2 Department of Medicine, Federal University of Fronteira Sul, Passo Fundo, RS, Brazil

Correspondence Address:
Jamir Pitton Rissardo
Av. Roraima, 1000 - Camobi, Santa Maria - RS 97105-900


Neurocysticercosis (NCC) is a specific form of cysticercosis that affects the central nervous system. It is caused by the tapeworm Taenia solium, which is often found in pigs. NCC is considered one of the “great simulator/mimickers” of other diseases. In this context, movement disorders (MDs) can occur in a small percentage of individuals with NCC. This review aims to evaluate the clinicoepidemiological profile, pathological mechanisms, and historical features of NCC-associated MD. Relevant reports in six databases were identified and assessed by two reviewers without language restriction. A total of 71 reports containing 148 individuals who developed an MD related to NCC were identified. NCC-associated MD included parkinsonism (n = 47), ataxia (n = 32), chorea (n = 18), dystonia (n = 13), tremor (n = 8), myokymia (n = 6), myoclonus (n = 4), ballism (n = 1), tics (n = 1), and others (n = 18). The mean and median ages were 36.58 (standard deviation: 20.51) and 35 years (age range: 1–88 years), respectively. There was a slight predominance of female sex (52.17%). On follow-up, 58.90% of the individuals had a full recovery; two deaths were reported. We believe that the majority of cases reported were only diagnosed because patients had classical clinical manifestations generally investigated by neuroimaging, resulting in incidental findings suggestive of NCC, which were later supported by laboratory examinations. Therefore, the association between NCC and MD is probably underreported. Clinicians should be wary of this association, mainly in endemic areas for cysticercosis.

How to cite this article:
Rissardo JP, Caprara AL, Durante ═. Neurocysticercosis and movement disorders: A literature review.Brain Circ 2020;6:225-241

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Rissardo JP, Caprara AL, Durante ═. Neurocysticercosis and movement disorders: A literature review. Brain Circ [serial online] 2020 [cited 2022 Oct 1 ];6:225-241
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Neurocysticercosis (NCC) is a specific form of cysticercosis that affects the central nervous system (CNS). It is caused by the tapeworm Taenia solium (T. solium), which is often found in pigs. The association of cysticercosis and CNS infection was first extensively described in the early 20th century by English authors. This finding can be explained by the fact that many of the patients reported had a history of travel to work in India, Egypt, and Gibraltar, places known for a high incidence of cysticercosis. When these travelers returned to the UK, the British Army medics reported their possibly imported cases. In the 1930s, a large number of cases were reported by physicians of the Royal Army Medical Corps working at the Queen Alexandra Military Hospital at Millbank by the Thames River.[1]

This cestode infection is classified by the World Health Organization (WHO) as a “neglected tropical disease,” which represents a diverse group of communicable diseases prevailing in tropical areas in about 150 countries, affecting >1 billion people. Common endemic areas include Asia, Eastern Europe, and South America [Figure 1]. The WHO proposed in the early 2000s that effective control can be achieved when selected public health approaches are combined and applied locally.[2]{Figure 1}

Pigs are commonly the intermediate host for T. solium. Humans are the definitive host, but can serve as intermediate as well. NCC occurs due to the accidental ingestion of eggs of the pork tapeworm by humans, resulting in the development of the larval form of T. solium (cysticercus) in the brain [Figure 2].[3],[4] It is worth mentioning that NCC is only acquired from the fecal-oral route (ingestion of eggs), not via the ingestion of cysticerci in undercooked pork, which is associated with taeniasis.[3]{Figure 2}

When the invasion of the CNS occurs, the cysticerci usually develop in five main stages [Figure 3].[5],[6],[7] The existence of the noncystic stage is not unanimously accepted, but we included it because findings of its development are observable through neuroimaging even before the vesicular phase.[6] The other four are also known as Escobar's pathological stages, which depict the natural evolution of NCC, and are identified by pathological and radiological specific features.[5] These stages are the vesicular, colloidal (colloidal–vesicular), granular (granular–nodular), and calcific (nodular) stages.[7]{Figure 3}

Cysticercosis has an unremarkable presentation because the presence of cysts in most tissues is generally asymptomatic. Hence, the prevalence of NCC is likely underdiagnosed. The clinical manifestations can range from asymptomatic brain lesions to mimicking any neurological disorder, depending or not on the location of the cysticerci implantation.[4] It is noteworthy that, together with neurosyphilis and AIDS, NCC is considered one of the “great simulator/mimickers” of other diseases.[8] The most common presentation is seizures.[4] In endemic areas, NCC represents the etiology of an important percentage of adult-onset epilepsy. Some studies have found that NCC accounts for approximately one of every three epilepsy cases in developing countries.[9] In this context, movement disorders (MDs) usually occur in about 3% of individuals with NCC.[10] The mechanism related to NCC-associated MDs may be a direct toxic effect of the cysticerci, edema, hypoxia affecting the nerve axons, and secondary to meningeal inflammation. In this way, the present literature review aims to evaluate the clinicoepidemiological profile, pathological mechanisms, and historical features of NCC-associated MDs.



