Abstract
DEAR SIR,
Insomnia has generally been attributed to psychological or psychiatric causes. We wish to describe two unusual cases of acute onset insomnia. In both cases, there was an inability to achieve any type of sleep unless aided with benzodiazepines. One of the patients was sleep-deprived for days and started to have hallucinations. We are hypothesizing that these presentations may be secondary to damage to the ventrolateral preoptic nucleus (VLPO).
The first case concerns a 62 year old European woman who was referred to our insomnia service. Her presenting complaint was inability to sleep for the last 3months following cardiac surgery secondary to a mitral valve problem. Before surgery, her typical sleep pattern entailed going to bed at 10PM and waking up refreshed at 6AM. After the surgery, she was awake and alert continuously for 7 days. Onthe 7th day, she began to hallucinate and hear voices from the fridge. She also heard a high-pitched buzzing noise which later sounded like music. She went to her general practitioner (GP) and was prescribed zopiclone. She began taking 3.75mg zopiclone intermittently (4 days on and 2 days off). She was able to sleep with zopiclone for 4 h, waking up refreshed. She would have a sleep latency of 1 h. Once she was able to sleep, she had no middle-of-night or early morning awakenings. Her perceptual disturbances resolved after the first sleep. During the 2 days off the zopiclone, she would lie in bed aware of everything happening around her and unable to sleep. She also tried melatonin, nortryptilline and amitriptyline with no success. She did not report symptoms of sleep-talking, sleep-walking, abnormal limb movements or snoring.
There were no complications during surgery. There were no neurological symptoms or deficits before or after surgery. There was no past psychiatric or relevant sleep history. She also had no family history of psychiatric or sleep disorders. She suffered no nightmares or post-traumatic stress disorder (PTSD) symptoms from the surgery.
In terms of her medical history, she had mitral valve incompetence from rheumatic fever, which wasrepaired 3months earlier as described. She had two discs fused in her spine 20 years ago and had also had ahysterectomy 20 years ago. She had renal stones in the past. She had no substance abuse or dependence.
On mental state examination, the patient was an engaging cheerful European woman who established good rapport. There were no abnormalities of speech, thought processes, thought content, perceptions, mood, insight or judgement. There were no safety concerns.
A continuous sleep log was performed for 3 weeks which confirmed that without hypnotics the patient had no sleep. Different treatment options were discussed and she felt that she was happy to continue with zopiclone.
The second case concerns a 71 year old European man who reportedthat 5months before presentation he had a sudden loss of ability to fall asleep with no obvious precipitant. Before this, he was a good sleeper with no significant problems. This continued for 5 days, after which he was prescribed benzodiazepines (temazepam 10mg nocte) by his GP with good effect. His current sleeping pattern was that he goes to bed around 10.15PM, reads forabout 30 min, takes his medicationaround 10.45PM, and has a sleep latency of approximately 10min with no middlenight awakenings. He reported that the main problem is the ability to fall asleep. Once he is able to sleep, the rest of his sleep is of good quality. There are no reports of nocturnal events such as gasping, snoring, sleep-talking sleepwalking or abnormal limb movements. On nights when he does not take medication, he remains fully awake the whole night with resulting poor concentration and low energy the following day. There are no other physical or neurological findings of note.
The patient has no psychiatric history and no evidence of any major mood, anxiety or psychotic disorder. He has no relevant family history. He does not use alcohol or other drugs. Medical history included post-nasal drip, osteoarthtitis and reflux oesophagitis controlled on Losec.
Mental state examination revealed an engaging man who established good rapport. There were no abnormalities of speech, thought processes, thought content, perceptions, mood, insight or judgement. There were no safety concerns. The patient was happy to continue with benzodiazepines as he obtains normal sleep on them.
These two reports are unusual cases of acute sleep onset insomnia in the elderly. In both cases, the two patients had no prior history of insomnia. They did not exhibit typical personality/ psychological features of individuals predisposed to insomnia. The acuity of the event is very unusual. Moreover, the severity is quite different from patients who suffer from insomnia. Most, if not all, patients with insomnia report some sleep, even if only a few minutes of superficial sleep in one night. In both cases, sleep onset did not occur at all without the use of benzodiazepines. In the first case, the patient started to hallucinate after many days of not sleeping. This is a phenomenon described with total sleep deprivation.
To our knowledge, similar cases have not been reported in the literature. We postulate that the aetiology may reflect the neuroanatomic basis of the regulation of sleep. It is known that the main ascending arousal pathways originate from two main sources. Cholinergic neurons in the pedunculopontine and laterodorsal temental noradrenergic locus coeruleus, serotonergic dorsal andmedian raphe nuclei and histaminergic tuberomammillary nucleus send major inputs directly to the cerebral cortex. Firing in both systems is necessary to produce a wakeful state. During sleep, the neurons contributing to the ascending arousal pathways are inhibited. The source of this inhibition has been tracked back to the VLPO. This cell group consists of neurons that contain GABA, galanin and two inhibitory neurotransmitters. These neurons provide inputs to the entire ascending arousal system. Ventrolateral preoptic nucleus neurons fire mainly during sleep and the two cases described may reflect lesions in this area, perhaps with a microvascular basis.1–3