Background: Isolated lower limb monoparesis is a rare clinical presentation of stroke, often mistaken for peripheral or spinal pathology. Infarcts in the anterior cerebral artery (ACA) territory, particularly involving the paracentral lobule, can present with contralateral lower limb weakness. Non contrast CT scan of brain which is usually the first investigation for suspected acute strokes could detect the ACS infarct in only 25%. 20 % of patients present with only isolated lower limb weakness and a normal NCCT brain in these cases may lead to erroneous localization of pathology to a peripheral cause. [1] Case Summary: We report three cases of patients presenting with isolated lower limb monoparesis due to ACA territory infarcts. Two patients underwent MRI brain with diffusion-weighted imaging (DWI) and one patient underwent urgent NCCT head, which was able to demonstrate the cerebral infarct. Lesions were localized to the medial frontal cortex, specifically the paracentral lobule. Timely imaging led to appropriate diagnosis and management with favorable outcomes. Conclusion: Central causes should be considered in patients presenting with lower limb monoparesis. ACA infarcts, though uncommon, are a critical differential diagnosis and can be accurately identified with neuroimaging.
Anterior cerebral artery (ACA) infarctions account for a small proportion of ischemic strokes. The ACA supplies the medial portions of the frontal and parietal lobes, including the paracentral lobule, which houses the motor cortex for the contralateral lower limb. Ischemia in this region can lead to isolated lower limb weakness, a finding more often attributed to spinal or peripheral nerve pathology. This uncommon presentation may delay diagnosis unless central causes are considered early. We present three cases of ACA territory infarcts with initial presentations as isolated lower limb monoparesis, highlighting the importance of neuroimaging in such clinical scenarios.
A 74 year old female presented with history of fall while getting up from sitting position which was associated with pain in left lower back and followed by weakness in left lower limb. These symptoms were sudden in onset and attributed to sudden jerk while trying to get up from sitting position. She denied any bladder/bowel issues.
In the emergency department, surgery resident initially evaluated her and decided to rule out a peripheral cause. Radiographs of LS spine and left hip revealed spondylotic changes in the lumbar spine and no abnormality in the left hip.
Neurological Examination: Grade 3/5 motor weakness in the left lower limb. Upper limbs and right lower limb strength were normal.
Imaging Findings:
- MRI Brain (DWI/FLAIR): Acute ischemic infarcts in the right half of genu and body of corpus callosum and right frontal lobe medial cortex involving the paracentral lobule. (Figures 1, 2 and 3)
Diagnosis: Right ACA territory acute ischemic infarct.
Management: Antiplatelet therapy and physiotherapy.
Outcome: Partial recovery with residual mild paresis at 3-month follow-up.
A 57-year-old male, old case of coronary artery disease presented with sudden-onset weakness in the right lower limb. He denied trauma, back pain, or bladder/bowel issues.
Neurological Examination: Grade 1/5 motor weakness in the right lower limb. Upper limbs and left lower limb strength were normal. Plantar reflex – mute on right and flexor on left.
Imaging Findings:
- MRI Brain (DWI/FLAIR): Acute ischemic infarcts in the left medial fronto-parietal cortex, left half of genu and body of corpus callosum. (Figures 4,5 and 6)
Diagnosis: Left ACA territory acute ischemic infarct.
Management: Antiplatelet therapy and physiotherapy.
Outcome: Partial recovery with residual mild paresis at 3-month follow-up.
A 63-year-old hypertensive and diabetic male developed right leg weakness over 24 hours.
Neurological Examination: Isolated right lower limb weakness (grade 2/5). No upper limb involvement or sensory loss. Normal power in left lower limb.
Urgent NCCT head was done for the patient.
Imaging Findings:
NCCT Head: Area of hypodensity (Average attenuation = 24 HU) in left half of genu and body of corpus callosum and adjacent left medial frontal cortex. (Figure 7)
MRI was not done for this patient as diagnosis was confirmed on NCCT head.
Diagnosis: Left ACA territory acute ischemic infarct.
Management: Dual antiplatelet therapy, statins, rehabilitation.
Outcome: Moderate improvement with assisted ambulation at 3 month follow up.
Isolated ACA territory infarcts are uncommon and account for 1.1% to 2.3 % of ischemic strokes [1,2,3,4]. The most frequent clinical findings include contralateral leg weakness, behavioral changes, and urinary incontinence. However, isolated lower limb monoparesis, as seen in our cases, is particularly uncommon and can mislead clinicians toward a peripheral diagnosis.
Isolated ACA territory infarction is relatively uncommon as compared to middle cerebral artery (MCA) territory infarction. It may be due to small diameter of the A1 segment of ACA as compared to that of MCA. The presence of the anterior communicating artery possibly plays an important role in emboli clearance [5]
The paracentral lobule is responsible for motor control of the lower limbs. Infarction in this area—especially when unilateral—can result in contralateral monoparesis without affecting the upper limbs or face. Imaging modalities such as MRI with diffusion-weighted sequences are essential in identifying acute infarcts. Vascular imaging (CTA or MRA) is valuable for assessing arterial patency and anatomical variants.
Prompt diagnosis and treatment with antiplatelets and supportive care result in good functional outcomes in most cases. The presence of vascular risk factors, such as hypertension, diabetes, and smoking, remains the most consistent predisposing factor for ACA infarcts. Peculiar manifestations of its clinical syndromes and the suspicion that many infarcts in this arterial territory are silent could result in the underdiagnoses of strokes involving the ACA or its branches [6]
Isolated lower limb monoparesis can be an atypical manifestation of ACA territory infarcts. A high index of suspicion and early imaging are critical for accurate diagnosis and timely management. Stroke should be considered in the differential diagnosis of acute monoparesis, especially in patients with vascular risk factors.
Figure 1(a), 1 (b) and 1(c): FLAIR hyperintensity in right half of genu of corpus callosum, right half of body of corpus callosum and right frontal paramedian cortex respectively.
Figure 2(a), 2(b) and 2(c): Areas appearing hyperintense on DWI, corresponding to areas of FLAIR hyperintensity.
Figure 3(a), 3(b) and 3 (c): Areas appearing hyperintense on DWI showing corresponding reduced ADC appearing hypointense on ADC images.
Figure 4(a), 4(b) and 4(c): FLAIR hyperintensity in left half of genu of corpus callosum, left half of body of corpus callosum and left fronto-parietal paramedian cortex respectively.
Figure 5(a), 5(b) and 5(c): Areas appearing hyperintense on DWI, corresponding to areas of FLAIR hyperintensity.
Figure 6(a), 6(b) and 6(c): Areas appearing hyperintense on DWI showing corresponding reduced ADC appearing hypointense on ADC images.
Figures 7(a), 7(b) and 7(c): NCCT head reveals hypodense areas involving left half of genu and body of corpus callosum and adjacent medial frontal lobe suggestive of acute ischemic infarct in the left ACA territory.
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