IntroductionMusical obsessions consist of intrusive recollections of music fragments that are experienced as unwanted. Otosclerosis is caused by an abnormal bone homeostasis of the otic capsule and represents a frequent cause of hearing impairment. Many conditions causing hearing loss have been associated with musical hallucinations, but the association between musical obsessions and hearing loss is frequently overlooked.Case presentationWe present the case of a 51-year-old Caucasian woman with a history of obsessive-compulsive disorder who developed musical obsessions soon after being diagnosed with otosclerosis. She was referred to our obsessive-compulsive disorder outpatient unit by her general psychiatrist. At the time of our first evaluation, she had severe musical obsessions that interfered with her social functioning and made her unable to follow conversations. She was started on 40mg of paroxetine and 2.5mg of aripiprazole, which led to significant improvement of her symptoms and of her social and work functioning.ConclusionsTo the best of our knowledge, this is the first report of musical obsessions in a patient with hearing loss due to otosclerosis and a history of obsessive-compulsive disorder. This case suggests that a differential diagnosis of obsessive-compulsive disorder should be carefully considered in patients with hearing impairment who complain of involuntary musical imagery, especially in those patients who have a previous history of obsessive-compulsive disorder.
BackgroundCapgras delusion is a delusional misidentification syndrome, in which the patient is convinced that someone that is well known to them, usually a close relative, has been replaced by an impostor or double. Although it has been frequently described in psychotic syndromes, including paranoid schizophrenia, over a third of the documented cases of Capgras delusion are observed in patients with organic brain lesions or neurodegenerative disease, including Parkinson’s Disease. Variants of Capgras involving animals or inanimate objects have also been described. The etiology of Capgras in Parkinson’s remains unclear, but may arise from a combination of factors, such as frontal lobe dysfunction and dopaminergic medication.Case presentationWe present the case of a 53-year old right-handed female with Parkinson’s disease who developed Capgras delusion during treatment with dopamine agonists and Levodopa/Carbidopa. She became convinced that her pet dogs and the plants in her garden had been substituted by identically looking ones. Our patient was initially treated with Quetiapine, with no improvement, and subsequently treated with Clozapine, which lead to partial regression of her symptoms. Neuropsychological Evaluation showed Mild Cognitive Impairment in Executive Functions.ConclusionsGiven the clinical history, onset and evolution of symptoms we believe our patient’s delusion resulted from the overlap of dopaminergic medication and Mild Cognitive Impairment in executive functions. Zoocentric Capgras, the variant we describe, has been rarely described in scientific literature, and we believe it is of interest due to its unusual characteristics.
Comorbidities among headaches and psychiatric disorders have been consistently reported in several clinical studies and reviews. In this paper, we review some recent clinical studies on migraine and tension-type headaches associated with mood, anxiety and somatoform disorders, focusing on therapeutic strategies for the psychiatric disorders.
Lack of insight, very frequent in schizophrenia, can be considered a deficit in Theory of Mind (ToM) performances, and is also found in other psychiatric disorders. In this study, we used the first- to third-person shift to examine subjects with psychotic and psychotic mood disorders. 92 patients were evaluated with SANS and SAPS scales and asked to talk about their delusions. They were asked to state whether they thought what they said was believable for them and for the interviewer. Two weeks later, 79 patients listened to a tape where their delusion was reenacted by two actors and were asked the same two questions. Some patients gained insight when using third-person perspective. These patients had lower SAPS scores, a lower score on SAPS item on delusions, and significant improvement in their SAPS delusion score at the second interview. Better insight was not related to a specific diagnostic group.
IntroductionWe describe a case of OCD and movement disorders associated with anti basal ganglia antibodies.MethodsA 17 year old patient was referred to our unit in February 2010 because of movement disorder. He denied personal or family history of psychiatric disorders and substance abuse other that occasional cannabis use. His symptoms had began 6 months earlier when he started presenting intrusive thoughts associated with various compulsions such as complex arm and leg movements and bizarre postures: he was treated with Olanzapine and Sertraline which lead to partial improvement of symptoms but he self-discontinuated the medication in january 2010. Upon admittance in february 2010 the patient showed obsessive thoughts associated with bizarre postures and upper limb complex movements.ResultsHe was treated with 100 mg of Clomipramine which lead to partial regression of symptoms. Autoimmunity screening was performed revealing anti neuron specific enolase and anti pyruvate kynase antibodies. The patient was treated with Desametasone which did not lead to any improvement.ConclusionsAnti neuron specific enolase and anti pyruvate kynase antibodies are directed against antigens specifically expressed in the basal ganglia. According to literature data these autoantibodies can be associated with movement disorders and OCD and we hypothesize that our patient's symtptoms were caused by autoimmunity. Although cortison was not successfull, recents reports in scientific literature have shown that other non psychopharmacological treatment, such as plasmapheresis, or IV immunoglobulins could be effective in similar patients: we are considering this as our next treatment option.
Objectives: Our goals were to evaluate if the presence of severe delusions negatively affects insight, regardless of diagnosis, and whether or not patients gain insight into their delusions when using a third person perspective. Methods: 92 delusional patients with psychotic and psychotic mood disorders were asked to speak about their delusions and were evaluated by means of the Scale for the Assessment of Positive Symptoms and the Scale for the Assessment of Negative Symptoms (SAPS and SANS). They were then asked to state whether they thought what they said was believable for them and for the interviewer. After two weeks 79 patients were evaluated with the same scales and listened to a tape where their delusion was re-enacted. They were then asked to state if what they heard was believable for them and for the interviewer. Results: 12 patients thought their delusions was unbelievable for the interviewer at first interview, and 17 patients did the same after the second interview; 4 patients stated what they heard from the tape after the second interview was unbelievable both for them and interviewer. Patients with better insight (patients who stated their delusion was not believable) had a lower SAPS score, a lower item delusion score and a significant improvement of item delusion score at second interview Conclusion: Several patients gain partial insight when using a third person perspective. The severity of delusions negatively affects insight, regardless of the patient´s diagnosis.
Introduction: A 34 year old man was referred to our unit for psychiatric evaluation. His psychomotor development was normal until the age of 12 , when he started showing progressive loss of cognitive skills and finalized motor activity. Symptoms rapidly worsened and by the age of 20 his language and motor skills were severly compromised. Starting at age 17 he had been treated with both 1st and 2nd generation antipsychotics which did not lead to any changes in symptoms. Family history was negative for psychotic or neurological disorders. The mother had alcohol abuse disorder and the younger sister was diagnosed with generalized anxiety disorder. Method: At the time of our evaluation patient was receiving 10 mg of Olanzapine. He was vigilant and passively cooperative to examination; he displayed physical immobility, waxy flexibilitas, stereotyped behaviour, camptocormia, echolalia, blunted affect and automatic and repetitive behaviour. Thought content was difficult to evaluate but he denied hallucinations or delusional thoughts. Results: BP was normal, as well as brain MRI and PET. Screening for Wilson's disease, metabolic diseases and fragile X Syndrome were negatve. DAT scan was also performed and showed no abnormalities. Medication withdrawal didn't lead to any changes in his status. Conclusions: The patient's symtoms fulfill the criteria for drug resistant Catatonic Schizophrenia. However the early onset of symptoms, the rapid deterioration of cognitive abilities, the early and extensive motor imparment and the complete resistance to drug treatment make this an interesting case for discussion about differential diagnosis.
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