Auditory hallucinations due to central nervous system lesions …

Douglas J Lanska MD MS MSPH

Neuro-Ophthalmology & Neuro-Otology

Updated 05.14.2024
Released 09.06.2015
Expires For CME 05.14.2027

Auditory hallucinations due to central nervous system lesions

Author: Douglas J Lanska MD MS MSPH

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Auditory hallucinations due to central nervous system lesions

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Introduction

Overview

This article describes the various types and locations of central nervous system lesions that can produce auditory hallucinations, either on a “release” or an “irritative” basis. Consequently, this article excludes various other conditions that can produce auditory hallucinations, including, for example, subjective tinnitus, objective tinnitus, and auditory hallucinations due to psychiatric disease (eg, schizophrenia, mania, psychotic depression, etc.), migraine, dementia, delirium or other acute encephalopathies, hallucinogens, or sensory deprivation.

Key points

	• Auditory hallucinations associated with lesions of the central nervous system may be simple (as with subjective tinnitus) or complex (voices or music).
	• Auditory hallucinations associated with lesions of the central nervous system may result from irritative or release processes. Those resulting from irritative processes (usually seizures) are typically brief (seconds or minutes), whereas those resulting from release mechanisms are typically prolonged (days to months).
	• Partial seizures may cause auditory hallucinations either in isolation during the awake state as a simple partial seizure, or as an aura (ie, the beginning of a symptom sequence leading to impairment of consciousness or a generalized seizure).
	• Auditory hallucinations associated with damage to brainstem structures involved in the central auditory pathways arise from release mechanisms and, consequently, tend to be prolonged and occur in association with central auditory processing disorders, including central hearing loss and impaired sound localization. These occur most commonly with acute lesions involving the pontine tegmentum.

Historical note and terminology

Canadian neurosurgeon Wilder Penfield (1891–1976) and his associates stimulated the exposed cerebral cortex of patients with uncontrollable neurologic seizures (53; 52).

Wilder Penfield

Canadian neurosurgeon Wilder Penfield in 1934. (Courtesy of McGill University Archives.)

Auditory hallucinations occurred only with stimulation of or near the temporal lobe cortex. Because the hallucinations often appeared to be reenactments of perceptions, Penfield concluded that electrical stimulation could activate engrams of prior experience. Penfield found that stimulation of the anterior transverse temporal gyrus of Heschl within the Sylvian fissure produced nonlinguistic simple sounds (eg, buzzing or whistling), whereas stimulation of the superior temporal gyrus produced experiential epileptic auditory hallucinations (eg, a voice or voices, music), with some differences between left and right (eg, with a trend for voices to result more often from stimulation of the superior temporal gyrus in the nondominant hemisphere) (52; 12). As summarized by Penfield and Perot,

there is a sharp functional frontier between the sensory and the interpretative areas . . . in the auditory cortex [the electrode may elicit] a ringing, humming or rumbling . . . but then, if the electrode is moved only a few millimetres away into the neighbouring cortex around these sensory areas, a response of a totally different order of neuronal organisation may result. There is no longer a sound but a voice, no longer a rumbling but music (52).

The auditory experiential responses arising from electrical stimulation of the auditory association cortex could be facilitated or inhibited by appropriately placed prior stimulation.

In 1986, Gregory Cascino and Raymond D Adams (1911-2008) reported three cases of auditory hallucinosis associated with brainstem lesions (08). They suggested that these might be due to a release mechanism, similar to what occurs with phantom limbs. A similar case was reported shortly thereafter by Douglas and Mary Jo Lanska and Mario Mendez in which further support was given for a release mechanism (44).

