0
Get Alert
Please Wait... Processing your request... Please Wait.
You must sign in to sign-up for alerts.

Please confirm that your email address is correct, so you can successfully receive this alert.

1
Letters   |    
Toluene Dependency, Psychosis, and Cerebellar Syndrome
Mohd Fadzli Mohd Isa, M.B.B.S.; Norzaini Rose Mohd Zain, M.Med., F.R.C.R.; Francesco Gaillard, M.Med., FRANZCR; Kok-Yoon Chee, M.D., M.Med.
The Journal of Neuropsychiatry and Clinical Neurosciences 2013;25:E42-E43. doi:10.1176/appi.neuropsych.12050111
View Author and Article Information

Dept. of Psychiatry and Mental Health, Hospital Kuala Lumpur, Malaysia
Dept. of Diagnostic Imaging, Hospital Kuala Lumpur, Malaysia
Dept. of Radiology, Royal Melbourne Hospital, Australia

Correspondence: Dr. Kok-Yoon Chee; e-mail: cheekokyoon@yahoo.com

Copyright © 2013 American Psychiatric Association

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.

 
Anchor for JumpAnchor for Jump
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.
 
Anchor for JumpAnchor for Jump
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.1

Fornazzari  L;  Wilkinson  DA;  Kapur  BM  et al:  Cerebellar, cortical, and functional impairment in toluene abusers.  Acta Neurol Scand 1983; 67:319–329
[CrossRef] | [PubMed]
 
Maruff  P;  Burns  CB;  Tyler  P  et al:  Neurological and cognitive abnormalities associated with chronic petrol sniffing.  Brain 1998; 121:1903–1917
[CrossRef] | [PubMed]
 
Lolin  Y:  Chronic neurological toxicity associated with exposure to volatile substances.  Hum Toxicol 1989; 8:293–300
[CrossRef] | [PubMed]
 
References Container

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.

+

References

Fornazzari  L;  Wilkinson  DA;  Kapur  BM  et al:  Cerebellar, cortical, and functional impairment in toluene abusers.  Acta Neurol Scand 1983; 67:319–329
[CrossRef] | [PubMed]
 
Maruff  P;  Burns  CB;  Tyler  P  et al:  Neurological and cognitive abnormalities associated with chronic petrol sniffing.  Brain 1998; 121:1903–1917
[CrossRef] | [PubMed]
 
Lolin  Y:  Chronic neurological toxicity associated with exposure to volatile substances.  Hum Toxicol 1989; 8:293–300
[CrossRef] | [PubMed]
 
References Container
+
+

CME Activity

There is currently no quiz available for this resource. Please click here to go to the CME page to find another.
Submit a Comments
Please read the other comments before you post yours. Contributors must reveal any conflict of interest.
Comments are moderated and will appear on the site at the discertion of APA editorial staff.

* = Required Field
(if multiple authors, separate names by comma)
Example: John Doe



Related Content
Books
Gabbard's Treatments of Psychiatric Disorders, 4th Edition > Chapter 11.  >
Gabbard's Treatments of Psychiatric Disorders, 4th Edition > Chapter 1.  >
Gabbard's Treatments of Psychiatric Disorders, 4th Edition > Chapter 1.  >
Gabbard's Treatments of Psychiatric Disorders, 4th Edition > Chapter 50.  >
Manual of Clinical Psychopharmacology, 7th Edition > Chapter 1.  >
Topic Collections
Psychiatric News
Read more at Psychiatric News >>
PubMed Articles