Auditory hallucinations due to central nervous system lesions

Douglas J Lanska MD FAAN MS MSPH (Dr. Lanska of the Great Lakes VA Healthcare System and the University of Wisconsin School of Medicine and Public Health has no relevant financial relationships to disclose.)
Originally released September 6, 2015; last updated January 30, 2017; expires January 30, 2020

This article includes discussion of auditory hallucinations due to central nervous system lesions, brainstem auditory hallucinosis, release hallucinations, and ictal hallucinations. The foregoing terms may include synonyms, similar disorders, variations in usage, and abbreviations.

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 (Penfield and Rasmussen 1950; Penfield and Perot 1963).

Image: Wilder Penfield
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) (Penfield and Perot 1963; Compston 2005). 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 (Penfield and Perot 1963).

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 3 cases of auditory hallucinosis associated with brainstem lesions (Cascino and Adams 1986). 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 (Lanska et al 1987).

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