Monoparesis as a manifestation of acute ischemic stroke is a rare disease entity. Depending on the study definition for monoparesis, its reported prevalence varies over a broad range from 0.7 to 4.1% [
Accordingly, we tried (1) to estimate the prevalence of monoparetic stroke potentially simulating peripheral neuropathy in our stroke cohort, (2) to investigate its lesion pattern, stroke mechanism, and initial neurologic findings, and (3) to discover its characteristic clinical features and prognosis by doing a cross-sectional and longitudinal comparison between patients with monoparetic and nonmonoparetic strokes.
We initially recruited 623 acute ischemic stroke patients who were consecutively admitted to the neurovascular or cardiovascular center of Sejong General Hospital within 7 days after symptom onset (between January 2011 and August 2015). From these patients, 16 patients with prestroke modified Rankin scale (mRS) ≥ 3 were excluded. Of the 607 patients, 31 patients (5.1%) were prospectively classified as having a monoparetic stroke and meticulously examined. Of 576 patients with nonmonoparetic strokes, 15 with incomplete study and 6 with no follow-up data of more than 6 months were excluded from this analysis. The Institutional Review Board of Sejong General Hospital approved this study, and informed consent was obtained from all included patients or their legal guardians to publish clinical details.
All survivors were followed up by outpatient clinic attendance. However, 126 patients were not followed up by our clinic at the time of this study. Of these, 93 patients’ condition could be ascertained by contacting patients themselves or their relatives via telephone interview. We scored mRS using a structured interview for accurate grading issued by the Korean Clinical Research Center for Stroke. 33 patients lost to follow-up were censored at their last clinic visit.
We monitored a major vascular event (stroke, acute coronary syndrome, or peripheral artery occlusion) and mortality after index stroke in our cohort. The nature of the vascular event and the cause of death were principally based on medical records from the treating physician at Sejong General Hospital. In the absence of such records, medical information was acquired from treating physicians at other institutions. Uncertain information was excluded from the study.
An ischemic stroke was defined as a focal neurologic deficit of an abrupt onset lasting > 24 hours with an evidence of new infarct lesions on brain imaging. A monoparetic stroke was defined as the presence of a motor deficit in either an arm (hand) or a leg, irrespective of sensory involvement but without facial weakness or speech disturbances. All the strokes were classified as large artery atherosclerosis (LAD), cardioembolism, lacune, two or more mechanisms, cryptogenic stroke, and other causes, according to the TOAST subtype classification system [
The clinical information included age, gender, history of hypertension, diabetes mellitus and hyperlipidemia (defined as a total cholesterol level > 200 mg/dl or a low-density lipoprotein cholesterol > 130 mg/dl at the time of presentation or a history of treatment), current cigarette smoking, a previous history of stroke and ischemic heart disease (defined as a known history or clinical demonstration of myocardial infarction or angina pectoris), atrial fibrillation, valvular heart disease, heavy alcohol consumption (>26 Soju drinks/month; about 20% alcohol), medication use (anthrombotics and statin) for ≥ 3 months at stroke onset, and the National Institutes of Health Stroke Scale (NIHSS) score at admission. All 586 patients underwent routine 12-lead ECG, transthoracic echocardiography, and 24-hour Holter monitoring. A total of 117 patients (20.0%) who could accept an esophageal transducer had transesophageal echocardiography for further investigation of the cardioembolic source (e.g., left atrial thrombus, atrial septal abnormality, or spontaneous echo contrast) requested by an attending physician.
All the included patients underwent 1.5-T magnetic resonance imaging (MRI) on admission. The MRI consisted of the diffusion-weighted image, gradient echo image, fluid-attenuated inversion recovery image, three-dimensional time-of-flight (TOF) intracranial MR angiography (MRA), and contrast-enhanced MRA, including extracranial carotid and vertebral arteries. Stenoses of brain vessels on MRA were classified as intracranial or extracranial atherosclerotic stenosis, based on the location of the arterial stenosis. More than 50% signal loss on MRA was considered to be significant to the categorization of a stenosis pattern.
