Case series of electrocardiograms in neurocardiology

CASE 1 Clinical presentation A 74-year-old Chinese woman presented with worsening right-sided weakness. She had a history of left parafalcine anaplastic meningioma, for which she underwent craniotomy and resection 2 years ago. She had also received adjuvant radiotherapy for the residual tumour, which was complicated by post-radiotherapy cerebral oedema. Acutely, there was no history of trauma, and she did not complain of headache or nausea. She had no chest pain or dyspnoea. Her heart rate was 82 beats/min, respiratory rate 20 breaths/min, blood pressure 142/75 mmHg, oxygen saturation 96% on room air and temperature 37.2°C. Neurological examination revealed right hemiplegia, while sensation was intact. Cranial nerve examination was normal. She had dual heart sounds and clear lungs on auscultation. What does her electrocardiogram (ECG) at presentation show [Figure 1a], compared to her ECG one year earlier [Figure 1b]?Figure 1: Case 1: ECGs at (a) presentation and (b) one year earlier.Her full blood count, creatinine and electrolytes were normal. A finger-prick glucose level showed a reading of 6.2 mmol/L. Computed tomography (CT) of the brain showed a left frontal lesion with surrounding oedema, regional mass effect and a midline shift of 5 mm to the right. Magnetic resonance imaging (MRI) confirmed a periventricular enhancing lesion measuring 4.6 × 4.5 × 5.1 cm [Figure 2].Figure 2: Axial MR image shows a left frontal periventricular enhancing lesion (arrowhead) measuring 4.6 × 4.5 × 5.1 cm, with surrounding oedema extending into the right frontal region, midline shift and effacement of the left lateral ventricle.ECG interpretation Both the ECG at presentation [Figure 1a] and that from one year earlier [Figure 1b] show normal sinus rhythm. Most notably, the ECG at presentation displays deep, symmetrical T-wave inversions and QT interval prolongation in the precordial leads, as well as in leads I, aVL and II. The J point is depressed by 1 mm in leads V2 and V3, but there are no other ST-segment abnormalities. In comparison, the ECG done one year earlier shows upright T waves, with physiological U waves visible in the precordial leads. Clinical course The patient’s cardiac enzymes were not elevated. She was admitted to the neurosurgical ward where intravenous dexamethasone was started. On consultation with a cardiologist, T-wave inversions were suspected to be cerebral T waves related to the intracranial lesion. Transthoracic echocardiography (TTE) and pharmacological myocardial perfusion imaging (MPI) were performed to exclude cardiomyopathy and myocardial ischaemia. Transthoracic echocardiography showed an ejection fraction of 55%, normal chamber sizes and regional wall motion abnormality of the basal inferior wall, while MPI did not demonstrate inducible ischaemia. She eventually underwent craniotomy and resection of the intracranial lesion. Histology from the lesion biopsy revealed features compatible with radiation necrosis. There was no recurrent meningioma or metastatic carcinoma identified. She was later discharged from hospital. An ECG was not repeated for this patient after her surgery, but normalisation of the cerebral T waves would be expected. CASE 2 Clinical presentation An 85-year-old Malay man presented to the emergency department after his colleagues witnessed him slumped over in his chair, apparently weaker on the left side. He had last been seen well 30 min earlier. Three years ago, he was diagnosed with hypertension, for which he was taking amlodipine 5 mg once daily. There was no history of trauma, headache, nausea or vomiting, and he was not taking anti-platelets or anti-coagulants. His vital signs were as follows: heart rate 84 beats/min, respiratory rate 18 breaths/min, blood pressure 228/131 mmHg, oxygen saturation 92% on room air and temperature 37.5°C. On physical examination, his Glasgow Coma Scale (GCS) score was E4V5M6. He had dysarthria, right-sided lower motor neuron facial nerve palsy, as well as weakness of the left upper and lower limbs. What does his ECG at presentation [Figure 3] show?Figure 3: Case 2: ECG at presentation.Computed tomography of the brain showed a 4.4 × 3.0 × 2.0 cm intraparenchymal haematoma within the right cerebellar hemisphere extending across the midline. There was also intraventricular haemorrhage with upstream hydrocephalus. The brainstem was superiorly displaced, with impending right cerebellar tonsillar herniation [Figure 4a]. While the patient was being assessed, his GCS score abruptly deteriorated to E1V2M2. He was intubated emergently and started on intravenous labetalol. After an urgent neurosurgical consult, he underwent emergency decompression surgery with evacuation of the right cerebellar haematoma and insertion of an external ventricular drain. He was admitted to the surgical intensive care unit (ICU) postoperatively, and repeat CT of the brain showed good decompression and clot evacuation [Figure 4b]. What does the routine ECG on Day 3 of admission [Figure 5] show?Figure 4: Case 2: (a) Pre- and (b) post-surgical axial and sagittal CT images of the brain show cerebellar bleed with intraventricular haemorrhage (arrowheads), which improved post-surgery. Asterisk <*> shows the external ventricular drain.Figure 5: Case 2: ECG on Day 3 of admission.ECG interpretation The ECG at presentation [Figure 3] shows sinus arrhythmia with clearly visible P waves preceding every QRS complex, while the ECG on Day 3 [Figure 5] shows an irregularly irregular rhythm with fibrillatory waves, diagnostic