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The Medical Consequences of Opiate Abuse and Addiction and Methadone Pharmacotherapy
Published in John Brick, Handbook of the Medical Consequences of Alcohol and Drug Abuse, 2012
Pauline F. McHugh, Mary Jeanne Kreek
Recently, reports of a progressive leukoencephalopathy have been seen in individuals who inhale the heated vapor of heroin, a practice known as “huffing” or “chasing the dragon,” and which appears to be on the rise in an attempt by opiate abusers to avoid the risks of needle use. The leukoencephalopathy consists of a vacuolization of white matter, which can be generalized throughout the central nervous system, although some reports suggest lesions are more likely to be seen in regions of poor blood perfusion, particularly the basal ganglia and cerebellum. The mechanism of the leukoencephalopathy is not known. The fact that it is most often seen in miniepidemics suggests that a particular unidentified contaminant may be to blame, although reports that only a few individuals using a particular supply of heroin have been affected suggest that an underlying genetic predisposition may also be necessary to develop the syndrome. Speculation that a toxic metabolite of heroin produced by heat vaporization may be a causative factor seems to have been invalidated by a report of an identical progressive leukoencephalopathy in an addict who was using heroin intranasally. Initially seen as pockets of miniepidemics in Europe over the past decade, cases have recently been reported in the United States (Celius and Andersson, 1996; Hill, Cooper, and Perry, 2000; Kreigstein et al., 1998; Rizzuto et al., 1997).
The neurologic approach
Published in Stanley Berent, James W. Albers, Neurobehavioral Toxicology, 2012
Stanley Berent, James W. Albers
In general, there are no conventional CT or MRI imaging abnormalities specific to any given neurotoxicant. There are some imaging abnormalities, however, that can result in a neuroradiology diagnosis of ‘toxic leukoencephalopathy’ (Filley & Kleinschmidt-DeMasters, 2001). ‘Leukoencephalopathy’ is the term used to reflect abnormalities of myelin and more general changes in cerebral white matter, and the abnormalities are believed to manifest primarily in neurobehavioral alterations (Filley, Heaton, & Rosenberg, 1990; Filley & Kleinschmidt-DeMasters, 2001). While, as mentioned elsewhere (see Chapter 5, for instance), neurobehavioral symptoms of this type are non-specific, in general the pattern of symptoms and signs associated with leukoencephalopathy mirrors the distribution and severity of white matter abnormality. That is, neurobehavioral or neurologic abnormalities are bilateral and diffuse, with mild cases exhibiting confusion and inattention, memory impairment, and emotional disturbance, without abnormal language function (Filley & Kleinschmidt-DeMasters, 2001). Of course, the differential diagnosis associated with imaging evidence of a toxic leukoencephalopathy includes numerous conditions associated with many different causes. One of the conditions initially attributed to ‘toxic’ leukoencephalopathy was chronic and massive exposure to toluene, in the form of ‘huffing’ (recreational toluene abuse) (Filley, et al., 1990). That situation, possibly in association with unrecognized hypoxia, produced MRI imaging abnormalities of cerebral atrophy and white matter changes characteristic of leukoencephalopathy. Further, the degree of white matter abnormality on MRI significantly correlated with neuropsychological impairments. Nonetheless, other conditions exist that may produce indistinguishable MRI white matter abnormalities, including hereditary and autoimmune demyelinating diseases, progressive multifocal leukoencephalopathy, acquired immune deficiency syndrome (AIDS), vasculitis, normal pressure hydrocephalus, and exposure to leukotoxic therapies including cisplatin or irradiation. Attribution to a toxic etiology from imaging evidence of a leukoencephalopathy will necessitate meeting criteria, such as Hill (1965), in order to establish causation. While objective documentation of neurologic or neurobehavioral deficits (i.e., the results from neuropsychological evaluation) is necessary (Schaumburg & Spencer 1987), the diagnosis of a leukoencephalopathy also requires that the neuroradiological abnormalities be present (Filley & KleinschmidtDeMasters, 2001). In the identification of imaging abnormalities characteristic of leukoencephalopathy, the results of MRI are the most sensitive of the imaging techniques because of the ability of MRI to image myelin, distinguish between gray matter and white matter, and identify primary and secondary loss of myelin to an extend which considerably exceeds that of CT (Frey, 2000).
