Letters to Editor Neurocysticercosis presenting as Parkinsonism 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 1a 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.
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 2a 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. 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.[1,3‑5] 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. [3‑5] 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
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
a
b
Figure 1: (a) Magnetic resonance imaging brain (T1‑W) showing multiple hypointense cystic lesions with eccentric mural nodule in case. (b) Magnetic resonance imaging brain (T2‑W) showing multiple hyperintense cystic lesions with eccentric hypointense mural nodule in case 1
656
a
b
Figure 2: (a) Magnetic resonance imaging brain (proton density imaging) showing cystic lesions having thin hypointense wall with eccentric hypointense nodule in bilateral basal ganglia in case 2. (b)Magnetic resonance imaging brain (T2‑W) showing cystic lesions having thin hypointense wall with eccentric hypointense nodule in bilateral basal ganglia in case 2
Neurology India | Nov-Dec 2013 | Vol 61 | Issue 6
Letters to Editor
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.
with cysticercosis. Report of three cases and review of the literature. Neurosurg Focus 2002;12:e2. Access this article online Quick Response Code:
Website: www.neurologyindia.com PMID: *** DOI: 10.4103/0028-3886.125276
Received: 18‑07‑2013 Review completed: 20‑08‑2013 Accepted: 18‑12‑2013
Prolonged thiamphenicol treatment associated sensory axonal polyneuropathy Sir, Thiamphenicol is a broad‑spectrum antibiotic and can cause dermatologic, gastrointestinal, hematologic and neurological side‑effects.[1,2] However neuropathy associated with thiamphenicol use is rather rare, hence this report.
References
A 35‑year‑old male patient was diagnosed with nongonococcal urethritis and received over 180 g of thiamphenicol in 4 months. He presented with tingling and pains in the lower limbs. Neurological examinations revealed unsteady gait. Pain sensation was slightly reduced in fingertips, but significantly reduced below the knee, with hyperalgesia below ankles. Vibration and position sensation lost below knees. Ankle reflexes were absent. Electromyogram of upper and lower limb muscles were normal. Nerve conduction study confirmed sensory neuropathy, mainly in lower limbs, predominantly axonal damage [Tables 1 and 2].
1.
Table 1: Motor nerve conduction study of limbs
Rohit Verma, Kuljeet Singh Anand1, B. B. Sharma2, Jyoti Garg1 Department of Psychiatry, Lady Hardinge Medical College and Smt. S. K. Hospital, Departments of 1Neurology and 2 Radiodiagnosis, Post Graduate Institute of Medical Education and Research, Dr. Ram Manohar Lohia Hospital, New Delhi, India E‑mail: [email protected]
2. 3. 4. 5. 6. 7.
Carabin H, Ndimubanzi PC, Budke CM, Nguyen H, Qian Y, Cowan LD, et al. Clinical manifestations associated with neurocysticercosis: A systematic review. PLoS Negl Trop Dis 2011;5:e1152. Cosentino 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. Verma A, Berger JR, Bowen BC, Sanchez‑Ramos J. Reversible parkinsonian syndrome complicating cysticercus midbrain encephalitis. Mov Disord 1995;10:215‑9. Sá DS, Teive HA, Troiano AR, Werneck LC. Parkinsonism associated with neurocysticercosis. Parkinsonism Relat Disord 2005;11:69‑72. Patel R, Jha S, Yadav RK. Pleomorphism of the clinical manifestations of neurocysticercosis. Trans R Soc Trop Med Hyg 2006;100:134‑41. Bianchin MM, Velasco TR, Takayanagui OM, Sakamoto AC. Neurocysticercosis, mesial temporal lobe epilepsy and hippocampal sclerosis: An association largely ignored. Lancet Neurol 2006;5:20‑1. DeGiorgio CM, Houston I, Oviedo S, Sorvillo F. Deaths associated
Neurology India | Nov-Dec 2013 | Vol 61 | Issue 6
Nerves
Left tibial nerve Right tibial nerve Left peroneal nerve Right peroneal nerve Left median nerve Right ulnar nerve
Proximal muscle Distal muscle Velocity Latency Amplitude Latency Amplitude (m/s) (ms) (mv) (ms) (mv) 14.7
10.2
4.7
12.3
41.0
13.8
8.5
4.3
12.3
43.2
12.2
5.2
4.0
5.8
41.5
11.5
5.0
4.2
5.2
46.6
7.7
12.6
3.7
13.1
57.5
7.7
16.1
2.5
17.6
55.8
657
Copyright of Neurology India is the property of Medknow Publications & Media Pvt. Ltd. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
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 2a 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. 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.[1,3‑5] 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. [3‑5] 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
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
a
b
Figure 1: (a) Magnetic resonance imaging brain (T1‑W) showing multiple hypointense cystic lesions with eccentric mural nodule in case. (b) Magnetic resonance imaging brain (T2‑W) showing multiple hyperintense cystic lesions with eccentric hypointense mural nodule in case 1
656
a
b
Figure 2: (a) Magnetic resonance imaging brain (proton density imaging) showing cystic lesions having thin hypointense wall with eccentric hypointense nodule in bilateral basal ganglia in case 2. (b)Magnetic resonance imaging brain (T2‑W) showing cystic lesions having thin hypointense wall with eccentric hypointense nodule in bilateral basal ganglia in case 2
Neurology India | Nov-Dec 2013 | Vol 61 | Issue 6
Letters to Editor
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.
