In 2015, an estimated 8.8% (more than 4 million people) were diabetic, globally (Koye, Magliano, Nelson, & Pavkov, 2018). Diabetes Mellitus (DM) (more commonly-used, ‘Diabetes’), whose nomenclature originates from Greek (for ‘siphon’) and Latin (sweet), is a condition caused by the underproduction of (corresponding to Type I- usually genetic), or pathological insensitivity to (corresponding to Type 2- usually acquired) the hormone, insulin. Insulin is produced by the Islets of Langerhans of the pancreas and regulates the transfer of blood glucose into body cells as fuel (Cowap & Parry, 2015). This is particularly important to the neural system and red blood corpuscles, as Cowap and Parry (2015) note that these cells “cannot use fats for energy—they can only use sugar” (p. 9). The pancreas also produces the antithesis of insulin, glucagon, and together with insulin, manages homeostatic control over the levels of glucose in the bloodstream. Cowap and Parry explain that Diabetes is diagnosed when the body can no longer maintain levels of blood glucose within the normal range (between 60 and 140mg/dL). Furthermore, Cowap and Parry describe the outcomes of excess (hyperglycemia) or insufficient (hypoglycemia) blood glucose, which can acutely cause coma and death, but chronically, may cause pervasive problems in multiple body systems. These include damage to the kidneys, nerves and vascular systems- which can correspondingly cause symptoms almost anywhere in the body.
How Does DM Relate to the Auditory-Vestibular System (AVS)
Naik and Tilloo (2018) cite multiple molecular processes in Diabetes Type 2 as a cause of vestibular disorders (VD). They describe “formation of advanced glycation end‑products, polyol formation, increased activity of protein kinase C, increased production of extracellular matrix proteins, and glycosaminoglycans” resulting in “microvascular damage termed as ‘Microangiopathy.’ “(p. 199) as the underlying mechanism. Likewise, Akinpelu, Ibrahim, Waissbluth and Daniel (2014) present animal and human temporal bone evidence for similar processes influencing the cochlea. Therefore, DM is also causal to sensorineural hearing loss (SNHL). Furthermore, Akinpelu, Ibrahim, Waissbluth and Daniel indicate that there is increased evidence of histological findings with increased length of clinical history. Xipeng et al. (2013) report that “prevalence of hearing loss in DM patients is twice that in normal individuals and that vertigo, tinnitus and hearing loss in DM patients are likely from inner ear diseases related to glucose metabolism disorders” (p. 84). The changes in the cochlea are not confined to older DM patients, nor only Type 2 DM. However, it is often only possible to detect fine changes in the cochlea in young patients with Distortion Product Otoacoustic Emissions (OAE) (Botelho, Carvalho da S., & Silva, 2014).
Naik and Tilloo (2018) found a significant association between the severity of VD, how well Diabetes Type 2 is controlled, and age, and conclude that in severe cases with a long duration, vestibular neuropathy is a probable aetiology. Also, due to peripheral neuropathy, poorer information obtained from somatosensory information can influence the vestibular system’s function due to reduced cerebellar modulation (Jáuregui-Renaud, Sánchez, Ibarra Olmos, & González-Barcena, 2009).
Ibraheem, Ramadan Hassaan and Mousa (2017) compared Diabetes Type 2 (oral insulin) and Type 1 patients and found similarity in both prevalence of VD and profiles of VD between two groups. However, they add that DM may lead to endolymphatic hydrops caused by disturbing the function of cells responsible for endolymphatic production (dark cells) in the vestibular labyrinth, affecting the sodium-potassium balance, and ultimately resulting in “elevation of the osmotic pressure that would absorb excess water into the endolymphatic space” (p. 141). The outcome could lead to the diagnosis of Meniere’s Disease with both auditory and vestibular correlates. Therefore, the relationship between Diabetes Mellitus and auditory-vestibular disorders, stems from vascular, neurological (including somatosensory) and metabolic pathologies.
Most commonly reported symptoms and patient presentation to Audiologists
Patients with VD caused by underlying DM Type 2, report increased frequency of symptoms of balance disturbance, generalised dizziness and problems with stability especially when changing body position, as well as instability on uneven surfaces (Jáuregui-Renaud, Sánchez, Ibarra Olmos, & González-Barcena, 2009). Naik and Tilloo (2018) note that more than 20% of their subjects had DM-induced unilateral Benign Paroxysmal Positional Vertigo (BPPV), with sudden onset vertigo lasting less than a minute, triggered by head position change, and with nystagmus in the plane of the affected canal. Ibraheem, Ramadan Hassaan and Mousa (2017) report patients with DM-linked endolymphatic hydrops (leading to Meniere’s Disease), with fullness, tinnitus, vertigo and fluctuating SNHL. In fact, SNHL will be a significant finding alongside VD of many DM patients (Naik and Tilloo, 2018). Walley, Anderson, Pippen and Maitland (2014) mention that patients may report a history of falls related to both vestibular and somatosensory changes. In DM Type 1, Klagenberg, Zeigelboim, Jurkiewicz, & Martins-Bassetto (2007) found that patients reported symptoms of headache, tinnitus and rotatory dizziness, with fewer also reporting hyperacusis, hearing problems and non-spinning dizziness. Vestibular symptoms can also be subclinical (not reported by the patient), despite medical investigation leading to the identification of a vestibular lesion (Kalkan, Bayram, Gökay, Cura, & Mutlu, 2018). Patients will also present with SNHL that is unexplained by age or other factors (Xipeng et al., 2013). The range of hearing loss configurations can be broad and should not be pre-characterised.
