Cranial Nerve VIII: Hearing and Vestibular Functions

| March 31, 2010 | 0 Comments

by Richard D. Sanders, MD, and Paulette Marie Gillig, MD, PhD
Dr. Sanders is Associate Professor, Departments of Psychiatry and Neurology, Boonshoft School of Medicine, Wright State University, and Ohio VA Medical Center, Dayton, Ohio. Dr. Gillig is Professor of Psychiatry and Faculty of the Graduate School, Department of Psychiatry, Wright State University, Dayton, Ohio

Psychiatry (Edgemont) 2010;7(3):17–22

Series Editor: Paulette M. Gillig, MD, PhD, Professor of Psychiatry, Department of Psychiatry, Boonshoft School of Medicine, Wright State University, Dayton, Ohio

Funding: There was no funding for the development and writing of this article.

Financial disclosure: The authors have no conflicts of interest relevant to the content of this article.

Key Words: psychiatry and neurology, hearing acuity, vestibular testing, deafness, vertigo, tinnitus, Meniere’s disease

Abstract

Cranial nerve VIII brings sound and information about one’s position and movement in space into the brain. The auditory and vestibular systems subserve several functions basic to clinical medicine and to psychiatry. This article covers the basics of cranial nerve VIII, hearing and vestibular systems, including common problems with hearing and balance, problems with hearing and balance that tend to be found in psychiatric patients, and some simple assessments of value in clinical practice.

Introduction

The eighth cranial nerve is deeply involved in clinical medicine. Hearing is of course central as patients generally hear our questions and we hear their answers. Routine assessment and treatment depend heavily on intact hearing. Some of the most common complaints in general medicine are vestibular (such as dizziness) and auditory (such as tinnitus and hearing impairment). This article covers the essential anatomy and physiology, abnormal clinical signs found in clinical psychiatry, and how to elicit these signs.

Relevant Anatomy and Physiology

Auditory system. The ear is commonly divided into outer, middle, and inner parts. The outer conducts air pressure waves to the tympanic membrane. The middle conducts pressure through the solid medium of the three ossicles, from the tympanic membrane to the oval window. The inner conducts waves through a fluid medium along the organ of Corti, triggering impulses in its hair cells, which correspond to specific frequencies. These form the auditory branch of the eighth cranial nerve and synapse on the ipsilateral cochlear nuclei in the rostral medulla. A majority cross over to join the lateral lemniscus, traveling rostrally to the midbrain inferior colliculus. From there, short neurons reach the medial geniculate nucleus, which projects via internal capsule to primary auditory cortex on the superior temporal gyrus.

Vestibular system. As with the acoustic branch, vestibular nerve impulses encoding motion and position originate in hairs within fluid-filled cavities. These cavities, the semicircular canals, utricle and saccule (collectively the labyrinth), are positioned so that any change or rotation is uniquely codified. The vestibular branch of the eigth cranial nerve closely adjoins the auditory. Its neurons synapse in vestibular nuclei, as well as in the rostral medulla. The vestibular nuclei project to many locations with intuitive relevance, including cerebellum, spinal cord, extraocular nuclei (nystagmus), parietal cortex (spatial orientation), vagal nucleus (vomiting), nucleus solitarius (nausea), and reticular formation (pallor, diaphoresis).

Signs and symptoms

Auditory system. Poor hearing acuity is a common and disruptive symptom. It affects about 10 percent of the population, with major effects on communication, social interaction, and cognition. At least 0.1 percent are congenitally deaf.[1] The most common causes of acquired hearing loss are noise exposure (sensorineural damage at the organ of Corti), otosclerosis (conductive damage at the middle ear ossicles), otitis media (middle ear inflammation interfering with conduction), cerumen impaction (mechanical blockage of the outer ear, interfering with conduction), presbycusis (age-associated sensorineural hearing loss), trauma, and Meniere’s disease (transient loss of hearing associated with attacks, sometimes permanent deficits after multiple attacks).