Clinical manifestations

Presentation and course

	• Postlesional auditory hallucinations after lesions of the central nervous system may be simple (as with subjective tinnitus) or complex (voices or music).
	• Postlesional auditory hallucinations resulting from irritative processes (usually seizures) are typically brief (seconds or minutes) whereas those resulting from release mechanisms are typically prolonged (days to months).
	• Initial ictal symptoms are often closely related to the physiological functions of the cortical circuits involved with the seizure locus and, consequently, such symptoms can provide localizing information.
	• When brain regions related to auditory integration are involved in the genesis of partial seizures, the seizure discharge can cause auditory hallucinations ranging from elementary sounds to complex hallucinations such as hearing spoken words, phrases, or music.
	• Auditory hallucinations that can occur due to damage to brainstem structures involved in the central auditory pathways may be unformed mechanical or seashell-like noises, voices (although individual words may be indistinct), or music.
	• Brainstem auditory hallucinosis is thought to arise from a release mechanism and, consequently, such hallucinations tend to be prolonged and occur in association with central auditory processing disorders, including central hearing loss and impaired sound localization.

Postlesional auditory hallucinations after lesions of the central nervous system may be simple (as with subjective tinnitus) or complex (voices or music). Those resulting from irritative processes (usually seizures) are typically brief (seconds or minutes), whereas those resulting from release mechanisms are typically prolonged (days to months). CNS structural lesions may result in auditory hallucinations by irritative processes or release mechanisms.

Ictal hallucinations. Auditory hallucinations are a rare initial manifestation of seizure and may occur with lesions in the posterior temporal lobe on one side (39). Lateral temporal seizures may have auditory (eg, buzzing, ringing) symptoms as the initial aura symptoms (40). Auditory aura in only one ear may lateralize a seizure to the contralateral hemisphere (40). A prefrontal-cingulate-auditory cortical network during epileptic seizures underlies the emergence of auditory verbal hallucinations, possibly through a transient deficit of self-monitoring for inner speech in focal epileptic seizures (45).

Currie and colleagues found that 17% of 514 patients with temporal lobe epilepsy experienced ictal auditory hallucinations (14). Partial seizures may cause auditory hallucinations either in isolation during the awake state as a simple partial seizure, or as an aura (ie, the beginning of a symptom sequence leading to impairment of consciousness or a generalized seizure) (02; 46; 09; 27; 36).

Initial ictal symptoms are often closely related to the physiological functions of the cortical circuits involved with the seizure locus, and, consequently, such symptoms can provide localizing information. Initial auditory hallucination in patients with temporal lobe seizures are associated with seizure onset limited to lateral structures (46).

When brain regions related to auditory integration are involved in the genesis of partial seizures, the seizure discharge can cause auditory hallucinations ranging from elementary sounds to complex hallucinations such as hearing spoken words, phrases, or music (52; 14). Ear plugging (ie, placing fingers in or covering the ears) is reported in some children with partial seizures as a response to an unformed, auditory hallucination localized to the superior temporal neocortex (09). In patients with more complex, formed auditory auras, ictal onset either from auditory association cortex in the temporal lobe or from the frontal lobe may be implicated (09). Unilateral ictal auditory hallucinations may occur in the ear (or side) contralateral to the side of the ictal focus, but they may also occur in the ear (or side) ipsilateral to the side of the ictal focus, and reports conflict on whether there is a contralateral predominance (23; 27). In any case, the unilateral perception of an auditory sensation does not definitively lateralize the lesion to the contralateral temporal neocortex (23). Verbal ictal auditory hallucinations result more often from left hemisphere foci, whereas nonverbal auditory ictal hallucinations result more often from right hemisphere foci (23; 27).

Musical hallucinations as a manifestation of epilepsy are uncommon but have been recognized in numerous case reports (01; 55; 11; 13; 68; 57; 21; 23; 04; 65).

Hallucinations with structural CNS lesions. Occasionally, auditory hallucinations can occur due to damage to brainstem structures involved in the central auditory pathways (08; 06; 44; 49; 20; 61; 67; 58). The sounds may be unformed mechanical or seashell-like noises, voices (although individual words may be indistinct), or music. These are thought to arise from release mechanisms and, consequently, tend to be prolonged and occur in association with central auditory processing disorders, including central hearing loss and impaired sound localization.

