heroin and Brain-Diseases

Heroin-associated spongiform leukoencephalopathy is a rare, and sometimes fatal, condition usually caused by vapor inhalation of heroin. The authors report a 41-year-old man who was diagnosed with delayed spongiform leukoencephalopathy three weeks after injecting heroin intravenously. He had been admitted to another hospital due to acute heroin overdose, which had occurred four hours after intravenous injection of an unknown amount of heroin. His clinical condition showed progressive improvement and he was discharged 12 days after admission. Three weeks after this episode, his cognitive functioning declined. Akinetic mutism, spasticity and hyperreflexia of all extremities were observed. Electroencephalography (EEG) and imaging of the brain showed typical characteristics of spongiform leukoencephalopathy. The three and six-month follow-up of the patient showed clinical improvement and this was corroborated through EEG measures and brain imaging. The discussion summarizes eight previously reported cases of intravenous heroin associated spongiform leukoencephalopathy and compares them to the authors'case.

Topics: Adult; Brain; Brain Diseases; Electroencephalography; Follow-Up Studies; Heroin; Humans; Injections, Intravenous; Leukoencephalopathies; Male

"Chasing the dragon" refers to the inhalation of heroin pyrolysate vapors produced when the freebase form of heroin is heated. Inhalation of these vapors can result in a rare toxic spongiform leukoencephalopathy. The patients may progress through 3 defined clinical stages, with one-quarter reaching the terminal stage, which invariably leads to death. Imaging and, in particular, magnetic resonance imaging (MRI) demonstrates white matter findings that are felt to be specific for this entity and essential in its early diagnosis. We present the typical imaging findings in a pictorial essay format, using images taken from 9 patients who presented within an 18-month period at UBC-affiliated hospitals. These findings include low computed tomography (CT) attenuation and high T2 MRI signal most commonly in the posterior cerebral and cerebellar white matter, cerebellar peduncles, splenium of the corpus callosum, and posterior limb of the internal capsules. In addition, there is often selective, symmetric involvement of the corticospinal tract, the medial lemniscus, and the tractus solitarius. We also present the variable diffusion-weighted imaging and apparent diffusion coefficient findings from 4 of our patients, which to our knowledge, have not been described in the literature.

Topics: Administration, Inhalation; Brain Diseases; Heroin; Humans; Magnetic Resonance Imaging; Narcotics

A spongiform leucoencephalopathy sometimes develops as a result of inhaling illicit heroin as well as due to carbon monoxide-intoxication. Clinically psychiatric symptoms precede a neurological deterioration. Some patients die. After a brief description of several epidemiological and historical-cultural aspects regarding the smoking of opiates, the typical neuroradiological signs such as hypodensity of the white matter in CCT and signal alterations in MRT, and neuropathological sequelae such as intramyelinic vacuolisation are listed. Pathophysiologically an edema of the white matter in the beginning is suspected. Second, a dysfunction of the mitochondria is addressed relying on the particular metabolism of the oligodendrocytes. Since smoking of heroin is an increasingly preferred way of application in all continents and therapeutic options are still lacking, the need of further explanation of the underlying processes is stressed.

Topics: Administration, Inhalation; Brain; Brain Diseases; Carbon Monoxide Poisoning; Heroin; Heroin Dependence; Humans; Magnetic Resonance Imaging; Tomography, X-Ray Computed

Although brain metabolism consumes high amounts of energy and is accompanied by intense heat production, brain temperature is usually considered a stable, tightly regulated homeostatic parameter. Current animal research, however, has shown that different forms of functional neural activation are accompanied by relatively large brain hyperthermia (2-3 degrees C), which has an intra-brain origin; cerebral circulation plays a crucial role in dissipating this potentially dangerous metabolic heat from brain tissue. Brain hyperthermia, therefore, reflects enhanced brain metabolism and is a normal physiological phenomenon that can be enhanced by interaction with common elements of an organism's environment. There are, however, instances when brain hyperthermia becomes pathological. Both exposure to extreme environmental heat and intense physical activity in a hot, humid environment restrict heat dissipation from the brain and may push brain temperatures to the limits of physiological functions, resulting in acute life-threatening complications and destructive effects on neural cells and functions of the brain as a whole. Brain hyperthermia may also result from metabolic activation induced by various addictive drugs, such as heroin, cocaine, and meth-amphetamine (METH). In contrast to heroin and cocaine, whose stimulatory effects on brain metabolism invert with increases in dose, METH increases brain metabolism dose-dependently and diminishes heat dissipation because of peripheral vasoconstriction. The thermogenic effects of this drug, moreover, are enhanced during physiological activation, resulting in pathological brain hyperthermia. Since brain hyperthermia exacerbates drug-induced toxicity and is destructive to neural cells, uncontrollable use of amphetamine-like drugs under conditions restricting heat dissipation from the brain may result both in acute life-threatening complications and clinically latent but dangerous morphological and functional brain destruction.