Available data suggest that hearing impairment is associated with mental illness and mental retardation.[2] Fetal alcohol syndrome is strongly associated with hearing impairment of several types.[3] Autism or autistic features may be specifically associated with deafness. Paradoxically, auditory hypersensitivity is quite common in autism.[4] Those who are deaf may be more impulsive and may have more personality disorders.[2,5] Those with acquired (but not hereditary) deafness are at higher risk for attention deficit hyperactivity disorder (ADHD).[5]

Hearing acuity deficits are present in at least two percent of people over 65 years of age.[6] Like visual deficits, they are thought to contribute to age-related psychopathology, including social withdrawal and depression.[7] Hearing deficits are also related to cognitive disability, although hearing aids may not bring sweeping improvements in cognition or behavior to the demented.[8]

Hearing deficit seems to be a risk factor for future psychosis in healthy young people.[9–12] It is uncertain whether the link between poor hearing and future psychosis might be due to reduced or distorted sensory input, or whether sensory disability is a less specific marker of early infection[13] or some other neurological handicap. Oddly, most studies find basic auditory acuity measures to be normal in schizophrenia[14–16] and late-life schizophrenia-like illness.[17–20] Low-level physiological responses, such as brainstem auditory-evoked potentials, are also normal,[21] but many deficits in performance and physiological response appear at many higher levels of processing.[21–24] Although low hearing acuity is a risk factor for psychosis, it is not a prominent finding in patients with psychosis.

Hearing loss is not a prominent feature of mood disorders,[25] but it is a common finding, along with weakness and fatigue, in mitochondrial diseases.[26] Thus, hearing loss in a patient with prominent weakness or fatigue should raise the question of mitochondrial disease.

Bilateral high-frequency loss is found in alcoholism, related to drinking time but not to age.[27] Alcohol acutely diminishes acuity across the frequency spectrum[28] and impedes central processing.[29] Cannabis seems to not have acute effects on auditory sensitivity, but it has interesting effects on higher order perception.[29,30]

Auditory hallucinations are among the most familiar symptoms in psychiatry, although reported by less than one percent of the adult population (except for sleep-associated hallucinations, which are common[31]) and about 75 percent of patients with schizophrenia. The symptom is accepted as unremarkable under certain circumstances, such as severe sleep deprivation and sleep onset. Some believe that healthy preliterate humans routinely hallucinated, as they seemed to in the stories of the Greek epic poet Homer and the Old Testament.[32]

Whether modern patients and ancient heroes, however, when it comes to the term auditory hallucination, most often we are referring to “voices” (intelligible speech), which is a particular type of complex hallucination. Much less common are musical hallucinations, which are strongly associated with deafness[13] and occasionally other neurological conditions.[33]

Tinnitus affects at least 30 percent of the population at some point, and leads at least 10 percent to seek medical attention.[34] Most tinnitus consists of a continuous higher-pitched tone. Called subjective tinnitus, it could be considered a rudimentary auditory hallucination. Strongly associated with acquired hearing loss, its mechanism is thought to involve disinhibition and cortical remapping, similar to the development of phantom limb pain after loss of normal sensory input. Subjective tinnitus should be distinguished from the uncommon objective tinnitus for which an explanation can be found. Objective tinnitus tends to be intermittent, often pulsatile, and lower pitched. Sources include audible turbulence in a vessel near the ear or abnormal activity of muscles in the palate or middle ear. Evaluation of tinnitus includes listening around the ear (especially if only one ear is affected) and evaluating hearing with audiometry. Audiologists are indispensible in the management as well as assessment of tinnitus.[35,36]

Vestibular system. First, it is worth noting that the complaint “dizzy” can include many symptoms associated with anxiety and orthostatic lightheadedness (presyncope), both very common in psychiatry. For present purposes, dizziness is a sense of being off balance. Dizziness is among the most common complaints in medicine, affecting at least 20 percent of the general population.[37] Vertigo, a type of dizziness, is a false sense that the self or the environment is moving, caused by asymmetric vestibular dysfunction. It has a one-year prevalence of about five percent in the general population.[38]