NCC was defined by the revised diagnostic criteria and degrees of diagnostic certainty for NCC by Del Brutto et al. [Table 1].[11] The majority of the studies featured neuroimaging findings. Cases without radiographic features were confirmed with histological demonstration of the parasite in biopsy material from neurosurgical interventions, identification of specific anticysticercal antibodies in cerebrospinal fluid (CSF), or cysticercosis outside the CNS associated with neurological impairment. The clinical characteristics and definitions of the MDs such as dystonia, restless leg syndrome, akathisia, dyskinesia, tremor, parkinsonism (PKN), tic, chorea, ballism, and myoclonus were obtained from the reference article by Jankovic and Tolosa.[12] In the cases where the non-English literature was beyond the authors' proficiency (English, Portuguese, Spanish, and German), and the English abstract did not provide enough data, such as articles in Korean, Thai, and Japanese, the Google Translate service was used.[13]{Table 1}

Search strategy

We searched six databases in an attempt to locate all reports about MDs associated with NCC that were published until 2020 in electronic form. Excerpta Medica (Embase), Google Scholar, Latin American and Caribbean Health Sciences Literature (Lilacs), Medline, Scientific Electronic Library Online (Scielo), and ScienceDirect were searched. The search terms used were “chorea, tremor, parkinsonism, myoclonus, ataxia, dystonia, myokymia, ballism, tic, dyskinesia, stuttering, restless legs syndrome, akathisia, restlessness, hyperkinetic, hypokinetic, bradykinesia, movement disorder.”[14] These terms were combined with “cysticercosis, neurocysticercosis” [Other 1 – Supplementary Material].[INLINE:1]

Inclusion and exclusion criteria

Case reports, case series, original articles, letters to the editor, bulletins, and poster presentations published up to June 2020 were included in this review with no language restriction. The two authors independently screened the titles and abstracts of all papers found in the initial search. Disagreements between the authors were discussed to establish consensus. Cases where the cause of MD was already known and the motor symptoms were not worsened or were not related to NCC were excluded. Cases that were not accessible by electronic means, including after a formal request E-mailed to the authors, were also excluded.

Data extraction

A total of 1,986 reports were identified from the search, of which 1,915 were excluded as they did not meet the inclusion and exclusion criteria [Figure 4]. When provided, we extracted MD type, authors, department, year of publication, country of occurrence, number of patients affected, age, sex, CSF analysis, neuroimaging features, patient's status at follow-up, and important findings of clinical history and management. The data were extracted by two independent authors, double-checked to ensure matching, and organized by whether or not the MD was caused by NCC.{Figure 4}

Statistical analysis

Categorical variables were represented as proportions; continuous variables were represented as mean, standard deviations (SDs), median, and range.

General data

A total of 71 articles containing 148 individuals presenting MDs related to NCC were reported [Table 2] and [Table 3].[10],[15],[16],[17],[18],[19],[20],[21],[22],[23],[24],[25],[26],[27],[28],[29],[30],[31],[32],[33],[34],[35],[36],[37],[38],[39],[40],[41],[42],[43],[44],[45],[46],[47],[48],[49],[50],[51],[52],[53],[54],[55],[56],[57],[58],[59],[60],[61],[62],[63],[64],[65],[66],[67],[68],[69],[70],[71],[72],[73],[74],[75],[76],[77],[78],[79],[80],[81],[82],[83],[84] Between 1903 and 2020, there were 81 patients from South America, 36 from Asia, 12 from Europe, 12 from North America, and 7 from Africa. The MDs encountered were PKN, ataxia, chorea, dystonia, tremor, myokymia, myoclonus, ballism, tics, and other not clearly defined. The mean and median ages were 36.58 (SD: 20.51) and 35 years (age range: 1–88 years), respectively. There was a slight female predominance (52.17%). On follow-up, more than half of the individuals (58.90%) had a full recovery. In addition, two deaths were reported due to the severity of other diseases co-occurring with NCC.[22],[73]{Table 2}{Table 3}

Interestingly, individuals with PKN had a higher frequency of complications. Moreover, those patients with a poor outcome had other associated clinical manifestations such as seizure, intracranial hypertension (ICH), cognitive impairment, and a focal neurologic deficit.

