Solvent abuse (toluene being the major component) is remarkably common, especially in young people with psychosocial stressors, and with chronic use can lead to numerous ill-effects, particularly affecting the central nervous system.
Solvent abuse is geographically widespread, and is particularly common among children and young adults with psychosocial stressors 1.
Clinical presentation is varied and depends on chronicity.
Acute exposure at high enough concentrations results initially in delerium, confusion and incoordination, and eventually (when higher concentrations are reached) hallucinations and psychosis. Decreased consciousness and coma can occur at still higher concentrations 3.
Chronic use, typically of a number of years, results in permanent neurological signs and symptoms including 1,3:
- insomnia: most common
- memory impairment
- cerebellar dysfunction
- temporal lobe epilepsy
The main constituent in most modern solvents is toluene (C7H8), also known as methylbenzene, a lipid-soluble aromatic hydrocarbon. When inhaled toluene is rapidly absorbed into the blood stream and distributed to lipid rich tissues (including the brain) where it accumulated. Demyelination and gliosis are histologically demonstrable in regions of abnormal T2 signal.
The cause of low T2 signal in the basal ganglia and thalami (see below) is uncertain, and could relate to iron deposition 1.
CT changes are non-specific and often absent. Generalised, age-inappropriate, cerebral volume loss may be seen 1.
MRI is the modality of choice for evaluation of cerebral changes related to toluene toxicity.
White matter T2 hyperintensity (focal and diffuse) is the most common finding, seen in approximately 50% of patients, typically after at least 4 years of abuse. Distribution of changes is widespread, typically affecting the periventricular / centrum semiovale, cerebellar hemispheres, internal capsule and brain-stem 1.
Thalamic hypointensity (best seen on T2 weighted images) is seen in 20%, with greater than expected reduced signal aso seen in the red nuclei, substantia nigra and dentate neuclei 1.
Cerebral and cerebellar volume loss, including thinning of the corpus callosum, with associate sulcal and ventricular dilatation is also recognised 1.
Other causes of thalamic hypointensity include metabolic disorders such as caeruloplasmin deficiency and lysosomal storage disorders 2.
- 1. Aydin K, Sencer S, Demir T et-al. Cranial MR findings in chronic toluene abuse by inhalation. AJNR Am J Neuroradiol. 2002;23 (7): 1173-9. AJNR Am J Neuroradiol (full text) - Pubmed citation
- 2. Autti T, Joensuu R, Aberg L. Decreased T2 signal in the thalami may be a sign of lysosomal storage disease. Neuroradiology. 2007;49 (7): 571-8. doi:10.1007/s00234-007-0220-6 - Pubmed citation
- 3. Caldemeyer KS, Pascuzzi RM, Moran CC et-al. Toluene abuse causing reduced MR signal intensity in the brain. AJR Am J Roentgenol. 1993;161 (6): 1259-61. AJR Am J Roentgenol (citation) - Pubmed citation
Toxic and metabolic encephalopathies
- overview by region
- white matter
- grey matter
- by agent/substance
- inhaled toxins
- oral toxins
- drugs (oral or IV)
- by systemic illness
- overview by region
- by substance
- Wernicke encephalopathy (vitamin B1)
- by substance
- Kearns-Sayre syndrome
- Leigh syndrome
- mitochondrial encephalopathy with lactic acidosis and stroke-like episodes (MELAS)
- myoclonus epilepsy with ragged red fibres (MERRF)
- mitochondrial deletion syndromes
- progressive cerebral poliodystrophy (also known as Alpers syndrome)
- trichopoliodystrophy (also known as Menkes disease)