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Table of Contents
REVIEW ARTICLE
Year : 2021  |  Volume : 4  |  Issue : 2  |  Page : 51-59

Chorea associated with infections: A narrative review


1 Department of Neurology, Shree Krishna Hospital and Pramukhswami Medical College, Bhaikaka University, Karamsad, Anand, Gujarat, India
2 Apollo Hospital, Greams Road, Chennai, Tamil Nadu, India

Date of Submission30-Mar-2021
Date of Decision20-Jun-2021
Date of Acceptance28-Jun-2021
Date of Web Publication30-Aug-2021

Correspondence Address:
Dr. Soaham Desai
Department of Neurology, Shree Krishna Hospital and Pramukhswami Medical College, Bhaikaka University, Karamsad, Anand, Gujarat.
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/AOMD.AOMD_12_21

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  Abstract 

In tropical countries like India, infections of the central nervous system (CNS) and their varied complications are often encountered. Movement disorders (MDs) are reported to be a complication of infectious diseases, and the spectrum of MDs differs in tropical countries from other developed countries. We screened three electronic databases to search for cases of chorea as a presenting feature of infections, collected cases, and series describing chorea associated with infections. The studies were identified later and data were extracted regarding study design, sample size, neurological assessment, and diagnostic workup including brain imaging and cerebrospinal fluid analysis. After a detailed review of 283 different articles in the selection, a total of 33 articles were included in the final manuscript. In this narrative review, we review the important contributions in the field of chorea related to infections and discuss the salient features of infections of the CNS which can present with chorea. The infections presenting with chorea include streptococcal infections, tuberculosis, neurosyphilis, Japanese encephalitis, herpes simplex encephalitis, and neurocysticercosis. The hypothesized mechanisms of infection-related dystonia are vasculopathy, space-occupying lesions, autoimmune reaction, and inflammation. Although chorea is considered to be a result of heredodegenerative, metabolic, or autoimmune disorders lesions, infections may also present with chorea, especially in tropical and developing countries.

Keywords: Chorea, infection, Sydenham chorea, tuberculosis


How to cite this article:
Yadav R, Vijay S, Desai S. Chorea associated with infections: A narrative review. Ann Mov Disord 2021;4:51-9

How to cite this URL:
Yadav R, Vijay S, Desai S. Chorea associated with infections: A narrative review. Ann Mov Disord [serial online] 2021 [cited 2021 Dec 1];4:51-9. Available from: https://www.aomd.in/text.asp?2021/4/2/51/324801




  Introduction Top


The common tropical infections such as tuberculosis, streptococcal infections, neurosyphilis, neurocysticercosis (NCC), and other infections are relatively rare in western countries. These infections can present with primary or secondary central nervous system (CNS) involvement. CNS involvement can have varied manifestations including encephalopathy, meningoencephalitis, headache, seizures, stroke, and rarely movement disorders (MD). CNS involvement by various infections may result in MDs. Infection-related MD can be hypokinetic ( Parkinsonism More Details) or hyperkinetic (tremors/chorea/dystonia/myoclonus). The pathophysiology of infection-related MD may be due to direct infection-related lesion or inflammation of various structures such as cortex/basal ganglia/brain stem/cerebellum/spinal cord secondary to vascular insult, autoimmune response, or related to drug therapy for the treatment of infection. Infection-associated chorea is generally described more in tropical countries.

The word chorea is derived from the Greek word meaning dance. Chorea is an MD that results from the continuous and unpredictable, random flow of muscle contractions leading to a dance-like appearance.[1] In the milder form, chorea appears like restlessness and the patient often tries to disguise the movements by converting them into semi-purposeful activity. In severe form, it causes continuous flow-like disabling and violent movements. Ballism is a variant of chorea characterized by large-amplitude flinging movements involving the proximal extremities. The key phenomenological feature of chorea to identify is the “randomness” in movements. The involuntary movements in chorea flit from one body region in an unpredictable manner. Chorea can affect various parts of the body and thus may cause difficulty with speech, swallowing, or gait. It disappears in sleep. Chorea is usually classified as primary (idiopathic, hereditary) or secondary (acquired).[2] Primary chorea disorder is usually insidious in onset, gradually progressive, and bilateral, whereas secondary chorea disorder is usually acute or subacute in onset and unilateral. There is lack of information on different infections which can present with chorea. We aim to assess infection-associated chorea in this narrative review. Sydenham’s chorea (SC) is the most common cause of childhood chorea in India, whereas Huntington’s disease and drug-induced chorea are common in adults.