In monoparetic stroke, lesion pattern and location were described as follows: (1) the presence or absence of cortical involvement, (2) multiple lesions (more than two topographically distinct lesions) or single lesion (uninterrupted lesion visible in contiguous territories) [
Statistical analyses were performed with SPSS software, version 18.0 (SPSS Inc., Chicago, IL). The independent
The mean age of 586 patients (313 men and 273 women) was 67.6 years (range: 18–97) at admission. Table
Comparison of clinical features between monoparetic and nonmonoparetic stroke patients at admission: number (%), mean ± SD.
Nonmonoparetic stroke |
Monoparetic stroke |
| |
---|---|---|---|
Age | 67.5 ± 13.7 | 68.8 ± 11.8 | 0.611 |
Female | 260 (46.8) | 13 (41.9) | 0.594 |
Hypertension | 371 (66.8) | 23 (74.2) | 0.396 |
Diabetes | 164 (29.5) | 12 (38.7) | 0.279 |
Hyperlipidemia | 287 (51.7) | 21 (67.7) | 0.082 |
Current smoking | 150 (27.0) | 8 (25.8) | 0.882 |
Previous stroke | 85 (15.3) | 2 (6.5) | 0.177 |
Ischemic heart disease | 115 (20.7) | 10 (32.3) | 0.127 |
Atrial fibrillation | 192 (34.6) | 9 (29.0) | 0.525 |
Valvular heat disease | 113 (20.4) | 5 (16.1) | 0.568 |
Alcohol | 92 (16.6) | 3 (9.7) | 0.310 |
Previous medication | |||
Antiplatelet | 221 (39.8) | 15 (48.4) | 0.344 |
Anticoagulant | 80 (14.4) | 6 (19.4) | 0.449 |
Statin | 145 (26.1) | 16 (51.6) | 0.002 |
Stenosis | 286 (51.5) | 14 (45.2) | 0.490 |
Stenosis pattern | 0.620 | ||
Intracranial and extracranial | 82 (14.8) | 3 (9.7) | |
Intracranial only | 157 (28.3) | 7 (22.6) | |
Extracranial only | 47 (8.5) | 4 (12.9) | |
No stenosis | 269 (48.5) | 17 (54.8) | |
TOAST classification | 0.505 | ||
Large artery atherosclerosis | 128 (23.1) | 9 (29.0) | |
Lacune | 85 (15.3) | 3 (9.7) | |
Cardioembolism | 207 (37.3) | 12 (38.7) | |
Two or more | 92 (16.6) | 3 (9.7) | |
Cryptogenic | 35 (6.3) | 4 (12.9) | |
Other causes | 8 (1.4) | 0 (0) | |
Nonlacunar | 470 (84.7) | 28 (90.3) | 0.392 |
Initial NIHSS | 6.6 ± 7.9 | 1.3 ± 1.0 | <0.001 |
Poor outcome | 191 (34.4) | 2 (6.5) | 0.001 |
NIHSS: the National Institutes of Health Stroke Scale. Poor outcomes indicate modified Rankin scale ≥3 at 3 months.
In a monoparetic stroke, the most frequent stroke subtype was cardioembolism (38.7%), followed by LAD (29.0%), cryptogenic stroke (12.9%), lacune (9.7%), and two or more mechanisms (9.7%, cardioembolism and LAD); most patients had nonlacunar strokes (90.3%). Initial NIHSS scores were far lower, and 6-month outcomes (mRS) were much better in this group compared with the nonmonoparetic stroke group. Moreover, monoparetic stroke was negatively associated with poor functional outcomes (6-month mRS ≥ 3) in univariate and multivariate logistic regression analyses (Table
Logistic regression analysis for poor outcomes (6-month mRS ≥ 3).
