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The Case of a nocturnal runner

Dr Thomas Elanjithara MRCPsych.
Staff Grade Psychiatrist
University Hospital Lewisham Lewisham High Street London SE13 6LW.

Dr Miriam Isaac
Speciality registrar in Psychiatry,
University College London.
London.
WC1E 6BT

Consent

The patient gave his written consent to publish this case report.

Abstract

Harmful sleep behaviours like REM sleep behaviour disorder (RBD) are increasingly identified in PTSD. The case report narrates the history of patient suffering both PTSD and sleep behaviour. It explains the mechanisms underlying the presentation, as an imbalance of adrenergic and cholinergic systems. Example of a treatment benefiting both PTSD symptoms and sleep behaviour using a combined adrenergic and serotonergic agent like Mirtazapine is described.

Key words: harmful sleep behaviour, PTSD. Adrenergic and serotonergic agent.

Case Presentation

Patient MA is a 38 years old single Asian man, who suffered a knife injury on his face, in November 2006. He was attacked by a group of hired men; during a forceful eviction from his rented accommodation. In March 2007, MA was referred to the mental health services with complains of disrupted sleep, “running out “of his bed, and poor energy during the day. He had moved in to live with his uncle by then .On a detailed assessment it became apparent that MA is suffering from symptoms of post traumatic stress disorder (PTSD) following the assault. He was attacked at night, when he was preparing to sleep. He was threatened to be killed and assaulted with knife across the face. He lost sight in right eye, but the left eye functions normally.
MA described having recurrent nightmares about group of men with knife coming to attack him. He also described running out of his bed when he has these dreams. According to him, he is able to fall in to sleep, but 2-3 hours in to sleep, he experiences nightmares. Most of the time he becomes fully awake, by the time he steps out of his bedroom. But other times he has gone out in to the street before becoming fully awake. He has accidentally fallen down few times during theses runs. His uncle, who he lives with, corroborated this information.
Since the alleged incident MA reports avoidance behaviour related to place where he was assaulted. His startle response was heightened and he was found to be irritable by his uncle’s family. MA reported no previous mental disorders. He reported no medical disorder including epilepsy, and denies use of alcohol or substances.
On serial outpatient assessments no signs of psychosis or mood disorder were found. Physical investigations and routine blood investigation were normal. At the initial assessment, his scores on Impact of Event- revised scale were: overall 1.32, Intrusion subscale 1.38, avoidance subscale 1.13, Hyper arousal subscale 1.5. By the time a polysomnography(PSG) was available, MA had responded to the treatment ( see below) and the sleep behaviour completely disappeared. Concurrent EEG was able to rule out seizure disorder. A CT scan of the brain ruled out any obvious pathological changes
The primary diagnosis of Post Traumatic stress disorder was made.
From the patient description and collateral information, an additional diagnosis of REM sleep behaviour Disorder (RBD) was also made( As per ICD 10 classification, it is best described as other non-organic sleep disorders, F51.8).

MA was started on Mirtazapine based on its efficacy in managing PTSD symptoms. The dose was increased from 15 mg at night to 30 mg in 7 days. He did not choose the psychological therapy offered.
With in the 2 weeks of starting mirtazapine, he reported less running incidences. By the 3rd week it completely disappeared.
However, he continued to have nightmares and other PTSD symptoms during the initial weeks of treatment. These symptoms improved gradually over the next few months. MA scored 0.30 on Impact of event score, after 6 months, indicating good improvement. HoNOS rating also showed overall functional and symptomatic improvement at follow up.
MA did not report any recurrences of the sleep behaviour.

Discussion

The International Classification of Sleep Disorders defines Rapid Eye Movement (REM) sleep behaviour disorder ( RBD) as a parasomnia characterised by intermittent loss of muscle atonia In REM sleep accompanied by motor activity associated with dream mentation. The minimal diagnostic criterion includes presence of limb or body movement associated with dream mentation along with one of the following-Harmful sleep behaviour, acting out of dreams, or disruption of sleep with abnormal behaviours. Polysomnograph(PSG) picks up these behaviours and movements, but it is not essential for the diagnosis, as set out in the guidance. MA described vivid nightmares of being attacked with knife, which starts 2-3 hours in to sleep. From his own description and collateral history from his family, it appeared that he was acting out the nightmares whilst running out. Also he would take few steps out of his bed before becoming fully awake. On few occasions he had fallen down and hurt himself, while running out.

