By Marcello Cherchi, MD PhD
For patients
Cocaine can cause problems in many parts of the body. In some people cocaine can cause hearing loss, tinnitus and dizziness.
For clinicians
Overview
Cocaine is extracted primarily from Erythroxylum coca and can be administered by inhalation, application to mucosal membranes, or injection (intravenously and intramuscularly). Pharmacologically, cocaine influences numerous neurotransmitter systems, including presynamptic monoamine reuptake, NMDA, and opioid receptors. Otovestibular effects are not well reported in the literature, but symptoms following cocaine use include hearing loss, tinnitus and disequilibrium. Ocular motor examination may reveal opsoclonus. Instrumented vestibular studies may show an altered vestibulo-ocular reflex. MRI of the internal auditory canals may reveal intralabyrinthine hemorrhage.
Introduction
Cocaine is a sympathomimetic tropane alkaloid that occurs naturally in several hundred Erythroxylum species of shrub; the cocaine consumed by humans is largely extracted from Erythroxylon coca (Roque Bravo et al. 2022). Cocaine can be ingested by chewing on the leaves of the plant. In industrialized countries cocaine is usually delivered in a more concentrated form through various routes (inhaled, applied to mucosal membranes, injected intravenously or intramuscularly).
Epidemiology
It has been estimated that of adults age 15 – 64 years, the proportion that have used cocaine in some form in the past year was 1% in South America, 1.2% in the European Union, and 2.1% in North America (Roque Bravo et al. 2022).
Pathophysiological mechanism of disease
Pharmacologically, cocaine functions primarily as a presynaptic monoamine reuptake inhibitor, thereby influencing the activity of dopamine, noradrenaline and serotonin neurotransmitter systems (Roque Bravo et al. 2022).
Cocaine has other pharmacologic effects as well (Roque Bravo et al. 2022). For example, cocaine can influence activity at NMDA, sigma‑ and kappa-opioid receptors. Cocaine can also block voltage-gated sodium channels and maintain them in an inactive state, and this property enables cocaine to function as a topical anesthetic.
Clinical presentation
Patell and colleagues (Patell et al. 2021) reported the case of a 32-year-old male who intranasally consumed 4 grams of cocaine daily for 2 days then presented with acute onset bilateral sensorineural hearing loss (Patell et al. 2021).
Physical examination
Physical examination of patients suffering from cocaine intoxication is usually dominated not by audiologic or vestibular symptoms, but rather by mania, myoclonus, cardiovascular symptoms, etc.
Ocular motor examination
Scharf reported the case of a 26-year-old woman who consumed cocaine intranasally and developed opsoclonus (Scharf 1989).
Testing: auditory
Animal studies report that cocaine alters auditory evoked potentials and diminishes cochlear blood flow (Shivapuja et al. 1993); repeated exposure to cocaine results in decreased adrenergic innervation of the cochlea (Shivapuja et al. 1994). Comparable studies in humans have not been published.
Testing: vestibular
Demer and colleagues (Demer et al. 1989) studied electronystagmography in 9 cocaine users and 9 healthy controls. They reported that saccades, tracking, vestibulo-ocular reflexes and caloric testing were similar between the two groups. However, “Extreme visual enhancement of VOR [vestibulo-ocular reflex] gain by 4x magnified vision was significantly impaired in cocaine abusers as compared with controls” (Demer et al. 1989).
Imaging
Nicoucar and colleagues (Nicoucar et al. 2005) reported the case of a 43-year-old male who consumed cocaine intransally then developed disequilibrium, and unilateral tinnitus and hearing loss. Brain MRI revealed an intralabyrinthine hemorrhage ipsilateral to the aural symptoms.
Treatment
The mainstay of treatment of cocaine-related symptoms is detoxification.
Notes
Cocaine is commonly consumed along with alcohol. Transesterification of both drugs produces cocaethylene, which has similar effects to cocaine, but has a longer half life (Pergolizzi et al. 2022), is very toxic, and particularly epileptogenic.
Our discussion has focused on the otovestibular effects of cocaine. Cocaine has well-documented toxicity on multiple organ systems, including the central nervous system, cardiovascular, respiratory, renal and hepatic system.
References
Demer JL, Volkow ND, Ulrich I, Krajewski K, Davis CM, Porter FI (1989) Eye movements in cocaine abusers. Psychiatry Res 29: 123-36. doi: 10.1016/0165-1781(89)90027-9
Nicoucar K, Sakbani K, Vukanovic S, Guyot JP (2005) Intralabyrinthine haemorrhage following cocaine consumption. Acta Otolaryngol 125: 899-901. doi: 10.1080/00016480510033658
Patell K, Al Armashi AR, Somoza-Cano FJ, Polanco VP, Ravakhah K (2021) Rare Case of Sudden Bilateral Sensorineural Hearing Loss After Cocaine Abuse. Am J Ther 29: e137-e139. doi: 10.1097/MJT.0000000000001421
Pergolizzi J, Breve F, Magnusson P, LeQuang JAK, Varrassi G (2022) Cocaethylene: When Cocaine and Alcohol Are Taken Together. Cureus 14: e22498. doi: 10.7759/cureus.22498
Roque Bravo R, Faria AC, Brito-da-Costa AM, Carmo H, Mladenka P, Dias da Silva D, Remiao F, On Behalf Of The Oemonom R (2022) Cocaine: An Updated Overview on Chemistry, Detection, Biokinetics, and Pharmacotoxicological Aspects including Abuse Pattern. Toxins (Basel) 14. doi: 10.3390/toxins14040278
Scharf D (1989) Opsoclonus-myoclonus following the intranasal usage of cocaine. J Neurol Neurosurg Psychiatry 52: 1447-8. doi: 10.1136/jnnp.52.12.1447-a
Shivapuja BG, Gu ZP, Liu SY, Saunders SS, Schoener EP (1994) Effects of repeated cocaine injections on cochlear function. Brain Res 668: 230-8. doi: 10.1016/0006-8993(94)90528-2
Shivapuja BG, Gu ZP, Saunders SS, Quirk WS (1993) Acute effects of cocaine on cochlear function. Hear Res 69: 243-50. doi: 10.1016/0378-5955(93)90114-g