Alarcón et al. in 2017 studied 23 individuals who developed MDs secondary to NCC.[10] They presented interesting conclusions, which changed many aspects of the current understanding of this infectious disease and abnormal movements. First, PKN was the most common MD in NCC, and was not related to the specific localization of the lesions. Second, individuals with chorea, dystonia, and tremor had a better prognosis than those who developed PKN. Third, chorea and dystonia were associated with specific lesions in the basal ganglia. It is worth mentioning that these characteristics were also found in our study and we will further discuss them in the following sections.

CHOREA – The first report

Pereira was probably the first to report a MD associated with tapeworm infection, published in 1903 on the “Clinical Notes” on “The Lancet.”[16] He described the case of a child who developed generalized chorea with a gastrointestinal infection, possibly taeniasis, without any heart involvement or a history of pharyngitis. After his publication, two other authors, Hodge in 1903 and Galbraith in 1904, reported similar cases.[15],[17] However, both patients had heart murmurs, which, in association with the chorea, could be the clinical manifestation of rheumatic fever caused by an autoimmune reaction to Group A β-hemolytic streptococci. Moreover, many drugs with unknown efficacy were attempted. Consequently, it is possible that these authors induced MDs in their patients, due to the use of substances that today are known to be extremely neurotoxic. Interestingly, Galbraith also wrote in 1903 that there was a distinct increase of chorea, which he correlated with the increased incidence of poliomyelitis at that time.[17]

Chorea, dystonia, and myoclonus affected a younger population when compared to the general data. Furthermore, chorea had the second-worst prognosis on follow-up because only about half of the patients had a full recovery. One death was reported by Bickerstaff in 1952.[22] He reported a patient with racemose NCC in which surgical excision of the lesion was tried, but she had extensive lesions in the arachnoid. The patient died of respiratory infections during hospitalization. Racemose NCC is characterized by the infection of the basal subarachnoid region. It is a relatively rare form of NCC with an appearance resembling “a collection of transient membranes forming a cluster like a bunch of grapes.”[85]

The cause of chorea in NCC could be explained by the mass effect, inflammation, hydrocephalus, or ischemia associated with the cysticerci. In this context, the majority of patients with neuroimaging showed at least one lesion localized in the basal ganglia region.[10] Another explanation for this involuntary movement could be an exacerbated immune response because many patients had alleviation of the symptoms when corticosteroids were started.[72],[82] In addition, others had ICH, and a ventriculoperitoneal shunt (VPS) was performed to alleviate the symptoms.[77] Vasculitis of the right middle cerebral artery was observed in one individual.[50] The presence of stenosis may lead to a change in the blood flow, and, due to this variable flux, abnormal movements can occur. This concept is supported by Echebarria, who studied patients with suspected NCC and established a correlation among the cerebral blood flow velocity and CSF pressure with the diagnostic criteria for NCC-associated MDs.[62]

One interesting fact is that in east Asian countries, the coinfection of NCC and Japanese encephalitis is being reported.[78] When these infections occur concomitantly, it is difficult to give a clear diagnosis of the main cause of the abnormal movements. We believe that specific features such as cystic lesions found in the basal ganglia associated with chorea are highly suggestive of chorea caused by NCC, as shown by this review and by Alarcón et al.[10]

PARKINSONISM – Diffuse brain inflammatory reactions?

Meyer (1906) and Felici (1938) were the first to associate PKN and cysticercosis; both studies contributed with the demonstration of postmortem microscopical analysis of the parasite.[22] Assis and Tenuto reported positive serum and CSF for cysticercosis in a patient with the association of PKN and ICH.[21]

The co-occurrence of PKN and ICH should be highlighted because almost half of the individuals reported in the literature [Table 2] with NCC and PKN had ICH. These clinical manifestations can be explained by the cerebral cysticercus causing edema or direct obstruction of the flow of the CSF, raising the intracranial pressure, and leading to the resting tremor and bradykinesia.[86] Cysts causing hydrocephalus have already been described in the fourth ventricle, perimesencephalic, meningeal, and brainstem areas. Alarcón et al. (2017) stated that PKN is not related to the specific localization of the lesions. This can be explained by the previously described hypothesis, even though the majority of the individuals reported by Alarcón et al. (2017) did not present any signs of ICH.

