Journal of Sleep Disorders: Treatment and CareISSN: 2325-9639

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Short Communication, J Sleep Disor Treat Care Vol: 7 Issue: 1

Brain Lesions and Sleep Onset REM Periods in Routine EEG

de Amorim IL1*, Silva C1, Peralta AR1-3 and Bentes C1-3

1Department of Neurosciences and Mental Health (Neurology), Portugal

2EEG/Sleep Laboratory, Hospital de Santa Maria-CHLN, Portugal

3Faculty of Medicine, University of Lisbon, Portugal

*Corresponding Author : Isabel Loucao de Amorim
Department of Neurosciences and Mental Health (Neurology). Hospital de Santa Maria, CHLN, Avenida Professor Egas Moniz, 1649-035 Lisbon, Portugal
[email protected]

Received: July 12, 2017 Accepted: February 20, 2018 Published: March 04, 2018

Citation: de Amorim IL, Silva C, Peralta AR, Bentes C (2018) Brain Lesions and Sleep Onset REM Periods in Routine EEG. J Sleep Disor: Treat Care 7:1. doi: 10.4172/2325-9639.1000205


Rapid eye movement (REM) sleep usually occurs after 90 minutes of consolidated sleep. Sleep onset REM Period (SOREMP) occurs when REM sleep latency is less than 15 minutes. It is a rare phenomenon, mostly associated with sleep deprivation and narcolepsy. Patients undergoing routine Electroencephalogram (EEG) studies for other reasons than sleep disorders can occasionally have SOREMPs. The objective of this study was to determine the frequency of patients with SOREMPS in routine EEG and to evaluate its possible etiologies. This is a retrospective study of all EEGs performed in the EEG/sleep laboratory from Hospital de Santa Maria-Lisbon, during last 6 years. EEGs with REM sleep were selected. Both ambulatory and EEGs performed in the acute setting were included along with Data for cranial CT-scan or MRI. In 6 years, only 8 patients had SOREMPs, among them, it was possible to obtain cranial MRI or CT-scan in 7 patients (one died). One patient with a psychiatric disorder, showed no lesions on MRI. The other 6 had lesions involving brainstem (n=5) or diencephalon (n=1). The etiologies were inflammatory (2), vascular (3) and infectious (1). All lesions except one were acute. These results suggest that when SOREMPs are detected, lesions involving REM sleep structures should be searched for.

Keywords: Sleep onset; REM periods; Rapid eye movement


Dement et al. [1] described in 1957 that NREM (non-REM) and REM (rapid eye movement) sleep alternate in a cyclic fashion every 90 minutes throughout the night. Sleep onset REM periods (SOREMPs) occurs when REM sleep latency is less than 15 minutes [2]. SOREMPs are a rare phenomenon that was first described by Vogel et al. [3] in 1960 and subsequent linked to narcolepsy by Rechtschaffen et al. [4] in 1963. Some years later, these reports were brought into question by studies in healthy young adults, as well as in patients with frequent periodic limb movements and sleep apnea, among whom multiple SOREMPs were found to be relatively common [5]. Recent data suggests that multiple SOREMP are not pathognomonic for narcolepsy [6]. In fact, presence of multiple SOREMPs supports the diagnosis of narcolepsy. However, other causes have to be excluded including drug withdrawal, REM sleep deprivation, obstructive sleep apnea and alcoholism, use of antidepressant therapy, major depression and circadian rhythm sleep-wake disorders [7-10]. Some reports also linked SOREMPs with different diseases like Prader-Wili syndrome, Kleine-Levin syndrome, Parkinson disease and periodic limb movements of sleep [11-14].

Patients undergoing routine Electroencephalogram (EEG) studies for other reasons than sleep disorders can occasionally have SOREMPs. In the literature there is no data regarding the diagnostic value of this finding. The objective of the present study was to determine the frequency of patients with SOREMPS in routine EEG and to evaluate its possible etiologies.


This is a retrospective study of all EEGs performed in the EEG/ sleep laboratory of the Department of Neurosciences and Mental Health of Hospital de Santa Maria-CHLN in Lisbon, during a period of 6 years (between 2010 and 2016). All routine EEGs (at least 30 minutes) and EEGs with sleep deprivation protocol (at least 60 minutes) were included, either from outpatient or inpatient studies. All of them included at least 19 EEG (10/20 International System), 2 EOG (Electrooculography), 1 ECG (Electroencephalography) and sometimes, 1 to 2 EMG (Electromyography) channels. All records were performed by experienced neurophysiology technicians and interpreted by clinical neurophysiology and semiology expert medical doctors (ARP+CB). Different variables were analyzed: Reason for the EEG, Accompanying neurological symptoms, Etiology of the disorder (namely in the acute setting), CT scan (cranial tomography scan) or MRI (magnetic resonance imaging) findings, Concomitant disorders, Usual medication, Medication at the time of the EEG and presence of sleep symptoms or sleep disorders upon follow up.