Topics: Animals; Brain; Brain Diseases; Cocaine; Fever; Heroin; Hot Temperature; Humans; Methamphetamine; Physical Exertion; Thermogenesis

Topics: Abscess; Adult; Animals; Autopsy; Blindness; Brain Diseases; Cerebrovascular Disorders; Endocarditis; Haplorhini; Hepatitis A; Heroin; Heroin Dependence; Humans; Male; Muscular Diseases; Myelitis, Transverse; Nervous System Diseases; New York City; Peripheral Nervous System Diseases; Quinine; Substance-Related Disorders; Tetanus

Topics: Acute Disease; Brain Diseases; Brain Injuries; Chronic Disease; Gas Poisoning; Heart Diseases; Heroin; Humans; Hypersensitivity; Iatrogenic Disease; Infusions, Parenteral; Kidney Failure, Chronic; Mountaineering; Pulmonary Edema; Radiography; Renal Dialysis; Sympathomimetics

The compulsion to seek and use heroin is frequently driven by stress and craving during drug-cue exposure. Although previous neuroimaging studies have indicated that craving is mediated by increased prefrontal cortex activity, it remains unknown how heroin administration modulates the prefrontal cortex response. This study examines the acute effects of heroin on brain function in heroin-maintained patients. Using a crossover, double-blind, placebo-controlled design, 27 heroin-maintained patients performed functional magnetic resonance imaging 20 minutes after the administration of heroin or placebo (saline) while drug-related and neutral stimuli were presented. Images were processed and analysed with statistical parametric mapping. Plasma concentrations of heroin and its main metabolites were assessed using high-performance liquid chromatography. Region of interest analyses showed a drug-related cue-associated blood-oxygen-level-dependent activation in the orbitofrontal cortex (OFC) in heroin-dependent patients during both treatment conditions (heroin and placebo). This activation of the OFC was significantly higher after heroin than after placebo administration. These findings may indicate the importance of OFC activity for impulse control and decision-making after regular heroin administration and may emphasize the benefit of the heroin-assisted treatment in heroin dependence.

Topics: Adult; Brain Diseases; Craving; Cues; Female; Gray Matter; Heroin; Heroin Dependence; Humans; Magnetic Resonance Imaging; Male; Narcotics; Neuropsychological Tests; Organ Size; Prefrontal Cortex

To evaluate the therapeutic effects of the glucocorticoid on heroin-induced spongiform leucoencephalopathy.. Twenty cases of heroin-induced spongiform leucoencephalopathy were randomly divided into the control group and the treating group with equal number. In the control group, the treatment was constituted by oral administration of vitamin B and coenzyme Q10 in a course of 1 month. In glucocorticoid treatment group, glucocorticoid (20 mg/d) for 10 d were given in addition to vitamin B and coenzyme Q10, and the dose of the glucocorticoid was gradually decreased afterwards. General observation and statistical analysis of function scores were performed in both groups before and 1, 6, 12 months after the treatment respectively.. No significant difference in function scores was observed between the 2 groups, while the results of observation before and after the treatment were significantly different (P<0.05). The most significant difference occurred when comparing the observations made 1 month and 6 months respectively after treatment (P<0.001).. Glucocorticoid has no obvious therapeutic effect on heroin-induced spongiform leucoencephalopathy, and rapid clinical recovery occurs within the initial 6 months of the treatment.

