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Table of Contents    
Year : 2017  |  Volume : 65  |  Issue : 2  |  Page : 389-391

An unusual cause of bilateral thalamic lesions

Department of Neurology, Gauhati Medical College, Guwahati, Assam, India

Date of Web Publication10-Mar-2017

Correspondence Address:
Dr. Ashok K Kayal
Department of Neurology, Gauhati Medical College, Guwahati, Assam
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/neuroindia.NI_293_16

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How to cite this article:
Bawri S, Das M, Goswami M, Kayal AK. An unusual cause of bilateral thalamic lesions. Neurol India 2017;65:389-91

How to cite this URL:
Bawri S, Das M, Goswami M, Kayal AK. An unusual cause of bilateral thalamic lesions. Neurol India [serial online] 2017 [cited 2023 Mar 31];65:389-91. Available from: https://www.neurologyindia.com/text.asp?2017/65/2/389/201856


The thalamus plays an important role in different brain functions including memory, emotions, sleep-wake cycle, executive functions, mediating general cortical alerting responses, processing of sensory (including taste, somatosensory, visual, and auditive) information and relaying it to the cortex, and sensorimotor control.[1] Bilateral thalamic lesions are uncommon. The lesions of these paired structures have a limited differential diagnosis that includes metabolic and toxic processes, infections, vascular lesions, and neoplasia. The differential diagnosis can be further narrowed down with the patient history, imaging characteristics, and the presence or absence of lesions outside the thalami.[2]

We describe the case of a 25-year-old girl who was referred to the Neurology Department for altered sensorium, quadriparesis, and episodes of right focal motor seizures with secondary generalization and occasional myoclonic jerks for 2 days. The girl had nausea and vomiting for which she was receiving homeopathic treatment 3 weeks prior to the development of neurological symptoms. There was no history of diplopia, visual loss, dysphagia, nasal regurgitation, and nasal intonation. There was also no history of fever, weight loss, cough, respiratory distress, and jaundice. There was no past history of abnormal behaviour, dystonia, or jaundice. She had a normal birth history, normal milestones, and her siblings were enjoying good health with normal birth and developmental history. General physical examination revealed a normal pulse rate of 84 per minute, regular blood pressure of 110/70 mmHg with anaemia. There was no icterus, or any lymphadenopathy. Neurological examination revealed that the patient was confused, had vertical gaze palsy with his pupils being bilateral normal sized, reactive to light. Rest of the ophthalmological examination was normal. The patient also had quadriparesis (power 3/5) with brisk deep tendon jerks with up going planter reflexes and no sign of meningeal irritation. Routine blood parameters showed a normal total leucocytic count with a high erythrocyte sedimentation rate of 78 mm after the end of the first hour and a hemoglobin of 10 gm% with a normal serum iron profile. Her renal function tests, liver function tests, serum ammonia, fasting blood sugar, thyroid profile, and ceruloplasmin level were normal. Her cardiac evaluation, including the electrocardiogram and echocardiography, was normal. Cerebrospinal fluid analysis was unremarkable along with negative findings on performing Mac Elisa for Japanese encephalitis, and on testing for West Nile virus, tuberculosis, cryptococcus, and Rickettsia. Initial computerized tomography (CT) scan of the brain was normal; subsequently, magnetic resonance imaging (MRI) of the brain with MR angiography (MRA) along with contrast study revealed T2 and fluid-attenuated inversion recovery hyperintensities involving bilateral dorsomedial nuclei without diffusion restriction [Figure 1]. Based on the history of homoeopathic treatment undertaken initially (since bismuth is often used for gastrointestinal symptoms), it was decided to test bismuth level, which was found to be high (3.88 µg/L; reference value: 0.0016–0.0029 µg/L). As the patient had a normal urine output and a normal renal profile, the decision for undertaking dialysis was delayed and the patient was managed conservatively. She was hospitalized for 3 months but recovered (she became conscious, oriented, with improved vertical gaze palsy, with a power 4-/5 in all limbs, and controlled seizures ) at the time of discharge. The repeat blood sample for bismuth level was within normal biological reference value (0.0016–0.0029 µg/L). Repeat MRI of the brain showed complete resolution of the intracranial lesions at the time of discharge of the patient [Figure 2]. Based on the history, clinical manifestations, and investigations, we attributed the bilateral thalamic lesions to bismuth toxicity.
Figure 1: Magnetic resonance imaging of the brain with magnetic resonance angiography along with contrast study revealed T2 and fluid-attenuated inversion recovery hyperintensities involving bilateral dorsomedial nuclei without diffusion restriction

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Figure 2: Normal magnetic resonance imaging of the brain with magnetic resonance angiography along with contrast study at the time of discharge

