Bilateral Lower Extremity Strokes: What You Need To Know

Strokes can present with a wide range of symptoms, and while lateralizing weakness, numbness, and speech changes are among the most common, in rare cases, patients may exhibit more subtle or atypical symptoms. Bilateral lower extremity weakness is one such atypical symptom, and it can be challenging to diagnose and treat. This symptom can be caused by various factors, including spinal cord lesions, brain stem stroke, or lesions within the frontal cortex. It is important for medical professionals to be aware of this rare presentation of stroke to ensure prompt diagnosis and treatment, improving patient outcomes.

Loss of dexterity in the bilateral lower extremities

The study found that the stroke patients had significantly greater root mean square errors in a force tracking task compared to the control subjects. This indicates an impairment in the ability to control muscle force during submaximal contractions in the knee extensor muscles. The study also found that the root mean square error of the affected limb was significantly related to motor function as determined by the Fugl-Myer assessment.

These results demonstrate that stroke patients can have impairment in the dexterity of both the affected and the unaffected lower extremities. This loss of dexterity can impact the patient's ability to perform daily activities and their overall quality of life.

It is important to note that the loss of dexterity in the bilateral lower extremities may vary depending on the severity and location of the stroke. Additionally, the recovery of dexterity may also depend on the timing and effectiveness of rehabilitation interventions. Further research is needed to better understand the factors that contribute to the loss of dexterity and to develop effective treatments for this condition.

Bilateral lower extremity weakness

The differential diagnosis for bilateral lower extremity weakness is broad and includes central and peripheral causes. Central causes include stroke, intracranial haemorrhage, spinal cord lesions (such as demyelinating disease, infarction, or compression caused by a herniated disc, abscess, hematoma, or tumour), and brain tumours. Peripheral causes include distal nerve disorders such as Guillain-Barré syndrome, neuromuscular endplate disorders, and myasthenic crisis. Toxic, metabolic, and endocrine causes of neurologic dysfunction, such as hypokalemic periodic paralysis, severe hypo/hypernatremia, hypo/hypercalcemia, hypophosphatemia, hypoglycemia, hyperglycemic nonketotic syndrome, botulinum toxin, and ciguatera poisoning, can also lead to bilateral lower extremity weakness.

In the case of isolated lower limb weakness following a hemorrhagic stroke, monoparesis (decreased muscle strength in one limb) can be the singular sign of a stroke. Monoparesis is more common in the upper limbs and occurs in approximately 4% of patients admitted with their first stroke. The majority of strokes are ischemic (80%), while the remainder are hemorrhagic. Purely motor strokes have been found to have a more favourable outcome compared to strokes with more extensive motor or sensory deficits.

Bilateral lower limb strengthening exercises have been found to be effective in improving balance in hemiparetic stroke patients. These exercises can also improve functional performance, including standing, transfers, stair climbing, and gait.

Impaired visuomotor skills in the unaffected lower limb

A study by Kawahira et al. (2005) investigated visuomotor skills in patients with stroke, focusing on the unaffected lower limb. The study found that these patients had significantly greater root mean square errors when compared to both the affected limb and the limbs of control subjects. This indicates a decreased ability to control muscle force during contractions in the knee extensor muscles. Furthermore, the study found a significant relationship between the root mean square error of the affected limb and motor function as assessed by the Fugl-Myer test. This suggests that the impairment in the unaffected lower limb is related to the overall motor function of the patient.

The underlying cause of impaired visuomotor skills in the unaffected lower limb following a stroke is not yet fully understood. However, it is believed to be related to the disruption of neural pathways and brain structures involved in visuomotor control. The pyramidal tract, which is responsible for transmitting motor signals from the brain to the spinal cord, may be affected, leading to impaired muscle control. Additionally, areas of the brain such as the posterior parietal cortex, which is involved in the recalibration of visually guided reaching, may also play a role in this condition.

The independence of impairments in proprioception and visuomotor adaptation after a stroke has been explored in recent research. Proprioceptive impairments are common after a stroke and can impact an individual's sense of body position and motion. Visuomotor adaptation, on the other hand, refers to the process of modifying movements in response to errors caused by visual disturbances. While both proprioceptive impairments and visuomotor adaptation can occur after a stroke, studies suggest that these impairments may be independent of each other. This means that the presence of one impairment does not necessarily indicate the presence of the other.

Further research is needed to fully understand the underlying mechanisms and potential treatments for impaired visuomotor skills in the unaffected lower limb following a stroke. It is crucial to recognise that stroke rehabilitation should not only focus on the affected limb but also address any impairments in the unaffected limb to optimise the patient's overall motor function and quality of life.

