Brain stem encephalitis with central neurogenic hyperventilation
- 1Department of Anaesthesiology, Nordland Hospital, Bodo, Norway
- 2Department of Neurology, Nordland Hospital, Bodo, Norway
- 3University of Tromso, Bodo, Norway
- 4Department of Anaesthesiology, Nordland Hospital, Bodo, Norway
- Correspondence to: R Salvesen Department of Neurology, University of Tromso, Nordlandssykehuset, N-8092 Bodo, Norway;
Central neurogenic hyperventilation (CNH) was defined by Plum and Swanson in 1959 as a syndrome of decreased PaCO2, raised PaO2 and respiratory alkalosis, in the absence of radiographic evidence of pulmonary congestion or inflammation.1 A 72-year-old man was increasingly dyspnoeic for the past 6 months before local hospitalisation. In this period he lost weight, and his gait became ataxic. He needed more sleep, started to shake and fainted twice. He was fully awake as he walked into the hospital. Arterial blood gas analyses showed pH 7.59, pCO2 1.9 kPa (14.3 mm Hg), bicarbonate 18 mmol/l, base excess−12 mmol/l and pO2 15.2 kPa (114 mm Hg). Arterial blood gas analysis using an arterial catheter during sleep gave the same results. He was breathing at a frequency of 30/min.
The patient was transferred to a central hospital. On arrival, he was fully awake, but had slurred speech. Eye movements were saccadic and dysconjugate when he looked upwards, and there was a slight proximal tetraparesis. Deep tendon reflexes were hyperactive and Babinski sign was positive on the left foot. Spirometry, thoracic x ray, computed tomography of the brain and thorax were normal. Examination of the cerebrospinal fluid (CSF) was carried out on three occasions: …