HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Abstract Figures Only Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Keogh, C. F. Articles by Graeb, D. A. Search for Related Content PubMed PubMed Citation Articles by Keogh, C. F. Articles by Graeb, D. A. Social Bookmarking                      What's this?

Neuroimaging Features of Heroin Inhalation Toxicity: "Chasing the Dragon"

¹ Department of Radiology, Vancouver Hospital and Health Sciences Centre UBC Site, 2211 Wesbrook Mall, Vancouver, B. C., V6T 2B5 Canada.
² Department of Neurology, Vancouver Hospital and Health Sciences Centre-UBC Site, Vancouver, B. C., V6T 2B5 Canada.

Received June 10, 2002; accepted after revision July 25, 2002.

 
Address correspondence to C. F. Keogh.

Abstract

Top Abstract Introduction Subjects and Methods Discussion References

 
OBJECTIVE. Our objective was to illustrate the dramatic neuroimaging findings of toxic leukoencephalopathy caused by heroin vapor inhalation.

CONCLUSION. Symmetric abnormality involving the cerebellar white matter and posterior limb of the internal capsule is characteristic of heroin vapor inhalation toxicity, although involvement may be more extensive, depending on the severity of the condition. MR imaging and CT appear to be essential for making this diagnosis because clinical history is often unreliable and findings at physical examination are nonspecific.

Introduction

Top Abstract Introduction Subjects and Methods Discussion References

 
Toxic leukoencephalopathy may be caused by a wide variety of agents, including occupational or environmental exposure, substance abuse, radiation, and chemotherapy [1]. The clinical and radiologic findings are often nonspecific, and an accurate diagnosis may be difficult without a known history of exposure to a particular agent. We present a series of patients with leukoencephalopathy with strikingly similar imaging features related to heroin vapor inhalation toxicity.

Subjects and Methods

Top Abstract Introduction Subjects and Methods Discussion References

 
Within a 5-week period, three patients who were 27-39 years old presented to local university-affiliated hospitals. A CT scan of the initial patient, a 27-year-old man with an altered level of consciousness and spastic paraparesis, revealed extensive symmetric low attenuation involving the cerebellum, brain stem, internal capsule, and cerebral white matter (Figs. 1A,1B,1C). Further evaluation with MR imaging showed dramatic symmetric increased signal in the cerebellar white matter and peduncles, the corticospinal tracts, and the cerebral white matter, particularly posteriorly. Of note was the selective involvement of the posterior limb of the internal capsule and sparing of the subcortical white matter (Figs. 1D,1E,1F). The patient's condition slowly deteriorated, and he died 6 weeks postadmission, after a seizure.

View larger version (121K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 1A. —27-year-old man found at home with decreased level of consciousness, aphasia, and spastic quadraparesis. Patient died after seizure 6 weeks after admission and underwent autopsy. Axial CT scan obtained through cerebellum shows symmetric white matter hypodensity with sparing of cortex.

View larger version (127K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 1B. —27-year-old man found at home with decreased level of consciousness, aphasia, and spastic quadraparesis. Patient died after seizure 6 weeks after admission and underwent autopsy. Axial CT scan obtained through brain at level of third ventricle shows symmetric white matter hypoattenuation in optic radiations and posterior limbs of internal capsule, simulating dragon's claws.

View larger version (114K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 1C. —27-year-old man found at home with decreased level of consciousness, aphasia, and spastic quadraparesis. Patient died after seizure 6 weeks after admission and underwent autopsy. CT scan, obtained cranially relative to A and B, shows more extensive white matter involvement.

View larger version (163K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 1D. —27-year-old man found at home with decreased level of consciousness, aphasia, and spastic quadraparesis. Patient died after seizure 6 weeks after admission and underwent autopsy. Axial T2-weighted MR image obtained through posterior fossa shows white matter hyperintensity in cerebellar white matter, sparing cortex and dentate nuclei. Superior, middle, and inferior peduncles were all involved. Note abnormal signal in pons involving corticospinal tracts (white arrow), medial lemnisci, and central tegmental tracts (black arrow). Findings resemble bearded (dentate nuclei) skull.

View larger version (164K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 1E. —27-year-old man found at home with decreased level of consciousness, aphasia, and spastic quadraparesis. Patient died after seizure 6 weeks after admission and underwent autopsy. Axial T2-weighted MR image obtained through midbrain shows hyperintensity in medial lemnisci and spinothalamic tracts (arrow), with sparing of adjacent substantia nigra and red nuclei. Image resembles bat staring at viewer.

View larger version (154K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 1F. —27-year-old man found at home with decreased level of consciousness, aphasia, and spastic quadraparesis. Patient died after seizure 6 weeks after admission and underwent autopsy. Axial T2-weighted MR image obtained through upper brain reveals extensive signal abnormality tending to preferentially involve posterior white matter. Subcortical white matter (arrows) is spared.

During the same week that the first patient was admitted, a 39-year-old man underwent MR imaging of the head for subacute onset of bradykinesia and ataxia. Although less dramatic, MR findings in this patient were remarkably similar to those of the first patient, with involvement of the cerebellar white matter, posterior limb of the internal capsule, and posterior cerebral white matter (Fig. 2A,2B,2C). The fluid-attenuated inversion recovery sequence (FLAIR) was the most sensitive for revealing the signal abnormality.