with cysticercosis. Report of three cases and review of the literature. Neurosurg Focus 2002;12:e2. Access this article online Quick Response Code:
Website: www.neurologyindia.com PMID: *** DOI: 10.4103/0028-3886.125276
Received: 18‑07‑2013 Review completed: 20‑08‑2013 Accepted: 18‑12‑2013
Prolonged thiamphenicol treatment associated sensory axonal polyneuropathy Sir, Thiamphenicol is a broad‑spectrum antibiotic and can cause dermatologic, gastrointestinal, hematologic and neurological side‑effects.[1,2] However neuropathy associated with thiamphenicol use is rather rare, hence this report.
References
A 35‑year‑old male patient was diagnosed with nongonococcal urethritis and received over 180 g of thiamphenicol in 4 months. He presented with tingling and pains in the lower limbs. Neurological examinations revealed unsteady gait. Pain sensation was slightly reduced in fingertips, but significantly reduced below the knee, with hyperalgesia below ankles. Vibration and position sensation lost below knees. Ankle reflexes were absent. Electromyogram of upper and lower limb muscles were normal. Nerve conduction study confirmed sensory neuropathy, mainly in lower limbs, predominantly axonal damage [Tables 1 and 2].
1.
Table 1: Motor nerve conduction study of limbs
Rohit Verma, Kuljeet Singh Anand1, B. B. Sharma2, Jyoti Garg1 Department of Psychiatry, Lady Hardinge Medical College and Smt. S. K. Hospital, Departments of 1Neurology and 2 Radiodiagnosis, Post Graduate Institute of Medical Education and Research, Dr. Ram Manohar Lohia Hospital, New Delhi, India E‑mail: [email protected]
2. 3. 4. 5. 6. 7.
Carabin H, Ndimubanzi PC, Budke CM, Nguyen H, Qian Y, Cowan LD, et al. Clinical manifestations associated with neurocysticercosis: A systematic review. PLoS Negl Trop Dis 2011;5:e1152. Cosentino 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. Verma A, Berger JR, Bowen BC, Sanchez‑Ramos J. Reversible parkinsonian syndrome complicating cysticercus midbrain encephalitis. Mov Disord 1995;10:215‑9. Sá DS, Teive HA, Troiano AR, Werneck LC. Parkinsonism associated with neurocysticercosis. Parkinsonism Relat Disord 2005;11:69‑72. Patel R, Jha S, Yadav RK. Pleomorphism of the clinical manifestations of neurocysticercosis. Trans R Soc Trop Med Hyg 2006;100:134‑41. Bianchin MM, Velasco TR, Takayanagui OM, Sakamoto AC. Neurocysticercosis, mesial temporal lobe epilepsy and hippocampal sclerosis: An association largely ignored. Lancet Neurol 2006;5:20‑1. DeGiorgio CM, Houston I, Oviedo S, Sorvillo F. Deaths associated
Neurology India | Nov-Dec 2013 | Vol 61 | Issue 6
Nerves
Left tibial nerve Right tibial nerve Left peroneal nerve Right peroneal nerve Left median nerve Right ulnar nerve
Proximal muscle Distal muscle Velocity Latency Amplitude Latency Amplitude (m/s) (ms) (mv) (ms) (mv) 14.7
10.2
4.7
12.3
41.0
13.8
8.5
4.3
12.3
43.2
12.2
5.2
4.0
5.8
41.5
11.5
5.0
4.2
5.2
46.6
7.7
12.6
3.7
13.1
57.5
7.7
16.1
2.5
17.6
55.8
657
Copyright of Neurology India is the property of Medknow Publications & Media Pvt. Ltd. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