In patients with musical hallucinosis due to focal brain lesions, the lesion does not consistently lateralize to the dominant or nondominant hemisphere (21; 23; 70; 71). The superior temporal sulcus is the most common site of pathology (04). The most frequent cause of musical hallucinations is hearing impairment (07), and in patients with musical hallucinations and Lewy body dementia, they may shift to another modality if hearing is corrected (48); other causes include social isolation, cognitive dysfunction, and medications (07).

Stroke. Poststroke psychotic disorders are most commonly attributed to right hemisphere lesions of the frontal, temporal, and/or parietal lobes or rinsular cortex (16; 33; 64; 50). Preexisting psychiatric disease may provide a behavioral susceptibility to develop delusions and hallucinations in these individuals (16). Although poststroke visual hallucinations are most typically associated with occipital strokes, auditory hallucinations are more commonly reported with a subcortical stroke than with strokes affecting the cortex (28), although they may occur with cortical lesions (51). It is important to emphasize that poststroke hallucinations do not require delusions or other evidence of psychosis.

CNS neoplasms. Central nervous system neoplasms can produce auditory hallucinations in 3% to 10% of patients (66; 14). Unformed auditory hallucinations have predominantly, but not exclusively, been reported with frontal and temporal lesions, usually on the side of the lesion (66). Formed auditory hallucinations occur predominantly with temporal lobe tumors, although they can also occur with frontal and parietal lesions (66). Patients with temporal lobe tumors occasionally present with auditory hallucinations or with bimodal auditory and visual hallucinations (66; 22; 15). Responsible tumors have included gliomas, oligoastrocytomas, and oligodendrogliomas (22; 15). In some cases, auditory hallucinations may occur due to treatment for cancer, eg, with temporal lobe damage after radiotherapy for nasopharyngeal carcinoma or with the development of chronic epileptic discharges after radiotherapy for oligoastrocytoma (41; 60). Other mass lesions involving the temporal lobe can present similarly, including cases with parasitic cysts (56).

CNS demyelinating disorders. Hallucinations are not uncommon in patients with multiple sclerosis, but they are seldom informative for clinical-pathologic correlation of auditory hallucinations because of several factors, including the following: a predominance of visual hallucinations, a frequent multiplicity of demyelinating plaques precluding precise localization, and frequent occurrence as part of an organic psychosis or as a result of medications (17).

Prognosis and complications

Auditory release hallucinations generally persist for weeks or months after the onset of a causative central nervous system lesion. They may gradually resolve with improvement or resolution of the underlying lesion. Ictal (irritative) auditory hallucinations are generally brief but may be recurrent.

Clinical vignette

Case 1. A 56-year-old nonalcoholic man developed a sudden severe headache, which was associated with slurred speech and right-sided weakness. He reported hearing low-pitched, slow, binaural “musical” sounds that were localized externally, but not associated with any auditory stimuli. He recognized these sounds as abnormal. He was severely hypertensive, with a blood pressure of 200/130 mm Hg. He was drowsy, but easily arousable, with a left Horner syndrome, downbeating nystagmus, right hypertropia, a left one-and-a-half syndrome (left gaze palsy plus left internuclear ophthalmoplegia), right facial hypesthesia to light touch and pinprick, left peripheral facial palsy, bilateral sensorineural hearing loss, inability to localize sounds with eyes closed, mild right hemiparesis, right-sided hyperreflexia, right Babinski sign, mild left-sided limb ataxia, and multimodal right hemihypesthesia. Head CT showed an acute left-sided dorsal pontine hemorrhage and prior small bilateral internal capsule lacunar infarctions. Head MRI showed that the hemorrhage involved the caudal half of the left pontine tegmentum. Pure tone audiometry showed moderate bilateral sensorineural hearing loss with poor speech discrimination on the left. Brainstem auditory evoked responses were normal on the right; on the left, only waves I and II were present with normal latencies, whereas all other waves were absent. Electroencephalography showed mild slowing, but no epileptiform discharges.