of new atrial fibrillation (AF). Although P waves in the initial ECG are bifid (lead II), their duration does not exceed 120 ms; hence, the ECG criteria for left atrial enlargement are not met. A review of the patient’s previous ECGs (not shown) all revealed sinus rhythm. Clinical course Subsequently, the patient spontaneously reverted to sinus rhythm without administration of anti-arrhythmic agents. Transthoracic echocardiography showed a left ventricular ejection fraction of 66% and a mildly dilated left atrium. He had a stormy stay in the ICU with difficult-to-control hypertension requiring multiple anti-hypertensive agents, ventilator-associated pneumonia and several failed extubation attempts. Unfortunately, he developed other infective complications during his hospital admission and eventually passed away. CASE 3 Clinical presentation An 86-year-old Chinese woman was brought to the emergency department by her family after being found unresponsive, with gaze deviation to the right and repetitive head nodding. She had a past medical history of hypertension, hyperlipidaemia, diabetes mellitus and Parkinson’s disease, for which she was on risperidone. Her vital signs were as follows: heart rate 60 beats/min, respiratory rate 20 breaths/min, blood pressure 156/74 mmHg, oxygen saturation 95% on room air and temperature 37.0°C. On physical examination, her GCS score was E4V4M6. Repeated head-nodding movements were observed, with occasional up-rolling of the eyes. Neurological examination of the cranial nerves and limbs was normal. What does her ECG [Figure 6] show?Figure 6: Case 3: ECG at presentation.Her full blood count, creatinine and electrolytes were within the normal range. Cardiac troponins were not elevated. Computed tomography of the brain showed an acute left thalamic intraparenchymal haematoma with surrounding oedema and mild focal mass effect [Figure 7a]. The on-call neurosurgeon who reviewed the patient started her on regular levetiracetam and recommended non-surgical management. She was also assessed by the on-call neurologist, who requested an MRI of the brain and an electroencephalogram (EEG). The MRI confirmed a left thalamic haematoma measuring 0.6 × 1.4 × 1.1 cm, with diffuse age-related cerebral atrophy. There was no hydrocephalus or midline shift [Figure 7a & b].Figure 7: (a) Axial CT image and (b) axial MR image of the brain show left thalamic haematoma (arrowhead in a and * in b). (c) Repeat axial CT image of the brain after one week shows expected evolution of the left thalamic haematoma (arrowhead).ECG interpretation The ECG at presentation [Figure 6] shows sinus bradycardia. The heart rate shows just under 60 beats/min, with a P wave before every QRS complex and a positive P wave in the inferior and lateral leads. A previous ECG (not shown) revealed normal sinus rhythm with a heart rate of 90 beats/min. Clinical course During recording of the EEG, the patient had intermittent right-sided facial twitching without accompanying epileptogenic activity. Therefore, the neurologist concluded that these abnormal movements were possibly tardive dyskinesia from chronic risperidone use for her Parkinson’s disease. A repeat CT of the brain 1 week later showed the expected evolution of the haematoma with stable surrounding oedema [Figure 7c]. A repeat ECG performed later during her admission showed resolution of the initial bradycardia [Figure 8].Figure 8: Case 3: ECG shows normal sinus rhythm at a heart rate of 80 beats/min.DISCUSSION The cardiovascular and central nervous systems interact via a complex network of cortical and subcortical structures, as well as through the autonomic nervous system and intracardiac nervous system, to form the heart–brain axis.[1] Therefore, neurological disease may affect the heart, including causing ECG changes and new-onset arrhythmias.[2,3,4,5,6,7] These ECG abnormalities are thought to result from neurogenic cardiac injury, mediated by elevated circulating catecholamines and neuroinflammatory responses.[8] Pathology involving certain areas of the brain that play key roles in the neurocardiac axis, such as the insular cortex, is more likely to be implicated.[2] ECG changes associated with neurological diseases T wave abnormalities Diffuse, deep, symmetrically inverted T waves, known as ‘cerebral T waves’, are classically seen in subarachnoid haemorrhage.[3] However, they may occur in any severe central nervous system trauma or pathology, particularly when there is raised intracranial pressure. These include large ischaemic strokes, intracranial haemorrhage, traumatic brain injury and supratentorial brain tumours.[4,9] Cerebral T waves have also been associated with echocardiographically detected wall motion abnormalities.[10] Case 1 had basal inferior wall motion abnormalities on TTE. While underlying undiagnosed ischaemic heart disease is a possibility, neurogenic myocardial stunning should be considered in the absence of known cardiac disease and with a normal MPI. Upright T waves of increased amplitude, often associated with QT prolongation, may also be observed following cerebrovascular events.[3] In contrast to case 1, case 2 did not display cerebral T waves despite significantly raised intracranial pressure. The prevalence of cerebral T waves was previously reported to be 2.1% in a study of 800 patients with ischaemic or haemorrhagic stroke.[11] Among patients with intracranial haemorrhage specifically, 13.8% were found to have T wave inversions.[12] Prolonged QT interval A prolonged QT interval is commonly seen following intracranial haemorrhage[2,3] and has also been reported in acute ischaemic stroke.