Fatal toxic leukoencephalopathy: clinical, radiological, and necropsy findings in two patients

Ryan, Aisling; Molloy, Fiona; Farrell, Michael; Hutchinson, Michael

doi:10.1136/jnnp.2004.047134

Cited by 84 publications

(75 citation statements)

References 10 publications

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“…Subsequent reports have been described across Europe [2,3,5,7,9,14,[20][21][22][24][25][26][27][28][29][30], in the USA [6,12,17], Austra- lia [23], Canada [8,11,13,16], as well as a few cases from Taiwan [10,18,19] and Hong Kong [15]. However, reports of heroin-associated leukoencephalopathy remain seldom considering the large number of heroin addicts.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Toxic Leukoencephalopathy after Heroin Abuse without Heroin Vapor Inhalation

Blasel

Hattingen

Adelmann³

et al. 2010

Clin Neuroradiol

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Section: Discussionmentioning

confidence: 99%

“…Moreover, as similar leukoencephalopathies have been reported in people using heroin by other means than inhaling heroin vapor [17,19,[22][23][24][25], it is arguable if heroin itself is toxic and/or if the way of heroin application matters.…”

Section: Discussionmentioning

confidence: 99%

Toxic Leukoencephalopathy after Heroin Abuse without Heroin Vapor Inhalation

Blasel

Hattingen

Adelmann³

et al. 2010

Clin Neuroradiol

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“…Clinical features included abulia, ataxia, speech abnormalities, spastic paraparesis, and hypotonia with prominent cerebellar and cerebral white matter destruction on MRI [70,71]. Although initially thought to be related to the inhalation of aluminum fumes, it is likely attributed to some unidentified impurity in the drug supply since reports of leukoencephalopathy have also occurred with intravenous heroin, inhaled oxycodone, and crack cocaine [72,73].…”

Section: Case Continuationmentioning

confidence: 99%

Case Files of the New York City Poison Control Center: Paradichlorobenzene-Induced Leukoencephalopathy

2010

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A 44-year-old man was brought to the emergency department by emergency medical services after he was discovered lying supine on his apartment floor. He was accompanied by his sister, who had decided to visit him after his absence from a family function. Worsening "bizarre" behavior had been noted by family members for 4 weeks, characterized by anorexia, social withdrawal, flat affect, and alogia. Prior to his illness, he was described as functional, independent, gainfully employed, and social.The patient had mild mental retardation and hypertension. There was no history of diagnosed psychiatric illness, although his family suspected pica. Medications included an unknown antihypertensive with which he was not compliant. He occasionally used marijuana and alcohol, without history of other abused drugs. The patient's sister reported significant weight loss over several months. There had been no apparent fevers, cough, vomiting, diarrhea, or convulsions. On physical examination, he appeared drowsy, was markedly cachectic, and emanated an atypical aromatic body odor. Initial vital signs were: blood pressure 154/90 mmHg, heart rate 98/min, respiratory rate 20/min, rectal temperature 37.4°C, and room air oxygen saturation 97%. Head, neck, chest, and abdominal examinations were unremarkable. He had dry, scaling, and ichthyotic skin. He was oriented to person and place, but not to time, date, or indication for hospitalization. Limited cranial nerve evaluation was normal. Pain and light-touch sensation were unaffected. Hyperreflexia (without clonus) and cogwheel rigidity were noted in both lower extremities; upper extremities were normal. Plantar reflexes were normal bilaterally. Muscle bulk, tone, and strength were normal. The patient was unable to stand without support and unable to ambulate, apparently due to impaired equilibrioception. He could follow simple one-step commands. He would speak a few words when asked simple questions, and he avoided eye contact.Serum electrolytes (sodium, potassium, chloride, calcium, and magnesium) and serum glucose were normal. Tests of hepatic and renal function were: AST 53

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“…Its pathophysiology, albeit unclear, is thought to involve a hypoxic-ischemic injury to the white matter of the cerebrum which results in widespread, confluent vacuolation of the latter, known as spongiform degeneration or leukoencephalopathy [5]. Neuroradiologic abnormalities are best seen in T2-weighted MRI brain scans which typically reveal bihemispheric white matter abnormalities [4]. Clinical outcomes can range from full recovery in some, over a 3-to 12-month period, to rapidly fatal in others [3,6].…”

Section: Discussionmentioning

confidence: 99%

“…Toxic leukoencephalopathy was first reported in 1982 and has been associated with exposure to a range of toxins including therapeutic drugs and illicit substances such as heroin and cocaine [2][3][4]. It principally affects white matter tracts, resulting in a spectrum of clinical features ranging from inattention and disorientation to dementia and death [1].…”

Section: Discussionmentioning

confidence: 99%

The Hazards of Recreational Drug Use: A Case of Toxic Leukoencephalopathy

Lavelle

Ismail

2015

J Neurol Res

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Toxic leukoencephalopathy is a disorder characterized by the alteration of myelin in white matter tracts secondary to exposure to neurotoxic substances. This case describes the neuropsychiatric presentation of toxic leukoencephalopathy. Brain imaging confirms a diagnosis of toxic leukoencephalopathy secondary to polysubstance overdose. The patient made a significant recovery following admission to hospital.

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Fatal toxic leukoencephalopathy: clinical, radiological, and necropsy findings in two patients

Cited by 84 publications

References 10 publications

Toxic Leukoencephalopathy after Heroin Abuse without Heroin Vapor Inhalation

Toxic Leukoencephalopathy after Heroin Abuse without Heroin Vapor Inhalation

Case Files of the New York City Poison Control Center: Paradichlorobenzene-Induced Leukoencephalopathy

The Hazards of Recreational Drug Use: A Case of Toxic Leukoencephalopathy

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