Forensic Evaluation of a Single Episode of a Disorder of Arousal in a Sleepwalking Defense: Cognitive Function Versus Prior Clinical History.

Introduction The clinical diagnosis of disorders of arousal (DOA) is based primarily on a clinical history including amnesia for episodes. The presence of amnesia means the patient cannot provide direct evidence. In a forensic setting, when the defendant has been charged criminally with violent actions or sexual related assaults allegedly during sleep, a sleepwalking defense may be presented. As opposed to clinical history, the prosecution generally focuses on the single episode of alleged DOA that resulted in the criminal charges against the defendant. The prosecution will argue that this episode of complex behavior was not consistent with a DOA. A past history of purported episodes is not proof that a recent single episode must be a DOA. However, most sleepwalking defenses rely heavily on standard clinical evaluations despite the fact they have no direct connection with the current criminally charged episode. The International Classification of Sleep Disorders (ICSD-3) General Diagnostic Criteria C for DOAs that states "limited or no associated cognition" should be present. Recent real time studies of DOAs have shown that during DOA episodes the prefrontal cortex (PRC) is deactivated while the motor cortex remains active. Conclusion The PFC is the location of almost all executive functions including inhibition, planning, memory, and many others. Thus, when the PFC is deactivated, these higher cognitive functions are not available. The presence of higher cognitive functions during an alleged episode of DOA would be inconsistent with a deactivated PFC and thus inconsistent with generally accepted brain activity during a NREM parasomnia. This would be direct evidence that the episode could not be a DOA but occurred during wakefulness. Clinical trial No.

Disorders of Arousal and timing of the first period of slow wave sleep: Clinical and forensic implications.

The timing of first period of slow wave sleep (SWS) is often used as a proxy for determining if and when Disorders of Arousal (DOA) such as sleepwalking are likely to occur or did occur in the past. In criminal cases employing a "sleepwalking defense" the prosecution may argue that nocturnal violence or sexually aggressive behavior occurred too early in the sleep period to be associated with SWS. Expert witness opinion on the expected latency to SWS (LSWS) has varied from minutes after sleep onset to ≥60 min. A search of PubMed was conducted for LSWS and for any reports of DOAs occurring from stage N2. A total of 21 studies reported LSWS in normal controls, clinically diagnosed sleepwalkers, in otherwise normal sleepers following different types of sleep deprivation and due to the effects of alcohol. Five studies reported episodes of DOA from N2 sleep. The shortest mean LSWS of 6.4 min was found with a combination of total sleep deprivation and alcohol. In a group of normal research subjects, a LSWS mean of 10.7 min was noted. LSWS in DOA patients occurred as early as a mean of 12.4 min. Two sleep studies performed on Kenneth Parks, acquitted of the murder of his mother-in-law by a sleepwalking defense, reported LSWSs of 9.7 and 10 min. Sleep deprivation but not alcohol was found to decrease LSWS significantly. Expert opinions on LSWS should be based on scientific peer reviewed publications documenting empirical sleep evidence and can be much shorter than is generally reported.

The neurophysiological and neurochemical effects of alcohol on the brain are inconsistent with current evidence based models of sleepwalking.

The DSM-5 and ICSD-3 have removed alcohol from the list of potential triggers for sleepwalking due to the lack of empirical evidence. Recent imaging and EEG based studies of sleepwalking and confusional arousals have provided a more data-based method of examining if alcohol is compatible with what is known about the neurophysiology and neurochemistry of sleepwalking. These studies have demonstrated a deactivation of the frontal areas of the brain, while the cingulate or motor cortex remains active and characterized activation in the form of beta EEG. This increase in activation is attributed to a decrease in the inhibitory activity the neurotransmitter GABAA. This cerebral excitability of the cingulate cortex of sleepwalkers is also present in the brains of sleepwalkers during wakefulness compared to normal controls. Alcohol is well established to have an inhibitory effect on the brain and specifically on the motor areas via the inhibitory effects of increased GABAA activity. Thus, the empirical data show sleepwalking is characterized by a decrease in the inhibitory activity of GABAA - permitting or facilitating motor activity while alcohol has the opposite effect of increasing GABAA and inhibiting motor activity. This is inconsistent with theories that alcohol is somehow a trigger or facilitator for sleepwalking.

