Stroke mimic in an acute rehabilitation unit patient with associated hypomagnesaemia

Abstract

This case report describes a patient who presented with acute left facial numbness and eyelid weakness prompting work-up, which demonstrated low suspicion for new stroke but revealed hypomagnesaemia as a potential differential diagnosis. Patient initially presented to the emergency department with left upper extremity weakness and was diagnosed with right basal ganglia infarction. Two weeks after transfer to the acute rehabilitation unit, patient suddenly complained of left facial numbness and eyelid weakness. However, brain imaging did not show any new acute infarct. Instead, laboratory results showed hypomagnesaemia at 1.50 mg/dL. Patient was therefore treated with intravenous magnesium leading to resolution of his symptoms. Up to 30% of acute stroke presentations are stroke mimics. Although hypomagnesaemia is less frequently seen as a mimic, its neuromuscular manifestations may present with similar symptoms. Patients will always benefit from a comprehensive evaluation for stroke symptoms, but it is important to consider the mimics as well.

Background

Stroke mimics are conditions with clinical signs that resemble the acute-onset cerebrovascular presentation of a stroke, but are instead another type of disease pathology.^1–3 The incidence of patients treated by stroke teams in the USA who are found to be experiencing a stroke mimic has been estimated to be 30%, indicating that the clinical phenomenon happens at a significant rate.² Furthermore, studies have found that among patients who were classified as having stroke mimics, metabolic disorder is consistently one of the most frequent final diagnoses among the common differential diagnoses of a suspected stroke.^{4 5} The most common metabolic conditions presenting as stroke mimics include hypoglycaemic, hypocalcaemia, hyponatraemia and hypothyroidism.²

Concern for a potential stroke mimic should not bar thrombolytic treatment in a patient suspected of having a stroke, given the narrow therapeutic time window within which antithrombolytic therapy can effectively mitigate stroke-related disability and mortality.^{1 6–8} However, once an acute stroke is deemed to be less likely, it is important to consider the stroke mimics to better treat the patient’s symptoms and to prevent future occurrence of similar episodes. This case report highlights a less common case of hypomagnesaemia presenting as a potential stroke mimic in an acute rehabilitation Unit (ARU) patient.

Case presentation

A 70-year-old-man with a medical history of diabetes mellitus type II, hypertension, benign prostate hypertrophy and colon cancer initially presented to the emergency department with symptoms of left upper extremity weakness for 1 day (>24 hours from onset of symptoms). On evaluation, the patient had strength of 4+/5 in the left upper extremity with decreased sensation also in the left upper extremity. The National Institutes of Health Stroke Scale (NIHSS) was 3. STAT CT scan and MRI brain without contrast showed subacute right basal ganglia infarct without midline shift or haemorrhage (figure 1). There were scattered periventricular white matter changes, likely microvascular and ischaemic. Patient was diagnosed with right basal ganglia infarction likely due to small vessel disease secondary to hypertension and was treated with aspirin 81 mg daily and clopidogrel daily. After medical optimisation, the patient was subsequently transferred to the ARU for rehabilitation where his left upper extremity weakness and decreased sensation improved.

Figure 1.

MRI brain without contrast on presentation to emergency department, showing subacute right basal ganglia infarction.

Two weeks into the patient’s ARU stay, patient complained of acute left upper facial numbness and left eyelid weakness that started that morning. On evaluation, patient was alert and oriented without any signs of confusion, dysarthria or aphasia. However, physical examination did not demonstrate new focal motor or sensory deficits and cranial nerves II–XII were intact. Patient’s bilateral upper extremities were noted to be 5/5 in strength when it was 4+/5 in the left upper extremity initially. Sensation was intact to light touch throughout bilateral upper and lower extremities, which is also an improvement from decreased sensation in the left upper extremity on initial admission. Additionally, cranial nerve V testing did not reveal objective findings of decreased sensation in the left face as patient noted, and cranial nerve VII testing revealed equal eyelid strength bilaterally, again without objective finding of left eyelid weakness. Patient did exhibit a left upper extremity pronator drift, which was present on previous neurological examinations. Vitals were within normal limits, with blood pressure 120/72 mmHg, heart rate 72 beats per minute, respiratory rate 18 breaths per minute, and oxygen saturation 100% on room air. Despite the normal neurological findings, a code stroke was called for a comprehensive evaluation given patient’s continued self-reported left upper facial numbness and eyelid weakness.