  Methodology Top


This article is a narrative review study and an attempt to highlight the infections associated with chorea. According to its nature as a “narrative review,” we did not graduate the articles, but we chose the most relevant contributions to the matter of this rare presentation of infection-associated dystonia. A literature search was independently conducted by two reviewers and reviewed all the cases reporting chorea in patients with proven CNS infections. We have followed Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines and searched three comprehensive electronic medical literature databases (PubMed, Embase, and Google Scholar) for articles on infection-associated dystonia from January 1, 1985. The literature search strategy was developed using a combination of Medical Subject Heading (MeSH) terms and keywords. The search strings were as follows: chorea, infection, virus, encephalitis, tuberculosis, streptococcus, mycoplasma, Japanese B encephalitis, varicella, SSPE, HIV, AIDS, malaria, NCC, dengue, and Whipple’s disease. We have also hand‐searched the reference lists of all the articles identified in the electronic search using common search engines (e.g., Google) to include further other studies or reports not identified by the search. Ethical approval was not required for this study. The search yielded studies reporting chorea among patients with different CNS infections. The studies were identified after a detailed search, and data were extracted regarding study design, sample size, neurological assessment, and diagnostic workup including brain imaging and cerebrospinal fluid (CSF) analysis. After a detailed review of 283 different articles in the selection, removing articles in non-English language, articles with incomplete details or contentious or analogous descriptions, a total of 33 articles were included in the final manuscript [Figure 1]. We shall discuss each of the infections (bacterial, viral, parasitic, and others) separately in this narrative review. [Table 1] enlists various infections that may present with MDs. [Table 2] enlists various infections which have been described to be present with chorea. [Table 3] enlists and describes the important diagnostic clues, mechanism of chorea, and treatment in different infections presenting with chorea.
Figure 1: Flowchart depicting search strategy for review of chorea associated with infections

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Table 1: Infections which can present with MDs

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Table 2: Infections causing chorea

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Table 3: Synopsis of different infection-associated choreas

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A. Bacterial infections and chorea

1. Streptococcal infection and chorea

SC is the commonest MD of childhood occurring between 5 and 15 years of age.[3] It is a well-characterized manifestation of acute rheumatic fever (RF), caused by an aberrant immune response to group A beta-hemolytic streptococci (GABHS). It is a relatively late complication of acute RF, occurring later than other complications such as carditis and arthritis. It usually occurs 4–8 weeks after streptococcal pharyngitis. The symptoms include insidious or abrupt onset of abnormal choreiform movements which usually affect all four limbs but may be more prominent on one side.[4] Hemichorea occurs in one quarter of patients. Other features of SC include tics, dysarthria, hypotonia, muscular weakness, hypometric saccades, and behavioral and neuropsychiatric abnormalities.[4] Some of the patients may develop severe hypotonia and may become bedridden, which is called “chorea paralytica.”[4] SC is a self-limiting condition with recovery occurring usually within few months. Pediatric autoimmune neuropsychiatric disorders associated with streptococcal infections (PANDAS) are another condition that presents with neuropsychiatric symptoms 7–14 days after streptococcal infection, but is distinct from SC. Patients with PANDAS may have tics that need to be differentiated from chorea. The absence of echocardiographic abnormalities, chorea, and RF helps differentiate SC from PANDAS.[5]

Pathophysiology of SC is believed to be due to molecular mimicry, i.e., antibodies against GABHS cross react with basal ganglia cells. Antibodies in SC activate calcium calmodulin-dependent protein kinase-II, which causes elevation of tyrosine hydroxylase level and release of dopamine. Antibodies have been identified against dopamine receptors D1 and D2 by enzyme-linked immunosorbent assay in patients of SC.[4] Magnetic resonance imaging (MRI) brain can be normal or may show hyperintensities on T2-weighted imaging (T2WI) in focal regions such as caudate nucleus and putamen. Positron emission tomography (PET) and single photon emission computed tomography (SPECT) imaging have been reported showing hypermetabolism and hyperperfusion in the basal ganglia region.[4]

