| Identifier |
walsh_2022_s3_c2 |
| Title |
The Nidus of the Neuropathy |
| Creator |
Heather McDonald, Adrian Budhram, J Alexander Fraser, Lulu LCD Bursztyn |
| Subject |
optic neuropathy, afferent visual pathways, vision loss binocular, optic tract, magnetic resonance imaging (MRI) |
| History |
A 57-year-old female presented with a one-year history of paresthesias, gait instability, slurred speech, peripheral; numbness, and fatigue. A non-contrast CT Head showed lower density in the corpus callosum. Follow-up MR Head showed; T2/FLAIR hyperintensity and diffusion restriction in the splenium of the corpus callosum, lentiform nucleus, dentate; nucleus, and left frontal lobe. Shortly thereafter, she reported decreased vision and colour perception in her left eye; (history right amblyopia). Six months later, she developed hyperacusis, limb weakness, and dysregulation of movements.; Repeat MR Head demonstrated more extensive high-signal change throughout the entire corpus callosum and new lesions; in the left internal capsule, caudate nuclei, anterior commissure, optic tracts, and red nuclei. The lesions in the dentate; nucleus had resolved. Past medical history was significant for migraine, ulcerative colitis and recurrent pouchitis treated; with metronidazole prophylactically for the past decade. She had multiple previous bowel surgeries including a colectomy.; She sustained whiplash from a motor vehicle accident 7 years ago. She previously worked in an automotive factory where; she was exposed to gas leaks. On exam, the patient was alert and oriented. BCVA measured 20/400 bilaterally. Pupils were; equal and reactive to light with a right RAPD. Extraocular movements were full without nystagmus. There was right; esotropia of 10PD. The remainder of the cranial nerve exam was normal. Slit lamp examination revealed mild cataracts; bilaterally and crowded, hyperemic discs with no pallor or hemorrhages. Power measured 5/5 throughout. Muscle; bulk/tone were normal, without spastic catch or clonus. Bilateral action and intention tremors, dysdiadochokinesia, and; heel-to-shin lower limb ataxia were present. Sensory exam demonstrated 50% decrease to pin prick in a glove and stocking; distribution. Deep tendon reflexes were normal throughout. Plantar reflexes were downgoing, pronator drift was absent,; and proprioception testing was normal. Gait testing demonstrated significant difficulty with tandem gait. EMG studies; revealed a length-dependent, predominantly sensory axonal polyneuropathy. |
| Disease/Diagnosis |
A diagnosis of metronidazole neurotoxicity was suspected based on suggestive MRI features and confirmed by symptom; resolution with discontinuation of the drug. Metronidazole neurotoxicity is a rare but very serious potential side effect of; the medication, characterized by peripheral neuropathy and encephalopathy, with classic findings on MRI (1).; Metronidazole is a nitroimidazole antibiotic that targets anaerobic bacteria and can easily cross the blood-brain barrier,; leading to high concentrations in the CNS (2). There are several theories regarding the pathogenesis of its toxic effects,; including its potential to bind RNA and cause reversible axonal swelling (3), but none have been fully validated. On average,; toxicity occurs approximately 54 days after initiating treatment, but can develop anywhere from 2 days to 8 years after; starting the antibiotic (1,2). The most classic findings on neuroimaging are hyperintense T2/FLAIR lesions seen in the; dentate nucleus. The patient's neuroimaging demonstrated these typical lesions initially, but not later in her course. She; had hyperintensities seen in the corpus callosum, which are also very common (44% of patients) (1). Characteristic; presenting signs and symptoms of metronidazole neurotoxicity include gait instability, dysarthria, limb discoordination, and; peripheral neuropathy; all of which the patient demonstrated (1,2). Altered mental status and seizures may also be present.; However, optic neuropathy in the context of metronidazole neurotoxicity is extremely rare. There are 11 cases of; metronidazole-induced optic neuropathy reported in the literature (4). The majority of patients (8/11) had reversible vision; loss which resolved spontaneously with discontinuation of metronidazole, but irreversible vision loss has been reported,; underscoring the importance of early diagnosis (4). Oculomotor disturbances including nystagmus, diplopia, abducens; paresis, saccadic pursuit disruption, and gaze palsies are reported in 23% of cases (1). Of note, Wernicke's encephalopathy; must be ruled out in these patients as it can present with a similar clinical and radiological picture (5). |
| Date |
2022-02 |
| References |
1. Sørensen, Karlsson, Amin, Lindelof. Metronidazole-induced encephalopathy: a systematic review, J Neurol, 267, 1-; 13, 2020.; 2. Kuriyama, Jackson, Doi, Kamiya. Metronidazole-induced central nervous system toxicity: a systematic review, Clin; Neuropharmacol, 34, 241-7, 2011.; 3. Bradley, Karlsson, Rassol. Metronidazole neuropathy, Br Med J, 2, 610-1, 1977.; 4. Peng, Wu, Lin. Metronidazole-Induced Irreversible Optic Neuropathy, Case Rep Ophthalmol, 12, 392-5, 2021. 5. Agarwal, Kanekar, Sabat, Thamburaj. Metronidazole-Induced Cerebellar Toxicity, Neurol Int, 8, 6365, 2016. |
| Format |
application/pdf |
| Type |
Text |
| Source |
54th Annual Frank Walsh Society Meeting |
| Relation is Part of |
NANOS Annual Meeting 2022: Walsh Session III |
| Publisher |
Spencer S. Eccles Health Sciences Library, University of Utah |
| Rights Management |
Copyright 2022. For further information regarding the rights to this collection, please visit: https://NOVEL.utah.edu/about/copyright |
| ARK |
ark:/87278/s60sakf4 |
| Contributor Primary |
Heather M. McDonald, BSc, MD |
| Contributor Secondary |
Adrian Budhram, J Alexander Fraser, Lulu LCD Bursztyn |
| Setname |
ehsl_novel_fbw |
| ID |
2100240 |
| Reference URL |
https://collections.lib.utah.edu/ark:/87278/s60sakf4 |
