The chemical senses of taste and smell play pivotal roles in human perception, influencing dietary preferences, nutritional intake, safety awareness, and overall quality of life. These senses are intricately interconnected, contributing significantly to the multisensory experience of flavor perception and olfactory identification.

Taste and smell disorders can arise from several etiologies. The cooccurrence of olfactory and taste disorders frequently aligns with shared etiological mechanisms [1]. Common causes, often shared by these disorders, can be categorized as neurodegenerative or nonneurodegenerative. Neurodegenerative etiologies, such as Alzheimer’s and Parkinson’s diseases, are often linked to chemosensory disorders [2-4]. Conversely, non-neurodegenerative disorders stem from various peripheral, central, and systemic factors (e.g., infections, injuries, medications, nutritional deficiencies, toxins, radiation and chemotherapy, metabolic and endocrine disorders, and neoplastic conditions) that contribute to these sensory impairments [5,6]. Traumatic brain injury (TBI), particularly following head trauma, is a significant precipitant for alterations in taste and smell perception [7-9].

Previous studies suggest that trauma-related taste dysfunction occurs in approximately 5% of cases [10]. Additionally, research has shown that approximately 6% of individuals experiencing post-traumatic anosmia also suffer from ageusia [11]. A study involving veterans with TBI explored sensory dysfunction in smell and taste, revealing a prevalence of 38.3% [12].

Mixed chemosensory disorders after head trauma encompass a complex interplay of taste and smell impairments. Thus, understanding and addressing these disorders are essential, as they significantly affect an individual’s well-being, dietary habits, and daily activities [13]. This case report endeavors to provide insights into the complexities of diagnosing and managing taste and smell impairments following TBI, emphasizing the significance of a multidisciplinary approach in comprehensively addressing mixed chemosensory disorders.

This study was conducted using a retrospective chart review, and ethical approval was exempted by the Chonnam National University Dental Hospital Institutional Review Board (Gwangju, Korea) (CNUDH-2023-023).

A 52-year-old male was referred to the Emergency Medical Center of Chonnam National University Hospital from a private hospital due to sudden dysarthria symptoms. A week prior, he had been involved in a car accident as a pedestrian, sustaining head and limb injuries, and he was receiving treatment at the private hospital. His medical history revealed four years of managing high blood pressure with medication and a recent diabetes diagnosis, for which he had started medication. During the physical examination, he displayed an alert mental state, scored 15 on the Glasgow Coma Scale, had equal and reactive pupils, and showed no apparent motor weakness.

A noncontrast brain computed tomography (CT) scan exhibited a faint linear high-density area in the left precentral gyrus, indicative of subarachnoid hemorrhage (SAH) (Fig. 1A), and a crescent-shaped isodensity region along the left cerebral convexity, suggestive of a subdural hematoma (SDH) (Fig. 1B). A subsequent brain magnetic resonance imaging (MRI) scan revealed fluid-attenuated inversion recovery images of hyperintensity in the sulci of the left precentral gyrus (Fig. 2A) and a crescent-shaped hyperintense lesion along the left cerebral convexity (Fig. 2B), confirming the presence of SAH and SDH, respectively. Susceptibility-weighted imaging revealed linear hypointensity in the precentral gyrus (Fig. 2C) and hypointense regions around the hyperintense lesion (Fig. 2D), supporting the SAH and SDH diagnoses by indicating the presence of associated blood products in both areas.

The patient was diagnosed with subarachnoid and subdural hemorrhage in the left frontoparietal region, and the proposed treatment plan included admission to a neurosurgery ward and conservative management.

The patient reported discomfort, an inability to detect salty or sour tastes, and diminished olfactory perception following the accident. Approximately 16 weeks post-treatment at the Emergency Medical Center, he underwent evaluation for olfactory function at the Department of Otolaryngology. A CT scan of the paranasal sinuses revealed no pathological changes or damage, indicating clear sinuses and an open osteomeatal unit. Olfactory function was assessed using a smell test kit (YSK olfactory function test; Kimex Co.), resulting in threshold, recognition, and discrimination scores of 6/12, 8/12, and 6/12, respectively. These results, indicating a decreased sense of smell, prompted the otolaryngologist to diagnose hyposmia.

