Giorgio Coccagna

Arterial pressure changes during spontaneous sleep in man

Abstract The systemic arterial pressure was measured continuously during spontaneous night sleep (using a catheter in the branhial artery) in eight normotensive subjects. The results can be summarized as follows: 1. 1. Arterial pressure decreased rapidly in the first part of the night and increased gradually in the second part. 2. 2. Pressure decreased progressively from when the subject was still awake to successive slow sleep stages: the difference in pressure between one stage and the next is significant. Pressure was slightly higher, but not to a significant degree, in REM stage than in stage 2. 3. 3. Variations of arterial pressure during a particular stage might be present both in stage 2 and in the REM stage. In stage 2, in some subjects, these variations became periodic from time to time, identifiable with the arterial pressure oscillations described by Sigmund Mayer; they were often accompanied by a respiratory periodicity. In the REM stage the increases in arterial pressure were more pronounced but not necessarily in relation to variations of arteriolar tone or of heart rate.

Some periodic phenomena arising during drowsiness and sleep in man.

In the course of numerous polygraphic recordings made on normal subjects and patients with sleep disturbances (Pickwickian syndrome, primary alveolar hypoventilation, restless legs syndrome and nocturnal myoclonus) we observed several vegetative and somatic phenomena which tended to oscillate or repeat themselves periodically every 20–30 sec during sleep, and especially during light sleep. The functional oscillations of this kind could involve the systemic arterial pressure, the pulmonary arterial pressure, cardiac rate, arteriolar tone, breathing, peripheral motoneurone excitability and the level of consciousness, both individually and simultaneously. It has been known for some time that systemic arterial pressure can present periodic oscillations at about every 30 sec (Meyer waves), especially in emergency situations; it has also been demonstrated experimentally that Mayer waves can be associated with periodic breathing and with cyclical oscillations of reticular tone, of pupil diameter and of the excitability of spinal motoneurones. During sleep, the physiological or pathophysiological situations which are the basis of these oscillatory phenomena could be represented by variations in pH, PCO2, and PO2 consequent on arterial hypotension or alveolar hypoventilation.

REM sleep behaviour disorder in Parkinson's disease: a questionnaire-based study

The aim of the study was to determine the clinical frequency and features of REM sleep behaviour disorder (RBD) in a large population of Parkinson’s disease (PD) patients using defined diagnostic criteria both for RBD and PD. Six trained neurologists used a semistructured questionnaire based on ICSD-R diagnostic criteria for RBD to evaluate 200 PD patients and their caregivers. Interobserver reliability for the diagnosis of RBD was “substantial” (Kappa 0.65). Five patients were excluded from the study because of an MMSE lower than 25. The demographic and PD clinical features were compared in the clinically defined RBD group and in those without RBD (NRBD). Then the RBD features during the last year were analysed in the affected group. Out of 195 patients, 66 fulfilled the ICSD-R criteria for RBD; 62 patients reported RBD during the last year (frequency 31.8%). RBD features: two or more episodes per week in 35.5%; upper limb movements in 87%; lower limb movements in 79%; vocalisations during events in 85%. RBD onset was before PD in 27% of patients; 69% of the RBD group had injured themselves or their caregivers during sleep. According to multivariate analysis, RBD was associated with male gender, age and PD duration. Brief training and the use of a semistructured questionnaire may help the neurologist in dealing with sleep disturbances in PD patients. The search for RBD symptoms in PD is highly recommended, especially in patients with a long disease duration, the risk of sleep-related injuries being high.

Motor pattern of periodic limb movements during sleep

Background: The pathophysiology of periodic limb movements in sleep (PLMS) in restless legs syndrome (RLS) is unclear. Objective: The authors neurophysiologically investigated PLMS in patients with idiopathic RLS in order to obtain information on the origin and pathophysiology of the movements. Methods: Ten patients with idiopathic RLS underwent electromyography with nerve conduction velocity (EMG-CV), somatosensory evoked potentials (SEPs), transcranial magnetic stimulation (TMS), nocturnal videopolysomnography, and multiple sleep latency test. The authors analyzed 100 consecutive PLMS for each patient to determine how frequently each muscle was involved in the PLMS; how frequently EMG activity started in a given muscle; and the time delay and pattern of activation between the first and the other activated muscles. Results: EMG-CV, SEPs, and TMS findings were all normal; in PLMS, leg muscles were those more frequently involved, often with alternation of side. Axial muscles were rarely and upper limb muscles sometimes involved. The tibialis anterior was the most frequent starting muscle. There was no constant recruitment pattern from one PLMS episode to another, even in the same patient. There was no ordinate caudal or rostral spread of the EMG activity. Conclusion: The recruitment pattern indicates the engagement of different, independent, and sometimes unsynchronized generators for each PLMS. The authors hypothesize an abnormal hyperexcitability along the entire spinal cord, especially its lumbosacral and cervical segments, as the primary cause of PLMS, triggered by sleep-related factors located at a supraspinal but still unresolved level.