Disorders of arousal from sleep and violent behavior: the role of physical contact and proximity.

STUDY OBJECTIVES: To review medical and legal case reports to determine how many appear to support the belief that violence against other individuals that occurs during Disorders of Arousal - sleepwalking, confusional arousal, and sleep terrors - is triggered by direct physical contact or close proximity to that individual and does not occur randomly or spontaneously. DESIGN: Historical review of case reports in the medical and legal literature. MEASUREMENTS AND RESULTS: A total of 32 cases drawn from medical and legal literature were reviewed. Each case contained a record of violence associated with Disorders of Arousal; in each, details of the violent behavior were available. Violent behaviors associated with provocations and/or close proximity were found to be present in 100% of confusional arousal patients and 81% of sleep terror patients. Violent behaviors were associated with provocation or close proximity in 40%-90% of sleepwalking cases, depending on whether the legal verdict and other factors were taken into account. Often the provocation was quite minor and the response greatly exaggerated. The specific manner in which the violence was triggered differed among sleepwalking, confusional arousals, and sleep terrors. CONCLUSIONS: In the cases reviewed, violent behavior directed against other individuals associated with Disorders of Arousal most frequently appeared to follow direct provocation by, or close proximity to, another individual. Sleepwalkers most often did not seek out victims, but rather the victims sought out or encountered the sleepwalker. These conclusions are tempered by several limitations: the selection of cases was not random and may not represent an accurate sample of violent behaviors associated with Disorders of Arousal. Also, final verdicts by juries in reported legal cases should not be confused with scientific proof of the presence or absence of sleepwalking. The pathophysiology of Disorders of Arousal with and without violent behavior could be associated with normally occurring deactivation of the frontal lobes during slow wave sleep (SWS) connected via atypically active thalamocortical pathways to the limbic areas. It is not known if the violent sleepwalker, confusional arousal patient, or sleep terror patient differs from other patients with these disorders. The conclusions of this case series await confirmation by the results of future sleep laboratory based studies.

Factors that predispose, prime and precipitate NREM parasomnias in adults: clinical and forensic implications.

Sleepwalking and related disorders are the result of factors that predispose, prime and precipitate episodes. In the absence of one or more of these factors sleepwalking is unlikely to occur. Predisposition to sleepwalking is based on genetic susceptibility and has a familial pattern. Priming factors include conditions and substances that increase slow wave sleep (SWS) or make arousal from sleep more difficult. These factors include sleep deprivation, alcohol, medications, situational stress and fever among others. The patient with a genetic predisposition to sleepwalking and with priming factors still requires a precipitating factor or trigger to set the sleepwalking episode in motion. Classical theories of sleepwalking were based primarily on case reports. Recently some of these theories have been tested in the sleep laboratory. Experimental sleep deprivation studies of sleepwalkers generally report an increase in complex behaviors during SWS, although one prominent study reported the opposite effect. However, the generally accepted theory that alcohol and medications can induce sleepwalking episodes remains entirely based on clinical and forensic case reports. Alleged cases of alcohol related sleepwalking often involve individuals lacking the generally accepted characteristics of sleepwalkers but with very high blood alcohol levels that could in and of itself account for complex behaviors noted without the presence of sleepwalking. Further, the effects of high levels of alcohol dramatically decrease SWS, a finding inconsistent with sleepwalking. Case reports of medication-related induction of apparent sleepwalking most often present a complex medical and psychiatric history associated with multiple medications. These patients often lack the clinical history and other criteria currently required for the diagnosis of sleepwalking. The medication-related behaviors may instead represent some other condition in an awake, but impaired patient. Sleep laboratory research has identified sleep disordered breathing, periodic leg movements, noise and touch among others as proximal triggers of sleepwalking episodes. Treatment of these triggers may result in resolution of sleepwalking without medication. Further sleep laboratory research is needed before experimental findings can be used for routine diagnostic and forensic purposes.

Hypersynchronous delta sleep EEG activity and sudden arousals from slow-wave sleep in adults without a history of parasomnias: clinical and forensic implications.

