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

Abstract

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

Multiple Sclerosis Disease Progression and Paradichlorobenzene

“…Our patient had elevated levels of blood PDCB at the time of presentation, consistent with her history of long-term mothball ingestion. 2 In many affected individuals, toxic effects persist and clinical deterioration occurs despite discontinuation of exposure to the toxin, a phenomenon known as "coasting," consistent with this patient's clinical course. 2 Again, the mechanisms underlying coasting are unknown.…”

Clinical Reasoning: A 12-year-old girl with headache and change in mental status

“…One prior case reported "symptoms of intracranial hypertension" 7 with many others reporting headache at the time of initial presentation. 3,8 However, elevated CSF opening pressure in association with PDCB exposure has not been reported previously and may explain the etiology of headaches in PDCB-related leukoencephalopathy. In several other cases, non-neurologic manifestations included a dry, ichthyotic rash with hyperpigmentation, 3,7 normocytic anemia, and acute hepatitis, all of which were seen in our patient.…”

Para-dichlorobenzene toxicity – a review of potential neurotoxic manifestations

“…(E) Extent of neuronal damage could be limited by preventing hyperthermia, hyper/hypoglycemia. (F) Renal excretion of PDCB following acute ingestion can be increased by preventing its deposition in adipose tissue by using intra venous fat emulsion agents, including propofol [Avila et al 2006;Hernandez et al 2010]. …”

“…Human volunteers following PDCB inhalation excreted 4.8-16.2% of 2,5-DCP in urine within 10 hours of exposure [Hernandez et al 2010]. …”