Approximately two weeks after the evaluation at the Department of Otolaryngology, the patient was referred to the Department of Oral Medicine for a detailed assessment of taste function. An oral examination showed the oral cavity to be in good condition. Both visual inspection and magnified clinical photographs indicated normal tongue and lingual papillae morphology. Salivary secretion rates measured at rest and upon stimulation were 0.2 and 2.2 mL/min, respectively, indicating no signs of xerostomia. Taste function was evaluated using a taste test kit (Taste Strips; Burghart Messtechnik GmbH), showing a general reduction in taste sensation bilaterally and specifically indicating ageusia for salty taste. Furthermore, electric taste-detection thresholds were assessed using an electrogustometer (EG-IIB; Nagashima Medical Instrument Co.) across the tip and posterior lateral border of both sides of the tongue. The measured values ranged from 24 to 34 dB (130-400 μA), significantly exceeding the normal threshold range.

Combining the findings from neurosurgery, otolaryngology, and oral medicine, the patient’s taste and smell symptoms were diagnosed as a mixed chemosensory disorder attributed to TBI resulting from head trauma.

Diagnosing mixed chemosensory disorders after head trauma poses several challenges due to the subjective nature of taste and smell perception and the multifactorial etiology of these impairments. This diagnosis often requires a multimodal approach that combines subjective patient reports and objective assessments [6,14]. Addressing the complexities of taste and smell alterations requires a comprehensive understanding of their clinical presentations and the use of various diagnostic tools to accurately characterize and manage these sensory impairments.

In this case, neurosurgery allowed for the initial identification and characterization of intracranial pathologies, such as subarachnoid and subdural hemorrhages, which may be linked to taste and smell irregularities. Advanced imaging techniques, such as CT and MRI, helped delineate structural changes impacting sensory function. The otolaryngologist was crucial in assessing olfactory function and nasal anatomy. Employing CT scans of the paranasal sinuses excluded local causes of olfactory dysfunction, ensuring no sinonasal pathologies were affecting smell perception. The expertise of the otolaryngologist in olfactory assessments using smell tests facilitated the diagnosis of olfactory deficits and the qualification of olfactory dysfunction. Furthermore, involving an oral medicine specialist contributed to the evaluation of taste disorders. Detailed examinations of oral cavity structures, including the tongue and lingual papillae, complemented by a chemical taste test and electrogustometry, helped identify taste impairments and assess the extent of dysfunction. The collaborative efforts among these specialties enabled a comprehensive evaluation of the patient’s chemosensory function.

TBI resulting from head trauma can lead to a spectrum of sensory disturbances, including taste and smell impairments [1,7,8]. Impact, acceleration–deceleration forces, or direct trauma to the head can cause shearing forces, contusions, hemorrhages, or diffuse axonal injury, affecting various brain regions associated with chemosensory perception [15-17].

In this case, brain imaging findings, particularly the presence of SAH in the left precentral gyrus and SDH along the left cerebral convexity, suggested the potential involvement of critical structures associated with taste and smell processing. The presence of SAH in the left precentral gyrus may have disrupted olfactory signal transmission. While the precentral gyrus is primarily known as the primary motor cortex—responsible for executing voluntary movements [18]—the precentral gyrus may have indirect connections or influences on olfactory processing pathways. Damage to the olfactory bulbs or neural pathways involved in olfactory perception may result in hyposmia or anosmia, contributing to the diminished sense of smell. Furthermore, SDH along the left cerebral convexity, situated near areas related to gustatory processing, may have affected taste perception. Disruption or damage to regions involved in gustatory perception, such as the insular cortex [19] or the frontal operculum [20], could lead to alterations in taste sensation or loss of taste modalities. However, the precise and direct correlation between these specific brain imaging findings and taste and smell alterations requires further investigation and detailed functional assessments to establish causality.

In conclusion, our report illuminated the intricacies involved with diagnosing and understanding mixed chemosensory impairments following TBI, emphasizing the critical role of electrosensory and chemosensory testing in unraveling these intricate sensory deficits. The findings underscore the importance of considering the involvement of the central nervous system in taste and smell disorders following head trauma, providing insights into potential brain regions affecting chemosensory perception.Furthermore, diagnosing mixed chemosensory disorders following head trauma requires a multimodal approach that combines subjective patient reports, objective assessments, and interdisciplinary evaluations.

No potential conflict of interest relevant to this article was reported.

Data sharing does not apply to this article, as no new data were created or analyzed in this study.

None.

Conceptualization: YGI. Project administration: JHK. Writing - original draft: YGI, SKK, CMS. Writing - review & editing: YGI, SKK, CMS, JHK.