Acta Neurol Belg DOI 10.1007/s13760-015-0432-1
LETTER TO THE EDITOR
Hypertensive encephalopathy associated with obstructive sleep apnoea syndrome Bengt Edvardsson
Received: 14 January 2015 / Accepted: 21 January 2015 Ó Belgian Neurological Society 2015
Keywords Obstructive sleep apnoea syndrome Hypertensive encephalopathy Neuroimaging Hypertension Hypertensive encephalopathy (HE) is a relatively rapidly evolving clinicoradiologic syndrome. It is characterized by confusion, cognitive changes, seizures and occasionally cortical blindness. Magnetic resonance imaging (MRI) usually displays bilateral subcortical parieto-occipital hyperintense lesions on T2 and FLAIR imaging [1]. Given the nonspecific constellation of symptoms associated with the syndrome in the acute hospital setting, HE can easily be missed [2]. Obstructive sleep apnoea syndrome (OSAS) is a common cause of secondary hypertension. HE in the setting of OSAS has not previously been reported. I describe a patient who developed HE associated with OSAS. The patient was initially misdiagnosed due to neuropsychiatric symptoms. A 59-year-old man presented with confusion, headache and blurred vision. He was recently diagnosed with OSAS. The 12-h polysomnography had showed an apnoea–hypopnea index of 49 events per hour which is compatible with a serious form of the disease. Continuous positive airway pressure (CPAP) therapy had not started yet. Blood pressure had been monitored earlier and he had been normotensive. There was no history of headache or other diseases. He denied alcohol intake but was a smoker. He used no medications. His height was 187 cm, his body weight was 92 kg and his BMI was 27.8 kg/m2. The headache was followed by nausea and vomiting. On B. Edvardsson (&) Department of Clinical Sciences, Neurology, Skane University Hospital, Lund University, 221 85 Lund, Sweden e-mail: [email protected]
presentation in the emergency department he was awake, but disoriented. On presentation, general physical and neurologic examination was normal apart from blurred vision. He was awake but still disoriented. Fundoscopic examination displayed bilateral papilloedema (grade IV hypertensive retinopathy). He had a blood pressure of 240/130 mmHg. Computer tomography including arterial/ venous angiography of the brain was essentially normal. Repeated blood pressure monitoring displayed marked hypertension. His blood pressure remained high, reaching 230/120 mmHg. The blood pressure was aggressively treated with intravenous drugs (labetalol and furosemide). An electroencephalogram showed diffuse slowing indicating an encephalopathy. Cerebrospinal fluid examination was normal apart from a high pressure of 28 mm H20. A brain MRI T2/FLAIR displayed an increased signal in the white matter on images throughout the parietal and occipital lobes on. No contrast enhancement was seen and diffusion-weighted imaging showed no signs of ischaemia (Fig. 1a). The MRI findings were consistent with HE. Oral antihypertensive treatment (labetalol 400 mg once daily, furosemide 40 mg once daily and felodipine 10 mg once daily) continued. CPAP therapy was started. An extensive clinical work-up has not provided any other explanation than OSAS for his HE. The patient was discharged after 3 weeks. An MRI after 6 weeks displayed marked regression of the abnormalities (Fig. 1b). At follow-up after 6 months and 1 year he felt well. His vision was normal as well as the fundi. A diagnosis of secondary hypertension due to OSAS was established. The patient is currently asymptomatic and his blood pressure varies within the normal range. He is continuing with antihypertensive treatment and CPAP therapy. The case study highlights a patient with HE in the setting of OSAS. OSAS is being more and more documented
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Acta Neurol Belg
OSAS is closely associated with the development of hypertension. The occurrence of severe hypertension is especially high in OSAS patients. About 50 % of patients with hypertension have concomitant OSAS and OSAS is the most prevalent secondary contributor to elevated blood pressure in patients with drug-resistant hypertension. The blood pressure is often not controllable despite therapy with three antihypertensive drugs from different classes. OSAS raises the blood pressure during both night and daytime and could cause a hypertensive emergency at any time. CPAP therapy reduces high blood pressure in hypertensive patients with OSAS. It also has a beneficial effect on cardiovascular mortality in patients with OSAS [4, 5]. The patient displayed many risk factors for OSAS as well as for hypertension such as smoking, male sex and age. Thus, OSAS and hypertension appear to be connected by an interaction of mechanisms [4]. HE can occur in the setting of OSAS. Patients with OSAS should have regular monitoring of blood pressure. Consequently, in people presenting with hypertension, and as might be the case, a resulting HE, OSAS should be considered a possible underlying cause.