[13] Occasionally, fusion of prominent U waves with the preceding T wave may result in a long QU interval, which can be mistaken for a prolonged QT interval. Severe QT prolongation of more than 550 ms in patients with intracranial haemorrhage has been associated with life-threatening ventricular arrhythmias, such as torsades de pointes degenerating into ventricular fibrillation, although this is rare.[5] ST segment changes Depression, and less commonly elevation, of the ST segment may occur with intracranial haemorrhage and other causes of raised intracranial pressure, including large brain tumours. These changes may be mistaken for acute ischaemia.[3,4] Ischaemic myocardial injury and infarction can occur after acute ischaemic stroke as part of the stroke–heart syndrome, and the patient’s clinical presentation and cardiac enzyme levels should be considered.[14] Case 1 had ST segment depression in leads V2 and V3 [Figure 1a] without chest pain or breathlessness, and cardiac enzymes were not elevated. Takotsubo syndrome, or stress cardiomyopathy, may occur in association with ischaemic stroke, intracranial haemorrhage and traumatic brain injury,[1] and may also produce ST elevation and T wave inversion on the ECG, closely mimicking that of an acute myocardial infarction.[15] Cardiac enzymes are often moderately raised. In stable patients, cardiac MRI is useful to distinguish Takotsubo syndrome from myocardial infarction and myocarditis.[15] Sinus bradycardia Sinus bradycardia may be seen in patients with central nervous system diseases.[3] It is due to neurally mediated autonomic dysfunction and may occur as part of Cushing’s reflex, in which raised intracranial pressure and the resultant cerebral ischaemia lead to a vasopressor response and elevated blood pressure to restore cerebral blood flow. The increased arterial blood pressure stimulates baroreceptors in the carotid bodies, causing vagally mediated bradycardia.[16] A similar vagal mechanism may be implicated in other bradyarrhythmias associated with raised intracranial pressure. Case 3 did not have evidence of raised intracranial pressure, and the sinus bradycardia was likely due to alterations in autonomic control. Atrial fibrillation Atrial fibrillation is a well-known risk factor for ischaemic stroke, through cardioembolism of an intracardiac thrombus. However, acute cerebrovascular events can also lead to autonomic imbalances and a catecholaminergic surge, thereby triggering new-onset AF. New-onset AF is more commonly associated with ischaemic stroke but can also occur in haemorrhagic stroke.[17] It is often difficult to attribute new-onset AF solely to an acute intracranial pathology, as other acute stressors may also contribute to its development. Case 2 developed AF [Figure 5] within the first 3 days of a massive cerebellar bleed, with spontaneous resolution to sinus rhythm. The patient had no electrolyte imbalances, normal thyroid function and was not septic at the time of AF development. However, AF occurred following emergent neurosurgery, which might have been a confounding factor. Of note, the TTE finding of a dilated left atrium in this case suggests an underlying abnormal atrial substrate predisposing to AF. Other tachy- and bradyarrhythmias Various arrhythmias have been reported in subarachnoid haemorrhage. Tachyarrhythmias include non-sustained ventricular tachycardia and paroxysmal supraventricular tachycardia, while bradyarrhythmias include sinoatrial block, sinus arrest and atrioventricular block.[5] The frequency and severity of arrhythmias are highest within the first 48 h of the acute bleed.[5] Life-threatening ventricular arrhythmias are uncommon.[5] Management considerations Electrocardiogram abnormalities and cardiac biomarker elevation can occur in acute neurological diseases. It is important not to attribute all cases to acute coronary syndromes without further evaluation. Starting anti-thrombotic therapy may be inappropriate or disastrous in cases where the inciting pathology is an intracranial haemorrhage. In the absence of cardiac symptoms, clinicians should be vigilant in identifying signs suggestive of an acute neurological insult and perform appropriate neuroimaging before starting anti-platelets. Echocardiography is useful to diagnose wall motion abnormalities,[10] and stress imaging in non-acute cases may reveal inducible ischaemia. Management of QT prolongation in acute neurological injury is largely supportive. Life-threatening ventricular arrhythmias, such as torsades de pointes, are uncommon and are typically associated with severe QT prolongation of more than 550 ms.[5] Electrolyte derangements should be corrected, and medications known to prolong QT interval should be avoided. CONCLUSION Electrocardiogram manifestations of neurological diseases are variable and often non-specific. They may reflect adverse neurological status but may also be due to acute cardiac complications. The overall clinical presentation, together with supportive imaging features, may help with diagnosis and management. Financial support and sponsorship Sia CH was supported by the Singapore Ministry of Health National Medical Research Council’s Transition Award (MOH-001368-00). Conflicts of interest Tan BYQ and Sia CH are members of the SMJ Editorial Board and were thus not involved in the peer review and publication decisions of this article. SMC CATEGORY 3B CME PROGRAMME Online Quiz: https://www.sma.org.sg/cme-programme Deadline for submission: 6 pm, 28 March 2026