Confusion after “Chasing the Dragon”: A case of delayed toxic leukoencephalopathy Nevares, A1; Morales, J1; Chadha, N1; Dorman, J2. 1Department of Medicine, 2Department of Neurology - John H. Stroger Jr. Hospital of Cook County DISCUSSION He had functional urinary- fecal incontinence, symmetric hyperreflexia in lower extremities and upgoing toes. INTRODUCTION T2 Delayed leukoencephalopathy has been described with: Inhaled heroin (“Chasing the Dragon”) spongiform leukoencephalopahy. Delayed post-hypoxic leukoencephalopathy (DPHL) Functional Arylsulfatase-A deficiency. Exposures to inhaled heroin and hypoxia were evidenced in this case. He developed the akinetic-mutism type of DPHL, which developed 3 weeks after “chasing the dragon” and the respiratory failure. MRI was consistent with leukoencephalopathy involving frontal, parietal, temporal and occipital areas, sparing the cerebellum, all of which supports the diagnosis of toxic leukoencephalopathy due to hypoxia, rather than “Chasing the Dragon” leukoencephalopathy, in which the high T2 signal intensities involve predominantly the cerebellum and posterior cerebrum. Toxic Leukoencephalopathy refers to a spectrum of leukoencephalopathies caused by iatrogenic, drug, hypoxic or infectious insults to the white matter. Few present with a delayed onset. “Chasing the Dragon”, which is the inhalation of heated heroin fumes, was first recognized as a cause of leukoencephalopathy in 1982 by Wolters and colleagues. We present a previously healthy 31 year old gentleman who developed an abrupt change in personality and impaired cognitive functions 3 weeks after “chasing the dragon” and subsequent respiratory failure. WORK UP HIV, syphilis screen were negative, sedimentation rate, TSH and B12 levels were normal. CSF had white blood cell count of 3/uL, red blood cells of 1/uL elevated proteins to 71mg/dL, with negative cultures. EEG showed diffuse slowing suggestive of bilateral hemispheric dysfunction. MRI demonstrated white matter high T2/FLAIR signal intensities involving bilateral frontal, parietal, temporal and occipital lobes. Patient was treated with amantadine for seven days and received physical therapy. FOLLOW UP CASE PRESENTATION Upon discharge, the patient was unable to independently perform his daily needs and only replied in monosyllabic words. At 5-weeks follow up, he was talkative and coherent, with adequate affect, but could not recall 3 words. At 8-weeks follow up, a cognitive linguistic quick test (CLQT) demonstrated: Mild attention impairment Moderate memory impairment Severe executive functions impairment Normal language Moderate clock drawing severity rating. Ten months from onset, he had returned to his baseline as per family members.   31 year old gentleman with no past medical history was brought to our institution with personality changes and odd behavior. One month prior, under the effects of alcohol and first-time heroin inhalation, he lost consciousness and reportedly remained unresponsive for 3 to 4 hours. Initial in-field intubation was attempted but unsuccessful until arrival to an outside facility, where he was admitted to ICU with respiratory failure requiring mechanical ventilation; pneumonia, acute kidney injury and rhabdomyolysis. He recovered and returned to his activities of daily living for two weeks, including his occupation as a painter, followed by one week of abrupt onset of change in personality and odd behavior. Upon presentation he was alert, but apathetic; he was mute with inappropriate smiling and followed simple commands. TEACHING POINTS Abrupt development of neuropsychiatric symptoms weeks after heroin inhalation or hypoxic insult, should prompt the clinician to recognize a delayed leukoencephalopathy. The distinction between DPHL and chasing the dragon spongiform leukoencephalopathy is best made based on radiological features and definitely but rarely pursued, by pathology. Most patients with DPHL will recover within 3 to 12 months, but impaired attention and executive functions can persist. FLAIR REFERENCES Shprecher, D.; Mehta, L. The Syndrome of Delayed Post-Hypoxic Leukoencephalopathy. NeuroRehabilitation. 2010 January ; 26(1): 65-72. Tormoehlen, L. Toxic Leukoencephalopathies. Neurol Clin 29 (2011) 591-605. Filley, C. Toxic Leukoencephalopathy. N Engl J Med. 2001 ;345(6): 425-32 Authors have no conflicts to declare …