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Table of Contents    
Year : 2022  |  Volume : 70  |  Issue : 4  |  Page : 1525-1533

MRI Spectrum of Toxic Encephalopathy—An Institutional Experience

Department of Neuroimaging and Interventional Radiology, National Institute of Mental Health and Neurosciences (NIMHANS), Bangalore, Karnataka, India

Date of Submission02-Apr-2020
Date of Decision08-Jul-2020
Date of Acceptance17-Jul-2020
Date of Web Publication30-Aug-2022

Correspondence Address:
Hima S Pendharkar
Additional Professor, Department of Neuroimaging and Interventional Radiology, 3rd Floor, Faculty Block, Neuro Centre, National Institute of Mental Health and Neurosciences (NIMHANS), Hosur Road, Bengaluru - 560 029, Karnataka
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0028-3886.355127

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 » Abstract 

Background: There are numerous toxins that affect our nervous system, both central and peripheral. Innumerable differentials exist in patients of acute encephalopathy and the list can be narrowed down with appropriate imaging. Specific neuroradiological features point to a particular diagnosis in a substantial number of cases.
Objective: Through this study, we aimed to demonstrate the varied imaging findings of toxic encephalopathy on MRI encountered at our institute.
Material and Methods: A retrospective analysis of the patients clinically diagnosed as toxic encephalopathy and referred for imaging between March 2015 and December 2019 was done. A total of 25 patients were included. Patient records were reviewed for clinical details, laboratory investigations, and treatment; the institute Picture Archiving and Communication System provided the imaging findings.
Results: Patients presenting were aged between 22 and 55 years (mean—34.3 years). Four patients (16%) presented with imaging findings characteristic of Marchiafava-Bignami disease and six patients (24%) had MRI findings of Wernicke encephalopathy. Three patients (12%) had methanol poisoning sequelae while imaging findings of nitroimidazole drug toxicity were observed in another three patients (12%). Two patients (8%) each of carbon monoxide poisoning and lead toxicity were seen. We had one patient (4%) each of isoniazid, methyl iodide, dextropropoxyphene toxicity, chronic toluene abuse, and hyperglycemia-induced hemiballismus-hemichorea.
Conclusion: Our study illustrates the amalgamated spectrum of MRI appearances in various subgroups of toxic encephalopathies. Imaging substantiated by relevant history and clinical manifestations can accurately diagnose the possible causative agent in the majority of the cases.

Keywords: Carbon monoxide, lead, Marchiafava, methanol, nitroimidazole, toluene, toxic encephalopathy, Wernicke
Key Message Toxic encephalopathy diagnosis in the clinical scenario is challenging. This study illustrates the amalgamated spectrum of MRI appearances in various subgroups of toxic encephalopathies. Imaging with a background clinical history can identify the possible causative agent in the majority of cases.

How to cite this article:
Biswas S, Pendharkar HS, Murumkar VS. MRI Spectrum of Toxic Encephalopathy—An Institutional Experience. Neurol India 2022;70:1525-33

How to cite this URL:
Biswas S, Pendharkar HS, Murumkar VS. MRI Spectrum of Toxic Encephalopathy—An Institutional Experience. Neurol India [serial online] 2022 [cited 2023 Jan 29];70:1525-33. Available from: https://www.neurologyindia.com/text.asp?2022/70/4/1525/355127

Toxic encephalopathies encompass a broad spectrum of entities, which by various pathomechanisms lead to alteration of central nervous system (CNS) functions that may present acutely or in a chronic stage.[1] Our brain remains at risk of damage from a multitude of toxins and their metabolites owing to the lipid content of myelin, an integral component of the nervous system.[2] Some agents are deliberately injected, inhaled, or ingested while others are accidentally encountered. Some toxins accumulate slowly leading to subtle- and insidious-onset clinical manifestations while others may cause profound and rapid CNS toxicity, sometimes leading to coma and death.[3]

