Solms [12] loosely grouped together 12 case reports in the literature and 10 of his own cases under the heading of dream/reality confusion (or ‘anoneirognosis’). These patients reported excesses of dreaming, ranging from increased frequency and/or vivacity of dreams to intrusions of dreaming and dream-like thinking into waking cognition. The principle justification for collecting these cases under a unitary nosological heading was that the focal lesions (representing a wide variety of pathologies) that cause ‘anoneirognosis’ were typically located in the transitional zone between the anterior diencephalon and basal forebrain. Kindred phenomena are, however, also observed with visual de-afferentation, peduncular hallucinosis, delirium, parkinsonian syndromes, Guillain–Barre syndrome and a variety of toxic and metabolic conditions. The common denominator in these cases may therefore simply be degradation of constraints on consciousness. Certainly, any suggestion at this stage that dream–reality confusion may be considered to be a focal symptom is unjustified.

Dream/reality confusion in parkinsonian syndromes is difficult to interpret. Increased dreaming and hallucinations are frequently seen with Parkinson’s disease (PD) but this may be iatrogenic. It is well established that hallucinations and excessive dreaming can be provoked by the administration of l-dopa, both in PD [87] (and in normal subjects, independently of any concomitant changes in REM sleep [88]. Accordingly, it has been shown that reduction of dopaminergic medication, and administration of dopamine blockers, reduces hallucinations and excessive dreaming in PD [89]. However, visual hallucinations in PD may also be an indication of the presence of Lewy body pathology, with involvement of parieto-occipital and limbic regions [90–92]. Excessive dreaming in parkinsonian syndromes may, therefore, have a different mechanism in cases with and without cortical Lewy bodies. In PD, hallucinations occur late in the course of the disorder, whereas they are an early feature of dementia with Lewy bodies (DLB).

Hallucinations and dream/reality confusion are also common in narcolepsy [92]. In these cases, hallucinations may accompany or follow attacks of cataplexy and sleep paralysis. Hallucinations of a presence of someone nearby (‘sensed presence’) or a pressure on the chest with breathing difficulties (‘incubus/succubus’), and floating/flying and ‘out of body’ experiences, are typical in these cases. Dreams can occur at sleep onset (at night or during daytime naps) as well as on awakening (Rosenthal’s syndrome). The retention of elements of normal waking mentation, such as volitional control or environmental awareness, is characteristic of narcoleptic dreams.

Various other rare disorders are associated with dream/reality confusion. Idiopathic hypersomnia manifests in excessive daytime sleepiness, prolonged unrefreshing sleep and ‘sleep drunkenness’ on attempting to wake up. Habitual dreaming, hypnagogic hallucinations and sleep paralysis are common in these cases [91]. Kleine–Levin syndrome is a rare disorder characterised by recurrent episodes of hypersomnia, compulsive eating behaviour and various psychopathological changes like hypersexuality, irritability or apathy. Hallucinations, delusions and ‘dreamy states’ are reported in 14–24 % of patients with KLS [93]. In fatal familial insomnia, a variant of Creutzfeldt–Jakob disease (CJD), progressive insomnia is coupled with an oneiric stuporous state in which patients perform complex, jerky movements that correspond to dream content which patients are later able to report [94]. Dream/reality confusion with hallucinations also occurs in sporadic CJD [95].

In populations without neurological disorders, excessive dreaming has been reported as a primary complaint in certain sleep clinics [96]. A study comparing these patients to controls revealed that complaints of excessive dreaming were related to significant microstructural changes, including increased arousals, intrasleep awakenings, period leg movements, alpha–delta sleep and REM density; however, no macrostructural changes were noted, and no differences in REM sleep and sleep onset latencies were apparent. Excessive dreamers were also found to be significantly more stressed, fatigued and anxious than controls, and to have more headaches.

Nocturnal seizures (and complex partial seizures in particular) sometimes present as recurring nightmares [97, 98]. Solms [12] identified 24 cases of this type in the literature and nine in his own series. Of theoretical interest is the fact that such nightmares typically occur during non-REM sleep. The content of the nightmares frequently coincides with that of the patient’s typical aura or ‘dreamy state’ seizures [12, 98, 99]. Penfield was able to artificially generate a waking aura resembling the recurring nightmare in one case by stimulating exposed cortex in the region of the epileptogenic focus [100–102]. Successful pharmacological or surgical treatment of the seizure disorder invariably results in disappearance of the recurring nightmares. These facts further support the interpretation of the nightmares in these cases as seizure equivalents (and indeed as non-REM phenomena).

