Obstructive sleep apnoea presenting as a stroke mimic

Abstract

Obstructive sleep apnoea (OSA) is never considered the aetiology of focal neurological symptoms or in the differential of stroke-like symptoms. Although it is a risk factor for stroke and can produce global neurological symptoms, such as confusion and decreased consciousness, it has never been reported to produce focal neurology. This case describes a patient with OSA, diagnosed through polysomnography, who had multiple presentations of focal stroke-like symptoms and signs, despite initial optimal post-stroke management. Symptomatic cessation was only achieved after the patient received continuous positive airway pressure therapy.

Background

Obstructive sleep apnoea (OSA) is not considered a differential diagnosis of stroke-like presentations¹ while it is a known risk factor for strokes and cardiovascular diseases.² This paper reports a man who presented with dysphasia and right-sided weakness, a presentation typical of a left middle cerebral artery stroke, who had multiple similar presentations, despite initial thrombolysis and stroke management. His stroke workup and thorough investigations, considering stroke mimics, were unremarkable. He was later sent for polysomnography (PSG) and found to have severe OSA and prescribed continuous positive airway pressure (CPAP) and had no further presentations.

Case presentation

A caucasian male in his late 80s, body mass index of 23.1, presented to hospital with blurred vision, slurred speech, right-sided weakness and drowsiness which occurred acutely, while driving.

He had a background of rheumatoid arthritis, hypertension, gastro-oesophageal reflux disease, benign prostate hyperplasia, diverticular disease, polymyalgia rheumatic and had undergone several abdominal surgical procedures. He was on the following relevant medications: leflunomide; candesartan; dutasteride/tamsulosin; pregabalin; indapamide; prednisolone; and recently ceased taking hydroxychloroquine.

At presentation, he needed two assistants to mobilise. On examination, his observations were stable and he was afebrile. He was drowsy but rousable, orientated to person, place and time. He had mild dysarthria and multi-directional nystagmus. He had no facial asymmetry and no focal neurology in his full examination. His stroke imaging series showed no acute bleeding, and his condition was managed as a stroke with thrombolysis complemented with dual antiplatelets and a statin. He achieved neurological recovery and was discharged.

He represented, 1 day after discharge, with recurrent symptoms on waking. He had an unremarkable neurological examination and workup and was discharged without any further issue.

He represented a day later, following his second discharge, complaining of a further episode on waking. Examination failed to reveal focal neurology.

Investigations

During his first presentation, his haematology and blood biochemistry including lipids, cholesterol and haemoglobin A1c (HbA1c), were unremarkable. His cardiograph (ECG) showed normal sinus rhythm. His cerebral CT stroke series showed no bleed, no hyperdense vessel (figure 1A), and no perfusion mismatch (figure 1B). It did show a heavily calcified posterior circulation and irregularity of the right-sided posterior inferior cerebellar artery (PICA) (figure 1C). His transthoracic echocardiogram showed no likely embolic source. The MRI of his brain showed a small focus of acute diffusion weighted image change in the right basal ganglia (putamen) and was diagnosed, at the time, as a right basal ganglia stroke (figure 1D).

Figure 1.

(A) Non-contrast CT brain did not show any intracranial bleed nor any hyperdensities. (B) CT cerberal perfusion did not demonstrate any territorial reductions in flow or volume. (C) CT neck and brain angiogram did not demonstrate any occlusions and showed symmetrical arterial supply to the cerebral hemispheres. (D) A T2 weighted MRI brain only showed a small focus of acute infarction in the right basal ganglia (putamen) and did not show a left-sided lesion.

On his second and third presentations, his CT stroke series and his MRI brain were unchanged from his first admission. An electroencephalogram (EEG) did not demonstrate any significant findings at his second presentation. He underwent another brain MRI on his third presentation, which showed resolution of the previous right basal ganglia restricted diffusion. A sleep-deprived EEG, at his third presentation, showed focal left frontotemporal slowing, with associated phase reversal, which was not present in a further study. A limbic encephalitis and anti-neuronal antibody panel were performed on his cerebro-spinal fluid (CSF), obtained at lumbar puncture, with no abnormal findings.