Treatment of SC includes antibiotics therapy and symptomatic treatment with dopamine antagonists and/or anti-epileptics, with immunomodulatory therapy.[4] Antibiotic penicillin is first-line therapy for SC and is also known to be effective in reducing the frequency of RF and SC recurrences. Neuroleptic drugs such as dopamine antagonists are used for the treatment of chorea. Haloperidol 1–3 mg/day or olanzapine 5–10 mg/day have shown benefits in treating SC. A study suggests tetrabenazine in the dose of 25 mg twice or thrice daily to be effective in the treatment of SC.[6] Anti-epileptic drugs such as valproate and carbamazepine are effective in SC. In a comparison study of valproate, carbamazepine, and haloperidol, six patients of SC were in each group. The trial showed improvement in all six patients with valproate, five of six patients with carbamazepine, and only three of six patients with haloperidol. Thus, valproate was recommended as first choice of therapy for SC.[7] In the head-to-head comparison of carbamazepine and valproate for SC, CBZ (15 mg/kg/day) was seen to be equally effective as valproate (20–25 mg/kg/day).[8] Immunomodulator therapy is recommended in moderate-to-severe chorea and it appears to shorten the disease course. A study of oral steroid therapy (prednisone 2 mg/kg/day for 4 weeks followed by gradual discontinuation) and another study of injectable pulse followed by oral steroid therapy (intravenous methylprednisolone 25 mg/kg/day for 5 days followed by oral prednisolone tapering therapy starting at 1 mg/kg/day) showed benefits in SC with steroids. Plasma exchange (PE) and intravenous immunoglobulin (IVIG) have shown improvement in patients with severe SC. In one study comparing IVIG, PE, and oral prednisone, a reduction in the severity of chorea at 1 month in each group was IVIG 72%, plasmapheresis 50%, and oral prednisone 29%, respectively. Thus, the study suggested that IVIG therapy may hasten the recovery.

2. Tuberculosis and chorea

In India, Mycobacterium tuberculosis is one of the most common organisms responsible for CNS infection. MD has been described to occur in nearly 18% of patients of tuberculous meningitis (TBM). MDs in patients with TBM may be related to ischemic vascular lesion, hydrocephalus, direct effect of bacterial toxin, or tuberculoma-related structural dysfunction. Ischemic vascular insults present with hemiparesis or dystonia, and hydrocephalus presents with gait dysfunction, executive dysfunction, headache, and cranial nerve palsy. Tuberculosis-related chorea usually manifests as hemichorea and is often associated with tuberculoma involving the contralateral basal ganglia region; however, generalized chorea has also been described. In a study of 180 patients of TBM, 7 patients had chorea, out of which 4 had generalized chorea whereas 3 had hemichorea. Vascular lesions of deeper structures were more common among patients with MD in that study.[9] In a study evaluating manifestations of CNS tuberculomas, 16 out of 49 patients of tuberculoma had MD (chorea-7, tremor-5, dystonia-3, and myoclonus-1). The most common location of tuberculoma was supratentorial, and the basal ganglia tuberculoma was associated with MD. One patient with chorea expired during the follow-up period, whereas all other patients recovered after the full course of anti-tubercular therapy ATT. Kalita et al.[10] from India presented a patient with left-sided hemichorea due to right-sided striatal tuberculoma. There was an improvement in chorea following 1 week of ATT and steroid therapy and got completely relieved at 3 months. Thus, chorea is an uncommon form of MD in patients with CNS tuberculosis. MD due to CNS tuberculosis commonly responds to ATT and steroid treatment.

3. Syphilis and chorea

Syphilis is caused by Treponema pallidum. Syphilis is no longer a common disorder but is still a significant health problem, particularly in developing countries. Neurosyphilis may occur in up to 9% of patients with untreated syphilis. Few cases of neurosyphilis presenting with MD have been reported.[11],[12],[13] Most patients with basal ganglia involvement in neurosyphilis have been associated with HIV infection.