As with dream/reality confusion (which frequently co-occurs with nightmares), increased frequency of nightmares is associated with a wide range of toxic and withdrawal states and metabolic abnormalities. The grounds for detaching these two ‘excesses of dreaming’ from each other are not entirely clear. The common denominator here may therefore, once again, simply be general degradation of constraints on consciousness.

It is important to note that nocturnal panic attacks and sleep terrors are not instances of nightmares. Detailed dream recall is often lacking in such attacks [103, 104], although in certain studies dream content has been reported [105].

In this disorder, dreamed behaviours are physically acted out. This is due to disruption of pontomedullary mechanisms that induce REM atonia [106]. The enacted behaviours may be dramatic or even violent, and usually relate to vivid, frightening dreams. A fair proportion of cases injure their bed partners [107]. The disorder is most common in males, and onset is often in the sixth or seventh decade. RBD manifests mainly in the second-half of the sleep cycle (where REM is predominant). Increased slow-wave sleep, and increased periodic limb movements across all sleep stages are also seen [107–111].

Of special interest is the association of RBD with the parkinsonian syndromes. The presence of RBD in PD patients is associated with cognitive deficits and appears to predict dementia [112, 113]. Disorders with Lewy body pathology often involve RBD. The incidence of RBD in PD is 25–50 % and more than 50 % in DLB and MSA. In contrast, disorders without Lewy bodies rarely involve RBD. Notably, idiopathic RBD may present many years prior to the other symptoms of an incipient parkinsonian syndrome [107, 113–118]. The prognostic significance of RBD as a precursor to PD, DLB and MSA is now well established, resulting in the suggestion that the term ‘cryptogenic’ RBD should replace ‘idiopathic’ RBD [109, 111, 119, 120].

DA circuitry is also central to reward processing. The mesocortical–mesolimbic (MC-ML) DA system is defined as the ‘system [that] is formed by dopamine neurons located in the ventral tegmental area … which project to the nucleus accumbens, prefrontal cortex, septum, amygdala, and hippocampus’ [123]. This system has been termed the SEEKING system by Panksepp [139] and it is thought to ‘drive and energize many mental complexities that humans experience as persistent feelings of interest, curiosity, sensation seeking’ (p. 145). It is also involved in reward processing, which refers to ‘an instinctual affective and exploratory drive to seek biologically-important stimuli in the external or internal (‘intrapsychic’) environment’ (Perogamvros and Schwartz, p. 1936) [140].

Perogamvros and Schwartz [140] have proposed the reward activation model (RAM) of dreaming, which postulates that reward processing during sleep may contribute to the consolidation of memories with a high motivational/emotional relevance, as well as aid in the modulation of REM sleep through projections to REM generating brainstem structures. Due to the strong interconnections between the hippocampus and the ventral tegmental area—which drives DA activity in the MC-ML circuits—RAM proposes that activation of the hippocampus during sleep may stimulate the VTA and lead to reward activation during sleep; in turn, VTA activity can lead to the reactivation of certain memories in the hippocampus. It is thought that during SWS in particular, the reactivation of the ventral striatum and the hippocampal complex allows for the consolidation of ‘memory-reward associations’ [141]. Therefore—and as originally proposed by Freud [142]—‘the fabric of the dream-thoughts is respolved into its raw material’ (p. 543).

In support of motivational theories of dreaming are studies of addiction, which has been associated with activity in the MC-ML dopamine system [143]. It is common for abstinent drug addicts to have increased dream content related to finding and taking drugs, a phenomenon that Johnson [144] first termed ‘drug dreams’. As many as 80 % of acutely abstinent drug addicts experience drug dreams [145], which is related to drug craving in addicts and previous drug users [146–149]. Drug craving can be triggered by cues related to drug taking, both conscious and unconscious [150]. These types of drug-related cues have also been shown to be associated with the subsequent occurrence of drug dreams [151, 152]. In the absence of these drug-related cues, drug dreams tend to dissipate [145]. Drug dreams persist in drug addicts undergoing pharmacological treatment during abstinence, such as methadone treatment in heroin addicts and nicotine gum in smokers [153], (indicating that drug dreams do not merely result from physical withdrawal, but rather are a type of psychological withdrawal [145]. Furthermore, up-regulation of the MC-ML dopamine system—as measured indirectly by the Limbic System Activity Scale—has been associated with drug dreams [154]. The association between this up-regulation of the MC-ML dopamine system and the presence of drug dreams provides further evidence for this system’s role in the motivational aspects of dream genesis [145]. This line of research has been used to argue that not only is the DA system involved in dream genesis, but that the content of drug dreams favours a motivational impetus for dream genesis [144, 155].