From 8712 EEGs performed over 6 years, only 8 patients had SOREMPs (0.09%). All of them occurred during routine EEGs without sleep deprivation protocol. They happened only in hospitalized patients, in the acute phase of central nervous system disorders.

All patients performed the EEG due to consciousness disturbance. It was possible to obtain cranial MRI or CT scan in 7 patients (87.5%). One patient died before brain imaging. Imaging exams and EEGs were performed at the same investigation period. All except one patient had acute lesions involving the brainstem and diencephalus. MRI and CT scan lesions, etiologies and other patient variables are showed in Figure 1.

Figure 1: Characterization of all 8 patients about EEG, neurologic symptoms, imaging, personal background, medication at home and on EEG time and follow up. * Days of hospitalization until the EEG.

In four patients, the EEG was performed during neuroleptics/ antidepressive and benzodiazepines deprivation. These included the only patient whose MRI did not disclose any lesion, a patient with previous psychiatric pathology to whom usual medication with anafranil and olanzapine had been interrupted.

Neither of the 8 patients had personal background of sleep disorders.

It was possible to obtain follow-up information in 5 patients, 4 of whom died in the acute phase of the disease and 1 that did not report sleep problems.


This study shows that SOREMPs in routine EEGs and sleep deprived EEGs are rare. In fact only 0.09% of all the EEGs from our lab showed SOREMPs.

In multiple sleep latency tests, SOREMPS are mostly associated with narcolepsy, sleep deprivation and drugs withdrawal. The most striking finding of our study is that, in our sample of patients referred for routine EEG, 6 out of 8 patients presented with acute brain lesions in structures that play an important role in sleep wake cycle. In hospitalized patients, SOREMPs may, on a first glance, be attributed to the more common sleep [15] and drugs deprivation [16] associated to this setting. Our results argue against this possibility. As expected in an acute setting, 50% of our sample was deprived of drugs whose absence may cause REM rebound and SOREMPs and it is also reasonable to admit that sleep deprivation, though not accessed in our sample, due to the retrospective nature of our study, was also present. However, the infrequent occurrence of SOREMPs in all patients submitted to EEGs in our laboratory (many of which are inpatients, submitted to the same sleep and drug deprivation) and its close relationship to an acute lesion in brainstem and diencephalic structures argue for a causal effect between both phenomena.

The precise pathophysiological mechanisms of SOREMPs are not totally known, Some brain areas take a main role in REM sleep, like the brainstem and diencephalic structures. Of these areas, the dorsomedial pontine tegmentum assumes a significant role. This area lies adjacent and rostral to the sixth nerve nucleus and is known to be important for the generation of REM sleep [17]. At the same time, it is the origin of the cholinergic component of the ascending reticular activating system, which is crucial for maintaining wakefulness [18]. The ascending reticular activating system comprises the magnocelullar and dorsal raphe nuclei, with the rostrally adjacent nuclei reticularis pontis caudalis, coeruleus, laterodorsal tegmental and pedunculopontine nuclei. Recently, these nuclei, particularly the locus coeruleus, were shown to be the major synaptic target areas of the hypocretin [19,20]. Cases of symptomatic narcolepsy were described in patients with lesions of the hypothalamus, thalamus, midbrain, pons or other areas of the brain that are involved in REM sleep [21]. An isolated brainstem lesion may explain REM disturbances, like SOREMPs, but hypersomnia is more often observed in diencephalic lesions [22]. These structures represent areas that are involved in the hypocretin projection pathway [20] and the lesion of these pathways may lead to narcoleptic semiology, like SOREMPS. All our patients had concomitant consciousness disturbance, possibly due to impairment of the nearby reticular activating pathway. It is notable that this sign – SOREMPs in routine EEG, occurred in seriously ill patients, 50% of which died in the acute setting, suggesting a bad outcome.

In rare cases, chronic symptoms of narcolepsy can be seen during the course of a neurological disease process like vascular diseases, multiple sclerosis, head trauma, brain tumours, or degenerative disorders, if these diseases can cause lesions in strategic areas [17]. In our study, it was not possible to evaluate if this sign in the acute setting led to narcolepsy like symptoms upon follow up.

In summary, our data suggests that when SOREMPs are detected, especially in the acute setting in patients with concomitant consciousness impairment, lesions involving REM sleep structures should be actively looked for.


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