His drowsiness resolved over several days. His auditory hallucinations became “like people talking” (although he was unable to make out individual words) and later “like continuous rain falling on a roof.” The binaural sounds were somewhat worse (louder) in the left ear and unaffected by auditory stimuli. Three weeks after the hemorrhage, the sounds became intermittent “ringing” or “clicking” noises before eventually resolving over several months.

In this case, clinical, electrophysiologic, and radiologic data indicated a left lower pontine segmental hemorrhage involving the area of the left superior olivary nucleus, the trapezoid body, and the oral and intermediate acoustic striae. Severely impaired sound localization in combination with an absent wave III on the brainstem auditory evoked response study suggested involvement of the superior olivary complex (44).

Case 2. A 57-year-old man presented with dizziness, right-sided numbness, and evidence of brainstem dysfunction of unclear duration. Examination revealed gaze-evoked nystagmus, left abducens and facial nerve palsy, right-sided hemihypesthesia, and mild (presumably right) hemiparesis. MRI revealed a mass lesion in the dorsal pons. Two days later he developed fever, nuchal rigidity, and somnolence. A spinal tap showed purulent cerebrospinal fluid but results of gram stain and cultures were not reported. He was diagnosed with a brainstem abscess and meningitis.

With antibiotics and dexamethasone, his clinical condition improved. However, by the fourteenth day of hospitalization, he had developed or newly noted auditory symptoms, including bilateral hyperacusis, left-sided tinnitus, and auditory hallucinations localized to the right ear and reported as “boys’ choirs singing folk songs.” The patient was fully alert and oriented, had insight into the hallucinatory character of the musical sounds (after initially surmising that there was a celebration in the schoolyard next to the hospital), and had no evidence of a psychiatric disorder. Other clinical findings at the time localized the lesion to the left pons: left-sided one-and-a-half syndrome, left nuclear VII nerve palsy, and mild right hemiparesis and hemihypesthesia. The musical hallucinations resolved five weeks after their onset.

A follow-up MRI on hospital day 17 showed involvement of the central auditory pathways above the cochlear nuclei on the left, including the dorsal acoustic striae, the trapezoid body, the superior olivary complex, and the lateral lemniscus; in addition, there was involvement of the olivocochlear bundle and the nucleus raphe magnus of the reticular formation. The ventral and dorsal cochlear nuclei in the rostral medulla were not involved. A brainstem auditory evoked response study on hospital day 13 demonstrated delayed “latencies” (apparently absolute latencies) of peaks III and V on the right, and of peak V on the left; a follow-up brainstem auditory evoked response study was normal a month later. Pure tone audiometry on day 23 reportedly showed a slight high-frequency left sensorineural hearing loss and a moderate pantonal right sensorineural hearing loss (61).

Case 3. A 56-year-old woman was admitted to a psychiatric unit after threatening her husband with a knife. She reported a 1-week history of suicidal and homicidal command hallucinations instructing her to overdose on nonsteroidal antiinflammatory drugs and kill her husband. A brain MRI revealed an acute right occipital lobe infarct with hemorrhagic transformation, as well as old ischemic infarcts within the right parietal and frontal lobes. The patient’s symptoms resolved without antipsychotic medications.

Acute right occipital stroke (MRI)

Diffusion-weighted MRI showing (A) an acute right occipital stroke in a patient presenting with auditory command hallucinations, along with old infarcts in the (B) parietal and (C) frontal lobes. (Source: Ido F, Badran R, Dmytruk ...