Univariate |
|
Multivariate |
| |
---|---|---|---|---|
OR (95% CI) | OR (95% CI) | |||
Monoparesis | 0.132 (0.031–0.561) | 0.006 | 0.123 (0.028–0.543) | 0.006 |
Age ≥65 years | 3.624 (2.414–5.441) | <0.001 | 2.120 (1.336–3.363) | 0.001 |
Female | 2.540 (1.782–3.622) | <0.001 | 1.716 (1.120–2.628) | 0.013 |
Hypertension | 1.191 (0.821–1.727) | 0.358 | 1.017 (0.655–1.578) | 0.940 |
Diabetes | 1.452 (1.004–2.101) | 0.048 | 1.375 (0.900–2.102) | 0.141 |
Hyperlipidemia | 1.067 (0.755–1.508) | 0.713 | 0.858 (0.571–1.290) | 0.461 |
Previous stroke | 2.296 (1.446–3.644) | <0.001 | 1.740 (1.053–2.874) | 0.031 |
Ischemic heart disease | 1.313 (0.870–1.982) | 0.195 | 1.150 (0.704–1.881) | 0.577 |
Atrial fibrillation | 1.666 (1.165–2.383) | 0.005 | 1.748 (1.137–2.686) | 0.011 |
Smoking | 0.347 (0.221–0.545) | <0.001 | 0.722 (0.412–1.265) | 0.255 |
Alcohol | 0.333 (0.186–0.595) | <0.001 | 0.671 (0.339–1.329) | 0.253 |
Stenosis | 2.496 (1.743–3.574) | <0.001 | 2.322 (1.499–3.597) | <0.001 |
OR: odds ratio; CI: confidence interval.
Of 31 monoparetic strokes, 19 (61.3%) and 12 (38.7%) involved arm and leg each. 12 patients (38.7%) had no significant proximal weakness in the involved limb (motor score of NIHSS = 0) at admission. Only 3 patients (9.7%) had a grave weakness corresponding to a motor score ≥2 on NIHSS. A total of 10 patients (32.3%) had sensory symptoms. Upper motor neuron signs were found in only 11 patients (35.5%). The most frequently-found upper neuron sign was hyperactive and asymmetric deep tendon reflex (32.3%), followed by the Chaddock sign (12.9%), Hoffman sign (9.7%) and the Babinski sign (3.2%). Most of the patients (80.6%) had a cortical lesion, and 64.5% of the patients had multiple lesions. The most frequently involved region was the precentral gyrus with additional regions (45.2%), followed by the medial frontal lobe (22.6%), subcortical regions (19.4%), the precentral knob area only (9.7%), and the parietal lobe only (3.2%) (Table
Initial neurologic findings and lesion patterns of patients with monoparetic stroke: number (%).
Total ( |
|
---|---|
Location of monoparesis | |
Arm | 19 (61.3) |
Leg | 12 (38.7) |
Motor score of NIHSS | |
0 | 12 (38.7) |
1 | 16 (51.6) |
2 | 2 (6.5) |
3 | 1 (3.2) |
Sensory involvement | 10 (32.3) |
Any upper motor neuron sign | 11 (35.5) |
Hyperactive deep tendon reflex | 10 (32.3) |
Babinski sign | 1 (3.2) |
Chaddock sign | 4 (12.9) |
Hoffman sign | 3 (9.7) |
Lesion pattern | |
Cortical involvement | 25 (80.6) |
Multiple | 20 (64.5) |
Lesion location | |
Precentral knob area only | 3 (9.7) |
Precentral gyrus with additional regions | 14 (45.2) |
Parietal lobe only | 1 (3.2) |
Medial frontal lobe | 7 (22.6) |
Subcortical regions | 6 (19.4) |
NIHSS: the National Institutes of Health Stroke Scale.
Lesion location and patterns on the diffusion-weighted image in monoparetic stroke. The white arrow indicates acute infarct lesion. (a) Precentral knob area only. (b) Precentral gyrus with additional regions. (c) Parietal lobe only. (d) Medial frontal lobe supplied from the anterior cerebral artery. (e) Corona radiata (posterior medial). (f) Medial medulla. (g) Centrum semiovale. (h) Internal border zone. (i) Rostral anterolateral pons.
The median follow-up period was 32.0 months (mean: 32.2; range: 6–70). During that period, 145 of the 555 patients (26.1%) with nonmonoparetic strokes died, whereas only 2 of the 31 patients (6.5%) with monoparetic strokes died due to cardiac disease (large atrial septal defect with Eisenmenger syndrome) and an unknown cause each. The cause of death in nonmonoparetic stroke group was as follows: brain herniation related to index stroke (14 patients, 9.7%), ischemic stroke recurrence (12 patients, 8.3%), heart failure (14 patients, 9.7%), acute myocardial infarction (5 patients, 3.4%), cancer (16 patients, 11.0%), pneumonia (17 patients, 11.7%), sepsis or other infections (7 patients, 4.8%), traumatic intracranial hemorrhage related to a fall (2 patients, 1.4%), spontaneous intracranial hemorrhage (3 patients, 2.1%), hemoptysis (2 patients, 1.4%), other causes (5 patients, 3.4%: aortic dissection in 1, small bowel infarct in 1, traffic accident in 1, renal failure in 1, and suicide in 1), and unknown cause (48 patients, 33.1%).