Besides ICH, other explanations based on the cysts' location appear to be insufficient, as it has been observed that NCC can affect distant brain regions from the cysticercus location. Therefore, maybe the assumption of Alarcón et al. (2017) that patients with PKN had more inflammation could explain these findings; in addition, different CSF protein levels in individuals with and without MDs further support this hypothesis. Moreover, perhaps the abnormal movements only occurred after a misleading inflammatory reaction caused by the parasite death and cystic degeneration.

Takayanagui and Jardim studied only individuals with NCC, in 1983, from their 238 patients, of which 2 developed PKN (0.40%);[26] in 1990, among 151 patients, only 1 developed PKN (0.66%).[32] Thus, the incidence of PKN in patients with NCC is probably rare, affecting <1% of the individuals. From another standpoint, it is often possible to observe these clinical manifestations in developing countries, where T. solium is more prevalent.[4] For example, Alarcón et al. (2017) assessed 590 individuals with NCC, among these, 23 patients (3.89%) presented PKN and others MDs.

Some individuals with PKN presented other less prominent or late-onset clinical manifestations, such as seizure, psychiatric symptoms, lower limb dystonia, blepharospasm, cognitive decline, ataxia, apraxia, and myokymia. Sharma et al. reported the interesting case of an individual with progressive supranuclear palsy syndrome and early cognitive decline.[68]

One common management was the VPS in the ICH cases, which not surprisingly alleviated the parkinsonian symptoms, possibly by the aforementioned mechanisms.[86] Prashantha et al. reported a case where only VPS and levodopa were attempted without any cysticidal drug, and the patient had a complete recovery.[60] In addition, some individuals presented levodopa-responsive PKN. In the case of Sá et al., the prescription of albendazole led to the alleviation of symptoms, and later reduction of the levodopa dose.[48] On the other hand, Lima et al. reported a case where albendazole worsened PKN symptoms.[69] Probably, the cysticidal drug would have caused an intense inflammatory reaction, which may be more commonly observed in forms involving intraventricular cysts and ependymitis/encephalitis.[87]

 MYOCLONUS – Cysticidal drugs should be tried

Only four cases of myoclonus (MCL) and NCC were found in the literature, so there is scarce clinical information about this involuntary movement. The MCL types were palatal, oculopalatal, and multifocal. No specific cystic location in the neuroimaging was associated with MCL; also, each article found lesions in a different location. The cysts were found in the dentate nucleus, meninges, pons, and frontal gyrus.

The source of MCL was subcortical in 75% of individuals. This feature was interesting because when compared with drug-induced MDs that specifically affect determined neurotransmitters, a microscopical lesion would theoretically lead to abnormalities in electrodiagnostic studies.[88] However, only the study of Puri et al. revealed an electroencephalogram with the presence of generalized synchronous as well as the asynchronous, nonperiodic paroxysmal discharge of polyspike, spike, and sharp waves with well-modulated alpha background activity.[33]

In one individual, cysticidal drugs were not attempted. It is noteworthy that he was the only that did not have a complete recovery.

 Dystonia – Maybe it is a vascular mechanism

Jiménez-Jiménez et al. reported the first case of NCC and dystonia (DTN); unfortunately, neuroimaging was only performed years after the first presentation, which may cast doubt on the possibility of the etiological diagnosis.[34] The DTN types reported in the literature were focal (blepharospasm, cervical, scalp, and writer's cramp), segmental (Meige syndrome), and hemidystonia.

More than 70% of the patients had at least one lesion localized in the basal ganglia region. Other areas affected were the thalamus, cortical and subcortical regions of the frontal lobe, parietal lobe, and temporal lobe.

All the patients that had a full recovery received cysticidal medication (albendazole or praziquantel). In 2016, Yoganathan et al. reported the case of an individual who developed Meige syndrome and PKN with a Japanese encephalitis and NCC coinfection.[78] This case reaffirms what was previously stated that the presence of specific features of NCC should always be searched in these patients, as we already exemplified in chorea cases.

Alarcón et al. (2017) proposed that DTN and chorea may be due to vascular mechanisms, which involve the perforating branches of the middle cerebral artery, leading to cerebral ischemia, blood–brain barrier damage, and increased levels of excitatory neurotransmitters, as already observed in altered glycemic states.[89] This hypothesis could partially explain the fact that the majority of the DTN and chorea cases had small cystic lesions, without edema or distortion of adjacent structures by pressure. Nevertheless, this does not explain why some individuals had unspecific localized lesions or active cysts localized in the basal ganglia.[45]

Myokymia (MKM)– Exceptionally highly reported

Myokymia (MKM) is an abnormal movement uncommonly reported with systemic diseases. However, from the group of systemic diseases, NCC seems to be the most commonly associated with MKM. In a review by Alarcón and Giménez-Roldán about MDs and systemic diseases, they only found reports of MKM related to NCC.[90]