When a patient complains of vestibular symptoms or unexplained hearing loss, the possibility of DM in the case history should be confirmed. However, the audiologist should bear in mind that the patient may not yet be diagnosed and should therefore probe for the symptoms of Diabetes. Confirmation thereof, should lead to physician referral. Other than changes in balance or equilibrium, these are: unexplained thirst; unexplained weight loss; frequent urination; increased hunger; general fatigue; changes in vision and changes in hearing; skin sensitivity or itching; paraesthesia; nausea and vomiting; repeat episodes of candida and delayed healing (Cowap & Parry, 2015).
Probable audiometric and vestibular test findings
Test findings may be quite varied due to the substantial array of resultant vestibular problems that may originate with DM. However, in most cases the severity of the hearing loss and the severity of the vestibular function is associated with the severity of the underlying DM, the time since diagnosis, the quality and type of control (including patient compliance), and the age of the patient (Ibraheem, Ramadan Hassaan & Mousa, 2017; Naik & Tilloo, 2018).
While a few patients may present unilaterally, most diabetic patients present with bilaterally symmetrical, sloping or flat sensorineural hearing loss which is usually slowly progressive (Ciorba, Aimoni & Bovo, 2012; Ferreira et al. 2016). Speech discrimination may vary, with some as expected for the severity of the loss, and some people, with poorer discrimination than expected when neuropathy is not only cochlea (peripheral) in origin. Naik and Tilloo (2018) demonstrated mostly absent otoacoustic emissions in moderately controlled DM, all absent in poorly controlled (severe) DM subjects, but mixed results in well-controlled (mild) subjects. Poor control of DM may also result in an acquired auditory neuropathy, where ABR most commonly would demonstrate an inverted ABR waveform when the stimulus polarity is changed (Winston & Stoner, 2013).
Similarly, the extent of vestibular symptoms and severity may vary, dependent on site of lesion in the vestibular system (and periphery), severity and clinical history of the DM itself. Patients with peripheral neuropathy will have proprioceptive changes affecting generalised balance and stability, and vision (retinopathy) (Walley, Anderson, Pippen & Maitland, 2014). These deficits can be demonstrated with a positive Romberg Test (https://www.physio-pedia.com/Romberg_Test) or for more detail, using computerized dynamic posturography ( https://www.dizziness-and-balance.com/testing/posturography.html). A significant proportion may also present with DM-precipitated BPPV with a positive Dix-Hallpike (Naik and Tilloo (2018), and some with endolymphatic hydrops, demonstrating fluctuating audiogram, pathological cVEMP, unilateral weakness on calorics with Electronystagmography (ENG), and abnormally large summating potentials using ECochG ( Fetter, 2014).
Current research on Vestibular Function in Diabetes Mellitus
Despite the long history of Diabetes (1552 BC), science does not know everything about it, and how it impacts the body (McCoy, 2009). Current research on vestibular dysfunction and DM is focused on identifying optimum vestibular test protocols. This would be in aid of identifying which parts of the vestibular system are specifically affected by DM and improving the generalisability of the results. Vestibular Evoked Myogenic Potentials (VEMP) is a possibility (Bayram, 2019). Additionally, there is a need to identify the presence of vestibular changes in both symptomatic and asymptomatic patients, where Cervical VEMP (cVEMP) shows promise (Kanumuri, Chaitanya, Nara, & Kumar Reddy, 2018). Motivating for a vestibular assessment and vestibular monitoring to become part of the regular battery of tests for every DM patient is supported by research that suggests a strong correlation between worsening VD and poor glycemic control (Naik & Tilloo, 2018). Strengthening the relationship of causality between DM and VD is supported by a literature review of 14 studies reviewed by Gioacchini et al. (2018). More detail is sought on the precise mechanisms of certain predisposed types of VD, such as otolithic vulnerability causing BPPV (D’Silva et al., 2017).
What can an Audiologist bring to Diabetic care?
Diabetes Mellitus is at epidemic proportions, doubling globally between 2000 and 2015 (Koye, Magliano, Nelson, & Pavkov, 2018). The condition is expensive due to its pervasive effects on many systems in the body, and the resultant comorbidity is disabling, causing significant distress and leading to depression in many people (Chima, 2017). Audiologists should be part of the Diabetes solution. Since both hearing and vestibular function show a significant causal correlation with Diabetes, we can play an important role in early identification. This leads to better management and reduces the risks of damage to vital systems, such as the cardiovascular system. In addition, since we have the capacity to provide regular follow up, we can also counsel patients more regularly about their compliance with their treatment. Non-compliance is one of the factors that drive poorer vestibular and cochlear outcomes, and therefore more rapidly progressive results could alert the audiologist to a patient who is not taking care of their condition optimally. Early intervention and management of both vestibular rehabilitation and cochlear stimulation using amplification is likely to be more effective and improve the experience of daily living, reducing depression, cognitive decline and increasing independence (Weinstein, 2019). This is because critical structures have not yet become so damaged as to yield poor results. Audiologists can ensure good vestibular compensation and consistent hearing aid use, coupled with regular check-ups are most likely to help manage the patient’s outcomes over the long term.
This makes the Audiologist a vital part of “team Diabetes”.
Finally, on a lighter note, did you know that in the early 16th century “people known as “water tasters” diagnosed diabetes by tasting the urine of people suspected to have it. If urine tasted sweet, diabetes was diagnosed. It wasn’t until the 1800s that scientists developed chemical tests to detect the presence of sugar in the urine.” (McCoy, 2009, para. 4).
Yuck! But I guess we use the tools we have at hand!
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