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Othello Syndrome in association with Primary Hyperparathyroidism
Goggins, Emerson and Nowers
Othello syndrome is a content specific delusion characterised by the unshakeable false conviction of the spouse's infidelity and can arise from a number of psychiatric and organic disorders. We present the case of an elderly woman who developed the delusion of her husband's infidelity while at the same time demonstrating evidence of cognitive impairment. She was concomitantly diagnosed with primary hyperparathyroidism. This case highlights the first complete report of Othello syndrome in association with primary hyperparathyroidism.
The Othello Syndrome in association with Primary Hyperparathyroidism
The term Othello Syndrome was first coined by John Todd in 19551. It has also been referred to as pathological, morbid or delusional jealousy and describes a content specific delusion characterised by the unshakeable false belief of the spouse's infidelity 2, 3. Non psychotic jealousy has also been seen as a part of a narcissistic or paranoid personality disorder4. It is thought to occur most often in association with chronic alcoholism and as a feature of affective disorders and schizophrenia 3. Organic causes of delusional jealousy have also been described 3, 5, 6, 7, 8.
While most reports of Othello Syndrome have not included adequate neurological evaluation it has been estimated that in at least 30% of cases in the recent literature most probably had a neurological basis for their delusion of infidelity 9.
We present the case of a previously happily married elderly woman who developed the delusion of her husband's infidelity while at the same time demonstrating evidence of cognitive impairment. The case represents the first complete report of Othello syndrome in association with hypercalcaemia secondary to primary hyperparathyroidism.
A 75 year old lady was admitted to an acute old age psychiatric unit detained under Section 3 of the Mental Health Act 1983. She had developed the delusional belief that her husband was having an affair with a neighbour. She began to act on her belief system accusing her neighbours of “covering up for him”. In the month preceding admission she was increasingly agitated and aggressive towards her husband. Her husband vehemently denied the accusation stating that it was absurd. Her daughter agreed explaining that he had recovered from a myocardial infarction and he rarely socialised. She had no past psychiatric history or history of alcohol abuse or learning disability.
Over the previous 12 to 18 months her family had noticed that she was becoming increasingly forgetful. This appeared insidious in onset and slowly progressive. She began to loose weight and appeared sullen, low in mood and irritable. She denied feeling depressed. She was self caring but increasingly relied upon her husband to undertake the majority of activities of daily living such as cleaning, cooking and shopping.
She was assessed by a psychiatrist on a domiciliary visit at the request of her general practitioner where a diagnosis of the Othello Syndrome was made. Cognitive impairment was noted and she was referred to a Day Hospital for a Memory Disorders assessment, however she refused to attend.
She was commenced on the atypical antipsychotic quetiapine and the sedating antidepressant mirtazepine however as she believed that there was nothing wrong with her, her compliance was poor.
Medical history and investigations
She described herself as feeling very well and in particular she denied any bone pain, aches, constipation, polyuria, polydipsia or cognitive problems.
Her physical examination was unremarkable. In particular central nervous system examination revealed no focal neurological signs. Her neck felt entirely normal on palpation.
On investigations her corrected calcium was found to be consistently between 3 to 3.4 mmol/litre. Her parathyroid level varied between 24 and 30 pmol/L. Her serum phosphate was low at 0.78 mmol/L consistent with primary hyperparathyroidism.
Other haematological and biochemical investigations were normal. Her chest X-ray revealed a slightly over inflated lungs with fibrocalcified opacities in both upper zones consistent with old healed Tuberculosis. Her heart size was normal. A scan of her parathyroid glands revealed an adenoma in the right upper pole and she was diagnosed with primary hyperparathyroidism. She refused to have a brain scan.
Surgical resection of the adenoma was recommended however she refused this. A further psychiatric assessment determined that she had mental capacity to refuse surgical intervention. Of note her decision was not influenced by her pathological jealousy. She stated that she did not feel that the benefits outweighed the risks.
Memory difficulties were reported to have begun at least a year prior to her first psychiatric assessment. A Folstein Mini Mental State Examination revealed a score of 20 out of 30.
