Biomedical subjects
Publications and source records attributed to G Coccagna.
After 1 year of exposure to trichloroethylene, reversible neuropsychological impairment and persistent EEG paroxysms were observed in one patient. The improvement of neuropsychological performances and the persistence of severe EEG abnormalities after withdrawal of the toxin suggest "functional" cerebral damage after prolonged exposure to trichloroethylene.
In order to evaluate autonomic nervous system changes occurring before nocturnal headache attacks, we studied three subjects (one male, two females) suffering from chronic migraine. All three patients underwent a nocturnal polygraphic recording including continuous monitoring of systemic arterial pressure and heart rate. Two subjects showed increases and irregularities of arterial pressure before awakening with headache. These changes began during N-REM sleep and lasted during REM sleep preceding the awakening with headache. Heart rate did not change before the attacks. These findings do not support the hypothesis that autonomic instability during REM sleep represents the precipitating factor of the attacks.
In a case of common migraine and in two cases of cluster headache we monitored the arterial pressure and the heart rate by means of polygraphic recordings before, during and after headache attacks. During migraine attacks the arterial pressure did not show significant changes; the heart rate increased. During cluster attacks the arterial pressure increased with frequent hypertensive peaks; the heart rate on average slowed down and showed marked irregularities.
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Polygraphic findings during spontaneous nocturnal sleep of 2 patients suffering from Shy-Drager syndrome are reported. In both patients, total sleep time was reduced--sleep latency and awakening periods during the night being increased. Considerable reductions of rapid eye movement (REM) stage and, in 1 patient, also of deep non-REM (NREM; stages 3-4) were found. No apneas were recorded. In normal subjects, systemic systolic and diastolic pressure decreases during all the sleep stages; in our patients, arterial pressure values rose progressively during NREM sleep stages and showed a further increase in REM sleep. In all the sleep stages, sudden phasic swings of systemic arterial pressure were observed.
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Patients suffering from Pickwickian syndrome or primary hypoventilation syndrome present apneas of a predominantly obstructive type which follow one another without interruptions throughout the duration of sleep. It is not possible to ascribe the somnolence of these patients to carbonarcosis, because in most cases Pa CO2, though high during sleep, presents normal values or slightly higher than normal values during wakefulness. Obstructive apneas are the cause of this syndrome: the elimination of obstructive apneas by means of tracheostomy leads to a complete clinical recovery. Before they began to suffer from hypersomnia, all these patients had been snoring heavily for many years. Snoring is therefore a fixed stage in the evolution of this disease. The fact that the overall clinical and polygraphic characteristics of these syndromes are identical suggests that they all constitute a single nosographic entity, which we have called "hypersomnia with periodic apneas".
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Twenty-one prepubertal children of small stature, 10 boys and 11 girls, aged from 4-3 to 12-8 years, were studied. Their height was less than 3rd centile, and during the preceding year all had a growth rate less than 4-5 cm/year. Arginine and L-dopa tests were given, and the release of growth hormone (GH) during monitored sleep was investigated. On the basis of the electroencephalogram and horizontal electro-oculogram, sleep was divided into stages 1-2-3-4 and rapid-eye-movement. All the children had a GH response greater than 8 ng/ml in at least one of the two pharmacological tests, and were therefore accepted as not suffering from GH deficiency. In all 21 children during sleep there was at least one secretory peak with GH greater than 8 ng/ml. Of a total of 46 secretory peaks recorded, 22 (48%) took place during deep, slow sleep (stages 3-4), 10 (22%) during light sleep (stage 2), 10 (22%) during REM sleep, and 4 (8%) during wakening. In 4 patients (19%) no secretory peak was observed during stages 3-4, even though there were peaks at other times. The data (a) show that it is essential to monitor GH throughout the night to ascertain with certainty the presence or absence of physiological secretory peaks of GH; (b) emphasise the rare disagreement between pharmacological and physiological tests; (c) suggest the use of this physiological test for GH secretion in those cases where the insulin test may be hazardous.
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.
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We describe a syndrome characterized by acquired micrognathia, hypersomnia, and periodic apneas during sleep. Six patients affected with the syndrome underwent nocturnal and diurnal polygraphic recordings that demonstrated that during sleep there is an uninterrupted succession of apneas, primarily the obstructive type, analogous to those observed in Pickwickian syndrome. Simultaneous recording of pulmonary and systemic arterial pressure during sleep and repeated blood gas analyses have shown that as soon as the apneas appear there is a decisive increase in pulmonary and systemic pressure and serious alveolar hypoventilation. The hemodynamic and ventilatory changes are even more intense during rapid eye movement sleep. Tracheostomy, performed on five of our patients, is the only treatment producing complete clinical remission of the syndrome.
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.