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Solvent Neurotoxicity (Chronic toxic encephalopathy, or CTE)

Timothy C. Hain, MD  Page last modified: February 15, 2015

Overview

Chronic solvent inhalation, also called "chronic painter's disease", is associated with unsteadiness, headache, and psychological disturbances. This is attributed to cumulative slow damage to the lipophilic nervous system. A large body of literature has been created, frequently authored by Scandanavian nationals, perhaps related to a very high level of interest or perhaps the funding availability for study of solvent toxicity in the Scandanavian countries.

Critical reviews of CTE often conclude that the literature has been overly enthusiastic about endorsing the existence of toxicity (Rebert and Hall, 1994), and initial impressions of decreased intellectual performance associated with solvents is sometimes retracted (Gade et al, 1988).

Mechanism:

Solvents are often lipophilic, which enables them to be absorbed by fatty tissue and penetrate the nervous system.

Diagnosis:

CTE is a diagnosis of exclusion, made primarily by combining a history of chronic exposure to solvents , with a constellation of otherwise rather common and somewhat subjective symptoms of unsteadiness, headache, and trouble thinking. Diagnostic criteria are "all over the map" (van Hout et al, 2001). Improvement after removal from solvent exposure is sometimes proposed as a diagnostic criteria (Feldman et al, 1999). This is sensible, but of course, vulnerable to bias.

"Objective" studies, such as pathology, are generally unable to document substantial damage (Nielson et al, 2006).

Neuropsychological studies suggest a fairly high prevalence of "suboptimal performance", meaning not trying (van Hout et al, 2003). However, test performance is adversely correlated with duration of exposure, suggesting that there is also a real effect.

Hearing testing is not correlated with CTE (Niklasson et al, 1998), but reduced visual suppression, prolonged saccadic latency, and reduced posturography scores are sometimes found (Niklasson et al, 1997; Ledin et al, 1991).

MRI imaging has been reported to show decreased signal in the basal ganglia on T2-weighted images, and "diffuse hyper intensity" according to Thuomas et al, 1996. These are unusual finding that ordinarily would not be noticed on MRI. CTE does not cause brain atrophy (Triebig and Lang, 1993; Orbaek et al, 1987), although contrary to this idea, it is well known that ethanol does cause atrophy of the superior vermis of the cerebellum.

Psychological tests show reduced thinking ability (Nilson et al, 1996; Odkvist et al, 1992), that correlates with duration of exposure (Rasmussen et al, 1993). Sabbath et al (2014) divided solvents into subtypes of chlorinated, benzene, and petroleum, and compared 8 different psychometric tests. These included mini-mental, digit substitution, free and cued selective reminding test, phonemic fluency, semantic fluency, and two versions of the trail making test. For individuals with high lifetime solvent exposure, performance was significantly diminished in all tests but the Trail making test version A. Timing of these tests was also often slowed down. Solvents affect working memory, attention and processing speed. Cognitive deficits may never entirely resolve (Sabbath et al, 2014).

Treatment:

Treatment involves withdrawing the individual from exposure and time. In our experience at Chicago Dizziness and Hearing, we expect improvement over months.

Summary:

CTE is a diagnosis of exclusion that combines the elements of long term exposure to solvents, intellectual deterioration, and exclusion of alternatives.


REFERENCES

Copyright August 3, 2016 , Timothy C. Hain, M.D. All rights reserved. Last saved on August 3, 2016