Studies of penetrance and anticipation in five autosomal-dominant restless legs syndrome pedigrees

Restless legs syndrome (RLS) can occur with an autosomal‐dominant mode of inheritance. To determine if there are distinguishing features of RLS pedigrees which might clarify molecular mechanisms of pathogenesis, five pedigrees with 81 affected members were analyzed for age of onset, sex ratio, and transmission pattern. One‐factor analysis of variance of ages of onset between generations was carried out, and segregation ratios were calculated for each generation. These kindreds showed an autosomal‐dominant mode of inheritance and a male:female ratio of 1:1.4 (p = 0.15). One of the five analyzed pedigrees shows some evidence of reduced penetrance. In two of the five analyzed pedigrees, there is statistical support for anticipation (p < 0.05). These variations in penetrance and anticipation suggest possible genetic heterogeneity.

Sleep-related breathing impairment in myotonic dystrophy.

SummaryRespiratory failure has been described in myotonic dystrophy; it worsens during sleep but its central or peripheral origin has yet to be determined. Moreover, patients may present severely disturbed sleep and daytime somnolence. Eight patients with mild to moderate myotonic dystrophy were studied to assess breathing function while awake and during sleep by means of the pulmonary function tests, nocturnal polysomnographic examination and the multiple sleep latency test (MSLT). Three patients had restrictive respiratory defects; none had signs of airway obstruction. All patients had very disrupted nocturnal sleep. Of six patients who underwent the MSLT only two showed a mild tendency to sleep during the day. Six patients had pathological apnoea plus hypopnoea index [(A+H)I] and there was a prevalence of central apnoeas. The apnoeas occurred while resting but awake and throughout all sleep stages. Only two patients (the ones with the least vital capacity) had episodes of progressive oxygen desaturation during rapid eye movement sleep, similar to those found in other restrictive disorders and in chronic obstructive pulmonary disease. It is concluded that the breathing pattern characteristic of our myotonic dystrophy patients was the occurrence of central apnoeas both at rest while awake and during sleep.

Breathing During Sleep in Man in Normal and Pathological Conditions

This is a brief presentation of the data collected during ten years of research into the behavior of respiration, alveolar ventilation, and pulmonary and systemic arterial pressure during 1–8

Alveolar hypoventilation and hyperosmnia in myotonic dystrophy.

A case of myotonic dystrophy accompanied by alveolar hypoventilation and hypersomnia is presented. Radiological studies and EMG examination of the intercostal muscles demonstrated that the respiratory muscles were affected by the disease, while polygraphic recordings showed that the alveolar hypoventilation and pulmonary hypertension worsened during sleep. The hypersomnia preceded the appearance of clinical signs of the muscular disease by many years and persisted even after treatment when the blood gas analysis values were greatly improved. During both diurnal and nocturnal sleep, the patient frequently fell asleep directly into a REM stage. The possibility is discussed that, concomitant with the respiratory musculature involvement, there is an alteration in the central nervous system in myotonic dystrophy which is at least partially responsible for both the alveolar hypoventilation and the hypersomnia.

Stiff-man syndrome associated with nocturnal myoclonus and epilepsy.

A case of stiff-man syndrome associated with primary generalised epilepsy is reported. In addition, nocturnal polygraphic recording revealed a nocturnal myoclonus. Detailed examination of the central nervous system did not show specific changes. There is no direct proof as to a spinal or supraspinal origin of the stiff-man syndrome. The absence of specific anatomical lesions may indicate a functional rather than a structural disturbance in its physiopathogenesis.

Effects of tracheostomy in two cases of hypersomnia with periodic breathing.

Two non-obese patients suffering from hypersomnia with periodic breathing, who presented predominantly obstructive apnoea persisting throughout sleep, underwent tracheotomy with placement of a permanent tracheal cannula. Before tracheostomy there was a serious state of alveolar hypoventilation with a marked rise in pulmonary arterial pressure which appeared during sleep. After tracheostomy breathing during sleep became regular, pulmonary arterial pressure became normal, and daytime drowsiness disappeared. These observations suggest that the obstruction of the upper air tracts during sleep represents the most important factor in the pathogenesis of hypersomnia with periodic breathing.