An inquest into the death of former world boxing champion Ricky Hatton, aged 46, concluded with a narrative verdict at Stockport Coroner’s Court (also referred to as South Manchester Coroners’ Court) on Friday, March 20. Senior Coroner for Manchester South, Alison Mutch, ruled that while Mr. Hatton died having suspended himself from a ligature, his intention remained unclear due to several contributing factors, leaving his family heartbroken and his legion of fans stunned.

A provisional cause of death of hanging had been given at a pre-inquest hearing. During the full inquest, Ms. Mutch stated that she could not be satisfied he intended to take his own life, citing that he left no note, was under the influence of alcohol, and showed microscopic evidence of Chronic Traumatic Encephalopathy (CTE), a brain disease often associated with repeated head impacts in contact sports like boxing.

Mr. Hatton was found unresponsive in the games room of his Hyde, Tameside, mansion on the morning of Sunday, September 14, 2024, by his long-time manager and agent, Paul Speak. Mr. Speak had arrived at approximately 6:30 AM to take Mr. Hatton to Manchester Airport for a planned flight to Dubai. Finding no answer at the intercom, he let himself in with his own key, discovered Mr. Hatton, and subsequently called the police and ambulance. The scene revealed an empty bottle of wine on a pool table and a half-drunk glass of wine on the bar, with lights off but music playing from a TV. No notes were found at the property, which was secure with no signs of disturbance.

A toxicology report confirmed that Mr. Hatton was significantly intoxicated, with 212mg of alcohol per 100ml of blood, more than twice the legal drink-drive limit. Evidence also indicated some cannabis use and previous cocaine use in his system, although there was no indication of recent cocaine intake in the hours before his death. Pathologist Dr. Neil Papworth, who conducted the post-mortem, identified damage to parts of Mr. Hatton’s brain, specifically mild CTE, characterized by chronic neuronal loss. While it was not possible to determine how Mr. Hatton was specifically affected by CTE, his relatives had noted a