Biological basis

	• Auditory hallucinations due to central nervous system lesions can result from lesions at any level of the central auditory pathways, including those in the pons and mesencephalon.
	• At a cerebrocortical level, auditory hallucinations can arise from an irritative process (eg, seizures) whereas more proximal lesions can interrupt ascending pathways and release spontaneous activity within cerebrocortical circuits, which is perceived as sound.
	• The “fast” ascending auditory system goes from the cochlea to the ipsilateral dorsal cochlear nucleus, which then decussates and ascends in the lateral lemniscus to the inferior colliculus in the midbrain, then to the medial geniculate body, and then to primary auditory cortex in the transverse temporal gyrus.
	• The slow(er) ascending system involves many more synapses and that may provide more information about the character of the sounds heard, such as location.
	• In the slow ascending auditory pathway, impulses from the cochlea synapse first in the ipsilateral ventral cochlear nucleus and then in the ipsilateral and contralateral superior olivary complex, with the crossing fibers forming the trapezoid body of the pontine tegmentum.
	• Effectively all auditory afferents travel through the midbrain in the lateral lemnisci and all auditory afferents synapse in the inferior colliculi before passing to the medial geniculate body in the thalamus and then to the primary auditory cortex.
	• In humans, the primary auditory cortex is located deep within the lateral fissure on a small patch of the transverse gyri of Heschl, on the upper surface of the temporal operculum, whereas the lateral superior temporal gyrus is involved in processing complex acoustic signals, including speech.

Auditory hallucinations due to central nervous system lesions can result from lesions at any level of the central auditory pathways, including those in the pons and mesencephalon (08; 06; 44; 49; 20; 61; 67; 42; 58). At a cerebrocortical level, auditory hallucinations can arise from an irritative process (eg, seizures or electrical stimulation) (62; 65), whereas more proximal lesions can interrupt ascending pathways and release spontaneous activity within cerebrocortical circuits, which is perceived as sound (42).

There is a “fast” ascending auditory system from the cochlea to the ipsilateral dorsal cochlear nucleus, which then decussates and ascends in the lateral lemniscus to the inferior colliculus in the midbrain, then to the medial geniculate body, and then to primary auditory cortex in the transverse temporal gyrus. There is also a slower ascending system that involves many more synapses and that may provide more information about the character of the sounds heard, such as location. In the slow ascending auditory pathway, impulses from the cochlea synapse first in the ipsilateral ventral cochlear nucleus and then in the ipsilateral and contralateral superior olivary complex, with the crossing fibers forming the trapezoid body of the pontine tegmentum. The superior olivary complex, located posterior (dorsal) to the trapezoid body, thus receives binaural input, and is, therefore, the first place in the central auditory system where binaural processing (stereo hearing) is possible. Different parts of this complex serve to measure the interaural time difference (the difference in time of arrival of sounds between the ears) and the interaural level difference (the difference in sound intensity between the ears). Fibers from the superior olivary complex in the slow ascending auditory system also pass through the lateral lemniscus to the inferior colliculus, and then to the medial geniculate body, and on to the primary auditory cortex. From the superior olivary complex to the transverse temporal gyri, the pathways incorporate signals pertaining to both ears.

Effectively all auditory afferents travel through the midbrain in the lateral lemnisci, and all auditory afferents synapse in the inferior colliculi, before passing to the medial geniculate body in the thalamus and then to the primary auditory cortex. In humans, the primary auditory cortex is located deep within the lateral fissure on a small patch of the transverse gyri of Heschl, on the upper surface of the temporal operculum, whereas the lateral superior temporal gyrus is involved in processing complex acoustic signals, including speech. Neurons from Heschl gyri ultimately project to a wide variety of other cortical processing areas, including Wernicke’s area in the parietal lobe.

Etiology and pathogenesis

As with visual hallucinations, auditory hallucinations may have an irritative basis (42). Electrical stimulation of the temporal cortex (in either hemisphere) may produce reports of auditory hallucinations (52), as can electrical stimulation of the anterior cingulate gyrus (62). Ictal auditory hallucinations are most common in patients with temporal lobe epilepsy but can occur less commonly with foci in other lobes. Complex auditory hallucinations (eg, voices or music) are typically associated with temporal cortex stimulation or irritation, whereas simple auditory hallucinations (such as tinnitus with hissing, buzzing, or ringing) can occur with cortical, subcortical, or insular stimulation or irritation.