In about 75 percent of cases, vertigo is caused by the more benign peripheral vestibular disorders, but the more sinister central lesions must be excluded. Central lesions (of the pons, medulla, or cerebellum) and peripheral lesions (of the semicircular canals, utricle, saccule, or vestibular nerve) can cause a similar presentation of vertigo, nausea, vomiting, ataxia, and nystagmus. Examination can accurately distinguish central from peripheral causes, which we will describe later. Patients with a peripheral vestibular lesion can usually stand (although often leaning toward the lesion), while those with a central lesion are often unable to stand without support. Dysarthria, incoordination, numbness or weakness—signs of damage elsewhere in the brain—suggest a central origin.[39,40]

The most common central causes of dizziness and vertigo are disorders of the vertebrobasilar circulation, migraine, multiple sclerosis, tumors of the posterior fossa, neurodegenerative disorders, and drug effects.[37,41] Common peripheral causes include benign paroxysmal positional vertigo (BPPV), Meniere’s disease, and vestibular neuritis. BPPV is the most common single cause of vertigo and is present in a significant proportion of elderly persons not seeking treatment for dizziness. In a nonspecialty setting, BPPV accounts for around 40 percent of vertigo cases, roughly 30 to 40 percent are due to vestibular neuritis/labrynthitis, about 10 to 15 percent are due to migraine, 10 percent are due to Meniere’s disease, and five percent are due to stroke.[38,41]

BPPV starts fairly abruptly, remits spontaneously after several weeks, and often recurs after months to years. Dizziness is always caused (or at least aggravated) by movement, but dizzy paroxysms last only seconds to minutes. BPPV is caused by debris in one of the vestibular organs, most often the posterior semicircular canal. It can usually be diagnosed without special tests (described later), and it can be readily treated without medication or surgery.[41]

Meniere’s disease is characterized by fluctuating, progressive, sensorineural hearing loss; spells of vertigo lasting minutes to hours with vestibular nystagmus; tinnitus (usually); a sense of fullness in the ears; and periods of remission and exacerbation. Its etiology seems to involve edema in the labyrinth.

Vestibular neuritis is a syndrome of acute unilateral vestibular failure, with vertigo, nausea, and unsteadiness, but no hearing changes. It often follows a viral syndrome. It generally remits in weeks to months. It is quite similar in presentation to stroke; in both, dizzy spells can last for days and there is little fluctuation in symptoms.[39,40]

Investigators of the early 20th century[42] found that patients with schizophrenia showed less nystagmus in response to vestibular stimulation than healthy controls. Modern vestibular research gives no clear answers regarding schizophrenia,[43] but there does seem to be an association between anxiety and impaired balance across species,[44] an excess of vestibular dysfunction in anxiety patients,[45] and an excess of anxiety among patients with vestibular disorders.[46] The most specific association is between agoraphobia and peripheral vestibular dysfunction.[45]

When confronted with acute vestibular signs and symptoms in routine psychiatric practice (nausea, dizziness or vertigo, nystagmus, impaired balance), it is important to think early of intoxication, particularly with ethanol or an anticonvulsant, or withdrawal, particularly from a serotonergic antidepressant.[47]

Examination Methods

Auditory system. Why not simply note whether or not “conversational hearing” is intact? This approach has inadequate sensitivity—around 50 percent.[6] Fortunately, another very efficient method is available, with at least 90-percent sensitivity and at least 80-percent specificity. This is the whispered voice test. Stand behind the patient, with your left arm extended about two feet to the patient’s ear. While occluding the left external auditory meatus with a finger in a rubbing motion (to ensure masking the left ear), whisper as softly as possible a letter, a numeral and another letter (e.g. “b, 8, g”). If the patient repeats the triplet correctly, move on to the other side (use an unrelated letter-number-letter stimulus). If there are any errors, whisper a new triplet to the same side. An abnormal result for an ear is if less than half of the letters or numbers are repeated correctly. For abnormal or questionable results, audiometric testing is in order.6
Having discovered a hearing deficit, one might inquire into its origins. A 512Hz tuning fork is useful for distinguishing sensorineural hearing loss (the problem is at the cochlea or beyond) from conductive hearing loss (sound waves are having trouble getting to the cochlea).