Bilateral lower limb strengthening exercises

Hip Exercise

• Lie prone on an examination table with the leg to be exercised positioned off the side.
• With a straight leg and dorsiflexed ankle, slowly raise the leg as high as possible without causing pain, then slowly lower it back down.
• Repeat this motion, starting with moderate assistance and progressing to minimal assistance.
• Ensure the pelvis is stabilized to prevent twisting or arching of the back.

Ankle Exercise

• Lie supine on an examination table.
• Starting with a relaxed ankle and foot position, dorsiflex the ankle and hold the position, then slowly lower the foot back down.
• Repeat this motion, starting with moderate assistance and progressing to minimal assistance.

Squats

• Stand with feet shoulder-width apart, head up, chest tall, and hands on hips or out in front.
• Sit back into a squat, keeping knees in line with toes, then push through the heels to stand back up.
• For an added challenge, try split squats or lunges, taking a step out with one foot and lowering the knee to the ground before pushing back up.

Hip Abduction

• Stand on one leg and lift the other leg out to the side without tipping the body.
• For support, use a chair or bar, and to progress the exercise, add a theraband around the ankles.

4-Point Kneel Hip Extension/ Donkey Kicks

• Start on hands and knees with hands under shoulders and knees under hips.
• Bend the moving knee to 90 degrees and kick it up towards the ceiling by activating the glutes.
• Keep the trunk steady and don't rock the hips or pelvis.

These exercises should be performed under the guidance of a qualified healthcare professional and tailored to the individual's needs and capabilities. It is important to ensure proper form and technique to avoid injury and maximize the benefits of the exercises.

Isolated lower limb weakness

The differential diagnosis for monoparesis can include lesions to the brain, spinal cord, and affected limb. Radiculopathy, myelopathy, myopathy, neuropathy, cerebral damage, ischemic lesions, and distal embolism are among the causes of monoparesis. It is important to differentiate between central and peripheral lesions to provide appropriate treatment. On physical examination, some key factors to consider are the pattern of muscle groups affected, the presence or absence of atrophy, fasciculations, or spasticity, hyperactivity of deep tendon reflexes, and the presence of extensor plantar reflexes.

When investigating a patient with monoparesis, further testing may be required to refine the differential diagnosis. This can include a complete blood count (CBC), electrolytes, glucose, coagulation status (international normalized ratio (INR) and partial thromboplastin time (PTT)), and creatinine. An electrocardiogram (ECG) should also be performed to look for cardiac arrhythmia, particularly atrial fibrillation, as it is associated with ischemic stroke.

If a central cause is suspected, initial imaging should include magnetic resonance imaging (MRI) or unenhanced cranial computerized tomography (CT) to look for infarction or hemorrhage. If there is a concern for metastatic brain lesions, a CT or chest x-ray may be necessary.

While monoparesis following a stroke is typically acute, it can be slow in onset, leading to misdiagnosis. The lack of additional clinical symptoms in monoparesis presentations provides challenges for determining the origin, so it is crucial to consider the possibility of stroke when presented with a patient exhibiting acute onset of purely motor monoparesis.

Case Study: Isolated Lower Limb Weakness Following Hemorrhagic Stroke

A 60-year-old male presented to the Emergency Department (ED) with an acute inability to bear weight on his left leg. He reported no numbness or other sensory changes and no history of trauma. The patient had a 50-pack-year smoking history and was diagnosed with type II diabetes mellitus 10 years prior. He also had a history of asymptomatic atrial fibrillation.

On examination, the patient appeared alert and oriented, with intact speech and facial function. His upper limbs had full strength, and the right leg had 5/5 strength. Left leg weakness of 3/5 was apparent throughout hip, knee, and ankle resisted motion tests. Bulk and tone were normal, with no fasciculation noted, and leg sensation was equal bilaterally. Tendon reflexes were brisk and symmetrical, except for a Babinski equivocal on the left.

The patient's ECG showed atrial fibrillation. Blood work revealed a well-controlled Hb A1C level, and chest x-ray was clear. Initial unenhanced CT imaging showed an intraparenchymal hemorrhage in the right frontal lobe with vasogenic edema. The lesion corresponded to the lower limb territory in the primary motor cortex of the precentral gyrus. A follow-up CT angiogram showed the intraparenchymal hemorrhage to be stable, with no evidence of venous sinus thrombosis, vascular malformation, hydrocephalus, or underlying mass lesions. The patient was diagnosed with a stable hemorrhagic stroke and admitted to the stroke unit for observation.

An MRI performed a week later revealed that the intraparenchymal hemorrhage in the high right frontal lobe was likely the result of amyloid angiopathy. The patient's muscle weakness improved significantly over the next two weeks, and he was discharged on anticoagulation therapy for his atrial fibrillation, along with aggressive risk factor control, including smoking cessation and diabetes management.

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