After discharge, he underwent all-night, in-hospital diagnostic PSG, with full 10/20 EEG prolonged video-monitoring, and was found to have severe, non-rapid eye movement (REM) OSA, with an apnoea/hypopnoea index (AHI) of 38 and an oxygen desaturation from an average of 95% to 83%, with a normal video-EEG study.

Differential diagnosis

Given the initial presentation of slurred speech and right-sided weakness, the patient was investigated for a cerebrovascular accident but had normal CT stroke series, apart from a heavily calcified posterior circulation and irregular right posterior inferior cerebellar artery. He was thrombolysed and placed on dual antiplatelets and a statin and neurologically resolved. He kept experiencing symptoms, with two further similar presentations, with unremarkable CT brain scan stroke series and full neurological function recovery each time. Investigation, with an MRI brain, showed a small focus of acute diffusion-weighted change in the right basal ganglia (putamen) and was diagnosed, at the time, as a right basal ganglia stroke which later showed resolution on subsequent MRI. Taken together, this made the diagnosis of a stroke less likely.

Medications were considered as a possible cause of his presentation, as the patient was on a number of medications, but these were unchanged, except the addition of dual antiplatelet therapy and a statin, following his initial stroke diagnosis. While it was possible that they could have caused a decreased level of consciousness, the reported asymmetric weakness, at the time of his initial presentation, was considered unlikely to be medication related. He had a further presentation and neither his history nor biochemical investigations showed changes that could be attributed to altered drug metabolism, which might have resulted in his recurrent symptoms.

He was also investigated for potential ictal activity but his EEGs did not reveal diagnostic features nor suggest seizures.

A lumbar puncture was performed to investigate causes of meningitis and encephalitis with an extensive CSF analysis panel resulting in no abnormal findings, eliminating both meningitis and encephalitis.

A post discharge, in-hospital, diagnostic PSG, with concurrent full 10/20 EEG prolonged video monitoring, demonstrated severe non-REM OSA with no signs of central apnoea. He was prescribed CPAP, subsequent to an in-hospital PSG, CPAP titration study, titrated to his AHI, and he has remained symptom free at the time of writing this article. This resulted in the diagnosis of OSA presenting as stroke mimic, something not previously reported in the stroke literature.

Treatment

The patient was initially thrombolysed, with alteplase, being initially diagnosed as a stroke, despite his symptoms not being representative of a right-sided PICA lesion. He achieved full neurological recovery, several days after admission and was discharged on atorvastatin, aspirin and clopidogrel, in addition to his regular medications.

The patient represented, a day after discharge, exhibiting similar symptoms and was found to have a postural drop on examination which was asymptomatic and was significantly improved after adding salt intake, oral hydration and ceasing candesartan, dutasteride/tamsulosin, pregabalin and indapamide. He was discharged without any further issues. He was commenced on carbamazepine, as a trial of therapy, due to the possibility of seizures, but subsequently developed light-headedness, disequilibrium and nausea and it was ceased.

He represented a day after his second discharge with similar symptoms but had no notable findings on examination or investigations. He was discharged without any further intervention after neurological recovery.

Drowsiness being one of the patient’s symptoms, he was sent for an all-night, diagnostic, in-hospital PSG and found to have severe, non-REM OSA without central apnoea and he was fitted with a small Fisher and Paykel Simplus Full face mask with appropriate headgear and humidification, following CPAP titration PSG, with CPAP set at 9 cm of water (H₂0) and he reported good CPAP tolerance. The CPAP was later increased to 10 cm H₂O at the 4 month follow-up and then 11 cm at the 7 month follow-up, in titration with his AHI.

