Abstract: In 1872, George Huntington presented his essay “On Chorea” to the Meigs and Mason Academy of Medicine and, in doing so, detailed a disease that would later bear his name. Huntington’s disease (HD) is a genetic, neurodegenerative disease that manifests as the loss of motor control, cognitive impairment, and mood and psychiatric changes in patients. These symptoms lead to the progressive loss of independence of patients, with severe symptoms ultimately resulting in death. The critical need for continued research into the pathology of HD is emphasized by the lack of a cure for HD thus far. The genetic origin of HD is a mutation in the interesting transcript 15 (IT15) gene encoding the huntingtin protein. A CAG (cytosine, adenine, guanine) expansion in the gene leads to the formation of a mutant huntingtin protein (mHTT) with an expanded polyglutamine sequence at the N-terminus. mHTT is cleaved into toxic fragments that can aggregate, form intracellular inclusions, and disrupt cellular processes which are hypothesized to lead to neurodegeneration. This contribution of mHTT to neurotoxicity is further postulated to result in the pathological atrophic changes that are hallmarks of the disease. One major pathological anatomical hallmark of HD is the atrophy of the striatum. Medium spiny neurons, which make up 90%–95% of neurons in the striatum, show particular vulnerability to degeneration in HD. The loss of these neurons is hypothesized to underlie motor impairment in HD. The atrophy of the cortex and basal ganglia is also well documented alongside striatal degeneration. Much like with the striatum, cortical atrophy is observed to underlie symptoms of HD, with atrophy of certain regions of the brain contributing to specific symptom profiles that patients present with. A better understanding of the contribution of regional degeneration of the brain to specific symptom profiles can possibly lead to targeted, symptom-specific therapies in the future (Palpagama et al., 2019; Testa and Jankovic, 2019).