Topics: Adult; Brain Diseases; Female; Glucocorticoids; Heroin; Humans; Leukoencephalopathy, Progressive Multifocal; Male; Treatment Outcome

At age 16, I injected morphine for the first time, and then started injecting heroin. By most standards, I was highly functioning, although I eventually became addicted. I was and remain socioeconomically privileged, but my relationship to heroin resulted in behaviors and consequences that I never could have conceived of, and which I sometimes strain to remember occurred. My life now is stable and conventional. Some aspects of my past addiction are unerasable, but the most salient of those are the social and legal consequences of having a criminal record-not any hallmarks of a chronic brain disease or disorder. I do not consider myself "in recovery." Rather, I am recovered, by standards both my own and derived from clinical nosology. I have been in sustained remission for over a decade. Yet feelings are not facts, as is often said. I still use alcohol, and occasionally (though not recently) I have used other drugs, so there remains the possibility that my brain is indeed "diseased" and I am not objectively recovered, my self-assessment notwithstanding. My aim in writing about my lived experience of drug use, addiction, and recovery is to highlight the heterogeneity of people's experiences and the insight that personal narratives can provide. Debates about the brain disease model of addiction are often confined to academia, with the real-world, unintended consequences of the "disease" label seldom considered. Stigmatization of people with addiction comes from moralizing about drug use but may also originate from well-intended labels. I posit that we should not need labels to care about addicted people and make scientifically informed treatment accessible. Addicted people deserve help because they either need or want it, regardless of labels that presume to describe the etiology or likely trajectory of their problems. I conclude that some labels, even those needed for clinical classification of human behavior, may be pernicious. Clinicians and researchers have an obligation to reflect more deeply on the implications of the disease conceptualization of complex human behaviors such as addiction.

Topics: Adolescent; Behavior, Addictive; Brain Diseases; Heroin; Humans; Substance-Related Disorders

A 26-year-old man with a 3-year history of heroin vapor inhalation developed spongiform leukoencephalopathy. T2-weighted magnetic resonance imaging showed characteristic high signals over subcortical white matter, including bilateral frontoparietal lobes, posterior limbs of internal capsules, splenium, occipital lobes, cerebellum and brainstem. Signal intensity of diffusion-weighted imaging was high, and apparent diffusion coefficient in corresponding areas was increased. Pathologic features of heroin induced spongiform leukoencephalopathy were unique, characterized by demyelination and vacuolar formation. 99m-Technetium-ECD SPECT and F18 FDG PET demonstrated decreased radiotracer uptake in the corresponding areas. 99m-Technetium-TRODAT SPECT showed no definite decreased uptake of radiotracer at basal ganglia, which suggests that the dopamine neurons were not affected.

Topics: Administration, Inhalation; Adult; Brain; Brain Diseases; Heroin; Humans; Male; Narcotics; Tomography, Emission-Computed, Single-Photon; Volatilization

Topics: Adult; Brain Diseases; Heroin; Heroin Dependence; Humans; Inhalation; Magnetic Resonance Imaging; Male

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

Topics: Administration, Inhalation; Adult; Brain Diseases; Heroin; Humans; Magnetic Resonance Imaging; Male; Narcotics; Tomography, X-Ray Computed

We present serial neuropsychological, magnetic resonance (MR) imaging and EEG changes in a case of widespread CNS myelinopathy due to intravenous heroin overdose complicated by a period of prolonged unconsciousness. Following recovery from the acute overdose, the subject had the delayed onset of akinetic mutism with urinary incontinence. Sequential formal neuro-psychological assessments over 9 months showed evolution from severe global cerebral dysfunction to moderate disturbance of frontal lobe function. Almost complete resolution of diffuse white matter signal changes, accompanied by the development of a degree of volume loss, was evident on serial MR imaging over the same period, and generalized arrhythmic delta-range slowing on the EEG evolved int o a near normal pattern.

Topics: Akinetic Mutism; Brain Diseases; Electroencephalography; Heroin; Heroin Dependence; Humans; Injections, Intravenous; Magnetic Resonance Imaging; Male; Middle Aged; Narcotics; Neuropsychological Tests; Recovery of Function; Unconsciousness

We report the case of a 41 year old patient who developed a severe cerebellar ataxia. MRI findings were suggestive of myelin damage with symmetrical involvement of the cerebellar hemispheres and, to a lesser extent, the decussation of the superior cerebellar peduncles, the corticospinal tracts and the centrum semiovale. He had been inhaling heroin for the last 5 years. Two years after stopping heroin, he showed clinical improvement with partial regression of the MRI lesions. MRI findings of leucoencephalopathy after heroin inhalation are well described in the literature, however longitudinal studies are rare. It is the purpose of this report to show that clinical and MRI features can be characteristic of this leucoencephalopathy and that regression of white matter lesions can be seen after heroin withdrawal.

