Sleepwalking2
Definition
Sleepwalking (SW, syn. somnambulism) consists of complex motor behaviours that interrupt night sleep. It is initiated during sudden arousals from slow wave sleep and culminates in a deambulatory activity with an altered state of consciousness and judgement [1].
Three Factors for SW
SW arises from genetic, developmental, somatic and psychological factors. Predisposing, priming and precipitating factors have been identified.
Predisposing Factors: Genetic Influences
The familial occurrence of SW was first documented in 1942 . The frequency of SW in firstdegree relatives is at least 10 times greater than in the general population. In a twin study monozygotic twins were found to be concordant for the symptom SW six times more than dizygotic twins. In the Finnish Twin Cohort the frequency of SW was similar in monyzygotic and dizygotic twins, however the concordance rate was also higher for monozygotic twins (0.55 vs. 0.32). The phenotypic variance related to genetic factors has been estimated to be about 57–66% in childhood SW and 36–80% in adult SW.
Priming Factors: Psychiatric and Neurological Influences
Current or past mental disorders are more common in patients with SW than in patients without SW . Schizoid, obsessive, compulsive, anxious, phobic, depressive symptoms or profiles have been found in patients with SW. Overall the link between psychopathology and SW is considered however to be weak [1] . Furthermore, a history of major psychological trauma appears to be rare in SW .
Several disorders of the central nervous system including stroke, head trauma, encephalitis, Tourette’s syndrome and migraine have been linked with (often adult) SW. In the absence of a specific correlation between SW and the topographical, pathological or neurochemical characteristics of these brain disorders the nature of the link between SW and neurological conditions (as this is the case also for psychiatricdisorders) appears to be non-specific one.
Triggering Factors: Precipitating Influences
Sleep fragmentation : This may be related to sleep disordered breathing, restless legs/periodic limb movements in sleep, internal stimuli (e.g., bladder distension) or external stimuli (light, noise) [1] . This may play a role in the observed association between SW and thyrotoxicosis. In a series of 74 adult sleepwalkers sleep disordered breathing was found ‘ only ’ in 25% of patients and periodic limb movements in 12% of patients.
Slow wave sleep rebound : This can be observed for example after sleep deprivation and at the beginning of CPAP treatment for sleep apnea. Experimentally a sleep deprivation of 36 hours has led to an increase in frequency and complexity of episodes during the recovery night compared with baseline in patients with SW.
Fever is often reported to trigger episodes of SW [1] .
Alcohol , often in combination of other factors, is not infrequently involved. Up to 10% of adult patients with SW consume alcohol at bedtime. Direct experimental evidence that alcohol may trigger or worsen SW is however lacking.
Several medications including zolpidem/benzodiazepines, thioridazine/neuroleptics, stimulants/aminergic (dopaminergic) drugs, antidepressants/serotonin reuptake inhibitors (e.g., paroxetin), antihistaminics and lithium may trigger SW episodes also in the absence of a positive history of SW . Nevertheless, only 4% of adult patients with SW consume psychotropic drugs.
Mental stress is often reported by patients as triggers of SW or as involved in increasing its frequency.
Pregnancy usually leads to a decrease of SW.
Possible Mechanism Model
Pathophysiological model of SW explain the simultaneous appearance of (1) complex motor behaviours (including deambulation) out of deep sleep in and (2) an impaired state of consciousness.
Animal and human data suggests that the variety of complex motor behaviours associated with SW could arise from the activation of neuronal networks in subcortical and brainstem regions responsible for the generation of (innate, archaic) emotional and motor behaviours. The activation of such ‘ central pattern generators ’ during SW, epileptic or psychogenic spells could explain the similar phenomenology of complex motor behaviours (including deambulation, eating, sexual activity, violent acts) seen with such different underlying conditions [2-4] .
The impaired state of consciousness typical of SW implies on the other hand an insufficient activation of prefrontal cortical areas necessary for purposeful behaviour/planning, insight/judgement and inhibition of emotional responses. These areas have been
shown by neuroimaging studies to be inactivated during physiological sleep. 1 The incomplete/difficult awakening of sleepwalkers from deep sleep could therefore correspond to a ‘ hypo-arousability ’ of (prefrontal?) cortical areas. This hypothesis could explain why factors that increase slow wave sleep (which exhibits maximal power over the prefrontal areas [5] ) trigger SW as well as the similarities between the mental state of sleepwalkers and that of normal subjects with protracted/difficult awakening from sleep (sleep inertia, sleep drunkenness).
One SPECT (single photon emission computed tomography) study supports the concept of state dissociation underlying SW. Compared to cerebral blood flow (CBF) data obtained in 24 subjects during wakefulness the CBF of a single patient during SW was found to be increased in the posterior cingulate cortex and cerebellar vermis and decreased in frontal and parietal association cortices ( Figure 9.4 ) [5] . This observation, in line with Broughton’s original suggestion of SW as an arousal disorder, suggests the presence of a specific activation of thalamo-cingulo-cortical pathways (implicated in the control of complex motor and emotional behaviour) while other thalamocortical pathways (including those projecting to the frontal lobes) remain inhibited. The appearance at the different ages and during different nights in the same patient of SW, sleep terrors, confusional arousals could be explained by the recruitment of distinct although partially overlapping thalamo-cingulo-cortical pathways.