The development of hearing in prelingually deaf children with white matter changes in the first year after cochlear implantation
Published in Acta Oto-Laryngologica, 2020
Min Shen, Yuan Li, Mo Long, Liyan Wang, Wei Liang, Zhongyan Chen, Yanfang Ma, Yuran Guo, Qingling Bi, Yang Zhang
The study recruited 21 children with white matter changes (group A) and 22 prelingually deaf children with normal white matter (group B), respectively. All patients included in group A should adhere to following inclusion criteria: (a) all patients had bilateral severe to profound SNHL without inner ear malformation. White matter changes were diagnosed by brain MRI. Hereditary progressive leukoencephalopathy was excluded. (b) The age of CI should be between 1 and 18 years old. (c) All participants’ mental and intellectual development were normal. (d) The subjects must be enrolled in a post-operative rehabilitative/educational programme. All patients included in group B should adhere to the same inclusion criteria as above except that normal white matter was indicted by MRI. Brain MRI and diffusion-weighted imaging (DWI) studies were performed 6 months later for children in the group A confirming that there had been no progression of the white matter lesion. Figure 1 shows examples of MRI images in one case with white changes and one case with normal white matter profile in the two groups. Approval from our Ethics Committee was obtained for this study.
An update on clinical, pathological, diagnostic, and therapeutic perspectives of childhood leukodystrophies
Published in Expert Review of Neurotherapeutics, 2020
Mahmoud Reza Ashrafi, Man Amanat, Masoud Garshasbi, Reyhaneh Kameli, Yalda Nilipour, Morteza Heidari, Zahra Rezaei, Ali Reza Tavasoli
“Leukoencephalopathy” is a term used to describe all diseases with exclusive or predominant CNS white matter abnormalities and can be divided into inherited and acquired forms. Over 100 inherited leukoencephalopathies were described (Supplemental Table 1). These conditions can be split into leukodystrophies and genetic leukoencephalopathies [10]. As leukodystrophies primarily affect CNS white matter; genetic leukoencephalopathies are systemic disorders with white matter involvement as their secondary findings. Since both groups have genetic etiology in nature, the differences can be attributed to the cell metabolic dysfunctions and the cardinal clinical symptoms of affected individuals due to a specified genetic defect [11,12]. Determining the type of heritable disorders with white matter involvement (especially the recent described ones) can sometimes be challenging based on their broad features and our limited knowledge about their pathophysiologic mechanisms. Furthermore, new categorizations are essential due to the overwhelming increase in number of inherited leukoencephalopathies. In fact, the current classification is fading away and “leukodystrophy” is used instead of “genetic leukoencephalopathy” in most recent studies [4].
Richard Bright’s observations on diseases of the nervous system due to inflammation
Published in Journal of the History of the Neurosciences, 2018
Case 19 was a girl in good health until age 2, when she developed impaired vision and convulsions, followed by general stiffness, spasmodic and rigid extension of the body and limbs. She died at age 3 years and 9 months. The autopsy showed a shrunken and hard brain, medulla oblongata, and part of the spinal cord (Fig. 6); effusion external to the brain; and soft pulpy cortex. The nerves were harder than usual, especially the optic nerve (p. 43). In the lungs “were a few milliary tubercles, some very transparent, others with yellow spots in their centres.” These appeared to be incidental findings, not related to the brain disease. A sister (Case 20) developed similar symptoms and died at nearly the same age (with no autopsy). These cases suggest hereditary leukoencephalopathy. Wilks (1859, p. 156), who mentioned this case in his lectures on pathological anatomy, ascribed the hardening of the white matter to inflammation.