Acute Atraumatic Pluriradiculopathy After Heroin Consumption To the Editor: Compressive neuropathy is the most frequent complication of the peripheral ner- vous system 1,2 after heroin consumption. Plexo- pathies, radiculopathies, and neuropathies without a traumatic cause are also described but are very uncommon and their prognoses are uncertain. 3–5 We present a case of an acute atraumatic pluriradiculopathy after heroin use. A 31-year-old man with regular drug abuse was admitted in the emergency department after suffering an abruptly right upper extremity weakness 2 hours after injecting intravenous heroin on his limb. The patient did not com- plain about pain or any sensory disorder and did not refer loss of consciousness after consump- tion, history of trauma, or other situations that could cause compression of the extremity. Physical examination revealed an areflec- tic flaccid paralysis proximally in the right upper extremity, without sensory disturbance. Creatine kinase (CK) levels were of 18,000 U/L, with a decrease to 8600 U/L a few hours later. Human immunodeficiency virus and hepatitis B virus serologies were negative, being positive for hepatitis C virus. The motor deficit still was remaining 2 weeks later, and a slight atrophy of the right infraspinatus muscle was already visible. A neurophysiological study was per- formed 23 days after the onset of symptoms showing fibrillation potentials and positive sharp waves in the biceps, extensor digitorum, extensor carpi radialis, palmaris longus, deltoid, and supraspinatus muscles with a neurogenic recruitment that was very poor in supraspina- tus and deltoid muscles. Sensory nerve con- duction studies were normal. This suggested a preganglionic involvement, affecting C5, C6, and C7 nerve roots. A magnetic resonance image of the brachial plexus and cervical spinal cord was performed, without compres- sive pathology at any point of the nerve pathway. Symptoms persisted for 1 month, and then progressively improved until com- plete recovery after 2 months. Heroin-related neuropathies without a traumatic cause are very uncommon. The clinical picture is acute, asymmetric, predomi- nantly proximal, painful, and associated with a sensory disorder. 6,7 There is no specific treat- ment, and the functional prognosis is variable. Symptoms appear 3–36 hours after consump- tion. There have been cases reported after snif- fed heroin, and in cases of intravenous abuse, the affected side does not always coincide with the side of the puncture. There are very few reports described, being the largest series of 6 patients, 8 4 with a plexus involvement (2 bra- chial and 2 lumbosacral) and 2 with an acute sensorimotor axonal neuropathy. All but one of these patients had elevated levels of creatine kinase. The prognosis was variable, and 2 pa- tients underwent nerve biopsy showing axonal loss with Wallerian degeneration. It has been proposed that there is a direct toxic effect either of the drug itself or its adulterants, as the mechanism of neurotoxicity 9 or rhabdomyolysis. 10–12 Proxi- mal regions of peripheral nerves lack perineu- rium, therefore nerve fibers are in contact with blood vessels in the absence of the blood–neural barrier. This anatomical consid- eration favors the liability at these locations of the peripheral nervous system (ie, roots) to certain immunologic (eg, Guillain–Barré syn- drome) or toxic (eg, cisplatin) phenomena. In summary, we describe a pluriradicular affectation after heroin consumption, which is very infrequent and poorly described. The reversibility of the deficit demonstrates the toxic, and sometimes transient, effect of the heroin and its adulterants in the peripheral nervous system. The peculiarity of our case is the absence of pain and sensory disorder, and the excellent and early recovery. This may suggest that in cases of heroin toxicity, the existence of a preganglionic disorder may be associated with a better prognosis. Miguel Ángel Rubio, MD* Alba León, MD† Antía Moreira, MD* Irene Navalpotro, MD* Journal of CLINICAL NEUROMUSCULAR DISEASE Volume 15, Number 3 March 2014 Copyright © 2014 by Lippincott Williams & Wilkins Letters to the Editor 87