Dizziness and Vertigo _________________________________________________________________________
Cervicogenic Vertigo Cervicogenic dizziness is characterized by imbalance, unsteadi- ness, disorientation, neck pain, limited cervical range of motion, and headache. It is closely related to changes in cervical spine position or cervical joint movement. Common etiologies are post-whiplash injury and inflammatory, degen- erative, or mechanical cervical spine dysfunction. The cause of imbalance, unsteadiness, and disorientation symptoms is suggested to involve pain, faulty cervical proprioceptive inputs, and disrupted signaling from upper cervical proprioceptor to vestibular nuclei [95]. Cervicogenic dizziness is diagnosed after mimics are ruled out, including central and peripheral vestibular disorders, vestibular migraine, labyrinthine concussion, cervical arterial dysfunction, and whiplash-associated disorder [95]. EXPOSURE TO TOXINS Lead or mercury exposure can be ototoxic and may cause vertigo through temporary or permanent damage to the inner ear or auditory nerve [96]. ADVERSE DRUG EFFECTS Dizziness or vertigo can occur as a direct side effect of medi- cation that resolves after discontinuation without cochleo- vestibular damage, or it may develop (and persist) secondary to cochleo-vestibular damage (ototoxicity). SIDE EFFECTS The list of drugs that may cause vertigo or dizziness is exten- sive and diverse. Medications consistently associated with dizziness include the antihypertensive drugs amlodipine and hydrochlorothiazide; the antibiotics ciprofloxacin, amoxicillin, and clavulanic acid; pantoprazole (a proton pump inhibitor); aripiprazole (an atypical antipsychotic); and atazanavir (a protease inhibitor). Selective serotonin reuptake inhibitors (SSRIs) such as paroxetine and sertraline can induce vertigo or dizziness as side effects or with abrupt cessation; mirtazapine may cause dizziness side effects [96]. Antiepileptic drugs in particular are linked to adverse effects on auditory or vestibular systems that may be reversible or irre- versible. Even at therapeutic dose ranges, long-term treatment with oxcarbazepine, carbamazepine, lamotrigine, phenytoin, valproate, gabapentin, or vigabatrin may result in auditory, central, and/or peripheral vestibular dysfunction [97].
OTOTOXIC DRUGS Ototoxic drugs can damage cochleo-vestibular structures, which may result in hearing loss, tinnitus, dizziness, or disequi- librium [98]. Cochlear damage can present acutely as tinnitus. Early hearing loss, which patients may not recognize, manifests in the highest frequencies (>4,000 Hz). With progression, the lower frequencies are affected, and patients may become profoundly deaf if the drug is continued. Stopping the drug early, before extensive damage, may prevent further loss. Par- tial recovery of auditory thresholds is possible, but the loss is usually permanent [98; 99]. Vestibular toxicity typically includes imbalance and visual symptoms. As with bilateral vestibulopathy, imbalance is worse in the dark or situations in which footing is uncertain; oscil- lopsia occurs when the head is moving. Patients do not present with nystagmus or vertigo complaints, because vestibulotoxicity is usually bilateral [98]. Ototoxicity is linked to more than 100 drug classes and more than 600 drugs [98; 185]. The best-known and most ototoxic are aminoglycosides, amiodarone, macrolides, vancomycin, loop diuretics, antineoplastic agents, salicylates, and antisep- tics. Aminoglycosides Aminoglycosides are the most vestibulotoxic of all ototoxic drugs. The introduction of streptomycin in 1944 for treatment of tuberculosis brought ototoxicity to clinical attention, as a substantial number of treated patients developed irreversible cochleo-vestibular dysfunction [98; 99]. The aminoglycosides remain widely used and differ in cochleo- vestibular toxicity. Kanamycin, amikacin, neomycin, and dihy- drostreptomycin are preferentially cochleotoxic. Gentamicin affects both cochlear and vestibular systems but is primarily vestibulotoxic, as are streptomycin, tobramycin, and netilmicin [98; 99]. The onset or progression of hearing loss can occur long after cessation of treatment, because aminoglycosides are cleared more slowly from inner ear fluids than from serum. Patients should be monitored for vestibulotoxic effects up to six months after discontinuation [98; 99]. Amiodarone Amiodarone is a widely used antiarrhythmic drug. Reports of amiodarone-induced vertigo and gait instability followed its introduction in the 1980s, and the drug was first implicated in bilateral vestibulopathy causality in 2017. The prevalence of bilateral vestibulopathy is as high as 81 per 100,000. Most cases are idiopathic, and amiodarone may account for a substantial proportion of bilateral vestibulopathy with unexplained causa- tion [100].
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