Document Type
Conference Proceeding
Publication Date
5-3-2024
Abstract
Introduction: Lithium is one of the mainstay treatments for bipolar disorder. Given its narrow therapeutic window, acute and chronic toxicity can develop. Acute toxicity includes gastrointestinal and cardiac manifestations whereas chronic toxicity manifests as neurologic, thyroid, and renal dysfunction. The therapeutic range of lithium is 0.6 to 1.2 mmol/L. With chronic use, lithium may be toxic at 1.2 mmol/L or greater (1). Neurological toxicity includes tremors, hyperreflexia, nystagmus, ataxia, confusion, and even seizures, however, rare reports have shown peripheral neuropathy as a manifestation. Case: A 40-year-old male with a history of bipolar disorder complicated by lithium induced chronic kidney disease stage 3 and hypothyroidism presented for acute on chronic severe bilateral lower extremity burning pain and paresthesias. The patient described a gradual two month progression of worsening painful paresthesias beginning in the great toes bilaterally and spreading up both feet to the level of the ankles. The pain worsens with weight bearing. He took no pain medication for his symptoms. The patient was evaluated previously in the outpatient setting a few months prior where no metabolic correlation was found and electromyography demonstrated severe bilateral lower extremity neuropathy and atrophy. Due to the on-going severity of his symptoms, he presented to the hospital for evaluation. On exam, sensation to pinprick was decreased distally and hyperesthesia and allodynia to light touch were evident in bilateral feet. There was no evidence of focal motor deficit, upper extremity or facial symptoms. No sensory level was appreciated, strength, tone and bulk were adequate, and reflexes were symmetric bilaterally. CT and MRI of the brain were negative for acute intracranial process. MRIs of the spine showed degenerative changes out of proportion to his symptom severity. Laboratory studies for an inflammatory/autoimmune process were negative making vasculitis less likely. The patient was started on Gabapentin. The neuromuscular team was consulted who expressed concern for lithium induced peripheral neuropathy considering the patient’s hospital admission for lithium toxicity (levels up to 2.14 mEq/L) three months prior coincided with his symptom onset. Given the patient’s concurrent lithium induced thyroidopathy and nephropathy, recommendation to permanently discontinue lithium is maintained with concern that this peripheral neuropathy, although rare, is secondary to toxic lithium levels. Discussion: The differential diagnosis of peripheral neuropathy is broad including metabolic, systemic, structural, and even toxic causes. Despite being extremely rare, Faravelli et al. has reported that chronic lithium use at therapeutic levels has been associated with peripheral neuropathy (1). Here, we present this atypical neurologic symptom that must be considered in an individual taking lithium with no other overt cause as prompt discontinuation of the treatment is imperative. Given that this patient is fairly young and healthy, we anticipate that he will have a much better recovery from his peripheral neuropathy than someone of advanced age with comorbidities, again pointing to the importance of early suspicion.
Recommended Citation
Biel A, Xin V, Moazzam M, Berghea R. Not-so-typical neurologic effects: unraveling lithium toxicity. Presented at: American College of Physicians Michigan Chapter and Society of Hospital Medicine Michigan Chapter 2024 Resident and Medical Student Day; 2024 May 3; Troy, MI.
Comments
American College of Physicians Michigan Chapter and Society of Hospital Medicine Michigan Chapter 2024 Resident and Medical Student Day, May 3, 2024, Troy, MI