Outcome and follow-up

Since his discharge, 7 months prior, the patient reports, and CPAP compliance records confirm, 100% compliance with CPAP, for 8.5 hours each night, and he no longer experiences any, slurring of the speech, unilateral or bilateral weakness nor drowsiness. At his first follow-up, 4 months post-discharge, his CPAP was titrated according to his AHI. It was further increased at his 7 month follow-up. These improvements were all in the absence of any medication changes.

Discussion

OSA typically causes lethargy, excessive daytime sleepiness and headache.³ This patient had stroke-like features, which resolved following treatment of non-REM OSA. Although OSA increases the risk of cardiovascular disease and ischaemic strokes,² there is no literature reporting OSA causing focal neurology and a misdiagnosis of stroke.²

This patient had dysarthria and hemiparesis, suggesting a left middle cerebral artery lesion, not identified with CT nor cerebral MRI but sufficient to provoke thrombolysis. Imaging demonstrated heavily calcified posterior circulation and irregular right-sided PICA, clinically irrelevant and thought co-incidental. Despite thrombolysis, within the 4.5 hour time window,⁴ he represented. Seizures were considered, with focal EEG changes, but a carbamazepine trial was poorly tolerated, and it was ceased.

PICA lesions cause vertiginous symptoms and predominantly horizontal, ipsilateral nystagmus,⁵ not apparent in this patient and were not consistent with his observed multi-directional nystagmus, for which there was no satisfactory explanation, but it was self-limited even on subsequent presentations without specific treatment, and the PICA abnormality was considered long-standing. Various conditions cause stroke-like symptoms, including: seizures¹; migraines¹; encephalitis¹; hypoglycaemia¹ and tumours.¹ This patient underwent EEGs, MRI and CT imaging, blood biochemistry and CSF analysis, which eliminated these diagnoses. The potential right basal ganglia infarct was anatomically inconsistent with the presentation. It was concluded that the multi-directional nystagmus was likely an incidental finding and unrelated to the presentation for which investigations failed to identify any structural or biochemical cause to explain the clinical sign.

Diagnostic PSG demonstrated non-REM, severe OSA, without evidence of central hypopnoea nor central apnoea, and CPAP abolished further symptoms. Neither STOP BANG nor Epworth Sleepiness Scale (ESS) scores were performed at presentation with PSG offered based on symptoms. While hypoxia produces global neurological changes, including decreased consciousness and confusion,⁶ this case appears unique because hypoxia seems responsible for hemiparesis and dysarthria. Mild left-sided hypoperfusion, from atherosclerotic disease or asymmetric anatomy, was considered but CT angiography and CT perfusion studies refuted this. Hemispheric differences, in temporary cerebral vascular responses to hypoxia, could be possible⁶ but require more imaging and, as the patient responded completely to CPAP, he does not justify further investigation. Currently, it is impossible to determine the pathophysiology underlying the OSA causing his deficits.

This case indicates OSA should be considered, within the differential diagnosis, for focal neurological symptoms and signs, consistent with stroke, when all other available tests are negative. PSG should be considered when other stroke mimics have been eliminated.

Patient’s perspective.

I am relieved that the symptoms that I was having were not because of a stroke. I am also happy that using the CPAP machine has relieved all my symptoms, this has given me more energy and allowed me to enjoy my life. I have been 100% compliant with using the CPAP machine and have been using it every night. I am happy that I do not need to return to the hospital because of more symptoms.

Learning points.

• A broad range of differentials should be considered in patients presenting with focal neurological symptoms.

• STOP BANG and ESS scores might be considered when screening for focal neurology, even in cases where the patient phenotypic presentation does not suggest obstructive sleep apnoea (OSA).

• Non-rapid eye movement OSA can present with focal neurological features and should be considered within differential diagnoses in presentations with focal neurology.

• Polysomnography should be considered as a part of a stroke work-up when other investigations are unhelpful.

Ethics statements

Patient consent for publication

Consent obtained directly from patient(s).