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LETTER TO EDITOR
Year : 2013  |  Volume : 61  |  Issue : 6  |  Page : 656--657

Neurocysticercosis presenting as Parkinsonism

Rohit Verma1, Kuljeet Singh Anand2, BB Sharma3, Jyoti Garg2,  
1 Department of Psychiatry, Lady Hardinge Medical College and Smt. S. K. Hospital, New Delhi, India
2 Department of Neurology, Post Graduate Institute of Medical Education and Research, Dr. Ram Manohar Lohia Hospital, New Delhi, India
3 Department of Radiodiagnosis, Post Graduate Institute of Medical Education and Research, Dr. Ram Manohar Lohia Hospital, New Delhi, India

Correspondence Address:
Rohit Verma
Department of Psychiatry, Lady Hardinge Medical College and Smt. S. K. Hospital, New Delhi
India




How to cite this article:
Verma R, Anand KS, Sharma B B, Garg J. Neurocysticercosis presenting as Parkinsonism.Neurol India 2013;61:656-657


How to cite this URL:
Verma R, Anand KS, Sharma B B, Garg J. Neurocysticercosis presenting as Parkinsonism. Neurol India [serial online] 2013 [cited 2020 Mar 30 ];61:656-657
Available from: http://www.neurologyindia.com/text.asp?2013/61/6/656/125276


Full Text

Sir,

Clinical manifestations of neurocysticercosis (NCC) may depend on several factors such as the immune response the host to parasite, topography, number, size and stage of lesions in the brain. [1] Although some cases of NCC may remain asymptomatic, most have been reported to present with seizures, headache and raised intra cranial tension. [1] Movement disorders have been rarely described in association with NCC. [2] We report two cases of NCC presenting with features of parkinsonism.

Case 1: A 50-year-old female presented with insidious onset and progressive history of headache and vomiting for 3 months, slowness of movement and drooling of saliva, difficulty in swallowing and speaking and generalized seizures since 2 months. Neurological examination revealed low volume and hypo kinetic speech. Ocular movements were slow with reduced blink rate and a positive Meyerson's sign. Motor system examination revealed generalized rigidity and severe bradykinesia in axial and appendicular muscles. The gait was slow with reduced arm swing. There was gross postural instability on pull test. Brain magnetic resonance imaging (MRI) demonstrated multiple cystic lesions with mural nodule in bilateral basal ganglia [Figure 1]a and b. ELISA for IgM antibodies against Taenia solium was reactive. She was treated with albendazole 15 mg/kg/day along with steroids. She developed increasing headache, vomiting and alteration in sensorium while on treatment and died in spite of anti-edema and other resuscitative measures.{Figure 1}

Case 2: A 43-year-old man, a known case of multiple NCC with seizures was admitted with slowness of activities, stiffness of limbs (right more than left) and speech disturbances since 2 months. Neurological examination revealed dysathric speech. Gait was slow and short stepped with reduced arm swing. Meyerson's sign was positive with a reduced blink rate. There was rigidity in all four limbs (right more than left) and bradykinesia (right more than left). Brain MRI demonstrated multiple cysticercal lesions scattered within bilateral pallidum and putamen [Figure 2]a and b. ELISA for IgM antibodies against T. solium was reactive. He was treated with cysticidal drug along with steroids. The parkinsonian symptoms gradually improved and at the end of 2 weeks he was totally asymptomatic.{Figure 2}

A wide variety of movement disorders have been reported in patients with NCC, such as parkinsonism, choreoathetosis, hemi-chorea, unilateral tremor, myoclonus, blepharospasm and ataxia. [1],[3],[4],[5] It is common to find NCC lesions in the basal ganglia but, unlike our patients, clinical manifestation of these lesions is uncommon. [2] NCC presenting as parkinsonism has been previously reported in four cases. [3],[4],[5] There was brainstem cysticercotic ependymitis and midbrain encephalitis in three cases, but none reported direct involvement of basal ganglia by NCC. Response to levodopa as well as cysticidal therapy with albendazole was good, allowing later reduction of levodopa dosage in one patient and complete withdrawal in two others with complete recovery.

Parkinsonism observed in patients with NCC is possibly due to the multiple basal ganglia or midbrain lesions, or due to cysticercal encephalitis. [1] The location of lesion itself appears insufficient to cause any precise changes as it has been observed that NCC affects brain regions that are distant from location of the cysticerci. [6] Hence parkinsonism, which is commonly associated with lesions of the midbrain leading to disruption of nigrostriatal pathway, can be generated by NCC occurring at a different brain region than midbrain as in our cases.

Other causes of secondary and reversible parkinsonism were excluded in our cases by the absence of other neurological signs, laboratory tests (hematological and biochemical analysis, skiagram-chest and soft-tissues, electrocardiography, human immunodeficiency virus serology, ELISA for Toxoplasmosis, MRI brain) and a detailed drug history. Both of our cases were managed only with steroids and albendazole therapy and no anti-parkinsonian drugs were administered. Cysticidal drug should be used with caution since it may sometimes be detrimental, more commonly so in multiple NCCs. [7] Parkinsonism in NCC is reversible as was evident in our second patient, similar to earlier reports.

To the best of our knowledge, this is probably the first case series in which anatomically symmetric cysticercal lesions within basal ganglia were associated with a clinical syndrome of bilateral parkinsonism. These cases draw attention to the inconsistent manifestations of NCC and also emphasize the importance of excluding a diagnosis of NCC in patients with parkinsonism from endemic areas, as symptoms can sometimes be reversible if diagnosis and its etiology are established early.

References

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