Slow Eye Research Articles

Spontaneous attentional failures reflect multiplicative interactions of chronic sleep loss with acute sleep loss and circadian misalignment

ObjectivesAcute and chronic sleep loss and circadian timing interact such that, depending on their combination, small or very large performance decrements are observed in tasks of attention. Here, we tested whether such nonlinear interactions extend to a physiological measure of spontaneous visual attentional failures, indicating a fundamental principle of sleep-wake regulation. MethodsNine healthy volunteers completed an in-laboratory 3-week forced desynchrony protocol consisting of 12 consecutive 42.85-hour cycles with a sleep-wake ratio of 1:3.3. The protocol induced increasing chronic sleep loss, while extended wake (32.85 hours) and sleep episodes (10 hours) occurred at multiple circadian phases. Attentional failure rate was quantified from continuous electrooculograms (number of 30-second epochs with slow eye movements/h of wakefulness) as a function of time since scheduled wake (acute sleep loss), week of study (chronic sleep loss), and circadian (melatonin) phase. ResultsDuring the first ∼8 hours awake, attentional failure rate was low, irrespective of the week. During the following wake hours, attentional failure rate increased steadily but at a faster rate in weeks 2 and 3 compared to week 1. The effects of acute and chronic sleep loss on attentional failure rate were magnified during the biological night compared to the biological day. ConclusionsA single extended sleep episode can only temporarily reverse attentional impairment associated with chronic sleep loss. Multiplicative effects of acute and chronic sleep loss—further amplified during the biological night—substantiate the interaction of 2 homeostatic response mechanisms and caution against underestimating their disproportionate combined impact on performance, health, and safety.

Measuring optokinetic after-nystagmus: potential for detecting patients with signs of visual dependence following concussion

Concussed patients with chronic symptoms commonly report dizziness during exposure to environments with complex visual stimuli (e.g. supermarket aisles, busy crossroads). Such visual induced dizziness is well-known in patients with vestibular deficits, in whom it indicates an overreliance on visual cues in sensory integration. Considering that optokinetic after-nystagmus (OKAN) reflects the response of the central network integrating visual and vestibular self-motion signals (velocity storage network), we investigated OKAN in 71 patients [17 (23.9%) females, 30.36 ± 9.05 years old] who suffered from persistent symptoms after a concussion and presented clinical signs suggesting visual dependence. Data were retrospectively compared with 21 healthy individuals [13 (61.9%) females, 26.29 ± 10.00 years old]. The median values of the slow cumulative eye position and of the time constant of OKAN were significantly higher in patients than in healthy individuals (slow cumulative eye position: 124.15 ± 55.61° in patients and 77.87 ± 45.63° in healthy individuals—p = 0.012; time constant: 25.17 ± 10.27 s in patients and 13.95 ± 4.92 s in healthy individuals—p = 0.003). The receiving operating curve (ROC) estimated on the time constant had an overall area under the curve of 0.73. Analysis of the ROC suggests that a test measuring the OKAN time constant could obtain a sensitivity of 0.73 and specificity of 0.72 in determining the origin of the visual-related disturbances in those patients (threshold 16.6 s). In a subset of 43 patients who also performed the Sensory Organization Test (SOT), the proposed OKAN test was twice as sensitive as the SOT. This study suggests that concussed patients with persisting visual symptoms may have an underlying impairment of the velocity storage mechanism and that measuring the OKAN time constant can objectify such impairment.

The Clinical Significance of the Failure to Perceive Vertigo in the Postcaloric Period Despite a Robust Caloric Response.

Purpose The purpose of this project was to explore the association between the perception of motion during caloric testing and two tasks associated with central vestibular processing: postural stability and visuospatial memory. Method This was a prospective study of 25 patients who were found to have nonvestibular etiologies of their symptoms and normal vestibular function test results and who underwent caloric testing with a mean maximum slow phase eye velocity for each irrigation of 15° or greater. Following each caloric irrigation, patients were asked whether they had any sensation of movement. Patients were grouped based on the presence or absence of motion during the caloric exam (motion perception vs. absent perception). Postural stability was assessed using computerized dynamic posturography, and visuospatial memory was assessed using a memory match card game application. Results There were no significant differences between groups on any measures of peripheral vestibular function. However, the Absent Perception Group showed greater postural instability during Condition 5 of posturography and performed significantly worse on a task of visuospatial working memory. Both age and absence of motion perception predicted abnormal performance on measures of postural stability and visuospatial working memory. Conclusions There appears to be clinical implications to a lack of motion perception during the caloric exam in patients with an otherwise normal peripheral vestibular system. Based on the current findings, we are unable to determine whether differences in postural stability and visuospatial memory were due to age or a central vestibular processing deficit.

