Musical Hallucinations: Interplay of Degenerative Brain Disease, Psychosis, and Culture in a Chinese Woman


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Midbrain lesions give rise to hallucinations that are usually auditory in nature if the lesions are pontine (Cascino and Adams, 1986; Lanska et al., 1987; Murata, 1994). The hallmark of pontine hallucinations is that they are often musical, complex, and structured, although elementary auditory hallucinations, such as the buzzing of bees or chiming of bells, may occur as well (Cascino and Adams, 1986; Lanska et al., 1987; Murata et al., 1994). We report a case of musical hallucinations (MH) that demonstrates the complex interaction between midbrain and cortex, the plasticity of psychiatric symptoms, as well as the interaction between psychopathology and culture.Case ReportThe patient, a 51-year-old Chinese woman who speaks only Cantonese, came to the United States from Hong Kong at age 45. She reported no personal or family psychiatric history and no history of substance abuse. At age 41, she presented with left-side tremor and gait disorder and was hospitalized in Hong Kong. Magnetic resonance imaging (MRI) revealed diffuse cerebral atrophy. No treatment was given. While the tremor spontaneously remitted, she continued to have a gait problem. Ten days before her admission to our inpatient psychiatry unit, her gait disorder worsened (she could not walk without support). Additionally, she had an abrupt onset of auditory hallucinations, consisting of mourning chanting of Buddhist monks. She developed delusional thinking that the chanting of the monks indicated that she would soon be dead. She also believed spirits were injecting worms into her blood which were eating her brain and that spirits were pushing her, causing her to fall. She had poor sleep and appetite.On mental state examination, she was alert but had severe psychomotor retardation, fixed eye contact, and low rate and volume of speech. There was no formal thought disorder. Her Mini-Mental Status Examination score was 25. Neurological examination showed severe hypokinesia, shuffling, unsteady, slightly wide-based gait, cog wheel rigidity predominant in the upper extremities, mild fine action tremor, reduced vertical gaze (Parinaud syndrome) and up-beating vertical nystagmus on downward gaze. The motor force, sensations, and cranial nerves were within normal limits.MRI revealed diffuse cerebral atrophy and small pons (see Figure 1). The electroencephalogram showed continuous generalized slowness predominant on posterior lobes. Audiogram, auditory evoked potentials, and blood levels of folate, vitamin B12, triiodothyronine, thyroxine, and thyroid-stimulating hormone were normal. Results of the rapid plasma reagin test were negative.She experienced partial improvement in psychotic symptoms after treatment with Risperidone (up to 3 mg p.o. b.i.d.) and Benadryl for her Parkinsonian syndrome and was discharged. She was rehospitalized after 2 weeks with the same presentation. Risperidone was discontinued and treatment with Permax was initiated, starting at a low dose (0.05 mg) that was progressively increased. Both Parkinsonism and psychotic symptoms improved for 6 weeks until the dose of Permax was increased to 0.5 mg, at which point the patient became psychotic again. She believed a man was spraying fire on her, although she only heard the hissing noise of the fire and did not see the man. She also reported hearing the hissing of snakes, although she denied seeing them. The psychosis did not improve with decreasing, then discontinuing, Permax.After six electroconvulsive therapy (ECT) treatments, she showed significant improvement in the extrapyramidal symptoms (she could walk unassisted) and complete remission of the psychosis. Although she refused to return for follow-up after discharge, her husband reported she was doing well 3 months later.DiscussionThe pathophysiology of MH is still widely debated.

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