British Journal of Radiology (2007) 80, e243-e246
© 2007 British Institute of Radiology
doi: 10.1259/bjr/40137535
MRI findings in methanol intoxication: a report of two cases
V Arora, MBBS, MD
I B S Nijjar, MBBS, MD
A S Multani, MBBS, MD
J P Singh, MBBS, MD
R Abrol, MBBS, PhD
R Chopra, MBBS, MD
and
R Attri, MBBS, MD
Nijjar Scan and Diagnostic Centre, 51/1, Court Road, Amritsar, Punjab, India
Correspondence: Dr Vijinder Arora, MRI Section, Nijjar Scan Centre, 51/1 Court Road, Amritsar, Punjab, 143001, India. E-mail: dr_vijinderarora{at}yahoo.co.in
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Abstract
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Methanol is a highly toxic substance and acute methanol poisoning produces severe metabolic acidosis and serious neurological symptoms, including severe visual impairment, extrapyramidal signs and coma. Its similarity to ethanol in appearance and odour leads to accidental use. We present two cases of accidental methanol intoxication and discuss the MRI findings.
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Introduction
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Methanol poisoning is a rare but extremely hazardous form of intoxication, generally occuring after suicidal or accidental events. Major methanol poisoning affects the optic nerve and the central nervous system with a predilection for basal ganglia, resulting in symptoms of visual disturbances, blindness, drowsiness, seizures and coma [1, 2]. When a large amount of methanol is ingested, death usually occurs within 3 days [3]. The surviving patient can show permanent sequelae of blindness and motor dysfunction, including rigidity, hypokinesis and other Parkinson-like signs [1, 3, 4]. We present two cases of methanol intoxication and their MR findings.
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Case report
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Patient 1
A 28-year-old man accidentally ingested spirit mistaking it for alcohol. 12 hours after ingestion he had nausea with vomiting and extreme drowsiness. He was referred for an MRI scan 24 hours after ingestion. MRI demonstrated bilateral putaminal lesions, appearing hyperintense on T2 weighted (T2W) images (Figure 1a
) and hypointense on T1 weighted (T1W) images (Figure 1b), suggestive of non-haemorrhagic necrosis. No abnormal signal was identified in the optic nerves. About 10 hours after MRI examination, the patient developed blurred vision and motor dysfunction including rigidity and hypokinesis.
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Figure 1. Turbo spin-echo T2 weighted (a) and spin-echo T1 weighted (b) axial images showing abnormal signal in the putamen bilaterally.
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Now, 5 months later, the patient is well oriented but has persisting visual and extrapyramidal symptoms.
Patient 2
A 50-year-old man with a history of chronic alcoholism presented to the emergency department with headache, dizziness, nausea, vomiting, sudden blurred vision and a fall in the bathroom 16 hours after drinking large quantities of what he thought was locally brewed alcohol. Neurological examination showed extrapyramidal signs and diminished reflexes, and 6/36 vision was established by eye examination. Fundus examination showed a blurred disc margin and hyperemic spots on the retina. A cranial MR study, performed on the sixth day after ingestion, demonstrated bilateral, symmetrical hyperintensities with central hypointensities on T2W images in the putaminal region (Figure 2a), appearing hypointense and hyperintense on T1W images (Figure 2b). High signal intensity on T2W images in the external and internal capsules suggested oedema. In addition, peripheral white matter lesions were identified in both temporal and frontal lobes, with sparing of a thin rim of subcortical white matter (Figure 3a,b).
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Figure 2. Turbo spin-echo T2 weighted (a) and spin-echo T1 weighted (b) axial images showing haemorrhagic necrosis of the putamina.
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Figure 3. Turbo spin-echo T2 weighted axial images showing peripheral white matter hyperintensities in the (a) temporal and (b) frontal lobes (arrows).
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Discussion
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It has been known for more than 80 years that methanol produces several types of toxicity in the human nervous system [5]. Coma and death can develop. In rare cases, complete recovery can follow even a severe intoxication if prompt treatment is instituted. The extent of permanent damage to the central nervous system, retina and optic nerve is related to the amount of methanol ingested [3, 5, 6]. Blindness is the most common symptom and persists after recovery from intoxication [3].
Bilateral basal ganglia lesions have been well documented in early clinicopathological studies. However, why methanol is so selective in its toxicity to the central nervous system has not been well described. One early hypothesis attributed the predilection for putaminal damage to the pattern of venous drainage in the lenticular nucleus [7]. More recent evidence has related methanol toxicity to the relatively greater susceptibility of the optic nerve and basal ganglia to anoxia and ischaemia, possibly as a consequence of their high metabolic rates [8]. Accumulation of a higher concentration of methanol in these areas has also been suggested [7].
The mechanism of methanol toxicity has been closely linked to the effect of formic acid generated from methanol by alcohol dehydrogenase [3, 9, 10]. The initial toxicity is caused by the methanol itself, but this alone does not cause lasting neurological sequelae [4, 11]. The latent period corresponds to the time period during which methanol is converted to formic acid, which is responsible for the acidosis and the toxic effects [9].
The characteristic clinicopathological findings of methanol intoxication are optic neuropathy and bilateral putaminal haemorrhagic and non-haemorrhagic necrosis [12]. Deep and peripheral white matter lesions have also been reported in the literature [13–17], with some reports mentioning sparing of the subcortical white matter [18]. In addition to bilateral haemorrhagic necrosis of the putamen and caudate nuclei and extensive subcortical necrosis, symmetric bilateral necrosis of the pontine tegmentum and optic nerves can occur, which may indicate a poor prognosis [19].
Bilateral putaminal necrosis is by no means specific to methanol toxicity and can also be seen in Wilson's disease, Leigh's disease, Kearns–Sayre syndrome and striatal degeneration associated with Leber's optic atrophy [1]. In addition to these pathologies, carbon monoxide inhalation and hypoxic/anoxic injuries such as near drowning should be considered in the differential diagnosis. However, in carbon monoxide poisoning, the specific focus of toxicity is the globus pallidus, and hypoxic/anoxic injuries additionally involve the caudate nucleus and other central grey nuclei [12].
In methanol intoxication, putaminal necrosis is usually permanent; however, in some series, significant regression of the neurological findings and disappearance of extrapyramidal symptoms are reported [12].
Treatment is by drug elimination (e.g. haemodialysis) and inhibition of the metabolism of methanol to toxic formic acid by competitive inhibition of the enzyme alcohol dehydrogenase (with ethyl alcohol or fomepizole) [20].
Our report illustrates the usual effects of methanol intoxication on the nervous system. The lesion site may be restricted to the putamen, as in our first case and in most similar reports in the literature, or may also involve the white matter, as seen in our second case. In conclusion, when symmetrical lesions are detected in the basal ganglia and white matter along with sudden visual disturbance, methanol intoxication should be considered in the differential diagnosis. Early diagnosis may improve the prognosis in the acute phase.
Received for publication April 28, 2006.
Revision received July 7, 2006.
Accepted for publication July 14, 2006.
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Abstract
Introduction