Parkinsonism, tremors, laryngeal dystonia, ataxia, and myoclonus are other MDs reported in patients with neurosyphilis. The mechanism of MD in neurosyphilis may be due to small or large vessel vasculitis-induced infarction or due to inflammation because of direct parenchymal spread.[14] MD and basal ganglia lesion in neurosyphilis patients are commonly associated with HIV infection. But chorea without basal ganglia lesion on MRI may be present in patients with neurosyphilis without HIV infection. Thus, it can be concluded that in a patient having chorea, normal MRI with positive CSF examination and serological test for syphilis are essential to rule out a rare reversible disorder. Neurosyphilis is treated by intravenous penicillin or ceftriaxone for 2–4 weeks (in patients who are hypersensitive to penicillin). Lumbar puncture should be performed at 3–6 months after treatment and every 6 months thereafter until the CSF white blood cell count is normal and the CSF-Venereal Disease Research Laboratory (VDRL) is nonreactive. If the CSF white blood cell count does not decrease 6 months after therapy or the CSF-VDRL does not decline four-fold (or becomes nonreactive if the initial titer is <1:2) after 1 year of therapy, retreatment would be required. In addition, retreatment would also be required if there is an increase in the CSF white blood cell count, or a four-fold increase in CSF-VDRL titer, in any follow-up CSF sample. If repeat lumbar puncture is not feasible, normalization of the serum RPR titer may be used as a surrogate for the success of neurosyphilis treatment.

4. Lyme disease and chorea

Lyme neuroborreliosis is caused by spirochete Borrelia burgdorferi (BB). Many patients present with Bannwarth syndrome, which is characterized by painful lymphocytic meningo-radiculitis with or without paresis.[15] Extrapyramidal symptoms are seen in <2% of patients in Lyme disease. Though MDs are rare in Lyme disease, chorea and ataxia have been described as a symptom of Lyme disease. Piccolo et al.[16] in 1998 described a case of Lyme disease having widespread chorea and behavioral disturbances. Hansen and Lebech[17] studied 187 patients with neuroborreliosis over 6 years from 1985 to 1990. CNS involvement in early neuroborreliosis was rare (seen in 4%). Diagnosis of Lyme disease is based on inflammatory CSF with positive anti-BB antibodies. High-dose intravenous penicillin resulted in the normalization of clinical features and CSF picture in 91% of the patients.

Chorea may be a rare symptom of neuroborreliosis. CSF in neuroborreliosis usually shows lymphocytic pleocytosis and positive for IgM or IgG antibodies against Borrelia burgdorferi.[18] MRI features in neuroborreliosis are nonspecific, may be normal, or may show cerebral white matter hyperintense foci on T2WI, nerve root, or meningeal enhancement. MD in neuroborreliosis responds to antibiotic therapy for Lyme disease.

B. Viral infections and chorea

1. Human immunodeficiency virus (HIV) and chorea

HIV infection results in an immune deficiency in patients making them highly susceptible to opportunistic infections. Infections such as toxoplasmosis, cryptococcosis, and tuberculosis are commonly associated with HIV. They can cause lesions involving basal ganglia, diencephalon, and brain stem structures resulting in MD.[18] Many studies have reported chorea in patients with acquired immunodeficiency syndrome (AIDS). In one of the older studies, Rosso et al.[18] in Brazil reviewed 2460 HIV patients admitted between 1986 and 1999. Out of these patients, 28 (2.7%) patients had MD; among whom 6 (21.4%) had hemichorea/hemiballismus, 14 (50%) had parkinsonism, 4 (14.2%) had myoclonus, 2 (7.2%) had painful legs moving toes, 1 (3.6%) had hemidystonia, and 1 (3.6%) had Holmes tremor.[19] All the patients with hemichorea/hemiballismus in this study were found to be due to toxoplasmosis of CNS. In the study by Piccolo et al. in 1999, a retrospective analysis of five patients with AIDS, chorea was caused by toxoplasmosis, progressive multifocal leukoencephalopathy (PML), herpes simplex encephalitis (HSE), and probably due to iatrogenic cause.[20] Chorea was resolved with pyrimethamine-sulfamethopyrazine treatment in patients with toxoplasmosis and zidovudine with HIV encephalitis. Hemichorea/hemiballismus in HIV patients is highly suggestive of CNS toxoplasmosis according to some experts.[20] In CNS toxoplasmosis, toxoplasma IgG is found to be positive and usually, CD4 counts are reduced below 100/µL. MRI may show typical ring-enhancing lesions at parietal/frontal lobes, thalamus, basal ganglia, and CM junction.[20] In HIV patients with MRI brain showing ring-enhancing lesions, toxoplasma and CNS lymphoma are the common differentials to be considered in developed countries, whereas in tropical countries, tuberculosis also is to be considered. Ancillary imaging studies such as thallium 201 SPECT, perfusion MRI, MRI spectroscopy, and PET scan have been suggested to help in differentiating between toxoplasma and CNS lymphoma; but they have limited sensitivity and specificity. Similarly, CSF study with cytology for lymphoma also has limited sensitivity. A trial of empiric therapy for possible toxoplasma may be considered as an alternative to brain biopsy in certain toxoplasma-seropositive patients with characteristic radiographic findings. In patients who do not show regression in repeat imaging after toxoplasma treatment, stereotactic brain biopsy is important for final diagnosis. The treatment of CNS toxoplasmosis is done with sulfadiazine, pyrimethamine, and leucovorin for 6 weeks, and response to treatment is assessed by serial brain imaging.