Yang et al. described a case of hemifacial spasm secondary to arachnoiditis due to a cyst in the cerebellopontine angle, in which the cysticercus was removed and the facial nerve was liberated with complete recovery of the symptoms.[84] This case was probably the first to show neurosurgical intervention in MKM associated with NCC. The cases reported by Revuelta Gutierrez et al. and Razdan et al. of MKM caused by subarachnoid NCC were both treated by a course of corticosteroids.[41],[64] The MKM had the second-best prognosis, where > 80% of the patients had a full recovery. However, it is worth mentioning that only six cases were found investigating the literature.

Keane in 1993 reported the case of a young adult male who presented with facial spasms accompanied by pretectal signs, and neuroimaging revealed obstructive hydrocephalus.[36] A VPS was performed with complete resolution of the symptoms. After about 3 years, the patient presented with similar symptoms, and the VPS was revised; after 1 month, he had a full recovery. Beydoun in 1994 reported a similar case presentation, but VPS was not performed and the patient did not have a full recovery.[37]


In sum, MDs associated with NCC already reported in the literature were PKN, ataxia, chorea, dystonia, tremor, myokymia, myoclonus, ballism, and tics. More than half of the individuals were from South American countries and about 25% from Asian countries. The most common MD reported was PKN. In addition, individuals who developed PKN had the worst prognosis of any other MD associated with NCC, except for ballism and tics, each with one case reported in the literature. Generally, individuals with chorea and dystonia have more specifically localized lesions. Due to the rarity of the clinical manifestations presented in this review, it is worth mentioning that case reports were included in the study. Because of this, an important limitation of the study is that it is not a systematic review. We believe that the majority of the cases presented in the literature were only reported because patients had classical clinical manifestations that prompted neuroimaging investigation, which was suggestive of NCC, and later supported by laboratory examinations. Therefore, the association between NCC and MD is probably underreported. Clinicians should be highly suspicious of this association, mainly in endemic areas for cysticercosis.