0069 Spectral Analyses of Slow Wave Sleep and Rapid Eye Movement Sleep are Associated with Changes in Continuous Nocturnal Blood Pressure

0069 Spectral Analyses of Slow Wave Sleep and Rapid Eye Movement Sleep are Associated with Changes in Continuous Nocturnal Blood Pressure

0193 Sleepiness and Slow Rolling Eye Movements are Increased During Autonomous Versus Manual Driving

0193 Sleepiness and Slow Rolling Eye Movements are Increased During Autonomous Versus Manual Driving

Clinical and genetic analysis of spinocerebellar ataxia type 7 (SCA7) in Zambian families

BackgroundTo date, 43 types of Spinocerebellar Ataxias (SCAs) have been identified. A subset of the SCAs are caused by the pathogenic expansion of a CAG repeat tract within the corresponding gene. Ethnic and geographic differences are evident in the prevalence of the autosomal dominant SCAs. Few descriptions of the clinical phenotype and molecular genetics of the SCAs are available from the African continent. Established studies mostly concern the South African populations, where there is a high frequency of SCA1, SCA2 and SCA7. The SCA7 mutation in South Africa (SA) has been found almost exclusively in families of indigenous Black African ethnic origin.ObjectiveTo present the results of the first clinical description of seven Zambian families presenting with autosomal dominant SCA, as well as the downstream molecular genetic analysis of a subset of these families.MethodsThe study was undertaken at the University Teaching Hospital in Lusaka, Zambia. Ataxia was quantified with the Brief Ataxia Rating Scale derived from the modified international ataxia rating scale. Molecular genetic testing for 5 types of SCA (SCA1, SCA2, SCA3, SCA6 and SCA7) was performed at the National Health Laboratory Service at Groote Schuur Hospital and the Division of Human Genetics, University of Cape Town, SA. The clinical and radiological features were evaluated in seven families with autosomal dominant cerebellar ataxia. Molecular genetic analysis was completed on individuals representing three of the seven families.ResultsAll affected families were ethnic Zambians from various tribes, originating from three different regions of the country (Eastern, Western and Central province). Thirty-four individuals from four families had phenotypic features of SCA7. SCA7 was confirmed by molecular testing in 10 individuals from 3 of these families. The age of onset of the disease varied from 12 to 59 years. The most prominent phenotypic features in these families were gait and limb ataxia, dysarthria, visual loss, ptosis, ophthalmoparesis/ophthalmoplegia, pyramidal tract signs, and dementia. Affected members of the SCA7 families had progressive macular degeneration and cerebellar atrophy. All families displayed marked anticipation of age at onset and rate of symptom progression. The pathogenic SCA7 CAG repeat ranges varied from 47 to 56 repeats. Three additional families were found to have clinical phenotypes associated with autosomal dominant SCA, however, DNA was not available for molecular confirmation. The age of onset of the disease in these families varied from 19 to 53 years. The most common clinical picture in these families included a combination of cerebellar symptoms with slow saccadic eye movements, peripheral neuropathy, dementia and tremor.ConclusionSCA is prevalent in ethnic Zambian families. The SCA7 families in this report had similar clinical presentations to families described in other African countries. In all families, the disease had an autosomal dominant pattern of inheritance across multiple generations. All families displayed anticipation of both age of onset and the rate of disease progression. Further clinical and molecular investigations of the inherited ataxias in a larger cohort of patients is important to understand the natural history and origin of SCAs in the Zambian population.