2. Japanese encephalitis (JE) and chorea

JE is the leading cause of epidemic encephalitis in Asia. It is transmitted by the vector (culex mosquito) from reservoirs such as pigs and bats. JE is caused by JEV which is a zoonotic flavivirus. Common clinical features of JE are fever, seizures, altered sensorium, and extrapyramidal symptoms.[21] The specific IgM antibodies can be detected in CSF, serum, or both in approximately 75% of patients by the third day of onset of disease and nearly all are positive by the seventh day of onset. MRI shows hyperintense or mixed intensity lesions on T2WI in the bilateral thalamus in JE. SPECT shows hypoperfusion in the thalamus, frontal cortex, and lentiform area consistent with a crucial role of the thalamus and its connections in the genesis of MD in JE. Substantia nigra may also get involved in JE. In 2010, Misra and Kalita[22] studied 209 patients with encephalitis; out of the 209 patients, 68 patients had JE, 53 had dengue, 15 had HSE, 11 had miscellaneous [mumps and Epstein–Barr virus (EBV)], and 31 patients had a nonspecific infection. MDs were found to be the most common in JE patients (67.6%). Chorea, myoclonus, and dystonia were grouped with dystonia for statistical analysis. Common MD in JE was parkinsonism, dystonia, or a combination of both. Five patients had athetosis, and three of them had chorea affecting both lower limbs. JE-induced N-methyl-D-aspartate (NMDA) receptor encephalitis can occur in up to 4.7% of the patients. Among the four patients with choreoathetosis following JE encephalitis, three subsequently had positive antibodies to NMDA receptors.[23] There is no definitive treatment in the form of an anti-viral drug for JE. Patients with seizures are treated with supportive measures, anti-edema measures, and anti-seizure medicines.

3. Herpes simplex virus and chorea

Herpes simplex virus type 1 is one of the most common causes of viral encephalitis worldwide. HSV encephalitis (HSE) is not commonly associated with chorea but may occur in children on relapse of HSE. Tay et al.[24] reported a patient with HSV encephalitis who developed MD 21 days after acyclovir treatment. He had developed athetosis, myoclonus, and oro-lingual choreiform movements. Repeat CSF for HSV was negative. However, later he had tested positive for both serum and CSF anti‐N‐methyl‐d‐aspartate receptor (anti-NMDAR) antibodies. This case report highlighted the importance of testing for NMDAR antibodies in patients with HSE developing MD later. Rathi and Rathi[25] in 2011 also reported a case of an 11-year-old boy having HSV1 encephalitis who recovered after acyclovir therapy but developed choreoathetosis after 2 weeks, which was relieved after anti-inflammatory therapy. Pulickal et al.[26] in 2013 reported a case of a 14-month-old child with human herpesvirus 6 encephalitis who developed fever and multiple seizure episodes followed by chorea associated with regression of developmental milestones. His seizures and chorea were resolved after treatment with levetiracetam, foscarnet, and IVIG. However, it was not clear whether chorea was related directly to viral infection or due to post-viral autoimmune reaction. In most cases of HSV encephalitis with chorea, the chorea occurs as a biphasic disease with HSE followed by encephalitis associated with anti‐NMDAR or anti-dopamine 2 receptor antibodies. In a systematic literature review of 43 patients, the most frequent type of MD during NMDAR encephalitis was choreoathetosis (73%), followed by dyskinesia (53%), ballismus or hemiballismus (23%), dystonia (17%), athetosis (10%), and stereotypies, posturing, intentional tremor, and myoclonus (3%).[27] These MDs occurred as generalized in 48% and the orofacial region was involved in 69% of the patients. Early recognition and initiation of IV antiviral agents along with IV steroids or IV immunoglobulins may improve the outcome.