In some situations, these conditions may present with characteristic neuroradiological findings. Imaging evidence can be substantiated by proper history, clinical evaluation, and often laboratory findings for arriving at a correct diagnosis. Innumerable differentials exist in patients of acute encephalopathy and the list can be narrowed down with appropriate imaging. The geographical distribution of lesions and the anatomical structures involved can help in reducing the list of differentials in patients with a positive history of acute or chronic toxin exposure. Toxic encephalopathy usually results in symmetrical involvement of the cortices and deep gray structures of the brain.[2]

 » Material and Methods Top

Our study was retrospective in nature and comprised patients who were diagnosed with various toxic leukoencephalopathies between March 2015 and December 2019. Patients were identified by extensively searching the neuroradiological database and archived MRI reports in the Picture Archiving and Communication System institute using the following key words—”Toxic encephalopathy,” “Drug-induced toxicity” and names of all possible exogenous and endogenous neurotoxins (including the ones which we have discussed in our article). Subsequently, the records were reviewed for clinical history, symptoms at presentation, imaging findings on MRI and CT, and relevant laboratory findings (when indicated). Our study group comprised 25 patients. MRI was done on two scanners—1.5 Tesla (Magnetom Aera, SIEMENS) and 3 Tesla (Achieva, PHILIPS) using the following standard sequences—axial T1, T2, fluid attenuated inversion recovery (FLAIR), susceptibility-weighted imaging (SWI), and diffusion-weighted imaging (DWI), sagittal T2, coronal T2, and post-contrast T1 images (Gadolinium was used as a contrast agent).

 » Results Top

Clinical details

A total of twenty five patients (males = 19; females = 6) were included in our study. The subjects were aged between 22 and 55 years (mean age—34.3 years). Eleven patients (44%) were chronic alcoholics. There were two females with a pregnancy of about 5 months and a history of recurrent episodes of vomiting followed by drowsiness. The clinical presentation of all the patients is summarized in [Table 1].
Table 1: Patient demographics, clinical features, and imaging findings

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Imaging findings

Cases 1–4 showed white matter hyperintense signal intensity on T2/FLAIR (periventricular region being most commonly involved). Corpus callosum involvement was noted in all the four cases. Restriction on DWI (Diffusion weighted imaging) was noted in cases 1, 2, and 3 [Figure 1]c, [Figure 1]h & [Figure 1]j. Case 1 showed peripheral enhancement of the lesions in the corpus callosum and white matter [Figure 1]e. With a background history and relevant MRI findings, these cases were diagnosed as Marchiafava-Bignami disease (MBD).
Figure 1: Marchiafava-Bignami disease. Case 1: (a)-Sagittal T2: Callosal hyperintensity (arrows); (b) Axial fluid attenuated inversion recovery (FLAIR): Callosal (short arrows) and subcortical white matter hyperintensity (long arrows); (c and d) Axial diffusion-weighted imaging (DWI) and apparent diffusion coefficient (ADC): restriction within the lesions (arrows); (e) Post-contrast T1: peripheral enhancement. Case 2: (f) axial T2: Callosal and periventricular white matter hyperintensity (arrows); (g and h) axial DWI: restricted diffusion in centrum semiovale and corpus callosum (arrows). Case 3: (i) sagittal T2: callosal hyperintensity (arrows); (j) axial DWI shows diffusion restriction within the genu and splenium of the corpus callosum

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Symmetrical T2/FLAIR hyperintensity involving the mammillary bodies, medial aspect of both thalamus, and tectum was noted in the cases numbered 5–10 with diffusion restriction in three cases (6, 8, and 9) in the above mentioned regions. Two patients (no. 7 and 9) were non-alcoholic pregnant females. None of the patients showed any contrast enhancement [Figure 2].
Figure 2: Wernicke encephalopathy. Case 5: (a and b) axial FLAIR showing symmetrical hyperintensity in the mamillary bodies (arrows-A) and thalami (arrows-B). Case 6: (c) axial T2 shows tectal hyperintensity (arrow); (d) axial DWI shows restriction in bilateral medial thalami (arrows). Case 8: (e and f) axial DWI and ADC showing restriction in mamillary bodies (short arrow) and tectum (long arrows). Case 9: (g) axial FLAIR showing hyperintensity in the periaqueductal grey matter (arrow); (h) axial DWI image shows restriction in both medial thalami (short arrows) and right basal ganglia (long arrow)

