eMedicine Specialties > Neurology > Neurotoxicology

Methanol: Differential Diagnoses & Workup

Author: Kalyani Korabathina, MD, Department of Neurology, University of South Florida College of Medicine
Coauthor(s): Selim R Benbadis, MD, Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, University of South Florida School of Medicine, Tampa General Hospital; David Likosky, MD, Clinical Instructor, Department of Neurology, University of Washington
Contributor Information and Disclosures

Updated: Mar 15, 2007

Differential Diagnoses

Arsenic
Seizures and Epilepsy: Overview and Classification
Cocaine
Subdural Hematoma
Complex Partial Seizures
Transient Global Amnesia
Head Injury
Uremic Neuropathy
Hyperammonemia
Viral Encephalitis
Inhalants
Viral Meningitis
Multi-infarct Dementia
Paraneoplastic Encephalomyelitis

Other Problems to Be Considered

Ethylene glycol intoxication
Carbon monoxide poisoning
Pseudoseizure
Any cause of altered mental status with acidosis and potential cardiovascular collapse

Workup

Laboratory Studies

  • Renal profile: Significant methanol ingestion leads to metabolic acidosis, which is manifested by a low serum bicarbonate level. The anion gap is increased secondary to high lactate and ketone levels. This is probably due to formic acid accumulation (Jacobsen, 1986).
  • Serum osmolality: Methanol ingestion results in an elevated osmolar gap. This is a nonspecific finding because it may represent the presence of a low molecular weight solute, such as ethanol, other alcohols, mannitol, glycine, lipids, or proteins.
    • A serum glucose measurement is required to calculate the expected plasma osmolality. Calculated osmolality requires a serum glucose measurement (calculated osmolality (mOsm/kg) = 2[Na+] + [glucose/18] + [BUN/2.8]).
    • The osmolar gap can be calculated using a set formula. To find the osmolar gap, take the measured plasma osmolality and subtract the calculated osmolality.
  • Serum amylase: Hemorrhagic pancreatitis has been described in as many as two thirds of the patients.
  • Serum methanol level: Definitive diagnosis of methanol toxicity requires a confirmed increase in the serum methanol level with gas chromatography. Peak levels are achieved 60-90 minutes after ingestion, but they do not correlate with the level of toxicity and thus are not a good indicator of prognosis.

Imaging Studies

  • CT scanning
    • CT scanning may reveal the characteristic changes of bilateral putaminal necrosis with varying degrees of hemorrhage, in addition to involvement of the cerebral white matter. However, the lesions may not be well localized when compared with MRI findings.
    • Moreover, often the initial CT scan is normal and several days may elapse before lesions become evident.
  • Magnetic resonance imaging
    • Characteristic findings are bilateral putaminal necrosis with or without hemorrhage, probably as a result of the direct toxic effects of methanol metabolites. This finding is certainly not specific for methanol toxicity because it can be seen with other diseases, such as Wilson disease, Leigh disease, and stroke (Blanco, 2006).
    • Other findings that have been described include cerebral and intraventricular hemorrhage, diffuse cerebral edema, cerebellar necrosis, subcortical white matter necrosis, optic nerve necrosis, and even enhancement of necrotic lesions (Blanco, 2006).
    • In a series of 4 patients, MRI performed within 2 weeks of methanol intoxication demonstrated changes in the putamen of all 4 patients (Hantson, 1997). Three of these patients had white matter lesions within the occipital/frontal lobes. Interestingly, in patients who recovered without extrapyramidal symptoms, the lesions regressed within several weeks. The authors recommend MRI as both a prognostic tool and to differentiate methanol intoxication from other conditions, such as hypoglycemia and carbon monoxide poisoning.

Other Tests

  • Electroretinography/visual evoked response: Two cases of methanol toxicity were evaluated using these studies. Characteristic findings correlated well with pathologic results and postulated toxicity. Loss of retinal sensitivity was coupled with scotomata in both patients evaluated. In addition, decreased amplitudes were found on visual evoked response testing, although latencies were normal (McKellar, 1997).

More on Methanol

Overview: Methanol
Differential Diagnoses & Workup: Methanol
Treatment & Medication: Methanol
Follow-up: Methanol
References
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References

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Further Reading

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Keywords

organic solvent, formaldehyde, formate, alcohol dehydrogenase, ADH, methanol ingestion, methanol toxicity, methanol intoxication, antifreeze ingestion, perfume ingestion, paint solvent ingestion, photocopying fluid ingestion, windshield washing fluid ingestion, shellac ingestion, inhalation of methanol, methanol fumes, methanol poisoning

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Contributor Information and Disclosures

Author

Kalyani Korabathina, MD, Department of Neurology, University of South Florida College of Medicine
Kalyani Korabathina, MD is a member of the following medical societies: American Academy of Neurology
Disclosure: Nothing to disclose.

Coauthor(s)

Selim R Benbadis, MD, Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, University of South Florida School of Medicine, Tampa General Hospital
Selim R Benbadis, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Sleep Medicine, American Clinical Neurophysiology Society, American Epilepsy Society, and American Medical Association
Disclosure: Nothing to disclose.

David Likosky, MD, Clinical Instructor, Department of Neurology, University of Washington
David Likosky, MD is a member of the following medical societies: American Academy of Neurology, American College of Physicians-American Society of Internal Medicine, and American Heart Association
Disclosure: Nothing to disclose.

Medical Editor

Jonathan S Rutchik, MD, MPH, Assistant Professor, Department of Occupational and Environmental Medicine, University of California at San Francisco
Jonathan S Rutchik, MD, MPH is a member of the following medical societies: American Academy of Neurology and Association of American Physicians and Surgeons
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Nestor Galvez-Jimenez, MD, Program Director of Movement Disorders, Department of Neurology, Division of Medicine, Director of Neurology Residency Training Program, Cleveland Clinic Florida
Nestor Galvez-Jimenez, MD is a member of the following medical societies: American Academy of Neurology, American College of Physicians, and Movement Disorders Society
Disclosure: Nothing to disclose.

CME Editor

Matthew J Baker, MD, Consulting Staff, Collier Neurologic Specialists, Naples Community Hospital
Matthew J Baker, MD is a member of the following medical societies: American Academy of Neurology
Disclosure: Nothing to disclose.

Chief Editor

Nicholas Y Lorenzo, MD, Chief Editor, eMedicine Neurology; Consulting Staff, Neurology Specialists and Consultants
Nicholas Y Lorenzo, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Neurology
Disclosure: Nothing to disclose.

 
 
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