The fundamental cause of state dissociation in SW remains unknown. The existence of different predisposing, priming and triggering factors of SW as well as of different forms of SW prove that the dynamic physiological reorganization that the brain undergoes at the transition from one state to another (in the case of SW from deep sleep to lighter sleep/wakefulness) represents a complex and fragile process that undergoes developmental maturation and can be impaired by different (neurological, psychological, pharmacological…) factors.
Possible Pathway
The association of SW with migraine suggests the possible involvement of the serotonin system in both. This hypothesis is further supported by the observation that several factors known to trigger SW (including fever, lithium and antidepressants) activate the serotoninergic system [7] . The involvement of cholinergic and GABA(A) pathways has been proposed based on theoretical speculations and the result of transcranial magnetic stimulation studies in awake sleepwalkers [7] . Considering the essential physiological role of the hypocretin (orexin) system in state stabilization [7] and the fact that narcolepsy represents the dissociated disorder ‘ par excellence ’ [7] , an involvement of this hypothalamic system – possibly with the dopamin system (which is known to interact with the hypocretin system [7] ) – appears also to be possible.
[1] American Academy of Sleep Medicine (2005). The International Classification of Sleep Disorders , 2nd Edition. American Academy of Sleep Medicine, Rochester .
[2] Berntson , G.G. and M icco , D.J. ( 1976 ) Organization of brainstem behavioral systems . Brain Res Bull 1 : 471 – 483 .
[3] Mahowald , M. and Schenck , C.H. ( 2000 ) Parasomnias: Sleepwalking and the law . Sleep Med Rev 4 : 321 – 339 .
[4] Tassinari , C.A. , Rubboli , G. , Gardella , E. , et al. ( 2005 ) Central pattern generators for a common semiology in fronto-limbic seizures and in parasomnias. A neurotologic approach . Neurol Sci 26 : 225 – 232 .
[5] Werth , E. , Achermann , P. and Borbély , A. ( 1997 ) Fronto-occipital EEG power gradients in human sleep . J Sleep Res 6 : 102 – 112 .
[6] Bassetti , C. , Vella , S. , Donati , F. , Wielepp , P. and Weder , B. ( 1999 ) SPECT during sleepwalking . Lancet 356 : 484 – 485 .
[7]
Sleepwalking (SW, syn. somnambulism) consists of complex motor behaviours that interrupt night sleep. It is initiated during sudden arousals from slow wave sleep and culminates in a deambulatory activity with an altered state of consciousness and judgement [1].
Three Factors for SW
SW arises from genetic, developmental, somatic and psychological factors. Predisposing, priming and precipitating factors have been identified.
Predisposing Factors: Genetic Influences
The familial occurrence of SW was first documented in 1942 . The frequency of SW in firstdegree relatives is at least 10 times greater than in the general population. In a twin study monozygotic twins were found to be concordant for the symptom SW six times more than dizygotic twins. In the Finnish Twin Cohort the frequency of SW was similar in monyzygotic and dizygotic twins, however the concordance rate was also higher for monozygotic twins (0.55 vs. 0.32). The phenotypic variance related to genetic factors has been estimated to be about 57–66% in childhood SW and 36–80% in adult SW.
Priming Factors: Psychiatric and Neurological Influences
Current or past mental disorders are more common in patients with SW than in patients without SW . Schizoid, obsessive, compulsive, anxious, phobic, depressive symptoms or profiles have been found in patients with SW. Overall the link between psychopathology and SW is considered however to be weak [1] . Furthermore, a history of major psychological trauma appears to be rare in SW .
Several disorders of the central nervous system including stroke, head trauma, encephalitis, Tourette’s syndrome and migraine have been linked with (often adult) SW. In the absence of a specific correlation between SW and the topographical, pathological or neurochemical characteristics of these brain disorders the nature of the link between SW and neurological conditions (as this is the case also for psychiatricdisorders) appears to be non-specific one.
Triggering Factors: Precipitating Influences
Sleep fragmentation : This may be related to sleep disordered breathing, restless legs/periodic limb movements in sleep, internal stimuli (e.g., bladder distension) or external stimuli (light, noise) [1] . This may play a role in the observed association between SW and thyrotoxicosis. In a series of 74 adult sleepwalkers sleep disordered breathing was found ‘ only ’ in 25% of patients and periodic limb movements in 12% of patients.
Slow wave sleep rebound : This can be observed for example after sleep deprivation and at the beginning of CPAP treatment for sleep apnea. Experimentally a sleep deprivation of 36 hours has led to an increase in frequency and complexity of episodes during the recovery night compared with baseline in patients with SW.
Fever is often reported to trigger episodes of SW [1] .