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Bismuth is the heaviest stable element and was discovered around 10 years ago. Paul et al.,[3] highlighted the fact that bismuth toxicity, while being rare, should be considered in a patient with progressive neurological decline. In the case series by Loiseau et al.,[4] the authors found a long prodromal phase followed by a phase characterized by four signs, that is, severe confusion, myoclonus, lack of coordination on standing or walking (astasia-abasia), dysarthria, and less commonly, paresthesia, hallucination, and seizures.[3],[4] However, the exact incidence is not well-known. Bismuth has beneficial effects for humans because it eradicates certain pathogens such as Helicobacter pylori and Pseudomonas aeruginosa but also has adverse side-effects, as indicated by cases of encephalopathy, renal failure, and suspected cyto- and genotoxicity.[5] Bismuth is readily absorbed, transported in the blood serum by human serum transferrin [6],[7],[8] and enters the central nervous system by a retrograde axonal transport route, breaching the blood–brain barrier [9],[10] [Table 1].
Table 1: Review of literature

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The thalamus integrates several important cortical functions as it contains strategic nuclei. Bilateral abnormalities of the thalamus are noted in different acute and chronic clinical situations such as metabolic and toxic processes, infections, vascular lesions, and neoplasia, and although MRI is the modality of choice for evaluation, the correct diagnosis can be made only by taking all relevant clinical and laboratory information into account.[11]

As the mechanism of bismuth toxicity has not been well-described, it is difficult to predict the treatment. The primary treatment is the removal of the bismuth compound from the patient's intake. The role of chelators such as D, L-2, 3-dimercaptopropane-1-sulfonic acid (DMPS) as a remedy is unclear. Our patient had confusion, myoclonus, seizures, and quadriparesis with increased blood bismuth level and an abnormal MRI, which later became normal with resolution of symptoms, without the chelation therapy.

Based on the history, clinical manifestation, and investigations, we attributed the bilateral thalamic lesions to bismuth toxicity, which to the best of our knowledge, is not well-reported.

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Conflicts of interest

There are no conflicts of interest.

 ╗ References Top

Renard D, Castelnovo G, Campello C, Bouly S, Le Floch A, Thouvenot E, et al. Thalamic lesions: A radiological review. Behav Neurol 2014;2014:154631.  Back to cited text no. 1
Smith AB1, Smirniotopoulos JG, Rushing EJ, Goldstein SJ. Bilateral thalamic lesions. AJR Am J Roentgenol 2009;192:W53-62.  Back to cited text no. 2
Reynolds PT, Abalos KC, Hopp J, Williams ME. Bismuth toxicity: A rare cause of neurologic dysfunction. Int J Clin Med 2012;3:46-8.  Back to cited text no. 3
Loiseau P, Henry P, Jallon P, Legroux M. Iatrogenic myoclonic encephalopathies caused by bismuth salts. J Neurol Sci 1976;27:133-43.  Back to cited text no. 4
Thomas F, Bialek B, Hensel R. Medical use of bismuth: The two sides of the coin. J Clinic Toxicol 2012;S3:004. doi: 10.4172/2161-0495.S3-004.  Back to cited text no. 5
Diaz-Bone RA, Van de Wiele T. Biotransformation of metal(loid)s by intestinal microorganisms. Pure Appl Chem 2010;82:409-27.  Back to cited text no. 6
Boertz J, Hartmann LM, Sulkowski M, Hippler J, Mosel F, Diaz-Bone RA, et al. Determination of trimethylbismuth in the human body after ingestion of colloidal bismuth subcitrate. Drug Metab Dispos 2009;37:352-8.  Back to cited text no. 7
Sun HZ, Zhang L, Szeto KY. Bismuth in medicine. In Metal Ions in Biological Systems, Metal Ions and Their Complexes in Medication. New York, USA: Marcel Dekker; 2004. p. 333-78.  Back to cited text no. 8
Stoltenberg M, Schionning JD, Danscher G. Retrograde axonal transport of bismuth: An autometallographic study. Acta Neuropathol 2001;101:123-8.  Back to cited text no. 9
Hegde AN, Mohan S, Lath N, Lim CC. Differential diagnosis for bilateral abnormalities of the basal ganglia and thalamus. Radiographics 2011;31:5-30.  Back to cited text no. 10
Siram R, Botta R, Kashikunte C, Pal PK, Yadav R. Chronic encephalopathy with ataxia, myoclonus, and auditory neuropathy: A case of bismuth poisoning. Neurol India 2017;65:186-7.  Back to cited text no. 11
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  [Figure 1], [Figure 2]

  [Table 1]


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