INTERNATIONAL JOURNAL OF GERIATRIC PSYCHIATRY, VOL. 5: 133-135 (1990)

KLEINE-LEVIN SYNDROME IN A 74-YEAR-OLD FEMALE

R. BROWN Senior Registrar in Psychiatry, Fazakerley Hospital, Longmoor Lane, Liverpool, L9 7AL, UK

AND

M. T. MALCOLM Consultant Psychiatrist, Department of Psychiatry, Clatterbridge Hospital, Clatterbridge Road, Bebington, Wirral,

Merseyside, Lh3 4JY. UK

SUMMARY

Kleine-Levin syndrome characteristically occurs in young men. We describe a case in a 74-year-old woman suggesting that the syndrome may not be confined to a particular age group or to the male sex.

KFY WORDS-Kleine-LeVin, hypersomnic, hyperphagia, elderly woman.

The Kleine-Levin syndrome has been described in detail by Kleine (1929, Levin (1936) and Critchley (Critchley and Hoffman, 1942; Critchley, 1962). The characteristic features are episodes of hyper- somnia alternating with voracious overeating lasting days or weeks, separated by long periods of normal health. Onset occurs mainly in the age group 12-21 years (Critchley, 1962).

Premorbid personality is normal. There is presumed to be a disorder in the hypothalamic or prefrontal regions (Bray and Gallagher, 1975). Lithium has been effective in the treatment of this syndrome (Ogura et al, 1976).

A 74-year-old retired female accountant with no past personal or family history of psychiatric illness and a normal premorbid personality had been well until May 1987 when she had been treated with antibiotics for a chest infection. Her daughter reported that in June she had suddenly become irritable and began to overeat ravenously. Her diet included frozen pizzas, a raw leg of lamb and gallons of milk. She would eat from others’ plates at the dinner table. She began stealing from shops and running up bills totalling a thousand pounds. Her weight increased from 87 kg to 112 kg in three months. In September she began to oversleep for periods of 12-18 hours. She smoked over 80 cigarettes a day and during periods of somnolence

Correspondence to first author

her clothes and furniture sustained many burn- holes. There was a degree of confusion such that a diagnosis of dementia had been considered, yet careful questioning on occasions showed her to be normally orientated and well able to do mental arithmetic. Her daughter reported verbal aggres- sion and bad temper on waking or if prevented from overeating.

She was admitted in October for observation. No neurological deficit was elicited on physical examination. A random blood glucose was 16-5 pl/ l with a fasting blood glucose of 6.6 pI/L The glucose tolerance test showed an elevated blood glucose of 14.8 p1/1 at one hour with a glycosuria of 2++ at two hours. The FSH level of 40 IU/I and LH level of 28 IU/ l were normal for a postmenopausal woman and thyroid hormone levels were normal. A third/fourth generation of IGE CT scan of the brain showed no abnormality. Clinical dementia tests were normal. She was treated with a weight- reducing diet and her weight fell to 107 kg.

Over the next few months she had three short- term relief admissions. Her weight fell to 97 kg and her overeating lessened though she would still try to steal food from the kitchen. By December her symptoms of hyperphagia and hypersomnia re- turned. She had no recollection for events over this period of one month. Subsequently her excessive sleeping and eating became reestablished. At no time did she express any symptoms of elation or depression.

0885-6230/90/020136--03$05.00 0 1990 by John Wiley & Sons, Ltd.

Received I6 March 1989 Accepted 6 July 1989

134 R. BROWN AND M. T. MALCOLM

DISCUSSION

In terms of onset, progression and symptoms, this case is typical of the Kleine-Levin syndrome. A febrile illness preceded the sudden onset of the patient’s irritability and hyperphagia. She then began to sleep for 12-18 hours and was aggressive when aroused by her family or prevented from eating. Between these periods her behaviour was normal and she had no recollection of events during those periods. She did become disorientated at times on returning from shopping. The above symptoms are typical of the syndrome. However, hypersexuality, difficulty in thinking and speech, and elation with visual or auditory hallucinations, which may occur in this syndrome, did not occur in this patient. No gross biochemical abnormality was found nor expected (Thompson et al., 1985).

In Kleine-Levin syndrome there is presumed to be a disorder in the hypothalamic region of the brain precipitated by either a viral infection or head injury (Critchley, 1962). Various hypothalamic disorders were associated with hyperphagia and obesity. From collected published reports, Bray and Gallagher (1975) described a constellation of associated symptoms and signs of varying fre- quency occurring in a series of 69 patients with hypothalamic obesity due to tumours: headache 72%, impaired vision 72%, impaired reproductive function 56%, diabetes insipidus polyuria 35%, somnolence 40%, behavioural changes (hyper- phagia/ hypersexuality) 20%, convulsions 7%. They noted that trauma, inflammatory disease and leukaemia causing damage to the hypothalamus may also result in hypothalamic obesity. Hethering- ton and Ranson (1942) identified damage to the ventromedial nucleus of the hypothalamus as the cause of hypothalamic obesity. Bray and Gallagher (1975) found that profound hypothalamic obesity could occur without any impairment of gonado- trophin, thyroid or adrenal function if lesions were highly localized to the ventromedial nucleus and this was the case with our patient. Hypothalamic obesity is the result of hyperphagia and not hypometabolism (Stevenson, 1969). Weight gain is rapid and is due to enlargement of existing adipose cells not hyperplasia (Hirsch, 1969; Bray and Gallagher, 1975). Abnormal glucose tolerance tests and obesity are frequently associated but return to normal with a weight-reducing diet (Ogilvie, 1935), as was the case with our patient.

A possible pathogenic sequence for the develop- ment of hypothalmic obesity has been proposed by

Stevenson (1969). Injury to the ventromedial hypothalamus releases central vagal centres and increases vagal firing to the B cells of the pancreas. The increased secretion of insulin lowers blood glucose levels which in turn induces food-seeking behaviour (hyperphagia) via the lateral hypo- thalamic nucleus. Bray and Gallagher’s studies (1975) of eight hypothalamically obese patients support the above proposed mechanism. Fasting levels of insulin in hypothalamically obese patients were higher than in patients with essential obesity, who are obese because of abnormal mitochondria1 lipid enzymes.

It appears therefore that any insult to the hypothalamus, and in particular the ventromedial nucleus, may result in a constellation of symptoms and signs corresponding to Kleine-Levin syn- drome.

Critichley (1962), in his authoritative review of the world literature, allowed a case aged 44 years at onset but rejected three others aged 48, 56 and 66 years as ‘not convincing’, ‘dubious’, ‘dissimilar’, respectively. He insisted it was a disorder occurring in young men, but this view prevents recognition in other age groups. Gallinek (1962) and Gilbert (1984) report occasional cases in women. Gallinek (1962) described a case aged 46 years at onset and concluded: ‘The syndrome is not confined to a particular age group or to the male sex, as had been assumed in the past by some authors’. Drake (1987) described a case in a 60-year-old woman with frontal and subcortical lacunar infarctions demon- stratable by brain CT scan.

The present case has features typical of the Kleine-Levin syndrome but is most unusual in the age of onset, 74 years. This suggests that this syndrome, previously thought to occur only in the young, can occur in the elderly, as injury to the hypothalamic region from whatever cause can occur at any age.

ACKNOWLEDGEMENTS

The authors wish to thank Mrs J. Robinson and Mrs P. Ashmore for their invaluable assistance.

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