Slow eye movementsを呈した急性小脳性失調症の一例

Slow eye movementsを呈した急性小脳性失調症の一例

Doubt, and: Incorrigible

Doubt, and: Incorrigible Safiya Sinclair (bio) DOUBT I There’s nothing of the dinosaurs in these bones—no blue fern locked in the carbon fossil, spirals trillingon spirals recoiling; question collapsing on itself. Nothing carbon can claim to know of me;three-hocked hydra pressed neat in my iron bonebinding these ragged and unlikely molecules, echo clamming the garden dark as a bell,thickening the Sunday crows like old London’swretched rats, leaping and furring, giving birthto themselves. The sermon if you please, is disease. II Ring Gethsemane.I shall be late. Turning my handsabout some troubling verse,my bald body stretched over the silent ether, news of your illness,your boundless assassins. Still trying to pick a dim soundout the clamorous tomb, a bronze chimeI can fix my brow upon. [End Page 322] But somewhere in Kingstonyou are one with the mud,lungs graveled in limestone,mouth ajar, a jawbone stillbegging the silent answer. Only doubt unfurlsin the wind of disquiet; my bodythen too young and too unknowing, now wanting,only wanting to say yes. III Too late at this hour to weanyour heart’s wild membranestill boomed against that flickeringmemory. Against all my careful inventions of love.Blackness in.Blackness out— or something clever you might sayin the blue field where I dream you, wide vectors of tyrannosauruslocked with Nero’s crumbled spine. Where our whole beggaring rabbleis spinning to a blur, all these vast oceansstill coming to a boil. [End Page 323] IV Find my body now at its empty page.Blanched beyond the darkness. Think a thumbprint of sandin Eve’s mitochondria. Where I unburied my own shelland found there no great design.A plain boneto be cast off in a nameless storm;these atoms flung wide and reboundin the ocean’s keening, giving birth to my old selveson a faceless shore. [End Page 324] INCORRIGIBLE All night I wrestled with it—the onerous verse, trying to salt the wound;there are worse things one could fix a gloom upon, I suppose. But I fight to tack it down,the indefinite I, I, iamb; to tease this venom out—its cerasee vine grown thick as my hair, pulling at my limbs, the fur of my mouth.Opening my hand in the fissure of my throat,a gutted fish, I am raking rut out. Beached now on his shore,blanched bone-white, I am watching my grandfather stranglea bucket full of conger eels. Waist-deep in the sea’s phlegm, each finger a purposeful hook, today he is putting light out.From the almond dusk, sun-roasted stiff, spinningtheir brittle halves around, he offers each to me like an eager child, until something in the eel’s eye claps me shut—a dull movement I cannot comprehend. Needto trawl some meaning from our grief; to shake the vaguer shadows out—to rack the placewhere something once moved. Suck the marrow out.Pity the body who knows itself gone apart. How shaking his rough hands gentle round my head,grandfather laughs like a loon, wolf-throated,snapping this stasis like a nylon line. A frightened net of sparrows comes loose in the air;weaving through a thicket of sandflies, picking life out.Are they watching us? Ourselves one drunk [End Page 325] sound in the soundless sea. Grandfather, dizzying.Pity the owl-moth that struck with all its might,night’s shutters unopening. Moon at my window, one slow eye, known-woundI am salting as proof of existence. Pine this self amongst the greenAdirondacks, its blank hem of fog unfurling where something else movesin the eye’s swift blink—beneath its greying leaves,life’s dark unstirring flashed its incorrigiblescream of light. [End Page 326] Safiya Sinclair SAFIYA SINCLAIR was born and raised in Montego Bay, Jamaica. Her first full-length collection, Cannibal (University of Nebraska Press, 2016), won the 2015 Prairie Schooner Book Prize in Poetry. She is the recipient of a 2016 Whiting Writers’ Award and a 2015 Ruth Lilly & Dorothy Sargent Rosenberg Fellowship from...

Modeling the formation and dynamics of cortical waves induced by cholinergic modulation

States of arousal, or consciousness with the brain are regulated largely by the neurotransmitter acetylcholine (ACh). Specifically, ACh is likely responsible for the transition between slow wave sleep (SWS; where ACh is absent) and rapid eye movement sleep or waking states (where ACh is high). Patterns of neural activity within the cerebral cortex corresponding to these states are markedly different. During SWS there are traveling waves of intense activity in the cortex while in other states locally organized stationary patterns occur [1]. From a functional perspective, stationary patterns are likely to be important for working memory and attention dynamics while traveling waves could lead to synaptic renormalization [2]. The mechanism for how changes on the cellular level are translated to patterns on the network level is not understood. In this work we give a model for the action of ACh on a network of neurons of the Hodgkin-Huxley type with a current that is regulated by ACh that induces spike-frequency adaptation (SFA) [3]. The cells are coupled in a center-surround scheme. When SFA is minimal (such as in waking or REM sleep state, high ACh) patterns of activity are localized and easily pinned to regions defined by enhanced recurrent excitation. Increasing the level SFA is present (by increasing ACh), traveling waves of activity naturally arise. Depending on the strength of inhibitory coupling within the network, SFA is able to induce a wide variety of dynamical regimes (Figure ​(Figure1).1). We present a detailed mechanism that shows that the level of inhibition sets the spatial extent of network activity and that SFA defines the temporal scope, which is directly modulated by ACh in the model. These model calculations give unique insights into the role and significance of ACh in determining patterns of cortical activity and functional differences arising from these patterns. Figure 1 An illustration of the dynamics sampled by scannig inhibitory strength,(wi e), and gKs . In this model gKs is increased to simulate decreasing ACh levels. In a general sense, the spatial scope of activity is determined by the excitatory/ inhibitory balance, ...