She had poor recall and disorientation to time with inattention. The National Adult Reading Test estimated her premorbid IQ to be within the average range for her age.
On memory assessment her immediate verbal recall was very severely impaired. In addition delayed verbal recall was severely impaired as was visual recognition memory. On executive functioning her verbal fluency was slightly impaired. The Weigls colour form sorting test was normal. The Hayling and Brixton test was impaired and her clock drawings were abnormal. With respect to language testing she could follow command but the Boston Naming Test indicate borderline impairment. On visuospatial testing the visual form discrimination test indicated she scored in the low average range.
Overall neuropsychometric testing suggested severe memory impairment and poor executive function with some preservation of language and visuospatial abilities suggestive of cerebrovascular disease rather than Alzheimer's disease.
Course in hospital
She was recommenced on quetiapine and her morbid jealousy somewhat subsided. After 9 weeks in hospital her husband was keen for her to be discharged and this was agreed. Following discharge she has been supported by the community mental health team.
This case highlighted the complexity of managing a competent patient refusing medical treatment for a condition that has been linked to multiple neuropsychiatric manifestations.
Our patient refused certain investigations such as a brain scan and she refused surgical intervention for her parathyroid adenoma. As a result it is unclear as to whether or not her hypercalcaemia was having a deleterious effect on her mental state or whether she was developing a dementing illness such as vascular dementia. The differential diagnosis of paraphrenia was also considered but was considered less likely in light of her significant cognitive impairment.
Primary hyperparathyroidism is characterised by hypercalcaemia, hypophosphataemia and a high level of parathyroid hormone. In persons greater than 60 years of age the incidence may be as high as 0.2% with a prevalence of 1.0% or greater in this elderly population 10-14. Patients may remain asymptomatic for years.
The neuropsychiatric manifestations of primary hyperthyroidism are common possibly occurring in more than half of all cases. The precise mechanism responsible for the production of the neuropsychiatric symptoms remains unknown although it has been speculated that high calcium levels are integral to mediating this pathology14. Neuropsychiatric symptoms associated with primary hyperparathyroidism span from a range of affective, anxiety, cognitive and psychotic presentations. In approximately 80% of cases the aetiology of the disorder is a single solitary usually benign adenoma resulting in overproduction of parathyroid hormone increases in serum calcium and decreases in serum phosphate 10. Surgical removal of the adenoma almost always reverses neuropsychiatric symptoms 14.
This case illustrates the importance of carrying out a full organic screen in patients with new onset psychopathology in old age.
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9. Malloy PF, Richardson ED. The frontal lobes and content-specific delusions. J Neuropsychiatry Clin Neurosci. 1994 Fall;6(4):455-66.
10. Potts JT diseases of the parathyroid gland and other hyper- and hypocalcemic disorders, in Harrison’s Principles of Internal Medicine, 15th ed. New York, McGraw-Hill medical, 2001, pp 2205-2220
11. Heath DA. Primary hyperparathyroidism. Clinical presentation and factors influencing clinical management. Endocrinol Metab Clin North Am. 1989 Sep;18(3):631-46.
12. Zahrani AA, Levine MA. Primary hyperparathyroidism. Lancet. 1997 Apr 26;349(9060):1233-8.
13. Wermers RA, Khosla S, Atkinson EJ, Hodgson SF, O'Fallon WM, Melton LJ 3rd. The rise and fall of primary hyperparathyroidism: a population-based study in Rochester, Minnesota, 1965-1992. Ann Intern Med. 1997 Mar 15;126(6):433-40.
14. Watson LC, Marx CE. New onset of neuropsychiatric symptoms in the elderly: possible primary hyperparathyroidism. Psychosomatics. 2002 Sep-Oct;43(5):413-7.
First author: Dr Raymond Goggins, Specialist Registrar, Cossham Memorial Hospital, Lodge Rd, Bristol, BS15 1LF
Catherine Emerson, Clinical Psychologist, Cossham Memorial Hospital, Lodge Rd, Bristol, BS15 1LF
Dr Mike Nowers, Consultant Psychiatrist, Cossham Memorial Hospital, Lodge Rd, Bristol, BS15 1LF
First Published December 2004