STUDY OBJECTIVES: To determine the frequency of classical markers of non-rapid eye movement (NREM) parasomnias--hypersynchronous delta sleep (HSD) electroencephalogram waves and sudden arousals from slow-wave sleep (SWS)--in patients without histories of somnambulism or other NREM parasomnias. DESIGN: Retrospective review. SETTING: Sleep disorders center laboratory. PATIENTS: 82 consecutive patients without a history of parasomnias who underwent diagnostic polysomnograms; 57 men and 25 women, mean age 48+/-13.3 years, were included without regard to diagnosis or findings. All patients had at least 30 seconds of stage 3 or 4 sleep during the polysomnogram. MEASUREMENTS AND RESULTS: The primary diagnosis of all but 4 patients was obstructive sleep apnea (mean respiratory disturbance index, 30 +/- 23.6 [range, 2.7-117] per hour of sleep). Polysomnograms were then reviewed for the presence of HSD and SWS arousals. A total of 235 arousals (mean, 2.9 +/- 2.7; range, 0-14) from stage 3 or 4 sleep were noted. Eight-five percent of all patients had at least 1 SWS arousal and 45% had 3 or more SWS arousals; 85.1% of all arousals from SWS were secondary to sleep-disordered breathing, and 5.9% were secondary to leg movements. At least 1 episode of HSD (mean, 1.4 +/- 1.6; range, 0-9) was noted in 65.8% of patients. CONCLUSIONS: HSD and SWS arousals were a common finding in patients without clinical histories of sleepwalking or other parasomnias but who were found to have frequent respiratory-related arousals during sleep. HSD and SWS arousals thus have a low specificity for NREM parasomnias and, without further research, are not useful for the objective confirmation of parasomnias in clinical evaluations and in the forensic evaluation of sleepwalking as a legal defense.

Prevalence and comorbidity of nocturnal wandering in the U.S. adult general population.

As noted by Ohayon et al., nocturnal wandering (NW) is not synonymous with sleepwalking. NW may also refer to wandering during the night due to epilepsy. Alcohol intoxication can also result in drunken behavior while awake, but this type of cognitive impairment may be undistinguishable from other forms of NW. Dementia and CNS drug effects can also result in NW.

Alcohol-induced blackout as a criminal defense or mitigating factor: an evidence-based review and admissibility as scientific evidence.

Alcohol-related amnesia--alcohol blackout--is a common claim of criminal defendants. The generally held belief is that during an alcohol blackout, other cognitive functioning is severely impaired or absent. The presentation of alcohol blackout as scientific evidence in court requires that the science meets legal reliability standards (Frye, FRE702/Daubert). To determine whether "alcohol blackout" meets these standards, an evidence-based analysis of published scientific studies was conducted. A total of 26 empirical studies were identified including nine in which an alcohol blackout was induced and directly observed. No objective or scientific method to verify the presence of an alcoholic blackout while it is occurring or to confirm its presence retrospectively was identified. Only short-term memory is impaired and other cognitive functions--planning, attention, and social skills--are not impaired. Alcoholic blackouts would not appear to meet standards for scientific evidence and should not be admissible.

Sleep driving: sleepwalking variant or misuse of z-drugs?

Sleep driving is most often classified as a variant of sleepwalking, but should be distinguished from impaired driving due to misuse or abuse of sedative/hypnotic drugs. Z-drugs; zolpidem and zopiclone in particular, have been associated with the majority of reported cases of impaired driving. Numerous studies have found z-drugs in driving under influence (DUI) related police stops, arrests and accidents. Impaired drivers are reported to have 1) blood levels of z-drugs that exceed therapeutic ranges 2) failed to take the medication at the correct time or remain in bed for sufficient time and/or 3) combined z-drugs with other central nervous system (CNS) depressants and/or alcohol. Consistent with CNS depression, z-drug-impaired drivers may demonstrate cognitive function at low levels with drivers still able to understand and respond to questions while sleepwalkers are completely unable to understand or interact with police. Z-drug-impaired drivers are often severely physically impaired, unable to stand up or maintain balance while sleepwalkers are able to stand and walk unaided. Sleep driving and impaired driving due to z-drugs may overlap. Sleep driving and drug-impaired driving are statistically rare events, but due to the billions of doses prescribed each year may still result in numerous DUI related arrests and accidents.