Investigations

During the code stroke, basic metabolic panel, complete blood count, calcium, magnesium and STAT CT head without contrast were ordered. Blood results at the time of presentation were normal (table 1) except a low magnesium level at 1.50 mg/dL (reference range 1.8–2.4). Thyroid function tests at admission were normal and were not repeated at this presentation. ECG showed normal sinus rhythm. CT of the brain showed expected evolution of the right basal ganglia infarct, now much less conspicuous than on prior examination. There were no acute intracranial haemorrhages, large territory infarcts or midline shift.

Table 1.

Laboratory results obtained during episode of left upper facial numbness and eyelid weakness

Test	Result	Flag	Units	Reference range
Sodium	138		mmol/L	136–146
Potassium	4.8		mmol/L	3.5–5.3
Chloride	105		mmol/L	95–110
Carbon dioxide	25		mmol/L	21–31.0
Urea nitrogen	19		mg/dL	5–25
Creatinine	0.78		mg/dL	0.66–1.28
Glucose	83		mg/dL	70–110
Calcium	9.2		mg/dL	8.4–10.2
Magnesium	1.50	Low	mg/dL	1.8–2.4
Phosphorous	3.3		mg/dL	2.5–4.9

Differential diagnosis

The top differential diagnosis for this patient’s acute left facial numbness and eyelid weakness is new ischaemic stroke, given patient’s recent history of basal ganglia stroke. However, the repeat CT of the brain did not show any new or worsening signs of ischaemic or haemorrhagic stroke. The neurology team, who was present during the code stroke, determined that there was no need for repeat MRI of the brain given very low suspicion for a recurrent stroke.

Transient ischaemic attack (TIA) is also high on the differential. Per chart review, patient’s initial basal ganglia stroke was thought to be secondary to small vessel disease due to hypertension, as patient has a history of hypertension and his blood pressure was noted to be up to 249/129 on presentation to the emergency room. However, this risk factor was well controlled during his ARU stay. Patient’s systolic blood pressure was kept between 90 and 120 mmHg throughout and even during the code stroke episode, his blood pressure was noted to be within normal limits at 120/72 mmHg.

Other risk factors for TIA were also evaluated to weigh its likelihood as a possible explanation for patient’s symptoms. Telemetry throughout hospitalisation did not demonstrate signs of atrial fibrillation and patient had a Zio Patch previously that did not record any atrial fibrillation. Echocardiogram on initial work-up did not demonstrate vegetation or thrombus formation and did not show patent foramen ovale. Magnetic resonance angiography of the head and neck did not demonstrate carotid stenosis that may contribute to ischaemic strokes. Therefore, although a TIA is a differential, this patient’s case warranted further investigation.

Other common stroke mimics include syncope, seizures and migraine, which were not present on history. Patient did not demonstrate a septic picture leading up to the episode, as his temperature, heart rate, respiratory rate and white blood count were all within normal limits. Hypoglycaemic, hypocalcaemia and hyponatraemia are less likely as well, as those laboratory values were all within normal limits at the time of presentation. The only noticeable abnormality on patient’s laboratory results was his hypomagnesaemia to 1.50 mg/dL. Although less commonly seen as a stroke mimic, hypomagnesaemia leads to symptoms such as weakness and tetany, which are similar to signs of an acute stroke. Therefore, hypomagnesaemia was considered as a possible and treatable differential for patient’s left facial numbness and eyelid weakness.