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Conflicts of interest

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1Singh G, Sander JW. Historical perspective: The British contribution to the understanding of neurocysticercosis. J Hist Neurosci 2019;28:332-44.
2World Health Organization. Taeniasis and Cysticercosis. World Health Organization. Available from: https://wwwwhoint/health-topics/taeniasis-and-cysticercosis#tab=tab_12020. [Last accessed on 2020 Sep 24].
3Prevention CfDCa. Cysticercosis, Biology; 2020. Available from: https://wwwcdcgov/parasites/cysticercosis/biologyhtml. [Last accessed on 2020 Sep 24].
4Lesh EJ, Brady MF. Tapeworm (Taenia solium, Taenia saginata, Diphyllobothrium, Cysticercosis, Neurocysticercosis), StatPearls. Treasure Island (FL): StatPearls Publishing; 2020. Available from: https://wwwncbinlmnihgov/books/NBK537154/. [Last updated on 2020 Aug 10].
5de Lange A, Mahanty S, Raimondo JV. Model systems for investigating disease processes in neurocysticercosis. Parasitology 2019;146:553-62.
6Estrada SS, Verzelli LF, Montilva SS, Acosta CA, Cañellas AR. Imaging findings in neurocysticercosis. Radiologia. 2013;55:130-41.
7Rodríguez Carnero P, Hernández Mateo P, Martín-Garre S, García Pérez à, Del Campo L. Unexpected hosts: Imaging parasitic diseases. Insights Imaging 2017;8:101-25.
8Rissardo JP, Caprara AL. Neurosyphilis-associated movement disorder: A literature review. Ann Mov Disord 2020;3:129-44.
9Caprara AL, Rissardo JP, Leite MT, Silveira JO, Jauris PG, Arend J, et al. Course and prognosis of adult-onset epilepsy in brazil: A cohort study. Epilepsy Behav 2020;105:106969.
10Alarcón F, Cedeño Y, de Yébenes JG. Parkinsonism and other movement disorders in 23 cases of neurocysticercosis. Parkinsonism Relat Disord 2017;42:47-53.
11Del Brutto OH, Nash TE, White AC Jr., Rajshekhar V, Wilkins PP, Singh G, et al. Revised diagnostic criteria for neurocysticercosis. J Neurol Sci 2017;372:202-10.
12Jankovic J, Tolosa E. Parkinson's Disease and Movement Disorders. 5th ed. Philadelphia: Lippincott Williams & Wilkins; 2006.
13De Vries E, Schoonvelde M, Schumacher G. No longer lost in translation: Evidence that Google Translate works for comparative bag-of-words text applications. Polit Anal 2018;26:417-30.
14Rissardo JP, Caprara AL. Bupropion-associated movement disorders: A systematic review. Ann Mov Disord 2020;3:86-98.
15Hodge RD. Tapeworm as a cause of chorea. Lancet 1903;162:1232-3.
16Pereira JA. Tapeworm as a cause of chorea. Lancet 1903;162:824.
17Galbraith HT. Tapeworm as a cause of chorea. Lancet 1904;163:1348.
18Broughton-Alcock W, Stevenson WE, Worster-Drought C. Cysticercosis of the brain: with report of a case. Br Med J 1928;2:980-2.
19Dixon HB, Smithers DW. Cysticercosis (Taenia solium). J R Army Med Corps 1935;2:91-8.
20Brotto W. Neurological aspects of cysticercosis. Arq Neuropsiquiatr 1947;5:258-94.
21Assis J, Tenuto RA. Intraventricular racemic cysticercus. Surgical excision. Arq Neuropsiquiatr 1948;6:247-53.
22Bickerstaff ER, Cloake PC, Hughes B, Smith WT. The racemose form of cerebral cysticercosis. Brain 1952;75:1-8.
23DE Assis JL, DE Campos EP, Franca LC. Parkinsonian syndrome in cerebral cysticercosis; anatomo-clinical study of a case. Arq Neuropsiquiatr 1955;13:44-9.
24Bickerstaff ER. Cerebral cysticercosis: Common but unfamiliar manifestations. Br Med J 1955;1:1055-8.
25Ronge J, Aidoo GA, Krüger G. Cysticercosis of the brain. Fortschr Neurol Psychiatr ihrer Grenzgebiete 1978;46:269-86.
26Takayanagui OM, Jardim E. Clinical aspects of neurocysticercosis: Analysis of 500 cases. Arq Neuropsiquiatr 1983;41:50-63.
27Cavalcanti CE. Calcified cysticerci in basal ganglia and Parkinson's syndrome: A case report. Arq Neuropsiquiatr 1984;42:183-6.
28Wie BA. Palatal myoclonus associated with cerebral cysticercosis. J Korean Neurol Assoc 1986;4:156-8.
29Bhigjee AI, Kemp T, Cosnett JE. Cerebral cysticercosis presenting with hemichorea. J Neurol Neurosurg Psychiatry 1987;50:1561-2.
30Barinagarementeria F, Del Brutto OH, Otero E. Ataxic hemiparesis from cysticercosis. Arch Neurol 988;45:246.
31Joubert J, Jenni WK. Treatment of neurocysticercosis. South African Med J 1990;77:27-30.
32Takayanagui OM. Neurocysticercosis: I. Clinical and laboratory evolution of 151 cases. Arq Neuro Psiquiatria 1990;48:1-10.