Conflict of interest interest.
The author declares that he has no conflict of
Informed consent Informed consent was obtained from all individual participants included in the study.
References Fig. 1 a MRI brain T2/FLAIR displaying increased T2 signal in the white matter throughout the parietal and occipital lobes consistent with HE. b MRI brain after 6 weeks displaying marked regression of the abnormalities
as a significant cause of medical morbidity and mortality. OSAS is a relatively frequent sleep disorder. It is typified by recurrent incidents of incomplete or complete collapse of the upper airway during sleep. It is defined by breathing disturbances during sleep with a minimum prerequisite frequency of 5 events per hour and lasting for at least 10 s. The prevalence of OSAS associated with accompanying daytime sleepiness is approximately 3–7 % for adult men and 2–5 % for adult women in the general population [3].
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1. Hinchey J, Chaves C, Appignani B et al (1996) A reversible posterior leukoencephalopathy syndrome. N Engl J Med 334:494–500 2. Lamy C, Oppenheim C, Mas JL (2014) Posterior reversible encephalopathy syndrome. Handb Clin Neurol 121:1687–1701 3. Punjabi NM (2008) The epidemiology of adult obstructive sleep apnea. Proc Am Thorac Soc 15:136–143 4. Konecny T, Kara T, Somers VK (2014) Obstructive sleep apnea and hypertension: an update. Hypertension 63:203–209 5. Bo¨rgel J, Springer S, Ghafoor J et al (2010) Unrecognized secondary causes of hypertension in patients with hypertensive urgency/emergency: prevalence and co-prevalence. Clin Res Cardiol 99:499–506
LETTER TO THE EDITOR
Hypertensive encephalopathy associated with obstructive sleep apnoea syndrome Bengt Edvardsson
Received: 14 January 2015 / Accepted: 21 January 2015 Ó Belgian Neurological Society 2015
Keywords Obstructive sleep apnoea syndrome Hypertensive encephalopathy Neuroimaging Hypertension Hypertensive encephalopathy (HE) is a relatively rapidly evolving clinicoradiologic syndrome. It is characterized by confusion, cognitive changes, seizures and occasionally cortical blindness. Magnetic resonance imaging (MRI) usually displays bilateral subcortical parieto-occipital hyperintense lesions on T2 and FLAIR imaging [1]. Given the nonspecific constellation of symptoms associated with the syndrome in the acute hospital setting, HE can easily be missed [2]. Obstructive sleep apnoea syndrome (OSAS) is a common cause of secondary hypertension. HE in the setting of OSAS has not previously been reported. I describe a patient who developed HE associated with OSAS. The patient was initially misdiagnosed due to neuropsychiatric symptoms. A 59-year-old man presented with confusion, headache and blurred vision. He was recently diagnosed with OSAS. The 12-h polysomnography had showed an apnoea–hypopnea index of 49 events per hour which is compatible with a serious form of the disease. Continuous positive airway pressure (CPAP) therapy had not started yet. Blood pressure had been monitored earlier and he had been normotensive. There was no history of headache or other diseases. He denied alcohol intake but was a smoker. He used no medications. His height was 187 cm, his body weight was 92 kg and his BMI was 27.8 kg/m2. The headache was followed by nausea and vomiting. On B. Edvardsson (&) Department of Clinical Sciences, Neurology, Skane University Hospital, Lund University, 221 85 Lund, Sweden e-mail: [email protected]