Postlesional auditory (“release”) hallucinations can result from lesions anywhere along the auditory pathway from the cochlea to the auditory cortex, including the brainstem, akin to Bonnet hallucinations with visual loss (08; 44a; 03; 26; 61; 32; 18; 42; 69; 19; 37; 38; 63). Persistent hallucinations over a period of weeks or months, with varied content, in association with hearing loss and in the absence of alcohol withdrawal, a thought disorder, alteration of consciousness, other positive motor or sensory phenomena, or epileptiform discharges on electroencephalography all support a release mechanism for such hallucinations (10; 08; 44). Cases of auditory hallucinosis associated with brainstem lesions most commonly involve acute or subacute lesions of the pontine tegmentum, although they can involve other areas, such as the medial geniculate nucleus (08; 06; 44; 49; 20; 24). Because the hallucinations developed in the setting of new-onset brainstem dysfunction, and because wave I was preserved in cases in which brainstem auditory evoked response studies were done (ie, thereby excluded severe dysfunction of the cochlear nerve, and cochlea for that matter), peripheral hearing loss does not account for such hallucinations.

In subjects with acquired deafness and musical hallucinosis undergoing PET studies of cerebral glucose utilization, the hallucinations have been associated with clusters of correlated activity in the posterior temporal lobes, the right basal ganglia, the cerebellum, and the inferior frontal cortices, but not with activity in the primary auditory cortices (26). This network of activity is similar to that demonstrated during the normal perception and imagery of patterned-segmented sound (26). Presumably, similar results would be obtained in patients with brainstem auditory hallucinosis.

Brainstem auditory hallucinosis has been reported with pontine hemorrhages; a brainstem arteriovenous malformation involving the pontine tegmentum with associated subarachnoid hemorrhage; a pontine abscess involving the pontine tegmentum; metastatic small cell carcinoma to the midbrain and involving the inferior colliculi; and acute rhombencephalitis due to listeria with an abscess in the middle cerebellar peduncle and with extensive surrounding edema (08; 44; 49; 20; 61).

Auditory illusions have also been reported with an infarct in the medial geniculate nucleus. A 49-year-old man suddenly heard louder sounds from a television that was playing a gunshot scene, but the sounds apparently persisted transiently after the television was switched off (palinacusis); the original sounds were described as the sound of roaring waves or clanging bells (24).

Similar modality-specific release hallucinations can occur experimentally or pathologically with unimodal sensory deprivation as with visual hallucinations in blindness (including Bonnet hallucinations with blindness due to ocular damage as well as similar hallucinations occurring in the blind hemifields of patients with strokes), phantom sensations after amputations, spinal cord injury or spinal anesthesia, and auditory hallucinations with deafness due to damage to the cochlea (30; 10; 47; 59; 29; 43).

Most reported cases of musical hallucinations in patients without psychiatric disorders have been in elderly people with acquired deafness due to damage to the inner ear, with the musical hallucinations appearing months to years after the development of hearing loss (59; 29; 05). Musical hallucinosis in deafness—whether due to damage to the inner ear or to damage to central auditory pathways—may involve widely distributed networks, including networks distinct from primary auditory cortex (26).

In a large single institution series, 393 subjects with musical hallucinations were identified and divided into five categories based on comorbid conditions: neurologic, psychiatric, structural, drug effect, and not otherwise classifiable (25). The mean age at onset of the hallucinations was 56 years (range 18 to 98 years), and about two thirds (65%) of the subjects were female. In 9% of subjects, the musical hallucinations were attributed to a focal brain lesion. Structural lesions associated with musical hallucinations involved both hemispheres, and almost all of them included involvement of the temporal lobe. Hearing impairment was common, particularly in the not otherwise classifiable category, where two thirds (67%) had hearing impairment. Those with a structural lesion were most likely to hallucinate modern music, whereas those with an underlying neurodegenerative disorder or isolated hearing impairment tended to hallucinate religious and patriotic music, and those with psychiatric disorders tended to hallucinate music that was mood-congruent.