Alcohol , often in combination of other factors, is not infrequently involved. Up to 10% of adult patients with SW consume alcohol at bedtime. Direct experimental evidence that alcohol may trigger or worsen SW is however lacking.
Several medications including zolpidem/benzodiazepines, thioridazine/neuroleptics, stimulants/aminergic (dopaminergic) drugs, antidepressants/serotonin reuptake inhibitors (e.g., paroxetin), antihistaminics and lithium may trigger SW episodes also in the absence of a positive history of SW . Nevertheless, only 4% of adult patients with SW consume psychotropic drugs.
Mental stress is often reported by patients as triggers of SW or as involved in increasing its frequency.
Pregnancy usually leads to a decrease of SW.
Possible Mechanism Model
Pathophysiological model of SW explain the simultaneous appearance of (1) complex motor behaviours (including deambulation) out of deep sleep in and (2) an impaired state of consciousness.
Animal and human data suggests that the variety of complex motor behaviours associated with SW could arise from the activation of neuronal networks in subcortical and brainstem regions responsible for the generation of (innate, archaic) emotional and motor behaviours. The activation of such ‘ central pattern generators ’ during SW, epileptic or psychogenic spells could explain the similar phenomenology of complex motor behaviours (including deambulation, eating, sexual activity, violent acts) seen with such different underlying conditions [2-4] .
The impaired state of consciousness typical of SW implies on the other hand an insufficient activation of prefrontal cortical areas necessary for purposeful behaviour/planning, insight/judgement and inhibition of emotional responses. These areas have been
shown by neuroimaging studies to be inactivated during physiological sleep. 1 The incomplete/difficult awakening of sleepwalkers from deep sleep could therefore correspond to a ‘ hypo-arousability ’ of (prefrontal?) cortical areas. This hypothesis could explain why factors that increase slow wave sleep (which exhibits maximal power over the prefrontal areas [5] ) trigger SW as well as the similarities between the mental state of sleepwalkers and that of normal subjects with protracted/difficult awakening from sleep (sleep inertia, sleep drunkenness).
One SPECT (single photon emission computed tomography) study supports the concept of state dissociation underlying SW. Compared to cerebral blood flow (CBF) data obtained in 24 subjects during wakefulness the CBF of a single patient during SW was found to be increased in the posterior cingulate cortex and cerebellar vermis and decreased in frontal and parietal association cortices ( Figure 9.4 ) [5] . This observation, in line with Broughton’s original suggestion of SW as an arousal disorder, suggests the presence of a specific activation of thalamo-cingulo-cortical pathways (implicated in the control of complex motor and emotional behaviour) while other thalamocortical pathways (including those projecting to the frontal lobes) remain inhibited. The appearance at the different ages and during different nights in the same patient of SW, sleep terrors, confusional arousals could be explained by the recruitment of distinct although partially overlapping thalamo-cingulo-cortical pathways.
The fundamental cause of state dissociation in SW remains unknown. The existence of different predisposing, priming and triggering factors of SW as well as of different forms of SW prove that the dynamic physiological reorganization that the brain undergoes at the transition from one state to another (in the case of SW from deep sleep to lighter sleep/wakefulness) represents a complex and fragile process that undergoes developmental maturation and can be impaired by different (neurological, psychological, pharmacological…) factors.
Possible Pathway
The association of SW with migraine suggests the possible involvement of the serotonin system in both. This hypothesis is further supported by the observation that several factors known to trigger SW (including fever, lithium and antidepressants) activate the serotoninergic system [7] . The involvement of cholinergic and GABA(A) pathways has been proposed based on theoretical speculations and the result of transcranial magnetic stimulation studies in awake sleepwalkers [7] . Considering the essential physiological role of the hypocretin (orexin) system in state stabilization [7] and the fact that narcolepsy represents the dissociated disorder ‘ par excellence ’ [7] , an involvement of this hypothalamic system – possibly with the dopamin system (which is known to interact with the hypocretin system [7] ) – appears also to be possible.
[1] American Academy of Sleep Medicine (2005). The International Classification of Sleep Disorders , 2nd Edition. American Academy of Sleep Medicine, Rochester .
[2] Berntson , G.G. and M icco , D.J. ( 1976 ) Organization of brainstem behavioral systems . Brain Res Bull 1 : 471 – 483 .
[3] Mahowald , M. and Schenck , C.H. ( 2000 ) Parasomnias: Sleepwalking and the law . Sleep Med Rev 4 : 321 – 339 .
[4] Tassinari , C.A. , Rubboli , G. , Gardella , E. , et al. ( 2005 ) Central pattern generators for a common semiology in fronto-limbic seizures and in parasomnias. A neurotologic approach . Neurol Sci 26 : 225 – 232 .
[5] Werth , E. , Achermann , P. and Borbély , A. ( 1997 ) Fronto-occipital EEG power gradients in human sleep . J Sleep Res 6 : 102 – 112 .
[6] Bassetti , C. , Vella , S. , Donati , F. , Wielepp , P. and Weder , B. ( 1999 ) SPECT during sleepwalking . Lancet 356 : 484 – 485 .
[7]
