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.

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.

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.

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.