Topics: Administration, Inhalation; Adult; Brain Diseases; Heroin; Humans; Magnetic Resonance Imaging; Male; Narcotics; Neurodegenerative Diseases; Remission Induction

Inhalation of heated heroin vapor ("chasing the dragon"), which is gaining popularity among drug users seeking to avoid the risks of parenteral drug administration, can produce progressive spongiform leukoencephalopathy.. We studied the clinical phenotype and course, MRI, MRS, and brain pathology in the first American patients described with this syndrome.. Two of the three heroin users studied inhaled heroin pyrolysate together daily over the course of 2 weeks. They developed ataxia, dysmetria, and dysarthria. Patient 1 progressed to an akinetic mute state with decorticate posture and subsequent spastic quadriparesis. Patient 2 developed a mild spastic quadriparesis and gait freezing. Patient 3 was asymptomatic following less heroin exposure. Brain MRI showed diffuse, symmetrical white matter hyperintensities in the cerebellum, posterior cerebrum, posterior limbs of the internal capsule, splenium of the corpus callosum, medial lemniscus, and lateral brainstem. MRS showed elevated lactate. Brain biopsy (Patient 1) showed white matter spongiform degeneration with relative sparing of U-fibers; electron microscopy revealed intramyelinic vacuolation with splitting of intraperiod lines. Progressive deterioration occurred in Patients 1 and 2 over 4 weeks. Both were treated with antioxidants including oral coenzyme Q, and clinical improvement occurred. Patient 1 recovered nearly completely over 24 months. Patient 2 improved, but developed a delayed-onset cerebellar hand tremor. Both still have white matter abnormalities on MRI and MRS.. Elevated lactate in white matter and the possible response to antioxidants suggests mitochondrial dysfunction in progressive spongiform leukoencephalopathy following inhalation of heated heroin vapor.

Topics: Administration, Inhalation; Adult; Antioxidants; Biopsy; Brain; Brain Diseases; Female; Heroin; Humans; Lactic Acid; Magnetic Resonance Imaging; Magnetic Resonance Spectroscopy; Male; Phenotype; Ubiquinone

Topics: Administration, Inhalation; Adult; Brain Diseases; Cocaine; Female; Heroin; Humans; Male; Substance-Related Disorders

Here we report the clinical and pathological findings in a 30-year-old drug addict in whom an intravenous injection of heroin led to reversible coma with respiratory depression and heart failure. On regaining consciousness, the patient was found to have rhabdomyolysis with renal failure requiring dialysis and peripheral neuropathy. Three weeks later his neurological condition suddenly deteriorated and delayed encephalopathy developed, leading to death 20 days later. The neuropathological study of the brain disclosed pale, spongy myelin with diffuse reactive astrogliosis and microglial proliferation, without hypoxic necrotic lesions. The cerebral and cerebellar cortices were unchanged. The absence of typical hypoxic lesions and the presence of spongiosis with massive astrocytosis distinguished this case from the previously reported cases of delayed leukoencephalopathy following severe hypoxia. An immunocytochemical study designed to exclude an underlying alteration of the metabolic oxidative pathway detected normal expression of the respiratory chain complexes IV, III and V. Despite the absence of an oxidative chain alteration in our patient, we cannot exclude the possibility that an individual predisposition played a pathogenetic role in this delayed leukoencephalopathy.

Topics: Adult; Brain Diseases; Demyelinating Diseases; Heroin; Humans; Immunohistochemistry; Injections, Intravenous; Male; Rhabdomyolysis; Substance Abuse, Intravenous

A 25-year-old man presented in March 1996 with progressive dysarthria, cerebellar ataxia, and dystonia, which began after he inhaled heroin vapor for a full day 2 months previously. The patient had a 2-year history of heroin inhalation. Magnetic brain stimulation showed waveform dysynchronization suggestive of motor pathway perturbation above the cervical spinal level. Brain computed tomography and magnetic resonance imaging revealed extensive symmetric white matter involvement of bilateral cerebral and cerebellar hemispheres and the brainstem, especially along the corticospinal tract. The clinical features, electrophysiologic manifestations, and imaging studies strongly indicated a lipophilic toxin-induced demyelinating process, mainly involving the central motor system, as the most likely cause of heroin leukoencephalopathy. This is the first reported case of heroin-related leukoencephalopathy in Taiwan.