C. Parasitic infections and chorea

NCC and chorea

NCC is commonly caused by accidental ingestion of Taenia solium. The most common presentation of intra-parenchymal NCC is a seizure, whereas intraventricular NCC may cause hydrocephalus and subarachnoid NCC may cause arachnoiditis.[28] MDs described to be associated with NCC are parkinsonism, tremors, dystonia, chorea, or myoclonus. Alarcón et al.[29] studied 590 patients of NCC, out of which 15 patients had parkinsonism, 5 had tremors, 2 had dystonia, and 1 had chorea. In a patient having chorea, an MRI brain lesion was found to be in the thalamus. NCC is treated with albendazole with steroids and anti-seizure drugs are added in patients having seizures.

D. Other infections with chorea (prion disease)

Creutzfeldt–Jacob disease (CJD) and chorea

CJD is a fatal neurodegenerative disease caused by prion proteins. There are four types of CJD: sporadic CJD (85%), genetic/familial CJD (14%), iatrogenic, and variant CJD (1%).[30] V-CJD occurs due to consumption of bovine spongiform encephalopathy-infected beef. Dementia, psychiatric features, painful sensory symptoms, and MD are common clinical features of variant CJD. Rapidly progressive mental deterioration, often with behavioral abnormalities, and myoclonus are two cardinal clinical manifestations of sCJD. Extrapyramidal signs such as hypokinesia and cerebellar manifestations are also common. CJD is distinguished from more common causes of dementia by its rapidly progressive course with prominent myoclonus and gait disturbance. Diagnosis is made on basis of clinical features, MRI (which can show diffusion restriction in bilateral caudate and putamen with cortical ribboning), EEG (showing periodic sharp wave complexes), and CSF 14-3-3 assay. Other autoimmune, infectious, malignant, and toxic-metabolic etiologies should be considered in the differential diagnosis. While the neuro-pathological examination is the gold standard test, brain biopsies are often not feasible at all centers. However, autopsies are important to definitively diagnose prion disease and determine its type. Histopathologic findings in prion disease consist of spongiform change, neuronal loss (particularly of cortical layers III–V) without inflammation, and accumulation of the abnormal prion protein detected by immunohistochemistry. Chorea is more common with vCJD and is included in its diagnostic criteria. There are several case reports describing chorea as a symptom of sporadic CJD.[30],[31],[32] The prevalence of chorea from a retrospective study of various confirmed CJD patients was 10–11%.[32],[33] However, sCJD and vCJD were not differentiated in the series. MDs in CJD are thought to be due to lesion involving striatum, thalamus, or midbrain. Thalamus is most commonly involved in vCJD, and thus chorea is a more common symptom associated with vCJD. There is no specific treatment available for the cure of CJD and it is a uniformly fatal disease. Treatment consists of symptomatic treatment for chorea, anti-seizure medicines for myoclonus, and supportive treatment.


  Conclusion Top


Chorea is one of the commonest forms of MD caused by CNS infection. The pathophysiology of chorea in CNS infections is commonly caused due to vascular lesion, auto-immune response to infection, or direct infection-related injury. The most commonly affected parts in infective chorea are the striatum, thalamus, and/or midbrain. CSF examination, brain imaging, and specific serological tests help in the diagnosis of the cause and mechanism of chorea. MRI usually shows basal ganglia lesions in patients with infection-related chorea. The majority of patients responds to therapy directed toward the causative pathogen. Symptomatic therapy for the treatment of chorea with tetrabenazine, antipsychotics, or benzodiazepines may be considered in severe cases or patients having nontreatable fatal disorders such as CJD.

Author contributions

1. Research project: A. Conception, B. Organization, C. Execution;

2. Statistical analysis: A. Design, B. Execution, C. Review and Critique;

3. Manuscript preparation: A. Writing of the first draft, B. Review and Critique.

R. Y.: 1BC, 3A; V. S.: 1AB, 2BC, 3B. S. D.: 1ABC, 2ABC, 3B.

Ethical compliance statement

The authors confirm that neither informed patient consent nor the approval of an Institutional Review Board was necessary for this work. We confirm that we have read the Journal’s position on issues involved in ethical publication and affirm that this work is consistent with those guidelines. Dr Soaham Desai would act as the guarantor and corresponding author of this article.

Conflicts of interest

No specific funding was received for this work. The authors declare that there are no conflicts of interest relevant to this work.

Financial support and sponsorship

No financial disclosures present for all the three authors.



 
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    Figures

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    Tables

  [Table 1], [Table 2], [Table 3]



 

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