Functional Consequences of Slow Drift Fixational Eye Movements in Patients with Central Vision Loss

Functional Consequences of Slow Drift Fixational Eye Movements in Patients with Central Vision Loss

EVALUATION THE STATUS OF SLEEP QUALITY IN ELDERLY PEOPLE IN KERMANSHAH CITY

Background and Aim: Sleeping is composed of two physiologic mode of slow and fast eye movement. Sleeping disorder in elderly people can cause different side effects such as falling, depression, mind disorders, irritability, tiredness, concentration problems, and so on. Current study was done with the aim of determining sleep quality among elderly people in Kermanshah. Materials and Methods: This current survey is a cross-sectional descriptive study which was performed among 100 elderly people in Kermanshah in 1392.The sample was selected according to the simple random sampling among the elderly people settling in Mehregan Sanatorium of elderly. The tools used for data collection were a questionnaire consisted of two demographic information parts and a questionnaire of Pittsburgh sleep standards, which were completed after interviewing the participants. Data was analyzed using SPSS16 software. Results: Mean age of participants was 66.7% ±2.7% years old. Most of the participants (67%), were undereducated. Half of them were women and the other half were men. 77.6% of participants were married and the others were single, widow, or got divorce. 10.2% reported having mental disorders history. 4.1% of participants in this study had used drugs before according to the achieved information from questionnaire. 39.8% of participants had moderate and 24.5% of them had severe sleep quality problems. Conclusion: The findings show that prevalence of improper sleep quality among elderly people is increasing which can cause serious problems. So, identifying effective factors in sleep quality in elderly people and designing proper intervention based on those factors in the direction of improving the quality of elderly people are suggested. Key Words: Elderly people, sleep quality , Kermanshah.

Preoperative sleep quality and inhalation anesthetic requirements: a sleep electroencephalography study

Background On the night before surgery, poor sleep quality due to anxiety is a frequently encountered problem. Objective This study aimed at determining the effect of preoperative sleep quality on intraoperative isoflurane requirements in patients undergoing elective surgeries and also offers an electroencephalography (EEG)-based classification of sleep quality. Patients and methods Twenty-seven adult male patients scheduled for elective open cholecystectomy with ages ranging from 20 to 40 years were included in this study. The night before the operation, the patients were subjected to an at least 8 h sleep EEG, which was scored for the following: total sleep time, percentage of slow wave sleep, and percentage of rapid eye movement sleep. Intraoperative isoflurane requirements were determined by recording the amount of inspired isoflurane concentration (every 2 min) needed to achieve an intraoperative bispectral index value between 40 and 60. Patients were classified according to sleep EEG into good sleepers and bad sleepers. Isoflurane requirements were first correlated with the EEG and then compared between the two groups. Results The inspired concentration of isoflurane in good sleepers was 1.15% (1.01-1.22%), whereas in bad sleepers it was significantly lower, at 0.99% (0.87-1.18%) ( P = 0.003). There was a positive correlation between isoflurane requirements and both slow wave sleep percentage ( r = 0.693; P = 0.003) and rapid eye movement sleep percentage ( r = 0.687; P = 0.005). Conclusion Patients suffering from poor sleep quality on the night before surgery need less intraoperatively inspired isoflurane concentration. This finding may have clinical importance in adjusting the isoflurane dose to meet patients' requirements, avoiding intraoperative complications. In addition, an EEG-based classification of sleep is offered.