If there is unilateral hearing loss, do the Weber test; otherwise, the test is misleading. Hold the vibrating fork firmly to the skull at a midline, and ask if it sounds louder on either side. If the bad side seems to be softer the damage is probably sensorineural. If the bad side seems to be louder, the damage is probably conductive. If they seem equal, the Weber is inconclusive. The Rinne test is a more accurate test, if conductive hearing loss is suspected. The patient is asked to report which seems louder, as bone and air conduction stimuli are applied. The simplest approach is to hold the tuning fork alternately to the mastoid (lightly but firmly) and about one inch from the ear, each for about two seconds. The tuning fork should be held so that its long axis is perpendicular to the line through the ear canals. If bone conduction is definitely heard better than air conduction (BC>AC), this is strong support for conductive hearing loss.[6]

Vestibular system. The horizontal head impulse test is a quick vestibulo-ocular reflex used to distinguish the more benign peripheral from the more ominous central lesions causing vertigo. Approaching a seated and relaxed patient from the front, grasp the head from both sides and instruct the patient to relax and (the examiner must do the work) fixate on your nose. Starting from about 20 degrees rotation off center, rapidly rotate the head to midline, observing the eyes. An abnormal response occurs when the head is rotated toward a vestibular lesion and consists of a quick corrective saccade (gaze shift) once the head stops moving. Without vestibular input, the patient cannot maintain fixation during the head rotation, requiring the adjustment. A normal result on this test (no corrective saccade seen) is strong evidence of central nervous system (CNS) involvement.[48]

Some cases with brainstem or cerebellar stroke may have false-positive head-impulse test results, but display skew deviation. Skew deviation is the vertical deviation of an eye. Ask the patient to fixate on a target, and alternately cover each eye for about two seconds. As the skewed eye is uncovered, it is noted to have deviated vertically. This finding suggests brainstem or cerebellar stroke. Thus, a positive head-impulse test supports a peripheral etiology, but skew deviation would over-ride this result in support of a central lesion.[49]

The Dix-Hallpike test is the acknowledged gold standard test to diagnose BPPV (specifically BPPV of the posterior semicircular canal, which comprises about 90 percent of BPPV). Start with the patient sitting upright with legs extended. Warn the patient that another brief episode of dizziness and nausea is likely to result from the test. Rotate the patient’s head about 45 degrees, then quickly help the patient assume a supine position with the head still rotated and hyperextended approximately 20 degrees. This extension may be achieved by supporting the patient’s head as it hangs off the table or by placing a pillow under the upper back. Then watch the patient’s eyes for about 45 seconds. If upwards, rotatory nystagmus occurs then the test is positive for BPPV. Nystagmus should take 5 to 20 seconds to develop after assuming the supine position. If nystagmus is predominantly downwards or lacks a rotatory component, a central lesion is more likely. After returning to a seated position and resting, the same exercise should be done to the opposite side.[41]

If the history is suggestive for BPPV, but the Dix-Hallpike test is negative on both sides, the supine roll test should be done. This is the best available test for lateral semicircular canal BPPV, which makes up about 10 percent of BPPV cases. The patient lies in a supine, flat position, facing the ceiling. After due warnings, rotate the head quickly to the right about 90 degrees, observing the eyes for nystagmus. In this case, a positive response consists of vigorous horizontal nystagmus (either toward the floor of the ceiling). After recovery, repeat the process with the head turned 90 degrees to the left.[41] If this test also produces no delayed nystagmus, BPPV is unlikely.

Summary

Auditory and vestibular problems are common in all patient populations, and particularly among certain groups of psychiatric patients. Poor auditory acuity detracts from social functioning and increases the risk for psychosis. Hearing acuity is very efficiently and accurately screened, and deficits can be assigned with reasonable accuracy to sensorineural or conductive causes. Vestibular problems are associated with anxiety, agoraphobia in particular. Acute vestibular complaints can usually be quickly and accurately diagnosed without using special tests, through history and examination.

