spine J Neurosurg Spine Volume 23 • August 2015 caSe report J Neurosurg Spine 23:159–165, 2015 I n Europe, it is estimated that around 13 million adults (15–64 years of age) have used cocaine at least once in their lifetime. 5 With the increasingly widespread illicit use of cocaine, a broad spectrum of clinical pathologies related to this form of drug abuse is emerging. The most frequently used method of administration of powdered cocaine is intranasal inhalation, or “snorting.” 18 Habitual nasal insuffation of cocaine powder often causes consid- erable damage to nasal mucosa; however, damage of the underlying perichondrium leading to nasal septum perfo- ration and destruction of the osteocartilaginous scaffold of the nose, sinuses, and palate is much less common. 25 In more severe cases, the destruction extends to the middle and superior turbinates and the lateral wall of the nose. 13 In some patients, hard and soft palate perforations may be present. Some individuals with severe destruction de- velop symptoms caused by propagating infections associ- ated with pseudotumor, proptosis, and diplopia. 13 Midline destructive lesions can be caused by a variety of specifc conditions other than cocaine abuse, including infections, neoplasms, sarcoidosis, and granulomatosis with polyan- giitis (GPA; Wegener’s granulomatosis). Their differentia- tion is important but may, at times, be very diffcult. 25 The correct diagnosis of cocaine-induced midline destructive lesions (CIMDLs) ultimately depends on a patient’s clini- cal history and documentation of drug abuse combined with the exclusion of other etiologies. 15 In the currently available literature, involvement of the craniovertebral junction or the spine in general in CIMDLs has never been reported. abbreviatioNS c-ANCA = cytoplasmic antineutrophil cytoplasmic antibody; CIMDL = cocaine-induced midline destructive lesions; GPA = granulomatosis with polyangi- itis; HNE = human neutrophil elastase; p-ANCA = perinuclear ANCA; VAS = visual analog scale. Submitted January 22, 2014. accepted November 12, 2014. iNclude wheN citiNg Published online May 8, 2015; DOI: 10.3171/2014.11.SPINE1471. diScloSure The authors report no conflict of interest concerning the materials or methods used in this study or the findings specified in this paper. Craniovertebral junction instability as an extension of cocaine-induced midline destructive lesions: case report carlo brembilla, md, 1 luigi andrea lanterna, phd, 1 andrea risso, md, 1 enrico bombana, md, 2 paolo gritti, md, 3 rosangela t rezzi, md, 4 giuseppe bonaldi, md, 5 and Francesco biroli, md 1 Departments of 1 Neurosurgery, 2 Infectious Diseases, 3 Anesthesia and Intensive Care, 4 Pathology, and 5 Neuroradiology, Pope John XXIII Hospital, Bergamo, Italy With the increasingly widespread illicit use of cocaine, a broad spectrum of clinical pathologies related to this form of drug abuse is emerging. The most frequently used method of administration of powdered cocaine is intranasal inhala- tion, or “snorting.” Consequently, adverse effects of cocaine on the nasal tract are common. Habitual nasal insuf fations of cocaine can cause mucosal lesions. If cocaine use becomes chronic and compulsive, progressive damage of the mucosa and perichondrium leads to ischemic necrosis of the septal cartilage and perforation of the nasal septum. Occa- sionally, cocaine-induced lesions cause extensive destruction of the osteocartilaginous structures of the nose, sinuses, and palate and can mimic other diseases such as tumors, infections, and immunological diseases. In the literature cur- rently available, involvement of the craniovertebral junction in the cocaine-induced midline destructive lesions (CIMDLs) has never been reported. The present case concerns a 44-year-old man who presented with long-standing symptoms including nasal obstruction, epistaxis, dysphagia, nasal refux, and severe neck pain. A diagnosis of CIMDL was made in light of the patient’s history and the fndings on physical and endoscopic examinations, imaging studies, and laboratory testing. Involvement of the craniovertebral junction in the destructive process was evident. For neurosurgical treatment, the authors considered the high grade of atlantoaxial instability, the poorly understood cocaine-induced lesions of the spine and their potential evo- lution over time, as well as cocaine abusers’ poor compliance. The patient underwent posterior craniovertebral fxation. Understanding, classifying, and treating cocaine-induced lesions involving the craniovertebral junction are a challenge. http://thejns.org/doi/abs/10.3171/2014.11.SPINE1471 Key wordS cocaine-induced midline destructive lesions; craniovertebral junction instability; craniovertebral junction fixation; cervical 159 ©AANS, 2015 Unauthenticated | Downloaded 12/16/22 06:10 PM UTC