33Puri V, Chowdhury V, Gulati P. Myoclonus: A manifestation of neurocysticercosis. Postgrad Med J 1991;67:68-9.
34Jiménez-Jiménez FJ, Molina-Arjona JA, Roldán-Montaud A, Agullá A, Santos J, Fernández-Ballesteros A, et al. Blepharospasm associated with neurocysticercosis. Acta Neurol (Napoli) 1992;14:56-9.
35Tansanee P. Neurocysticercosis presenting with Parkinsonism: A case report. Bull Dep Med Serv 1992;17:565-9.
36Keane JR. Cysticercosis: Unusual neuro-ophthalmologic signs. J Clin Neuroophthalmol 1993;13:194-9.
37Beydoun SR. Facial myokymia secondary to neurocysticercosis. Muscle Nerve 1994;17:1060-1.
38Keane JR. Tremor as the result of shunt obstruction: Four patients with cysticercosis and secondary parkinsonism: Report of four cases. Neurosurgery 1995;37:520-2.
39Verma A, Berger JR, Bowen BC, Sanchez-Ramos J. Reversible parkinsonian syndrome complicating cysticercus midbrain encephalitis. Mov Disord 1995;10:215-9.
40Singh UK, Sinha R, Suman S. An unsteady 12-year-old. Lancet 1996;347:1158.
41Revuelta Gutierrez R, Soto-Hernández JL, Suastegui-Roman R, Ramos-Peek J. Transient hemifacial spasm associated with subarachnoid brainstem cysticercosis: A case report. Neurosurg Rev 1998;21:167-70.
42Sawhney IM, Singh G, Lekhra OP, Mathuriya SN, Parihar PS, Prabhakar S, et al. Uncommon presentations of neurocysticercosis. J Neurol Sci 1998;154:94-100.
43Serrano-Dueñas M, Placencia M. Abnormal involuntary movements and hydrocephalus. Rev Ecuat Neurol 1999;8:42-6.
44Mathew I, Hassan KM. Neurocysticercosis presenting as reversible parkinsonian syndrome. J Assoc Physicians India 2001;49:288-9.
45Cosentino C, Velez M, Torres L, Garcia HH, Cysticercosis Working Group in Perú. Cysticercosis lesions in basal ganglia are common but clinically silent. Clin Neurol Neurosurg 2002;104:57-60.
46Frei K, Truong D. P931: Dystonia of the scalp secondary to cysticercosis. Movement Disorders 2002;17:284-5.
47Alárcon F. Movement disorders in neurocysticercosis: report of 15 patients. In: Willow, Marianne J, editor, Parkinson's Disease: New Research New York: Nova Science Publishers; 2005.
48Sá DS, Teive HA, Troiano AR, Werneck LC. Parkinsonism associated with neurocysticercosis. Parkinsonism & related disorders 2005;11:69-72.
49Scott JX, Devi A, Kumar TS, Moses PD. A rare presentation of neurocysticercosis in a young child. J Trop Pediatr 2005;51:254-5.
50Bouldin A, Pinter JD. Resolution of arterial stenosis in a patient with periarterial neurocysticercosis treated with oral prednisone. J Child Neurol 2006;21:1064-7.
51Cosentino C, Vélez M, Torres L, Garcia HH. Neurocysticercosis-induced hemichorea. Movement Disorders 2006;21:286-7.
52Jha S, Kumar R, Kumar R. Clinical pleomorphism of neurocysticercosis in children: Some unusual manifestations. J Pediatric Neurol 2006;4:103-9.
53Patel R, Jha S, Yadav RK. Pleomorphism of the clinical manifestations of neurocysticercosis. Trans R Soc Trop Med Hyg 2006;100:134-41.
54Suwatcharangkoon S, Boonkongchuen P, Pulkes T. P702: Tropical CNS infection and parkinsonism. Movement Disorders 2006;21:519.
55Verma R, Agarwal A, Kar AM. Hemichorea resulting from single enhancing computed tomography lesion. J Assoc Physicians India 2006;54:735-7.
56Hamed SA, El-Metaal HE. Unusual presentations of neurocysticercosis. Acta Neurol Scand 2007;115:192-8.
57Bhatia R, Desai S, Garg A, Padma MV, Prasad K, Tripathi M, et al. Isolated facial myokymia as a presenting feature of pontine neurocysticercosis. Mov Disord 2008;23:135-7.
58Garcia Ruiz PJ, Cabo I, Garcia Bermejo P, Ayerbe J. 788: DOPA-responsive parkinsonism and blepharospasm secondary to neurocysticercosis. Movement Disorders 2008;23:258.
59López IC, Bermejo PG, Espiga PJ, Tapia DQ. L-dopa sensitive parkinsonism in neurocysticercosis. Neurologia 2008;23:119-21.
60Prashantha DK, Netravathi M, Ravishankar S, Panda S, Pal PK. Reversible parkinsonism following ventriculoperitoneal shunt in a patient with obstructive hydrocephalus secondary to intraventricular neurocysticercosis. Clin Neurol Neurosurg 2008;110:718-21.
61Teive HA, Funke V, Bitencourt MA, de Oliveira MM, Bonfim C, Zanis-Neto J, et al. Neurological complications of hematopoietic stem cell transplantation (HSCT): A retrospective study in a HSCT center in brazil. Arq Neuropsiquiatr 2008;66:685-90.