References
1. Parving A. The need for universal neonatal hearing screening—some aspects of epidemiology and identification. Acta Paediatr Suppl. 1999;88:69–72.
2. Carvill S. Sensory impairments, intellectual disability and psychiatry. J Intellect Disabil Res. 2001;45:467–483.
3. Church MW, Kaltenbach JA. Hearing, speech, language, and vestibular disorders in the fetal alcohol syndrome: a literature review. Alcohol Clin Exp Res. 1997;21:495–512.
4. Gomes E, Pedroso FS, Wagner MB. Auditory hypersensitivity in the autistic spectrum disorder. Pro Fono. 2008;20:279–284.
5. Bailly D, Dechoulydelenclave MB, Lauwerier L. Hearing impairment and psychopathological disorders in children and adolescents. Review of the recent literature. Encephale. 2003;29:329–337.
6. McGee S. Evidence-based Physical Diagnosis. Philadelphia: Saunders; 2001.
7. Heine C, Browning CJ. Communication and psychosocial consequences of sensory loss in older adults: overview and rehabilitation directions. Disabil Rehabil. 2002;24:763–773.
8. Allen NH, Burns A, Newton V, et al. The effects of improving hearing in dementia. Age Ageing. 2003;32:189–193.
9. O’Neal P, Robins LN. Childhood patterns predictive of adult schizophrenia: a 30-year follow-up study. Am J Psychiatry. 1958;115:385–391.
10. David A, Malmberg A, Lewis G, et al. Are there neurological and sensory risk factors for schizophrenia? Schizophr Res. 1995;14:247–251.
11. Stefanis N, Thewissen V, Bakoula C, et al. Hearing impairment and psychosis: a replication in a cohort of young adults. Schizophr Res. 2006; 85:266–272.
12. van der Werf M, van Boxtel M, Verhey F, et al. Mild hearing impairment and psychotic experiences in a normal aging population. Schizophr Res. 2007;94:180–186.
13. Gordon AG. Schizophrenia and the ear. Schizophr Res. 1995;17:289–291.
14. Bartlett MR. The sensory acuity of psychopathic individuals: a comparison of the auditory acuity of psychoneurotic and dementia praecox cases with that of normal individuals. Psychiatr Q. 1935;9:422–425.
15. Ludwig AM, Wood BS, Downs MP. Auditory studies in schizophrenia. Am J Psychiatry. 1962;119:122–127.
16. Gruzelier JH, Hammond NV. Gains, losses and lateral differences in the hearing of schizophrenic patients. Br J Psychol. 1979;70:319–330.
17. Sjogren H. Paraphrenic, melancholic and psychoneurotic states in the presenile-senile period of life: a study of 649 patients in the functional division. Acta Psychiatr Scand. 1964;40 (Suppl 176):1–63.
18. Gurian BS, Wexler D, Baker EH. Late-life paranoia: possible association with early trauama and infertility. Int J Geriatric Psychiatry. 1992;7:277–284.
19. Almeida OP, Howard RJ, Levy R, David AS. Psychotic states arising in late life (late paraphrenia): the role of risk factors. Br J Psychiatry. 1995;166:215–228.
20. Prager S, Jeste DV. Sensory impairment in late-life schizophrenia. Schizophrenia Bull. 1993;19:755–772.
21. Pfefferbaum A, Horvath TB, Roth WT, et al. Auditory brain stem and cortical evoked potentials in schizophrenia. Biol Psychiatry. 1980;15:209–223.
22. Brenner CA, Krishnan GP, Vohs JL, et al. Steady state responses: electrophysiological assessment of sensory function in schizophrenia. Schizophr Bull. 2009;35:1065–1077.
23. Javitt DC. When doors of perception close: bottom-up models of disrupted cognition in schizophrenia. Annu Rev Clin Psychol. 2009;5:249–275.
24. Ford JM, Roach BJ, Jorgensen KW, et al. Tuning in to the voices: a multisite FMRI study of auditory hallucinations. Schizophr Bull. 2009;35(1):58–66.
25. Kallert TW. Acoustic and optical perceptual disorders in depressive diseases—an overview of results from experimental studies. Schweiz Arch Neurol Psychiatr. 1996;147:4–11.