Mortality was significantly higher in patients with nonmonoparetic strokes (
Cox proportional hazards models for mortality.
Univariate |
|
Multivariate |
| |
---|---|---|---|---|
HR (95% CI) | HR (95% CI) | |||
Monoparesis | 0.221 (0.055–0.893) | 0.034 | 0.229 (0.056–0.931) | 0.039 |
Age ≥65 years | 3.106 (2.045–4.716) | <0.001 | 2.143 (1.369–3.355) | 0.001 |
Female | 1.911 (1.373–2.661) | <0.001 | 1.246 (0.867–1.791) | 0.234 |
Hypertension | 0.973 (0.693–1.367) | 0.875 | 0.993 (0.681–1.449) | 0.971 |
Diabetes | 1.078 (0.760–1.527) | 0.674 | 1.083 (0.751–1.562) | 0.669 |
Hyperlipidemia | 0.771 (0.558–1.066) | 0.116 | 0.665 (0.467–0.947) | 0.024 |
Previous stroke | 1.492 (0.993–2.240) | 0.054 | 1.174 (0.776–1.777) | 0.446 |
Ischemic heart disease | 1.403 (0.970–2.031) | 0.072 | 1.522 (1.012–2.291) | 0.044 |
Atrial fibrillation | 1.644 (1.188–2.276) | 0.003 | 1.477 (1.032–2.112) | 0.033 |
Smoking | 0.369 (0.230–0.591) | <0.001 | 0.698 (0.409–1.193) | 0.189 |
Alcohol | 0.288 (0.147–0.565) | <0.001 | 0.467 (0.225–0.968) | 0.041 |
Stenosis | 1.629 (1.169–2.268) | 0.004 | 1.449 (0.990–2.120) | 0.057 |
HR: hazard ratio; CI: confidence interval.
Comparison of Kaplan-Meier curves between monoparetic (1) and nonmonoparetic (2) strokes.
In our stroke cohort, the prevalence of monoparesis was 5.1%, which is higher than that reported in previous studies [
In this study, there is no significant difference in basic characteristics between patients with monoparetic and nonmonoparetic strokes, except prestroke statin use. As expected in prior studies, the monoparetic stroke group had a better functional outcome on 6-month mRS compared to nonmonoparetic stroke group [
Although most of the lesions were located in cerebral cortices, several subcortical regions were also involved. Considering topographical convergence along the descending motor fiber pathway, a cerebral infarct causing monoparesis in the subcortical region tends to be rare and, if any, would possibly be small and solitary. Thus, only six of our patients (19.4%) had a lesion in such regions, and, of these, 3 cases (50%) were classified as lacune. Particularly, a somatotopic organization of motor fibers in corona radiata and rostral pons is relatively well known. Namely, motor fibers for arm and leg are arranged along the anterolateral-to-posteromedial axis in corona radiata and anteromedial-to-dorsolateral axis in the rostral pons, respectively [
Patients with monoparetic strokes had a significantly lower risk of mortality during a mean follow-up period of 2.7 years. Stroke recurrence and major vascular events were observed in 3 (9.7%) and 4 (12.9%) patients with monoparetic strokes, respectively. The recurrence rate is lower than that previously reported in another study (14% of recurrence over 1.7 years mean follow-up) [
The main limitation of our study was based on a small sample data of a single center, potentially leading to selection bias. Only 31 patients were recruited with monoparetic strokes. Therefore, our results might not be generalizable to other stroke populations. However, most studies to date have consisted of a small number of case series. In addition, in two prior large studies that included more than 50 patients [
Acute onset monoparesis should be carefully examined for the probability of stroke, though it is infrequently encountered, because of the paucity of upper motor neuron sign. Since monoparetic stroke seems mostly associated with cardiac or artery-to-artery embolism, detailed studies to detect potential embolic sources should be performed. It could have a better outcome in mortality and functional recovery. However, the risk of further vascular events including stroke recurrence does not seem to be lower compared to nonmonoparetic strokes.
The authors declare that they have no conflicts of interest.
This work was supported by the Soonchunhyang University Research Fund.