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Cases 11 to 13 had bilateral symmetrical putaminal hemorrhagic necrosis with blooming on SWI following country liquor intake. Among them, only case 12 had CT and MRI images at the time of acute presentation. Cases 12 and 13 showed bilateral optic atrophy on MRI. The above findings were sequelae of Methanol toxicity [Figure 3].
Figure 3: Methanol poisoning. Case 11: (a) axial T2 showing symmetrical putaminal cavitation (arrows); (b) axial SWI shows putaminal hemorrhagic necrosis (arrows). Case 12: (c) CT shows symmetrical hypodensity in bilateral putamina (arrows); (d) axial T1 showing symmetrical hyperintensity (arrows); (e) Follow-up after 1 year shows hemorrhagic cavities in bilateral putamina (arrows); (f) Follow-up coronal T2 shows bilateral optic atrophy (arrows). Case 13: (g) and (h) Axial T2 and SWI showing cystic cavities in the bilateral posterior putamina with peripheral hemosiderin rim (arrows)

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Three cases (No. 14, 15, and 16) showed symmetrical T2/FLAIR hyperintensity of bilateral dentate nuclei. Cases 14 and 16 also had splenial hyperintensity on T2 and FLAIR. Additionally, case 14 had symmetrical involvement of bilateral basal ganglia, inferior olivary nuclei, central tegmental tracts, optic chiasma, and optic tracts with evidence of diffusion restriction. Case 16 showed symmetrical hyperintensity of the middle and superior cerebellar peduncles, periaqueductal grey matter and medial thalami. These findings were attributed to nitroimidazole toxicity [Figure 4].
Figure 4: Nitroimidazole toxicity. Case 14: (a) sagittal T2 showing expansion and hyperintensity in corpus callosum splenium (arrow). Case 15: (b) axial FLAIR showing symmetrical hyperintensity in bilateral dentate nuclei (long arrows) and central tegmental tracts (short arrows); (c) axial DWI shows diffusion restriction in bilateral dentate nuclei (arrows). Case 16: (d) axial DWI showing diffusion restriction in the splenium (arrow); (e) sagittal T2 showing hyperintensity in the splenium (arrow); (f) axial FLAIR image shows splenial hyperintensity (arrow)

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Cases 17 and 18 had symmetrical T2/FLAIR hyperintensity of bilateral globus pallidus, periventricular and lobar white matter. DWI restriction was noted in the splenium and genu, bilateral globus pallidus, and parenchymal white matter in case 18. The imaging findings were consistent with carbon monoxide poisoning [Figure 5]a, [Figure 5]b, [Figure 5]c, [Figure 5]d.
Figure 5: (a-d): CO poisoning. Case 17: (a) axial T2 shows bilateral pallidal hyperintensity (arrows). Case 18: (b) axial T2 shows symmetrical globus pallidus hyperintensity (arrows); (c and d) axial DWI shows restriction in B/L centrum semiovale, subcortical white matter, corpus callosum, and globus pallidus (arrows). (e-h) methyl iodide toxicity. Case 19: (e-g) axial FLAIR showing symmetrical hyperintensity in bilateral dentate nuclei (long arrows-E), central tegmental tracts (short arrows-E), dorsal pons and SCP (arrows-F), posterior lentiform nuclei (arrows-G); (h) sagittal T2 showing long tract hyperintensity in the dorsal brainstem (arrow)

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Case 19 with methyl iodide toxicity had symmetrical T2/FLAIR hyperintensity involving bilateral dentate nuclei, globus pallidus, putamen, dorsal pons, periaqueductal grey matter, inferior olivary nuclei with bilateral hypertrophic olivary degeneration [Figure 5]e, [Figure 5]f, [Figure 5]g, [Figure 5]h.