26. Fattal O, Budur K, Vaughan AJ, Franco K. Review of the literature on major mental disorders in adult patients with mitochondrial diseases. Psychosomatics. 2006;47:1–7.
27. Wheeler DC, Dewolfe AS, Rausch MA. Audiometric configuration in patients being treated for alcoholism. Drug Alcohol Depend. 1980;5:63–68.
28. Upile T, Sipaul F, Jerjes W, et al. The acute effects of alcohol on auditory thresholds. BMC Ear, Nose and Throat Disorders. 2007; 7:4.
29. Fitzpatrick D, Eviatar A. The effect of alcohol on central auditory processing (comparison with marijhuana). J Otolaryngol. 1980;9:207–214.
30. Roser P, Juckel G, Rentzsch J, et al. Effects of acute oral Delta9-tetrahydrocannabinol and standardized cannabis extract on the auditory P300 event-related potential in healthy volunteers. Eur Neuropsychopharmacol. 2008; 18:569–577.
31. Ohayon, MM. Prevalence of hallucinations and their pathological associations in the general population. Psychiatry Res. 2000;97:153–164.
32. Jaynes J. The Origin of Consciousness in the Breakdown of the Bicameral Mind. Boston: Houghton Mifflin; 1976.
33. Sacks O. Musicophilia: Tales of Music and the Brain. New York: Knopf; 2007.
34. Heller AJ. Classification and epidemiology of tinnitus. Otolaryngol Clin North Am. 2003; 36:239–248.
35. Noble W, Tyler R. Physiology and phenomenology of tinnitus: implications for treatment. Int J Audiol. 2007;46:569–574.
36. Crummer RW, Hassan GA. Diagnostic approach to tinnitus. Am Fam Physician. 2004;69:120–126.
37. Karatas M. Central vertigo and dizziness: epidemiology, differential diagnosis, and common causes. Neurologist. 2008;14:355–364.
38. Neuhauser HK. Epidemiology of vertigo. Curr Opin Neurol. 2007;20:40–46.
39. Chan Y. Differential diagnosis of dizziness. Curr Opin Otolaryngol Head Neck Surg. 2009;17:200–203.
40. Kerber KA. Vertigo and dizziness in the emergency department. Emerg Med Clin North Am. 2009;27:39–50.
41. Bhattacharyya N, Baugh RF, Orvidas L, et al. Clinical practice guideline: benign paroxysmal positional vertigo. Otolaryngol Head Neck Surg. 2008;139(Suppl 4):S47–S81.
42. Angyal A, Sherman MA. Postural reactions to vestibular stimulation in schizophrenic and normal subjects. Am J Psychiatry. 1942;98:857–862.
43. Levy DL, Holzman PS, Proctor LR. Vestibular dysfunction and psychopathology. Schizophr Bull. 1983;9(3):383–438.
44. Kalueff AV, Ishikawa K, Griffith AJ. Anxiety and otovestibular disorders: linking behavioral phenotypes in men and mice. Behav Brain Res. 2008 10;186:1–11.
45. Jacob RG, Furman JM, Durrant JD. Turner SM. Panic, agoraphobia, and vestibular dysfunction. Am J Psychiatry. 1996;153:503–512.
46. Clark DB, Hirsch BE, Smith MG, et al. Panic in otolaryngology patients presenting with dizziness or hearing loss. Am J Psychiatry. 1994;151:1223–1225.
47. Black K, Shea C, Dursun S, Kutcher S. Selective serotonin reuptake inhibitor discontinuation syndrome: proposed diagnostic criteria. J Psychiatry Neurosci. 2000; 25:255–261.
48. Newman-Toker DE, Kattah JC, Alvernia JE, Wang DZ. Normal head impulse test differentiates acute cerebellar strokes from vestibular neuritis. Neurology. 2008;70:2378–2385.
49. Kattah JC, Talkad AV, Wang DZ, et al. HINTS to diagnose stroke in the acute vestibular syndrome. Three-step bedside oculomotor examination more sensitive than early MRI diffusion-weighted imaging. Stroke. 2009;40:3504.

Tags: , , , , , ,

Category: Neurology, Past Articles, Psychiatry

Leave a Reply

This site uses Akismet to reduce spam. Learn how your comment data is processed.