Treatment

Given the work-up, patient was treated with 2 mg of intravenous magnesium, which led to improvement of his magnesium level to 1.80 mg/dL and resolution of his symptoms. Subsequently, patient did not complain of any further left-sided facial numbness or weakness.

Outcome and follow-up

Patient’s magnesium level after the code stroke fluctuated between 1.60 and 2.00 mg/dL, still requiring a combination of intravenous and oral repletion. However, the patient did not note any further episodes of facial numbness or weakness. Patient was discharged home on one 400 mg magnesium oxide tablet per day, with continued magnesium laboratory draws via Home Health two times a week. Patient was recommended to follow-up with his primary care Provider closely, with a follow-up appointment scheduled for 1 week after discharge. Patient was also scheduled to follow-up with Neurology’s Stroke Clinic 2 weeks after discharge for continued monitoring.

Discussion

Although this ARU patient had a stroke mimic possibly due to multiple reasons, the associated hypomagnesaemia is a potential explanation especially because his symptoms improved following magnesium supplementation. Hypomagnesaemia occurs in 12 per cent of hospitalised patients and in 60%–65% of patients in the intensive care unit.^{9 10} Severe depletion is defined as magnesium level of <1 mg/dL, moderate as 1–1.5 mg/dL and mild as 1.6–1.9 mg/dL.¹¹ The major clinical manifestations of hypomagnesaemia include neuromuscular hyperexcitability (tremor, tetany, convulsions), weakness, delirium, arrhythmias, hypocalcaemia and hypokalaemia.¹² The most common causes of hypomagnesaemia include gastrointestinal losses such as diarrhoea, malabsorption and proton pump inhibitors, as well as renal losses such as diuretics use, antibiotics use, uncontrolled diabetes mellitus, alcoholism and hypercalcaemia. The cause of this patient’s hypomagnesaemia is unclear; however, diarrhoea is the most likely reason as the patient did note multiple days of diarrhoea the previous week. Patient was not taking any diuretics, antibiotics or proton pump inhibitors. Additionally, patient’s blood sugar levels were tightly controlled while in the hospital with sliding scale insulin, so his history of diabetes mellitus was less likely contributing to his low magnesium level. Treatment of hypomagnesaemia is mainly repletion, which led to resolution of patient’s symptoms.

A case report from Central University Hospital in Spain similarly described a case of hypomagnesaemia as a stroke mimic.⁸ A 73-year-old woman presented to the emergency department with acute aphasia and right hemiparesis. Patient had an NIH Stroke Scale of 21 comparable with severe stroke and thus received thrombolysis treatment. However, her neuroimaging did not demonstrate signs of acute ischaemic disease. Instead, her magnesium level was found to be 0.24 mg/dL and patient had been taking omeprazole for multiple years. After repletion of her magnesium to 1.7 mg/dL and stoppage of the proton pump inhibitor, patient’s symptoms slowly resolved.

Stroke mimics may account for up to 30% of all acute stroke presentations, most commonly seizures, syncope, sepsis, migraine, brain tumours and metabolic conditions.² Hypomagnesaemia is less frequently seen as a mimic; however, its neuromuscular clinical manifestations such as weakness and tetany may present similarly as stroke symptoms. Patients will always benefit from a comprehensive evaluation for acute stroke; however, once it is deemed less likely, it is important to consider the stroke mimics to better treat the patient’s symptoms and to prevent future occurrence of similar episodes.

Patient’s perspective.

‘My left face feels weird and weak, like my eyelid is shutting and I can’t lift it.’—Patient’s description of his symptoms

Learning points.

• If a stroke is suspected, first proceed with a comprehensive workup to evaluate for an acute ischaemic or haemorrhagic stroke.

• Stroke mimics may account for up to 30% of all stroke presentations.

• Most common stroke mimics include seizures, syncope, sepsis, migraine headaches, brain tumours and metabolic conditions.

• Hypomagnesaemia can cause neurological symptoms that may also mimic an acute stroke.