More recently, interest has centered on the use of sublingual buprenorphine for the treatment of heroin (and cocaine) abuse; this drug has both opioid agonist and antagonist properties; it mutes the effect of withdrawal, also serves as an aversive agent, and its abuse potential is relatively low. A randomized trial conducted by Fudala and colleagues has demonstrated the superiority over methadone of a combination of buprenorphine and naloxone combined with brief counseling in keeping opioid addicts in treatment and abstinent of abused drugs. This approach has been available in Europe for many years and has been adopted in the United States under a Department of Health–supervised program for primary care offices. In addition, there is evidence, based on animal experiments and experience with small numbers of addicts, that it may be useful for the treatment of dual dependence on cocaine and opiates (see Mello and Mendelson), but this has not been confirmed in other clinical trials.
Medical and Neurologic Complications of Opioid Use
In addition to the toxic effects of the opioid itself, the addict may suffer a variety of neurologic and infectious complications resulting from the injection of contaminated adulterants (quinine, talc, lactose, powdered milk, and fruit sugars) and of various infectious agents (injections administered by unsterile methods). The most important of these is HIV infection, but septicemia, endocarditis, and viral hepatitis may also occur. Particulate matter that is injected with heroin or a vasculitis that is induced by chronic heroin abuse may cause stroke by an incompletely understood occlusion of cerebral arteries, with hemiplegia or other focal cerebral signs. Amblyopia, probably as a result of the toxic effects of quinine in the heroin mixtures, has been reported, as well as transverse myelopathy and several types of peripheral neuropathy. The spinal cord disorder expresses itself clinically by the abrupt onset of paraplegia with a level on the trunk below which motor function and sensation are lost or impaired and by urinary retention. Pathologically, there is an acute necrotizing lesion involving both gray and white matter over a considerable vertical extent of the thoracic and occasionally the cervical cord. In some cases, a myelopathy has followed the first intravenous injection of heroin after a prolonged period of abstinence. We have also seen two cases of cervical myelopathy from heroin-induced stupor and a prolonged period of immobility with the neck hyperextended over the back of a chair or sofa.
In addition, we and others have observed instances of a subacute progressive cerebral leukoencephalopathy after heroin use, similar to ones that occurred in Amsterdam in the 1980s, the result of inhalation of heroin or an adulterant (Wolters et al; Tan et al). Most instances of this leukoencephalopathy are the result of inhalation of heated heroin vapor in a practice known as “chasing the dragon.” The clinical presentation has varied but generally includes stupor, coma, and death, after a latent period of hours or days. In one of our patients, the white matter changes were concentrated in the posterior regions of the hemispheres and in the internal capsules and, in one striking case, in the cerebellar white matter. The MRI is fairly characteristic—widespread white matter hyperintensity involving supratentorial and infratentorial structures, with a predilection for corticospinal fibers above and below the internal capsules, and with sparing of subcortical U-fibers and gray matter structures. The white matter is vacuolated, as indicated by Ryan and colleagues, with an appearance that simulates the spongiform change of prion disease. The pathophysiology is unknown but mitochondrial damage has been suggested. A similar leukoencephalopathy has also been reported in cocaine users, although a hypertensive encephalopathy or an adrenergic-induced vasculopathy may have played a role in these cases.