In patients with midbrain lesions, auditory hallucinations may also possibly occur by mechanisms similar to those that produce so-called peduncular (visual) hallucinations. A patient with multiple sclerosis experienced congruent visual and auditory hallucinations of deceased familiar people that persisted for several days (67). Magnetic resonance imaging revealed an isolated, predominantly left-sided lesion in the periaqueductal segment of the midbrain. Taylor and colleagues suggested that these hallucinations represented a variant of peduncular hallucinations involving two sensory modalities, possibly due to “deregulation of modulatory superior collicular activity and a release of cross-modal integrative functions of the superior temporal sulcus.” Other cases may involve this mechanism, although this is speculative. For example, bimodal visual and auditory hallucinations have been reported in association with an extraventricular neurocytoma in the cerebellum (34).

Diagnostic workup

	• Patients with new-onset auditory hallucinations should be clinically evaluated for hearing loss, psychiatric disease, migraine, dementia, delirium or other acute encephalopathies, metabolic derangements, and intoxications.
	• Medications and use of alcohol and illicit drugs should be carefully reviewed.
	• If there are focal central nervous system symptoms or signs or if clinical circumstances suggest the likelihood of a focal brain process (eg, head injury, disequilibrium, and increased falls risk, known cancer of a type that commonly metastasizes to the brain, etc.), brain imaging should be obtained, preferably with magnetic resonance imaging.
	• If there is clinical evidence of hearing impairment, pure tone audiometry and speech audiometry (including speech-in-noise testing) is appropriate.
	• If there is an inconsistency between relatively normal performance on pure tone audiometry and poor performance on speech testing, a central auditory disorder should be considered, and brain imaging should be obtained even if no focal symptoms or signs are evident.

Patients with new-onset auditory hallucinations should be clinically evaluated for hearing loss, psychiatric disease, migraine, dementia, delirium or other acute encephalopathies, metabolic derangements, and intoxications. Medications and use of alcohol and illicit drugs should be carefully reviewed. Evidence of focal central nervous system symptoms or signs should be sought clinically.

Diagnostic evaluation will be dictated by the results of clinical evaluation, but if there are focal central nervous system symptoms or signs, or if clinical circumstances suggest the likelihood of a focal brain process (eg, head injury, disequilibrium, and increased falls risk, known cancer of a type that commonly metastasizes to the brain, etc.), brain imaging should be obtained, preferably with magnetic resonance imaging. If there is clinical evidence of hearing impairment, pure tone audiometry and speech audiometry (including speech-in-noise testing) is appropriate. If there is an inconsistency between relatively normal performance on pure tone audiometry and poor performance on speech testing, a central auditory disorder should be considered, and brain imaging should be obtained even if no focal symptoms or signs are evident. Brainstem auditory evoked response (also known as auditory brainstem response) testing may provide further insights on the integrity of the auditory pathways and the involvement of specific auditory pathway structures. Electroencephalography can be considered to help establish or exclude an ictal basis, though this is not likely to be informative in cases in which there are persistent auditory hallucinations in the absence of cerebrocortical involvement (as determined from clinical and radiologic examinations).

Management

	• Patients typically have preserved insight with such hallucinations and may benefit from knowing that they may occur with brain lesions and, as such, do not represent a manifestation of mental illness.
	• Release auditory hallucinations due to disruption of central auditory pathways (ie, in the absence of an irritative process) typically do not respond to use of hearing aids or to treatment with antipsychotic medications or anticonvulsants.
	• Patients with ictal auditory hallucinations often respond to appropriate anticonvulsant therapy.
	• Even in the absence of epileptiform discharges or overt seizures on electroencephalography, an empiric trial of an anticonvulsant may prove helpful in some cases with lesions of the temporal lobe, especially when the lesion is unilateral.
	• Unilateral temporal lobe lesions could produce octal auditory hallucinations and would not be likely causes of release hallucinations because of bilateral representation of hearing in the cerebrocortical auditory centers.

