HFI often raises concern when first identified on medical imaging, but it is a relatively common finding. It is frequently discovered incidentally when a patient undergoes a CT scan or MRI for an unrelated medical issue. This article provides an assessment of HFI, analyzing its risks and health implications. The following sections detail the nature of HFI, its associated symptoms, and the current clinical approach to its detection and management.
Understanding Hyperostosis Frontalis Interna
Hyperostosis Frontalis Interna is characterized by the benign overgrowth of bone tissue on the inner table of the frontal bone of the skull. This bone growth is non-malignant and typically presents as bilateral and often asymmetrical thickening. The growth may manifest as sessile or nodular formations, and it can be focal or diffuse, generally sparing the midline.
HFI was first described in 1719 by Giovanni Battista Morgagni. Early descriptions sometimes linked it to a broader syndrome involving obesity, leading to misconceptions about its clinical significance. Today, HFI is largely understood as an isolated anatomical variation that is usually of no clinical consequence. The condition can sometimes extend beyond the frontal bone to involve the parietal bones, known as hyperostosis cranii interna.
Assessing the Risk of Symptoms and Complications
HFI is generally considered benign and asymptomatic in the vast majority of cases. Because it is often found incidentally, researchers have struggled to establish a direct causal link between the bone thickening and various reported symptoms. Historical literature associated HFI with a triad of symptoms, including chronic headaches, dizziness, and neuropsychiatric symptoms. Modern research often fails to confirm HFI as the direct cause of these issues, suggesting the correlation is due to the population studied, typically older adults undergoing brain imaging.
Severe, extensive bone growth is classified into specific grades, with the most advanced types occupying more than 50% of the frontal endocranium. In these rare instances, the excessive bone mass could reduce the intracranial volume. While extremely uncommon, excessive growth may lead to complications such as nerve impingement or increased intracranial pressure. However, patients with even advanced thickening are frequently asymptomatic, highlighting the low probability of these serious events.
Etiology and Common Risk Factors
The precise mechanisms causing HFI remain uncertain, but evidence suggests a multifactorial origin involving genetic, metabolic, and hormonal changes. A primary risk factor is sex and age, as the condition is overwhelmingly more common in women, particularly those past menopause. Post-mortem studies report a prevalence around 12% in the general population, with severe cases occurring most frequently in women over 65 years old.
The significantly higher prevalence in females has led to the “estrogen theory.” This theory posits that changes in estrogen levels play a role in stimulating the irregular bone growth, strongly associating HFI with the post-menopausal period. The condition is also sometimes observed in men with hormonal disturbances, such as atrophic testes, further supporting a link to endocrine function.
HFI also shows associations with metabolic conditions, as it was historically linked to Morgagni-Stewart-Morel syndrome, which included obesity and virilism. The presence of HFI is now often seen alongside features of metabolic syndrome, including obesity and diabetes, suggesting a complex interplay of systemic factors. Genetic predisposition may also contribute, demonstrated by ethnic differences in the age of onset and progression rate.
Detection and Clinical Management
HFI is most often diagnosed incidentally through CT scans or MRIs performed for other medical reasons. The characteristic appearance of irregular bone accretion on the inner frontal bone surface is usually sufficient for a radiological diagnosis. A crucial part of the diagnostic process is differentiating HFI from other, more serious conditions that can cause skull thickening.
Differential diagnoses include Paget’s disease of bone, a chronic disorder of accelerated bone remodeling, and other forms of hyperostosis affecting the skull. Unlike Paget’s disease, HFI does not involve biochemical markers of high bone turnover, such as elevated serum alkaline phosphatase. Therefore, the clinical management of HFI, especially in an asymptomatic patient, is conservative and involves observation.
Treatment for the bone thickening is generally not needed due to the condition’s benign nature. If a patient presents with associated symptoms, such as headaches or dizziness, these are managed individually rather than treating the underlying HFI bone changes. The focus remains on ruling out other causes and providing symptomatic relief, as the thickening itself usually poses no threat to long-term health.