Speedy eye movements in multiple sclerosis: Association with performance on visual and nonvisual cognitive tests

Objective: Eye movement difficulties in multiple sclerosis (MS) are common and may influence performance on cognitive tests. The following studies examined associations between a new measure of speedy eye movement speed and visual/nonvisual cognitive tests. Method: In Experiment 1, MS patients (N = 71) were administered cognitive tests and the Speedy Eyes Test (SET) as a measure of purposeful speedy eye movements under timed conditions. Experiment 2 was composed of MS patients (n = 60) and a neurologically healthy comparison group (n = 31) and examined group differences in an abbreviated version of the SET. Results: In both studies, slower eye movements were significantly associated with poorer performance on cognitive tests with a large effect size in Experiment 1 and a medium effect size in Experiment 2. Analyses in Experiment 2 also revealed significant group differences in an abbreviated measure of the SET, where MS patients had slower eye movements than the comparison group. Conclusions: Pending further research, the SET, a brief, inexpensive, and nontechnical measure of speedy eye movement, may serve as a visual/oculomotor indicator of cognitive impairment in multiple sclerosis.

Slow eye movement analysis in patients with obstructive sleep apnea/hypopnea syndrome

To determine whether slow eye movement (SEM) analysis performed comparably to standard sleep onset criteria at the multiple sleep latency test (MSLT) and the maintenance of wakefulness test (MWT) in patients with obstructive sleep apnea/hyponea syndrome (OSAHS). We compared SEM latencies with sleep latencies upon analysis of MSLT and MWT recordings artificially, in a population of 20 severe OSAHS patients that randomly underwent the 2 tests 2 days apart. They all answered the Epworth Sleepiness Scale. Mean SEM latency was different from standard sleep onset in the MSLT [(4.2 ± 1.9) min vs (5.3 ± 2.0) min, P < 0.001], and the MWT [(12 ± 10) min vs (13 ± 10) min, P < 0.001]. Mean SEM latency correlated significantly with the sleep latency at the MSLT (r = 0.958, P < 0.001) and at the MWT (r = 0.997, P < 0.001). Finally, the Epworth Sleepiness Scale score correlated with SEM latency at the MSLT (r = -0.580, P = 0.007), but not at the MWT. SEM latency was different from sleep latency that detected from EEG, but they correlated significantly with each other, thus providing a simplified way to evaluate sleepiness.

Effects of endolymphatic sac decompression surgery on endolymphatic hydrops

Conclusions: The present findings suggest that complete control of vertigo after endolymphatic sac decompression surgery (ESDS) does not always depend on improved vestibular function or reduced endolymphatic hydrops. Vertigo control is, however, associated with hearing stability.Objective: Among surgical treatments for intractable Meniere’s disease, ESDS is performed to preserve and improve inner ear function. We examined the correlation between changes in vertigo frequency and neuro-otologic function to understand the condition of the inner ear in patients whose vertigo was completely controlled after undergoing ESDS.Methods: This was a retrospective cross-tabulation study. Between 1997 and 2001, we treated 52 patients with intractable vertigo using ESDS and followed the patients regularly for 2 years. Postoperatively we evaluated and recorded changes in vertigo attack frequency, maximum slow phase eye velocity, worst hearing level, and glycerol test results according to modified American Academy of Otolaryngology–Head and Neck Surgery 1995 criteria.Results: We found no correlation between vertigo control and vestibular function. There was also no correlation between vertigo control and negative conversion of the glycerol test. There was a significant correlation between vertigo control and hearing control .

A Psychomotor Test for Assessment of Visuomotor Coordination during Performance of a Monotonous Target-Tracking Activity

Visuomotor coordination is required for successful performance of activities. Different types of tasks, such as getting into cars or working in static conditions require various coordination patterns with different levels of interaction between eye and hand movements. A psychomotor test was developed for analysis of impairments to visuomotor coordination induced by decreases in the level of arousal. The test is as follows: a small round spot (14 mm in diameter) was used as the target spot, and this moved across a monitor screen at a constant slow rate (12 mm/sec) in a circular orbit of diameter 70 mm with a period of 20 sec. Subjects were told: “Keep the mouse cursor inside the target object. If the cursor comes out of the moving target, this will be counted as an error.” Subjects’ reactivity levels were tested by introducing occasional presentations of an additional moving target, which had to be caught with the mouse as quickly as possible, with a click of the mouse button. The trajectory of the mouse cursor was recorded with a time resolution of 120 Hz. Eye movements were recorded using a contactless eye movement video detection system (Eyegaze Development System, LC Technologies, USA), which is based on reflection of infrared light from the cornea and allows the coordinates of gaze direction to be measured with a time resolution of 120 Hz. The monotonous nature of the test decreased the level of arousal and induced a drowsy state, which led to the occurrence of errors 30–40 min from the start of the experiment. The dynamics of the physiological level of arousal were identified electroencephalographically. Analysis of the time characteristics of slow tracking and fast saccadic eye movements and of hand movements showed them to be highly sensitive to decreases in work capacity induced by decreases in the level of arousal. Further development of this approach will facilitate the development of a contactless method for the rapid diagnosis of critical levels of drowsiness and for identifying the professional characteristics of human operators requiring high levels of visuomotor coordination.