Case 20 was a diagnosed case of multiple intracranial tuberculomas and was on antitubercular therapy. She now presented with progressive ataxia for 4 months. Her present MRI showed symmetrical non-enhancing T2/FLAIR hyperintensity in bilateral dentate nuclei, the ring-enhancing lesions had completely resolved (image not shown).

Cases 21 and 22 had symmetrical calcification in the cerebral grey-white junction, dentate nuclei, and cerebellum. Considering the history and elevated serum lead levels, the findings were diagnostic of lead poisoning [Figure 6]a and [Figure 6]b.
Figure 6: A-Lead poisoning. Case 22: (a and b) axial NCCT showing subcortical calcification at the grey-white junction (arrows-A) and bilateral cerebellar white matter (arrows-B). (c): Hyperglycemia induced hemiballismus and hemichorea. Case 23: (c) axial T1 showing left putaminal hyperintensity (arrow). (d-h): dextropropoxyphene toxicity. Case 24: (d and e) axial FLAIR and T2 showing symmetrical basal ganglia hyperintensity (arrow); (f) axial DWI shows restriction in bilateral caudate head and putamina (arrows); (g) coronal T2 shows symmetrical basal ganglia hyperintensity (arrows); (h) Post-contrast T1 image reveals no enhancement

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Unilateral T1 hyperintensity in the left putamen in case 23, a known diabetic with markedly elevated blood glucose level, was suggestive of hyperglycemia-induced hemiballismus-hemichorea (HIHH) [Figure 6]c.

Symmetrical T2/FLAIR hyperintensity with DWI restriction was noted in bilateral caudate nuclei and putamen in case 24, a case of dextropropoxyphene toxicity [Figure 6]d, [Figure 6]e, [Figure 6]f, [Figure 6]g, [Figure 6]h.

Case 25 had symmetrical T2/FLAIR hyperintensity involving both centrum semiovale, middle cerebellar peduncle, cerebellum and along white matter tracts in the internal capsule and brainstem. T2 hypointensity in bilateral thalami was also seen [Figure 7]. Mild volume loss was also seen in the supra and infratentorial brain parenchyma. These changes were secondary to toluene toxicity.
Figure 7: Toluene abuse. Case 25: (a) and (b) axial FLAIR image showing symmetrical hyperintensity in bilateral periventricular white matter (arrows-A) and peridentate white matter (arrows-B); (c) and (d) axial T2 showing hyperintensity in bilateral centrum semiovale (arrows-C), posterior limb of internal capsules (short arrow-D) and hypointensity in both ventrolateral thalami (long arrow-D); (e) axial T2 showing hyperintensity in bilateral middle cerebellar peduncle (short arrows) and corticospinal tracts (long arrows-E); (f) coronal T2 shows symmetrical hyperintensity in bilateral cerebral and cerebellar white matter (arrows)

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 » Discussion Top

The list of toxins affecting the central nervous system is ever-increasing; the clinical manifestations are usually varied with multicompartmental involvement. Such toxic encephalopathies usually result from various endogenous or exogenous toxins. Although adequate history taking and thorough clinical evaluation can point to the diagnosis of toxic encephalopathy, the cause sometimes remains elusive. Many times, it has been noted that the constellation of imaging findings leads to retrospective interrogation of the patient to elucidate the history of specific toxin intake or accidental/occupational exposure.