Topics: Administration, Inhalation; Adult; Brain Diseases; Heroin; Humans; Male; Substance-Related Disorders

Topics: Administration, Oral; Brain Diseases; Child, Preschool; Heroin; Humans; Male

A 20-year-old male heroin addict had a sudden onset of progressive medullary dysfunction and died within 12 days. Postmortem examination disclosed mycotic granulomas due to primary chromoblastomycosis strictly limited to the medulla oblongata and adjacent leptomeninges. Similar lesions were absent outside the central nervous system. Such pathologic lesions related to narcotic addiction have not been reported previously.

Topics: Adult; Brain Diseases; Chromoblastomycosis; Heroin; Humans; Male; Medulla Oblongata; Substance-Related Disorders

47 patients with spongiform leucoencephalopathy but no other consistent abnormalities, except brown pigmentation of the alveolar macrophages in the lungs, are described. 11 patients have died. Epidemiological studies indicate at the cause of the illness the inhalatory use of poisoned heroin vapours (pyrolysate). The heroin is primarily sold on the black market in Amsterdam. The Netherlands. Over 170 suspect heroin samples were collected for analysis of the possible poisonous factor. Although suspect, none of the samples could be unambiguously related to the observed illness. Chemical, toxicological, and histopathological investigations have not so far revealed the nature of the poisonous factor, but several neurotoxic agents that are known to cause comparable leucoencephalopathies have been ruled out. This appears to be the first manifestation of the poisonous potential of the unknown causative factor.

Topics: Adolescent; Adult; Brain; Brain Diseases; Female; Heroin; Heroin Dependence; Humans; Male; Netherlands; Smoke; Tomography, X-Ray Computed; Volatilization

Topics: Adolescent; Adult; Brain; Brain Diseases; Drug Contamination; Female; Heroin; Heroin Dependence; Humans; Male

Topics: Adult; Brain Diseases; Deglutition Disorders; Dexamethasone; Drug Hypersensitivity; Heroin; Humans; Male; Pons; Quadriplegia; Speech Disorders; Spinal Cord Diseases; Substance-Related Disorders

Topics: Adolescent; Adult; Brain Diseases; Heroin; Humans; Male; Paraplegia

Topics: Adolescent; Brain Diseases; Coma; Decerebrate State; Electroencephalography; Heroin; Humans; Hypoxia; Male; Neurologic Examination; Substance-Related Disorders; Time Factors; Vision Disorders

Topics: Adult; Brain Diseases; Encephalitis; Fungi; Heroin; Humans; Infections; Injections, Intravenous; Male; Morphine Dependence; Mycoses

Topics: Adult; Aged; Brain Diseases; Cerebral Cortex; Endocarditis, Bacterial; Female; Fungi; Granuloma; Heroin; Humans; Male; Meningitis; Middle Aged; Morphine Dependence; Substance-Related Disorders

Topics: Adolescent; Biliary Tract Diseases; Brain Diseases; Chemical and Drug Induced Liver Injury; Child; Chronic Disease; Electroencephalography; Exchange Transfusion, Whole Blood; Female; Hepatic Encephalopathy; Hepatitis; Heroin; Humans; Male; Methods; Neurologic Manifestations; Plasma Substitutes; Plasmapheresis

Topics: Adult; Anesthesia, General; Asphyxia; Barbiturates; Brain; Brain Diseases; Female; Forensic Medicine; Globus Pallidus; Heart Arrest; Heroin; Humans; Hypoxia, Brain; Injections, Intravenous; Male; Middle Aged; Morphine Dependence; Necrosis; Peptic Ulcer Perforation; Suicide

Topics: Adrenal Cortex; Adrenal Cortex Diseases; Brain; Brain Diseases; Heroin; Humans; Infant; Infant, Newborn; Infant, Newborn, Diseases; Intestinal Obstruction; Intestines