Answer by taking a quote from the following article:

Henry Gustav Molaison (February 26, 1926 - December 2, 2008), known widely as H.M., was an American memory disorder patient who had a bilateral medial temporal lobectomy to surgically resect the anterior two thirds of his hippocampi, parahippocampal cortices, entorhinal cortices, piriform cortices, and amygdalae in an attempt to cure his epilepsy. Although the surgery was partially successful in controlling his epilepsy, a severe side effect was that he became unable to form new memories. H.M. was widely studied from late 1957 until his death in 2008. His case played an important role in the development of theories that explain the link between brain function and memory, and in the development of cognitive neuropsychology, a branch of psychology that aims to understand how the structure and function of the brain relates to specific psychological processes.

Henry Molaison was born on February 26, 1926, and experienced intractable epilepsy that has sometimes been attributed to a bicycle accident at the age of seven. (This accident was initially reported to have occurred at age nine, but was corrected by the patient's mother at a later stage.) He had partial seizures for many years, and then several tonic-clonic seizures following his 16th birthday. In 1953, he was referred to William Beecher Scoville, a neurosurgeon at Hartford Hospital, for treatment.  Scoville localized Molaison's epilepsy to his left and right medial temporal lobes (MTLs) and suggested surgical resection of the MTLs as a treatment. On September 1, 1953, at the age of 27, Molaison's bilateral medial temporal lobe resection included the removal of the hippocampal formation and adjacent structures, including most of the amygdaloid complex and entorhinal cortex. His hippocampi appeared entirely nonfunctional because the remaining 2 cm of hippocampal tissue appeared to have atrophied and because the entire entorhinal cortex, which forms the major sensory input to the hippocampus, was destroyed. Some of his anterolateral temporal cortex was also destroyed.  After the surgery, which was partially successful in its primary goal of controlling his epilepsy, Molaison developed severe anterograde amnesia: although his working memory and procedural memory were intact, he could not commit new events to his explicit memory. According to some scientists, he was impaired in his ability to form new semantic knowledge, but researchers argue over the extent of this impairment. He also had moderate retrograde amnesia, and could not remember most events in the one- to two-year period before surgery, nor some events up to 11 years before, meaning that his amnesia was temporally graded. However, his ability to form long-term procedural memories was intact; thus he could, for example, learn new motor skills, despite not being able to remember learning them.  The case was first reported in a paper by Scoville and Brenda Milner in 1957. Near the end of his life, Molaison regularly filled in crossword puzzles. He was able to fill in answers to clues that referred to pre-1953 knowledge. For post-1953 information he was able to modify old memories with new information. For instance, he could add a memory about Jonas Salk by modifying his memory of polio.  He died on December 2, 2008.

Did he learn any tricks to deal with this?
Molaison regularly filled in crossword puzzles. He was able to fill in answers to clues that referred to pre-1953 knowledge.