Onset Of Auditory Hallucinations Research Articles

Editors' Note: Timing and Impact of Psychiatric, Cognitive, and Motor Abnormalities in Huntington Disease

Dr. McAllister and colleagues retrospectively analyzed the prevalence, timing, and functional impact of psychiatric, cognitive, and motor abnormalities in Huntington disease (HD) gene carriers in 6,316 individuals in the European HD Network (REGISTRY). They found that psychiatric and cognitive symptoms were common and functionally debilitating in HD gene carriers, with 42.4% of patients with HD reporting at least 1 psychiatric or cognitive symptom before motor symptoms, most commonly depression. However, the initial manifestation of HD was increasingly likely to be motor and less likely to be psychiatric as the age at presentation increased. The authors concluded that nonmotor symptoms should not be used to make a clinical diagnosis of HD because it was impossible to distinguish confidently between nonmotor symptoms arising from HD vs primary psychiatric disorders, particularly in younger premanifest patients. In response, Dr. Bird et al. argue that such a conclusion is too broad and negative, while agreeing that caution is needed and depression should not be used as a diagnostic factor. They argue that psychiatric, behavioral, and cognitive symptoms can be diagnostically meaningful in the setting of a positive genetic test, noting examples like the onset of auditory hallucinations, paranoid delusions, a sustained personality change, or decreased work performance with impaired cognition. They note that such symptoms are part of the diagnostic process for genetic forms of behavioral frontotemporal dementia, which is phenotypically similar to HD, and that earlier diagnosis can help connect patients and families to critical services. Responding to these comments, the authors note that clinical onset of HD is typically diagnosed using the emergence of specific extrapyramidal motor features. They agree that certain neuropsychiatric symptoms like apathy and increased aggression are more strongly suggestive of HD pathology. However, they caution that other commonly reported symptoms may reflect environmental sequelae or those related to the knowledge of their genetic status and should not be used on their own to make an HD diagnosis. This exchange highlights the clinical challenges of defining the onset of a complex neuropsychiatric disease like HD when one already knows the patient's genetic status. Nonetheless, the early diagnosis of HD in the appropriate clinical and genetic setting may allow for deployment of important patient resources. Dr. McAllister and colleagues retrospectively analyzed the prevalence, timing, and functional impact of psychiatric, cognitive, and motor abnormalities in Huntington disease (HD) gene carriers in 6,316 individuals in the European HD Network (REGISTRY). They found that psychiatric and cognitive symptoms were common and functionally debilitating in HD gene carriers, with 42.4% of patients with HD reporting at least 1 psychiatric or cognitive symptom before motor symptoms, most commonly depression. However, the initial manifestation of HD was increasingly likely to be motor and less likely to be psychiatric as the age at presentation increased. The authors concluded that nonmotor symptoms should not be used to make a clinical diagnosis of HD because it was impossible to distinguish confidently between nonmotor symptoms arising from HD vs primary psychiatric disorders, particularly in younger premanifest patients. In response, Dr. Bird et al. argue that such a conclusion is too broad and negative, while agreeing that caution is needed and depression should not be used as a diagnostic factor. They argue that psychiatric, behavioral, and cognitive symptoms can be diagnostically meaningful in the setting of a positive genetic test, noting examples like the onset of auditory hallucinations, paranoid delusions, a sustained personality change, or decreased work performance with impaired cognition. They note that such symptoms are part of the diagnostic process for genetic forms of behavioral frontotemporal dementia, which is phenotypically similar to HD, and that earlier diagnosis can help connect patients and families to critical services. Responding to these comments, the authors note that clinical onset of HD is typically diagnosed using the emergence of specific extrapyramidal motor features. They agree that certain neuropsychiatric symptoms like apathy and increased aggression are more strongly suggestive of HD pathology. However, they caution that other commonly reported symptoms may reflect environmental sequelae or those related to the knowledge of their genetic status and should not be used on their own to make an HD diagnosis. This exchange highlights the clinical challenges of defining the onset of a complex neuropsychiatric disease like HD when one already knows the patient's genetic status. Nonetheless, the early diagnosis of HD in the appropriate clinical and genetic setting may allow for deployment of important patient resources.

A commentary on: Affective coding: the emotional dimension of agency.

A commentary on: Affective coding: the emotional dimension of agency.

Is schizophrenia a spatiotemporal disorder of the brain's resting state?

Is schizophrenia a spatiotemporal disorder of the brain's resting state?

Editorial

Editorial

Hierarchical and Nonhierarchical Approaches in Psychiatric Diagnosis: A Case Report of Change in Psychiatric Symptoms and Diagnosis Over Time

The article reports the case of a 39-year-old male who was diagnosed with and treated for bipolar disorder. Over the past 18 months, the patient has experienced new onset of auditory hallucinations and worsening of his psychotic symptoms. The treating psychiatrists changed the diagnosis from bipolar disorder to schizoaffective disorder. The authors discuss hierarchical and nonhierarchical approaches to psychiatric diagnosis in relation to this case report.

Steady State Visually Evoked Potential Correlates of Auditory Hallucinations in Schizophrenia

This study attempted to localize regions of brain electrical activity associated with the onset of auditory hallucinations. Changes in Steady State Visually Evoked Potential (SSVEP) topography associated with the onset of spontaneous auditory hallucinations was studied in eight schizophrenic patients. The SSVEP elicited by a spatially uniform sinusoidally varying visual flicker was recorded using a 64-channel electrode helmet. A large and significant decrease in SSVEP latency in the right temporo/parietal region occurred in the second prior to the report of auditory hallucinations. A control task with matching motor movements produced no significant decrease in SSVEP latency in the same right temporo/parietal location. This finding suggests that activity of fine temporal resolution in the neural networks in the right temporo/parietal area may be implicated in the genesis of auditory hallucination, in conformity with certain neuropsychological theories.