# Reduced nicotine dependence following traumatic brain injury in an elderly patient: a case report and literature review

## TL;DR

An elderly man with a long smoking history stopped craving nicotine after a severe brain injury, suggesting TBI might disrupt brain circuits related to addiction.

## Contribution

This case report provides novel clinical evidence that traumatic brain injury may disrupt nicotine dependence through neurobiological changes.

## Key findings

- An 87-year-old man with 60 pack-years of smoking showed abrupt cessation of nicotine craving after severe TBI.
- The patient remained abstinent for six months without withdrawal symptoms or interventions.
- The case suggests TBI may affect mesolimbic dopaminergic circuits involved in nicotine reward processing.

## Abstract

Traumatic brain injury (TBI) can induce a range of neurological and behavioral changes, including potential effects on substance dependence. We present the case of an 87-year-old male with a longstanding history of heavy smoking (~60 pack-years) who demonstrated an abrupt cessation of nicotine craving following a severe TBI involving subdural hemorrhage, contusions, and subarachnoid hemorrhage. Clinical management included supportive therapy for intracranial pressure control and infection management. Nicotine dependence and craving were qualitatively assessed through repeated structured clinical interviews during hospitalization and outpatient follow-up. Remarkably, during the six-month follow-up, the patient remained abstinent without signs of withdrawal or nicotine craving and the use of pharmacological or behavioral interventions. This case highlights a rare but significant phenomenon suggesting that severe brain injury may disrupt mesolimbic dopaminergic circuits, including the ventral tegmental area (VTA) and nucleus accumbens (NAc), central to nicotine-related reward processing. We discuss potential neurobiological mechanisms post-injury, including dopaminergic dysfunction and health behavior adaptation. Further research is needed to elucidate the underlying pathways and clinical implications of TBI-associated changes in addictive behaviors.