RBD has been previously reported in patients suffering from degenerative neurological disorders like Parkinson’s disease and Lewy Body Dementia (DLB). The incidence rate in these groups of patients is between 19% and 77%. There is growing recognition of sleep behaviour disorders like RBD in PTSD patients. In a study done in Veteran Affairs Medical centre in North Carolina, USA, 56% patients with RDB were also found to have PTSD.

The exact mechanisms responsible for REM sleep and sleep behaviours like RBD, are not yet found. The authors present a simplified description of underlying mechanisms and postulates effects on chemical systems based on available research findings.
Physiological and lesioning studies have shown that pontine region in the brain stem seats the REM sleep control centres. This includes adrenergic system (situated in Locus ceruleus ( LC) and peri- LC alpha nucleus) and Cholinergic system situated in pedunculopontine nucleus (PPN) and laterodorsal tegmental nucleus ( LDT).Cholinergic input to LC is excitatory but adrenergic input in to PPN and LDT is inhibitory. Both these systems receive inhibitory input from serotonergic system situated in raphe nucleus. Cholinergic system is considered to be responsible for initiating and maintaining REM sleep. Adrenergic system from LC is responsible for slow wave sleep. Peri-LC adrenergic neurons send inhibitory signals to the spinal motor neurons during the sleep, producing muscle atonia. This inhibits the excitation caused by the cortical centres and brainstem, on the spinal motor centre during dreaming. When this balance is maintained, it makes sure the dreams are not acted out during the sleep, as there is inhibition of motor activity.

In conditions like DLB and Parkinson’s disease, there are degenerative changes to LC and peri-LC neurons. This results in relative lack of effective inhibition of spinal motor neurons resulting in acting out of dreams. In PTSD, brain sensitivity to noradrenalin is increased with suppression of cortical and hippocampal activity. It can cause dysregulation in noradrenergic system and the REM balance is affected. Also LC is found to have lesser number of neurons in chronic anxiety states and PTSD. When there is weaker firing from LC (adrenergic), there is relative disinhibition of cholinergic system at PPN. This imbalance causes less inhibitory control over spinal motor neurons and results in sleep behaviour.

Mirtazapine is an α 2 auto receptor blocker, and it enhances adrenergic transmission along with enhancing 5HT1A transmission, whereby resetting the dysregulation in the sleep physiology.
There are case reports of patients with neurodegenerative disease like Parkinson’s , exhibiting sleep behaviour, when started on Mirtazapine. The likely explanation is that because there are irreversible degenerative changes in LC, it fails to responds to the adrenergic transmission enhanced by Mirtazapine. This leaves the serotonergic inhibition to predominate and leads to precipitation of sleep behaviour like RBD.
Where as in case of patients with PTSD with no neurodegenerative diseases, there are more active neurons in LC, which responds to the enhanced adrenergic transmission by Mirtazapine and the balance between adrenergic and cholinergic system resets. This can result in disappearance of sleep behaviour.

Clonazepam has shown some effect in treating sleep behaviours in neurodegenerative disorders. SSRI and other antidepressants have mixed responses reported in this patient group.

Conclusion

This case history illustrates a combined adrenergic and serotonergic agent like Mirtazapine, used effectively in treating symptoms of PTSD and associated harmful sleep behaviour disorder in some one with no co-morbid neurodegenerative disorders known. This is a promising outcome in the light of previous findings of Mirtazapine induced sleep behaviour in a patient group with neurodegenerative conditions. It calls for careful patient selection (ruling out co-morbid neurodegenerative disorders in PTSD) and further controlled studies of treatment of PTSD associated sleep behaviours.

Declaration of interest- None

References

Boeve, BF, Silber, MH, Saper, CB, Ferman,TJ. (2007)
Pathophysiology of REM sleep behavior disorder and relevance to neurodegenerative disease .Brian 130(11): 2770-2788

Garcia-Rill, E. (1997) Disorders of Reticular activating system. Med Hypothesis 49: 379-387.

Hageman, I, Andersen, HS, Jergensen, MB. ( 2001) Post traumatic stress disorder: a review of psychobiology and pharmacotherapy. Acta Psychiatrica Scandinavica104:411-422.

Husain, AM, Miller, PP, Carwile ,ST. (2001) REM sleep behaviour disorder: Potential relationship to Post traumatic stress disorder. Journal of clinical neurophysiology 18(2):148-157.

Thomas , A , Bonanni,L, Onofrj,M.( 2007) Symptomatic REM sleep behaviour disorder. Journal of Neurological Sciences. 28:S21-S36.

First Published July 2008

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