View larger version (159K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 2A. —39-year-old man with bradykinesia and ataxia. Axial fluid-attenuated inversion recovery (FLAIR) image shows symmetrically increased signal in cerebellar white matter, peduncles, and pons (white arrow). As in patient shown in Figure 1A,1B,1C,1D,1E,1F,1G,1H, dentate nuclei are spared (black arrow).

View larger version (167K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 2B. —39-year-old man with bradykinesia and ataxia. Axial FLAIR image reveals symmetric abnormal signal in optic radiations (short arrow) and posterior limbs of internal capsule (long arrow). Anterior limb of internal capsule was spared in all patients.

View larger version (127K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 2C. —39-year-old man with bradykinesia and ataxia. Axial FLAIR image shows characteristic involvement of posterior white matter.

View larger version (97K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 1G. —27-year-old man found at home with decreased level of consciousness, aphasia, and spastic quadraparesis. Patient died after seizure 6 weeks after admission and underwent autopsy. Low-power photomicrograph of histopathologic specimen shows normal gray matter (white arrow) and subcortical white matter (curved arrow). Extensive spongiform degeneration and vacuole formation are present in deeper white matter (black arrow). (H and E)

View larger version (86K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 1H. —27-year-old man found at home with decreased level of consciousness, aphasia, and spastic quadraparesis. Patient died after seizure 6 weeks after admission and underwent autopsy. High-power photomicrograph of histopathologic specimen shows spongiform degeneration and vacuole formation. (H and E)

Regarding MR findings, specific questioning revealed that both men inhaled heroin vapor, a practice known as "chasing the dragon" or "chineseing" [2, 3]. The patients had indulged in this practice within the previous 3 weeks. The second patient was also taking methadone as part of a maintenance program.

Five weeks later, a 32-year-old man presented with dysarthria, bradykinesia, and ataxia. The patient was enrolled in a methadone program but had also inhaled heroin 2 weeks previously. CT and MR imaging showed abnormalities (Fig. 3A,3B) in a similar distribution as those of the other two patients, although not as extensive as those in the patient who ultimately died.

View larger version (113K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 3A. —32-year-old man with dysarthria, ataxia, and bradykinesia after inhalation of heroin vapor. Axial CT scan obtained through posterior fossa shows extensive hypodensity in cerebellar hemispheres, with sparing of dentate nuclei, similar to that in patients shown in Figures 1A,1B,1C,1D,1E,1F,1G,1H and 2A,2B,2C.

View larger version (137K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 3B. —32-year-old man with dysarthria, ataxia, and bradykinesia after inhalation of heroin vapor. Axial T2-weighted MR image shows symmetric signal hyperintensity in posterior limbs of internal capsule and optic radiations.

An autopsy was performed on the first patient, which revealed extensive spongiform degeneration of the white matter and formation of vacuoles in the same distribution as the MR abnormalities (Figs. 1G and 1H). These findings are characteristic of heroin inhalation toxicity as described by Wolters et al. [3].

Discussion

Top Abstract Introduction Subjects and Methods Discussion References

 
The term "chasing the dragon" appears to have originated in China in the 1920s and became a popular mechanism of heroin administration in the 1950s in Hong Kong because the drug was cheap but impure. A small quantity of powder is placed on aluminium foil, which is then heated underneath with a lighter or matches. The heroin liquefies into a reddish brown glob, which moves around on the foil and emits a white vapor. The glob or "dragon" is "chased" with the lighter underneath while the vapor is sucked through a straw or pipe. This method of administration avoids the dangers of IV use.

Leukoencephalopathy due to inhalation of heroin pyrolysate was first described by researchers in The Netherlands in 1982 [3]. Clinically, the condition has three stages, progressing from cerebellar signs and motor restlessness to pyramidal and pseudobulbar signs and, in a minority of patients, to a terminal stage characterized by spasms, hypotonic paresis, and ultimately death [3]. Symmetric spongiform degeneration occurs, particularly in the cerebral and cerebellar white matter and in corticospinal and solitary tracts [3].

The MR imaging findings reflected this distribution, with symmetric high signal on T2-weighted and FLAIR sequences in these areas (Figs. 1A,1B,1C,1D,1E,1F,1G,1H and 2A,2B,2C). Involvement of the cerebellum and the posterior limb of the internal capsule, with sparing of the anterior limb, appears to be a characteristic finding in this condition, helping to distinguish it from other causes of leukoencephalopathy such as toluene toxicity or reversible posterior leukoencephalopathy [4, 5]. Although sparing of the subcortical white matter has not been previously described in the imaging literature, it would appear to be typical of this condition. The reason for this striking pattern of involvement is unknown. Kriegstein et al. [2] have shown reduced N-acetyl aspartate and increased cerebral lactate on proton MR spectroscopy in this condition, postulating that these findings reflect mitochondrial toxicity [2].

