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PubMed1992

[Fulminant meningoencephalitis due to Listeria monocytogenes].

We present a case of meningoencephalitis due to Listeria monocytogenes type IV in a patient in which the diagnosis of small-cells malignant diffuse non-Hodgkin's lymphoma had been established. He was hospitalized with vague clinical manifestations and without showing any neurological focus. Hours later, he presented clinical brain stem semiology. Within a 24-hour period, Listeria monocytogenes was isolated from blood and cephalorhachidian fluid (being the first time that this microorganism had been isolated for the past 20 years in our laboratory). The patient evolved to a state of coma, with Cheyne-Stokes's respiration, abolition of pupillary reflexes, decerebration position and exitus laetalis. The affection of the central nervous system has been fully documented. However, its fulminant presentation, as in the case that we present here, is less frequent, although it has been described in the literature by other authors, like Finegold et al., with cases in which the interval between the onset of the neurological focality and death ranged from 8 to 16 hours. The antibiogram showed a wide sensibility to several groups of drugs, despite the fast evolution of the disease that prevented the modification of the initial antibiotherapy (Vancomicine and imipenem).

Acute Disease↗
PubMed1992

Right and left ventricular functional impairment and sleep apnea.

Obstructive sleep apnea may contribute to the development of pulmonary hypertension and RVF primarily through pulmonary vasoconstriction secondary to hypoxia. Several recent studies indicate, however, that intermittent apnea-related hypoxia is not sufficient to cause sustained pulmonary hypertension. These studies have been consistent in showing that pulmonary hypertension and RVF are almost invariably seen in the presence of diurnal hypoxia. Sustained pulmonary hypertension, therefore, appears to be associated with sustained hypoxia as is the case in COPD. Patients with OSA who have hypoxia while awake are, as a rule, obese and have mild-to-moderate diffuse obstructive airways disease. Thus, most cases of pulmonary hypertension in association with OSA result from a combination of OSA, obesity, and diffuse obstructive airways disease, a so-called overlap syndrome. However, from the therapeutic viewpoint, it is apparent that treatment of OSA by NCPAP or tracheostomy, in such cases, is usually sufficient to reverse pulmonary hypertension and RVF. More recent work has provided strong evidence that OSA can play a role in the pathogenesis of LV heart failure in patients with CHF of otherwise unknown etiology. It is likely that this occurs through a combination of increased LV afterload related to exaggerated negative Pit swings during obstructive apneas, to intermittent hypoxia, and to chronically elevated sympathoadrenal activity. Reversal of OSA by NCPAP in these patients may relieve LV heart failure. These findings add a new dimension to our understanding of the pathophysiologic effects of OSA on the cardiovascular system by demonstrating that the LV is a structure that may suffer functional impairment secondary to the stresses imposed by OSA. Finally, it has now become apparent that CSR in patients with CHF can cause symptoms of a sleep apnea syndrome when associated with intermittent hypoxia and arousals from sleep. Reversal of CSR during sleep by NCPAP can lead to alleviation of these symptoms and possibly to reduced cardiac dyspnea and LV systolic function as well. Taken together, this suggests that much more extensive use of polysomnography may be warranted in the investigation of cardiovascular disease. The reasons are compelling: sleep apnea disorders are common and eminently treatable conditions whose reversal can result in improved right and left heart function and symptomatic improvement in patients with impaired myocardial function.

Cheyne-Stokes Respiration↗
PubMed1991

[Oxygen saturation and sleep structure in patients with dilated cardiomyopathy].

It is known that patients suffering from severe cardiomyopathy may develop cyclic changes in breathing (Cheyne-Stokes-breathing) (2, 3). Coughing and dyspnea may be linked to periodic breathing. Specific detailed polysomnographic studies of sleep architecture and oxygen saturation have not been published. Eight patients suffering from dilatative cardiomyopathy (NYHA III-IV) were studied by pulse oximetry and polysomnography. Six of eight patients had severe breathing irregularities. These disturbances became manifest partially as Cheyne-Stokes breathing, partially as central sleep apnea. During these periods, oxygen saturation dropped as far as to 65 per cent of the original level.

Adult↗
PubMed1989

[Pathophysiology of dyspnea].

The sensation of dyspnea is related to pathologically increased breathing work as a result of hyperventilation and/or increased airway resistance. Low cardiac output resulting in tissue hypoxia provokes hyperventilation. In diffuse interstitial lung diseases, hyperventilation is combined with severely reduced lung compliance. In severe airway obstruction, hypoventilation is the result of excessively enhanced breathing work. Habituation and acute changes of situation have an important bearing on the subjective sensation of dyspnea.

Airway Resistance↗
PubMed1987

[Leigh's subacute necrotizing encephalomyelopathy due to decreased activity of the pyruvate dehydrogenase complex].

A new patient with Leigh's syndrome (subacute necrotizing encephalomyelopathy due to pyruvate dehydrogenase complex deficiency) is presented. A Turkish boy of consanguinously married healthy parents developed progressive muscle weakness since infancy. At the age of 3 years he was unable to sit, stand or walk. Clinical examination showed general muscle weakness, hypotonia, muscle hypotrophy, bilateral ptosis, partial bilateral external ophthalmoplegia, nystagmus, intention tremor and hypoactive tendon reflexes. The EEG showed diffuse slowing, the cerebral CT scan disclosed mild hydrocephalus e vacuo. Motor nerve conduction velocity was slightly decreased, the EMG revealed signs of neuropathy. In the biopsied muscle only a mild hypotrophy of type 2 fibres was found, no abnormal mitochondria could be detected. The sural nerve was slightly abnormal: loss of large myelinated axons, loss of unmyelinated nerves. CSF protein was elevated to 80 mg/dl, protein electrophoresis revealed the pattern of markedly impaired blood-CSF barrier. Serum lactate and pyruvate were permanently elevated. In the urine the excretion of alanine was raised. The clinical state deteriorated during intercurrent infections; somnolence, vomiting and Cheyne-Stoke's respiration occurred. At the age of 3 1/2 years the child died of pneumonia. In the liver tissue a decreased activity of the pyruvate dehydrogenase complex was found. Neuropathological examination of the brain demonstrated wide-spread changes of Leigh's spongiform encephalopathy. Several enzyme deficiencies have hitherto been associated with Leigh's syndrome: This patients confirms earlier findings that a subgroup of Leigh's syndrome is caused by pyruvate dehydrogenase complex deficiency.

Biopsy↗
PubMedDate not supplied

Cheyne-Stokes breathing and systemic arterial pressure periodic pattern during sleep in central alveolar hypoventilation.

This report refers to a 51 year old man with the clinical features of central alveolar hypoventilation (CAH). Polysomnographic recordings showed periodic breathing and central apnoeas associated with abnormal oscillations of systemic arterial pressure and heart rate during all sleep stages. Oxygen administration during sleep reduced hypoxia, while the periodic breathing and arterial pressure oscillations persisted. The authors suggest that an impairment of the brain structures that play a role in homeostatic adjustment of autonomic functions in connection with the sleep-wake cycle, is responsible for the unusual sleep-related disturbances shown by this patient.

Blood Gas Analysis↗