presentation in the emergency department he was awake, but disoriented. On presentation, general physical and neurologic examination was normal apart from blurred vision. He was awake but still disoriented. Fundoscopic examination displayed bilateral papilloedema (grade IV hypertensive retinopathy). He had a blood pressure of 240/130 mmHg. Computer tomography including arterial/ venous angiography of the brain was essentially normal. Repeated blood pressure monitoring displayed marked hypertension. His blood pressure remained high, reaching 230/120 mmHg. The blood pressure was aggressively treated with intravenous drugs (labetalol and furosemide). An electroencephalogram showed diffuse slowing indicating an encephalopathy. Cerebrospinal fluid examination was normal apart from a high pressure of 28 mm H20. A brain MRI T2/FLAIR displayed an increased signal in the white matter on images throughout the parietal and occipital lobes on. No contrast enhancement was seen and diffusion-weighted imaging showed no signs of ischaemia (Fig. 1a). The MRI findings were consistent with HE. Oral antihypertensive treatment (labetalol 400 mg once daily, furosemide 40 mg once daily and felodipine 10 mg once daily) continued. CPAP therapy was started. An extensive clinical work-up has not provided any other explanation than OSAS for his HE. The patient was discharged after 3 weeks. An MRI after 6 weeks displayed marked regression of the abnormalities (Fig. 1b). At follow-up after 6 months and 1 year he felt well. His vision was normal as well as the fundi. A diagnosis of secondary hypertension due to OSAS was established. The patient is currently asymptomatic and his blood pressure varies within the normal range. He is continuing with antihypertensive treatment and CPAP therapy. The case study highlights a patient with HE in the setting of OSAS. OSAS is being more and more documented
123
Acta Neurol Belg
OSAS is closely associated with the development of hypertension. The occurrence of severe hypertension is especially high in OSAS patients. About 50 % of patients with hypertension have concomitant OSAS and OSAS is the most prevalent secondary contributor to elevated blood pressure in patients with drug-resistant hypertension. The blood pressure is often not controllable despite therapy with three antihypertensive drugs from different classes. OSAS raises the blood pressure during both night and daytime and could cause a hypertensive emergency at any time. CPAP therapy reduces high blood pressure in hypertensive patients with OSAS. It also has a beneficial effect on cardiovascular mortality in patients with OSAS [4, 5]. The patient displayed many risk factors for OSAS as well as for hypertension such as smoking, male sex and age. Thus, OSAS and hypertension appear to be connected by an interaction of mechanisms [4]. HE can occur in the setting of OSAS. Patients with OSAS should have regular monitoring of blood pressure. Consequently, in people presenting with hypertension, and as might be the case, a resulting HE, OSAS should be considered a possible underlying cause.
Conflict of interest interest.
The author declares that he has no conflict of
Informed consent Informed consent was obtained from all individual participants included in the study.
References Fig. 1 a MRI brain T2/FLAIR displaying increased T2 signal in the white matter throughout the parietal and occipital lobes consistent with HE. b MRI brain after 6 weeks displaying marked regression of the abnormalities
as a significant cause of medical morbidity and mortality. OSAS is a relatively frequent sleep disorder. It is typified by recurrent incidents of incomplete or complete collapse of the upper airway during sleep. It is defined by breathing disturbances during sleep with a minimum prerequisite frequency of 5 events per hour and lasting for at least 10 s. The prevalence of OSAS associated with accompanying daytime sleepiness is approximately 3–7 % for adult men and 2–5 % for adult women in the general population [3].
123
1. Hinchey J, Chaves C, Appignani B et al (1996) A reversible posterior leukoencephalopathy syndrome. N Engl J Med 334:494–500 2. Lamy C, Oppenheim C, Mas JL (2014) Posterior reversible encephalopathy syndrome. Handb Clin Neurol 121:1687–1701 3. Punjabi NM (2008) The epidemiology of adult obstructive sleep apnea. Proc Am Thorac Soc 15:136–143 4. Konecny T, Kara T, Somers VK (2014) Obstructive sleep apnea and hypertension: an update. Hypertension 63:203–209 5. Bo¨rgel J, Springer S, Ghafoor J et al (2010) Unrecognized secondary causes of hypertension in patients with hypertensive urgency/emergency: prevalence and co-prevalence. Clin Res Cardiol 99:499–506