The particular chemical that causes heroin inhalation toxicity is unknown but is believed to be an occasional impurity that is activated by heating the drug over the aluminium foil.

In our study, all three patients had a definite history of chasing the dragon. Within the following month, two additional patients presented with similar imaging findings. Both patients were known to smoke crack cocaine, but further details could not be obtained. One patient was unresponsive on admission and subsequently died, and the other fled the emergency room after undergoing CT. These additional two patients may also have been dragon chasers, or alternatively, the toxic agent may be an impurity that can be added to heroin or cocaine and is only activated by heating. Unfortunately, samples of the drugs could not be obtained.

Heroin use and intoxication are associated with a number of other effects on the central nervous system, including hypoxic brain injury, transverse myelitis, and brain abscess. The imaging features of these manifestations, however, are nonspecific with regard to cause. Treatment is primarily supportive, although it has been suggested that coenzyme Q and vitamin supplements may be of benefit [2].

In summary, we presented three dramatic cases of toxic leukoencephalopathy related to heroin vapor inhalation. The condition involves the cerebral and cerebellar tracts, with characteristic involvement of the cerebellar and posterior cerebral white matter and the posterior limb of the internal capsule. Because of the illicit nature of the toxin and the variable, nonspecific clinical features, imaging, in particular MR imaging, is invaluable in making the diagnosis. Proton MR spectroscopy is not essential for the diagnosis but may help to elucidate the nature of the condition in the future. With changing practices of drug use, in part to avoid the risks of IV administration, further examples of this condition will likely be encountered.

Acknowledgments
 
We thank P. Chipperfield, T. Hurwitz, and D. Johnston for their information and advice regarding the patients and G. R. W. Moore for pathologic correlation.

References

Top Abstract Introduction Subjects and Methods Discussion References

 

1. Filley CM, Kleinschmidt-DeMasters BK. Toxic leukoencephalopathy. N Engl J Med 2001;345:425 -432[Free Full Text]
2. Kriegstein AR, Shungu DC, Millar WS, et al. Leukoencephalopathy and raised brain lactate from heroin vapor inhalation. Neurology 1999;53:1765 -1773[Abstract/Free Full Text]
3. Wolters EC, Stam FC, Lousberg RJ, et al. Leukoencephalopathy after inhaling heroin pyrolysate. Lancet 1982;2:1233 -1237[Medline]
4. Tan TP, Algra PR, Valk J, Wolters EC. Toxic leukoencephalopathy after inhalation of poisoned heroin: MR findings. AJNR 1994;15:175 -178[Abstract]
5. Hedley-Whyte ET. Leukoencephalopathy and raised brain lactate from heroin vapor inhalation. Neurology 2000;54:2027 -2028[Free Full Text]

CiteULike

Complore

Connotea

Del.icio.us

Digg

Reddit

Technorati

This article has been cited by other articles:

				M. Martin, R. A. Hurley, and K. H. Taber Is Opiate Addiction Associated With Longstanding Neurobiological Changes? J Neuropsychiatry Clin Neurosci, August 1, 2007; 19(3): 242 - 248. [Full Text] [PDF]

				I. G. Hagan and K. Burney Radiology of Recreational Drug Abuse RadioGraphics, July 1, 2007; 27(4): 919 - 940. [Abstract] [Full Text] [PDF]

				S. Molloy, C. Soh, and T.L. Williams Reversible delayed posthypoxic leukoencephalopathy. AJNR Am. J. Neuroradiol., September 1, 2006; 27(8): 1763 - 1765. [Abstract] [Full Text] [PDF]

				W.-C. Chang, C.-P. Lo, H.-W. Kao, and C.-Y. Chen MRI features of spongiform leukoencephalopathy following heroin inhalation Neurology, August 8, 2006; 67(3): 504 - 504. [Full Text] [PDF]

				E Bartlett and D J Mikulis Chasing "chasing the dragon" with MRI: leukoencephalopathy in drug abuse Br. J. Radiol., November 1, 2005; 78(935): 997 - 1004. [Abstract] [Full Text] [PDF]

				A Ryan, F M Molloy, M A Farrell, and M Hutchinson Fatal toxic leukoencephalopathy: clinical, radiological, and necropsy findings in two patients J. Neurol. Neurosurg. Psychiatry, July 1, 2005; 76(7): 1014 - 1016. [Abstract] [Full Text] [PDF]

				O. Halloran, S. Ifthikharuddin, and L. Samkoff Leukoencephalopathy from "chasing the dragon" Neurology, May 24, 2005; 64(10): 1755 - 1755. [Full Text] [PDF]

				K. Okamoto, S. Tokiguchi, T. Furusawa, K. Ishikawa, A. F. Quardery, S. Shinbo, and K. Sasai MR Features of Diseases Involving Bilateral Middle Cerebellar Peduncles AJNR Am. J. Neuroradiol., November 1, 2003; 24(10): 1946 - 1954. [Abstract] [Full Text] [PDF]

This Article Abstract Figures Only Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Keogh, C. F. Articles by Graeb, D. A. Search for Related Content PubMed PubMed Citation Articles by Keogh, C. F. Articles by Graeb, D. A. Social Bookmarking                      What's this?