Marchiafava-Bignami disease (MBD)

The first description of MBD was in 1903 by Marchiafava and Bignami.[4] It is usually seen in chronic alcoholics.[5] On MRI, T2, and FLAIR images reveal callosal hyperintensity with the involvement of the adjacent white matter. In the acute stage, the parenchymal lesions may show DWI restriction[6] as well as peripheral contrast enhancement. Three patients of MBD in our series had acute presentation: DWI restriction was present in all these three patients while one of them showed contrast enhancement [Case 1, [Figure 1]e]. The most important differential diagnosis of acute presentation is Wernicke encephalopathy (WE).[7]

Wernicke encephalopathy

WE results from a deficiency of thiamine.[8] It is usually seen in chronic alcoholics. Rare causes include post GI surgery, anorexia nervosa, chronic uremia, hyperemesis gravidarum of pregnancy, and parenteral therapy.[9] Two of our patients with WE were pregnant females with hyperemesis gravidarum.

MRI usually reveals altered signal intensity (hyperintense on T2/FLAIR) in the classical distribution—mammillary bodies, thalamus, periaqueductal grey, and midbrain tectum.[10] Atypical sites of signal changes include the dorsal brainstem, cerebellum (deep gray nuclei and white matter), midbrain (red nucleus and substantia nigra), corpus callosum, fornix, and caudate nuclei.[11] Of the six patients of WE in our study, five showed typical MRI findings while one patient had T2/FLAIR hyperintensity of the fornices.

Methanol toxicity

Methanol is often used as a less expensive substitute for the fortification of country-made liquors in developing countries.[12] Approximately, 85–90% of patients present with visual disturbances with about 25% being comatose at the time of admission.[3] All three of our patients had a history of ingestion of local country-made liquor.

CT usually depicts bilateral symmetric hypodense lesions in the putamina with hemorrhagic necrosis seen in 15–25% cases. MRI shows T1 hyperintensity and patchy T2 hypointensity in late acute/subacute stages of hemorrhagic necrosis with blooming on Susceptibility weighted imaging (SWI). Cystic cavitations in the putamen and optic nerve atrophy may be seen in chronic methanol poisoning survivors.[3] Two of our patients had optic nerve atrophy while all three showed cystic cavities in bilateral putamina.

Nitroimidazole toxicity

Metronidazole, tinidazole, and ornidazole are common nitroimidazole derivatives.[13] The findings of metronidazole toxicity on imaging were first illustrated by Ahmed et al.[14] The first case report on ornidazole toxicity by Taskapilioglu et al.[13] demonstrated symmetrical signal changes involving dentate nucleus, dorsal pons, and splenium. In addition to the classical imaging findings, two of our patients in this group also showed involvement of the central tegmental tracts, basal ganglia, medial thalami, and optic chiasma and tracts; one of these had ornidazole while the other had tinidazole toxicity. Peripheral neuropathy during treatment with ornidazole has been previously documented by Desbordes et al.[15] To our knowledge, imaging findings due to tinidazole toxicity have not been previously reported.

Carbon monoxide (CO) toxicity

CO exposure results from sources like partial fuel combustion and can prove fatal.[3],[16] On MRI, symmetrical T2/FLAIR hyperintensities are seen in both globus pallidus with the putamina and caudate nuclei being less affected.[3] Mild T1 hyperintensity may be seen in the lesions within the globus pallidus and substantia nigra reflecting the deposition of hemoglobin degradation products.[16] DWI may reveal symmetrical restriction in cerebral white matter. Basal ganglia changes may develop at a later stage.[17] CO can also lead to delayed leukoencephalopathy in the late subacute period with extensive white matter hyperintensities.[3]

Methyl iodide toxicity

Methyl iodide, a rare toxic inhalant, is usually encountered in the pharmaceutical industry.[18] Our patient worked in a chemical factory and had long-term occupational exposure to this agent.

The patient had symmetrical T2/FLAIR hyperintensities in bilateral dentate nuclei, dorsal pons, periaqueductal region, inferior olivary nucleus, and superior cerebellar peduncles with additional findings of basal ganglia involvement and hypertrophic olivary degeneration. Deshmukh et al.[18] described similar findings in their patient.