Patients typically have preserved insight with such hallucinations and may benefit from knowing that they may occur with brain lesions and, as such, do not represent a manifestation of mental illness.

Patients with release auditory hallucinations due to disruption of central auditory pathways (ie, in the absence of an irritative process) are difficult to manage. The hallucinations typically do not respond to use of hearing aids, or to treatment with antipsychotic medications or anticonvulsants. If the hallucinations are precipitated by mass effect or acute demyelination, they may benefit from measures that address the underlying disease process.

Patients with ictal auditory hallucinations often respond to appropriate anticonvulsant therapy. Even in the absence of epileptiform discharges or overt seizures on electroencephalography, an empiric trial of an anticonvulsant may prove helpful in some cases with lesions of the temporal lobe, especially when the lesion is unilateral. Unilateral temporal lobe lesions could produce octal auditory hallucinations and would not be likely causes of release hallucinations because of bilateral representation of hearing in the cerebrocortical auditory centers.

Outcomes

Outcomes generally depend on the underlying disease process. Release hallucinations are more difficult to manage than irritative hallucinations (eg, resulting from seizures). Release hallucinations may resolve spontaneously over weeks or months in conjunction with clinical improvement (eg, with treatment of a brainstem abscess or resolution of a brainstem hematoma). Patients with ictal auditory hallucinations often respond to appropriate anticonvulsant therapy.

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Patient Profile

Age range of presentation: 0 month to 65+ years
Sex preponderance: Female = male
Heredity: None
Population groups selectively affected: None
Occupation groups selectively affected: None

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Auditory hallucinations due to central nervous system lesions

Associated Disorders

Brainstem hemorrhage
Brainstem infarction
Central nervous system neoplasms
Cerebral hemorrhage
Cerebral infarction
- Demyelinating diseases of the central nervous system
- Epilepsy
- Multiple sclerosis
- Seizures
- Traumatic brain injury

Differential Diagnosis

subjective tinnitus
objective tinnitus
schizophrenia
mania
psychotic depression
- migraine
- dementia
- delirium
- acute encephalopathies
- hallucinogens
- sensory deprivation

Also Relevant

Central deafness
Cognitive aspects of central auditory disorders
Sensorineural hearing loss
Visual hallucinations in blindness

Auditory hallucinations due to central nervous system lesions …

Auditory hallucinations due to central nervous system lesions

Introduction

Overview

Key points

Historical note and terminology

Clinical manifestations

Presentation and course

Prognosis and complications

Clinical vignette

Biological basis

Etiology and pathogenesis

Epidemiology

Prevention

Differential diagnosis

Confusing conditions

Associated or underlying disorders

Diagnostic workup

Management

Outcomes

Media

References

Contributors

Author

Patient Profile

ICD & OMIM codes

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to access the full version.

Questions or Comment?

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Auditory hallucinations due to central nervous system lesions

Introduction

Overview

Key points

Historical note and terminology

Clinical manifestations

Presentation and course

Prognosis and complications

Clinical vignette

Biological basis

Etiology and pathogenesis

Epidemiology

Prevention

Differential diagnosis

Confusing conditions

Associated or underlying disorders

Diagnostic workup

Management

Outcomes

Media

References

Contributors

Author

Patient Profile

ICD & OMIM codes

This is an article preview. Start a Free Account to access the full version.

Questions or Comment?

Also in This Category

NF2-related schwannomatosis

Common maculopathies

Toxic and nutritional deficiency optic neuropathies

Third nerve palsy

Nystagmus

Metal neurotoxicity

Vascular cognitive impairment

Chronic progressive external ophthalmoplegia

This is an article preview.
Start a Free Account
to access the full version.