Visual influence on the slow oscillatory eye movement discovered during a visual fixation task

A slow oscillatory movement (SOM) has previously been discovered superimposed on the three well known components of fixational eye movements. The purpose of the present study was to explore the visual influence on the control mechanism of the SOM. Three tests with different fixation targets and backgrounds were prepared. The eye position during a fixation task on healthy test subjects has been recorded by the Chronos eye tracking device. The visual stimuli with no or less information triggered larger SOM amplitudes. None of the investigated conditions significantly influenced on SOM frequency.

On-off asymmetries of responses to caloric step stimuli

Rapid head movement was combined with continuous caloric irrigation of the external ear to evaluate the time courses of the on-step (null-to-supine repositioning) and off-step (supine-to-null repositioning) vestibulo-ocular reflexes (VOR) responses in eight healthy subjects. During continuous air-caloric irrigation, each subject's head was positioned with his/her lateral semicircular canal alternately placed in the null (horizontal) and activating (vertical) planes, and the time course of the slow phase eye velocity was evaluated. The resulting responses were characterized by estimates of activation and adaptation components, and their amplitudes and time constants were calculated. Comparisons of the on-step and off-step responses revealed the activation and adaptation components of the VOR to have similar amplitudes. On the other hand, the time constant for the activation component was prolonged for the off-step response, while that for the adaptation component was shortened. Null-to-supine and reciprocal vestibular stimulation during continuous caloric irrigation of the external ear canal elicited asymmetric VOR responses that exhibited differing time courses.

A case of apogeotropic nystagmus with brainstem lesion: An implication for mechanism of central apogeotropic nystagmus

We report a case showing apogeotropic nystagmus with the lesion of the brain stem, and discuss a possible mechanism of central apogeotropic nystagmus. The case was a 73-year-old male. We analyzed his nystagmus three-dimensionally. He showed apogeotropic nystagmus. Axis angles of slow phase eye velocity of his apogeotropic nystagmus were not in line with the axes perpendicular to the plane of horizontal semicircular canals, but with the patient's vertical axis. We then found that his nystagmus including the apogeotropic nystagmus was positioning, but not positional and that the direction of his positioning nystagmus was the same direction of postrotatory nystagmus after his head movement. His MRI scans showed an infarction around the prepositus hypoglossi nucleus of the brain. His apogeotropic nystagmus seemed to consist of a combination of prolonged postrotatory nystagmus after his head rotation to the left and right lateral position because the axis of postrotatory nystamus was in line with the axis of the head rotation. Therefore, it is suggested that a possible mechanism of central apogeotropic nystagmus is a prolonged postrotatory nystagmus after his head movement in the supine position due to the brain lesion involving the velocity storage mechanisms.

Topographical distribution of the locus coeruleus and raphe nuclei in the lizard Ctenosaura pectinata: Functional implications on sleep

The nature of sleep in reptiles has traditionally created intense discussion and has originated some controversy. Nevertheless, some authors have described a sleep phase analogous to sleep in endotherm vertebrates. It is known that in mammals, the locus coeruleus and raphe nuclei, located in the brain stem, are functionally related to the sates vigilance regulation. In contrast the presence of two sleep phases in the lizard Ctenosaura pectinata similar to slow wave sleep and rapid eye movement sleep have been described. Therefore we carried out studies of the brain stem of C. pectinata to search for cellular groupings related to the regulation of these sleep phases. We identified and described the topographical distribution of the locus coeruleus and raphe nuclei in the lizard C. pectinata. Results show that these nuclei that have been functionally related to vigilance states in mammals, are also present in C. pectinata. These nuclei are formed by fairly well defined cellular groupings placed in the brain stem.