Isoniazid toxicity

Patients with isoniazid neurotoxicity presents commonly with peripheral neuropathy and encephalopathy.[19] Our patient had findings similar to the cases described by Deepesh[20] and Prashant Peter.[21] In developing countries where tuberculosis is prevalent, isoniazid toxicity as a complication of antitubercular therapy must be considered in bilateral dentate hyperintensity, with differentials being metronidazole toxicity, enteroviral infections, or atypical WE.[20]

Lead toxicity

Neurotoxicity from heavy metals may be due to chronic or acute exposure.[21] Exposure usually occurs through inhalation or ingestion.[22] Chronic lead toxicity poisoning usually presents with a multitude of neurological symptoms.[23] Lead encephalopathy has been described in patients with oral intake of Ayurvedic drugs. The serum lead level in chronic poisoning is usually more than 40 micrograms/deciliter (normal value < 10).[24] Both the patients in our study had a long-term history of intake of Ayurvedic medicines. The serum lead levels were also elevated in both the patients [Case 21—75 μg/dL and case 22—82 μg/dL]. Lead intoxication results in bilateral symmetric calcification in the cortical grey-white matter junction, cerebellar hemispheres, and ganglio-thalamic regions[24] as was seen in both of our patients.

Hyperglycemia-induced hemiballismus and hemichorea (HIHH)

Patients with uncontrolled diabetes having nonketotic hyperglycemia can present with symptoms of HH, that is, involuntary movements on one side of the entire limb or of both limbs.[25] Although multiple theories behind chorea have been postulated, the exact pathomechanism remains to be elucidated.[26]

Unilateral striatal hyperdensity on non-contrast CT scan is often diagnostic. On MRI, T1 hyperintensity in the basal ganglia is usually seen with diffusion restriction. Signal intensity change may extend up to the cerebral peduncle of the midbrain.[27] Our case had T1 hyperintensity in the left putamen.

Dextropropoxyphene toxicity

Dextropropoxyphene and its various combinations are sold in our country in the trade name of Spasmo-Proxyvon.[28] Dextropropoxyphene is an opioid analog structurally related to methadone. Its L-isomers are responsible for antitussive action whereas analgesic effect resides in the D-isomers. Convulsions and delirium are the major effects of an overdose.

Our patient presented with an acute overdose of dextropropoxyphene. MRI showed symmetrical T2/FLAIR hyperintensity in bilateral basal ganglia with DWI restriction. Blood and urine toxicology evaluation was within normal limits. A thorough review of the existing literature showed no prior documentation of imaging findings of this entity. Hypoxia, secondary to drug-induced respiratory depression, may possibly have led to the basal ganglia signal changes.

Toluene abuse

Toluene, a major component of organic industrial solvents, is found in glues, paint thinners, and ink, and long-term abuse results in chronic solvent encephalopathy.[3] Sniffing is one of the most common methods of solvent abuse and prevalent among adolescents and young adults of the low socioeconomic strata.[29]

Hyperintense signal changes in the cerebral white matter (centrum semiovale and periventricular regions) are common, often extending to involve the subcortical U fibers, internal capsules, pons, and cerebellum. Chronic exposure is also associated with generalized parenchymal atrophy.[3]

Based on the extent of involvement, there may be diffuse or restricted white matter changes. Thalamic T2 hypointensity may be secondary to iron deposits or toluene partitioning into the cell membrane phospholipid layer.[30] Our patient had diffuse white matter changes, T2 hypointensity of bilateral thalami, and mild parenchymal volume loss.

 » Conclusion Top

Toxic encephalopathy has a broad spectrum and a combination of clinical approach and imaging with relevant laboratory investigations helps in arriving at a definitive diagnosis. We present the multifaceted imaging spectrum including both typical and atypical findings of various toxic encephalopathies that were encountered in our tertiary care institution. Through this article, we also present the imaging findings of tinidazole and dextropropoxyphene toxicity, which to our knowledge have not been previously published.

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Conflicts of interest

There are no conflicts of interest.

 » References Top

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  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7]

  [Table 1]


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