62Echebarria S. Mo-424: Neurocysticercosis, cerebral blood flow velocity (CBFV) and CSF-related movement disorders. Movement Disorders 2009;24:403-4.
63Munhoz R, Famelli H, Teive HA, Werneck LC. We-287: Infectious causes of parkinsonism. Movement Disorders 2009;24:182.
64Razdan S, Pandita KK, Pandita S. Reversible hemifacial spasm due to neurocysticercosis. Ann Indian Acad Neurol 2009;12:191-2.
65Balaji J, D M. Clinical and radiological profile of neurocysticercosis in South Indian children. Indian J Pediatr 2011;78:1019-20.
66Dewan P, Kaushik JS, Gomber S, Gupta A. Uncommon presentation of neuro-cysticercosis. South Afr J Child Health 2011;5:58-9.
67Karnik PS, Tullu MS, David JJ, Ghildiyal RG. Neurocysticercosis-induced hemiballismus in a child. J Child Neurol 2011;26:904-6.
68Sharma P, Garg RK, Somvanshi DS, Malhotra HS. Progressive supranuclear palsy like syndrome: Neurocysticercosis an unusual cause. Neurol India 2011;59:484-5.
69Lima PM, Munhoz RP, Teive HA. Reversible parkinsonism associated with neurocysticercosis. Arq Neuropsiquiatr 2012;70:965-6.
70Teive HA. A 38-Year-old Brazilian woman presenting with reversible parkinsonism associated with neurocysticercosis. Movement disorders 2012;2:57-9.
71Sarangi R, Sahoo S, Mohapatra S. Neurocysticercosis masquerading psychotic disorder: A case report. J Acute Dis 2013;2:79-81.
72Venkatarathnamma PN, Chandra Shekara MN, Srinivasa SV, Basavaih J. Phenytoin induced cerebellar ataxia and orofacial dyskinesia in a case of disseminated cysticercosis: A case report. Int J Clin Pharmacol Toxicol 2013;2:102-5.
73Verma R, Anand KS, Sharma BB, Garg J. Neurocysticercosis presenting as parkinsonism. Neurology India 2013;61:656-7.
74Gokhale AA, Tullu MS, Agrawal M, Gavali VS. Neurocysticercosis presenting as myoclonus: A rare manifestation. Indian J Trauma Emerg Pediatrics 2015;7:15-7.
75Sharma K, Chaudhary KP, Gupta RK. Unusual case of orbital neurocysticercosis involving lateral rectus, cerebellum and brain stem. Del Ophthalmol 2015;25:209-11.
76Singh G, Vikhe VB, Chaudhari H. Neurocysticercosis presenting as Hemiplegia: A rare case report. International J Interdiscip Multidiscip Studies 2015;2:20-2.
77Costa PS, Santiago IG, Lima WR, Santos CS, Rocha AV, Fortes PM. Racemose neurocysticercosis: A cluster of bad grapes. Int J Infect Dis 2016;48:5-6.
78Yoganathan S, Sudhakar SV, Thomas MM, Yadav VK. A tropical menace of co-infection of Japanese encephalitis and neurocysticercosis in two children. J Pediatr Neurosci 2016;11:140-4.
79Campos EM, Raslau FD, Salinas R, Di Capua D, Slevin JT, Villamar MF. Reversible manifestations of extraparenchymal neurocysticercosis. Clin Case Rep 2018;6:1400-1.
80Gupta S, Bhattad S, Khwaja GA. IP7/320: Lower limb monochorea as an unusual manifestation of motor cortex neurocysticercosis. Ann Indian Acad Neurol 2019;22:45-157.
81Anjana KK, Suresh VC, Poornima C, Madhuvan HS. An unusual presentation of neurocysticercosis as psychosis with tics. Arch Ment Health 2020;21:55-8.
82Kumar S, Garikapati A, Yarappa R, Chaturvedi S, Gupta A. Neurocysticercosis presenting as hemichorea: a case report. Asian J Gerontol Geriatr 2020;15:1-2.
83Oliveira SC, Monteiro DA, Silva GF, Santos LT, Ribeiro EM. Parkinsonism secondary to hydrocephalus caused by neurocysticercosis. Cureus 2020;12:e7887.
84Yang SY, Vásquez CM; Cysticercosis Working Group in Perú. Hemifacial spasm secondary to arachnoiditis due to neurocysticercosis: Clinical image. World Neurosurg 2020;143:180-2.
85Wiwanitkit S, Wiwanitkit V. Racemose cysticercosis: A summary of 5 reported Thai cases. J Neurosci Rural Pract 2015;6:451.
86Curran T, Lang AE. Parkinsonian syndromes associated with hydrocephalus: Case reports, a review of the literature, and pathophysiological hypotheses. Movement Disorders 1994;9:508-20.
87García HH, Evans CA, Nash TE, Takayanagui OM, White AC Jr. Botero D, et al. Current consensus guidelines for treatment of neurocysticercosis. Clin Microbiol Rev 2002;15:747-56.
88Rissardo JP, Caprara AL. Pregabalin-associated movement disorders: A literature review. Brain Circ 2020;6:96-106.
89Rissardo JP, Caprara AL. Movement disorders associated with hypoglycemia and hyperglycemia. Ann Mov Disord 2020;3:118-20.
90Alarcón F, Giménez-Roldán S. Systemic diseases that cause movement disorders. Parkinsonism Relat Disord 2005;11:1-8.