Toluene Dependency, Psychosis, and Cerebellar Syndrome

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Back to table of contents Previous article Next article LettersFull AccessToluene Dependency, Psychosis, and Cerebellar SyndromeMohd Fadzli Mohd Isa, M.B.B.S., Norzaini Rose Mohd Zain, M.Med., F.R.C.R., Francesco Gaillard, M.Med., FRANZCR, and Kok-Yoon Chee, M.D., M.Med.Mohd Fadzli Mohd IsaSearch for more papers by this author, M.B.B.S., Norzaini Rose Mohd ZainSearch for more papers by this author, M.Med., F.R.C.R., Francesco GaillardSearch for more papers by this author, M.Med., FRANZCR, and Kok-Yoon CheeSearch for more papers by this author, M.D., M.Med.Published Online:1 Apr 2013https://doi.org/10.1176/appi.neuropsych.12050111AboutSectionsPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InEmail To the Editor: We report on a 22-year-old man who has a 9-year history of glue-sniffing that evolved into a full-blown picture of psychological dependency that was characterized by craving and tolerance, which was subsequently followed by agitation, irritability, and physical struggle. It gradually ended with period of low mood, lack of motivation, and social withdrawal. The disturbance was punctuated by episodes of florid psychosis during intoxication, which included visual hallucination and disorganized behavior. After 6 years of chronic glue-sniffing, there was an insidious onset of bilateral, low-frequency intention tremors involving the upper limbs that gradually worsened and was accompanied by unstable gait, stuttering of speech, and blurring of vision. There was no history to suggest seizure disorder or any infection of the central nervous system. There was a 1-year delay before presentation to medical services due to shame and guilt feelings about coming out of the house because of the physical problems. Mental state examination (MSE) revealed presence of scanning speech and impairment of abstract thinking. He scored 26/30 on Mini-Mental State Exam (MMSE). He had bilateral, persistent, horizontal, pendular nystagmus, and bilateral intention tremors of the hands, broad-based gait, past pointing and dysdiadokinesia of the upper limbs, which were more prominent on the right side. Further examination revealed optic atrophy of the right eye, but sensorimotor functions were normal, and muscle wasting was absent.Blood and urine biochemistry that included measurements of serum lactate and ceruloplasmin were negative, as was the screening for other commonly abused substances. Magnetic resonance imaging (MRI) of the brain demonstrated extensive increased T2 signal in the white matter extending from the centrum semiovale, down the posterior limb of the internal capsule, and through the anterolateral pons, as well as the white matter of the cerebellar hemispheres (Figure 1). Low signal is seen in the deep gray-matter structures, particularly involving the thalami, globus pallidi, and dentate nuclei, as well as the red nuclei and substantia nigra (Figure 2). Widespread cerebral and cerebellar volume loss is also present, with marked thinning of the corpus callosum, without T2 signal change.FIGURE 1. There was extensive increased T2 signal in the white matter, extending from the centrum semiovale, down the posterior limb of the internal capsule, and through the anterolateral pons, as well as the white matter of the cerebellar hemispheres.FIGURE 2. Low signal is seen in the deep gray-matter structures, particularly involving the thalami, globus pallidi, and dentate nuclei, as well as the red nuclei and substantia nigra.T: thalamus; SN: substantia nigra; RN: red nuclei; DN: dentate nuclei; GP: globus pallidus.Treatment was initiated with propranolol 40 mg bid. This was discontinued after 3 months because of lack of efficacy, and he was started on treatment with amantadine 100 mg nightly, primidone 250 mg nightly, and supplemented with thiamine. Despite 6 months of the above treatments, there has been no improvement. He continues to sniff glue, albeit at a much lower frequency and amount.Peripheral neuropathy, cerebellar dysfunction, cranial nerve damage, cortical atrophy, encephalopathy, and dementia have all been attributed to result from prolonged and heavy exposure to inhalants.1,2 N-hexane and toluene adhere to lipid-laden myelin sheaths and neuronal membranes to start the demyelinating process.3 Cerebellar damage due to toluene was first reported three decades ago, and it commonly presents with tremors and ataxia, which correlate to the extent of sulci enlargement.1Dept. of Psychiatry and Mental Health, Hospital Kuala Lumpur, MalaysiaDept. of Diagnostic Imaging, Hospital Kuala Lumpur, MalaysiaDept. of Radiology, Royal Melbourne Hospital, AustraliaCorrespondence: Dr. Kok-Yoon Chee; e-mail: [email protected]comReferences1 Fornazzari L, Wilkinson DA, Kapur BM, et al.: Cerebellar, cortical, and functional impairment in toluene abusers. Acta Neurol Scand 1983; 67:319–329Crossref, Medline, Google Scholar2 Maruff P, Burns CB, Tyler P, et al.: Neurological and cognitive abnormalities associated with chronic petrol sniffing. Brain 1998; 121:1903–1917Crossref, Medline, Google Scholar3 Lolin Y: Chronic neurological toxicity associated with exposure to volatile substances. Hum Toxicol 1989; 8:293–300Crossref, Medline, Google Scholar FiguresReferencesCited byDetailsCited ByDrugs of abuse and ocular effects15 March 2021 | Clinical and Experimental Optometry, Vol. 104, No. 5Schizophrenia Research, Vol. 201The American Journal on Addictions, Vol. 27, No. 8Psychopharmacology, Vol. 232, No. 17Toluene related leukoencephalopathy15 March 2012 Volume 25Issue 2 Spring 2013Pages E42-E43 Metrics PDF download History Published online 1 April 2013 Published in print 1 April 2013