Most commonly, lacunar syndromes affect the elderly with long-standing hypertension. Otherwise, younger patients with lacunar syndromes may have a diagnosis of rare genetic conditions, such as CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy). The presenting complaint would usually not include cortical signs such as agnosia, aphasia, neglect, apraxia or hemianopsia. These lacunar infarcts usually cause symptoms over minutes to hours but may progress with a stuttering course. The clinical features and physical exam findings of lacunar syndromes are characteristic of the type of lacunar syndrome.

Pure motor hemiparesis: The patient presents with weakness on one side of the body (face, arm, and leg) without cortical signs and sensory symptoms. 

Pure sensory stroke: The patient presents with unilateral numbness of the face, arm, and leg without cortical signs or motor deficits. All sensory modalities will be impaired.

Ataxic hemiparesis: These patients present with unilateral limb ataxia and weakness that is out of proportion to the strength/motor deficit. Patients may also exhibit other ipsilateral cerebellar signs such as dysarthria, dysmetria, and nystagmus without exhibiting cortical signs.

Sensorimotor stroke: Patients present with weakness and numbness of the face, arm, and leg without cortical signs. Cortical function testing must be done meticulously to distinguish between a frontoparietal lobe (MCA) stroke and a subcortical stroke (posterior thalamus and internal capsule).

Dysarthria-clumsy hand syndrome: This is the least common of all lacunar syndromes. Patients present with facial weakness, dysarthria, dysphagia and dysmetria/clumsiness of one upper extremity.

Initial evaluation of a suspected lacunar stroke involves brain imaging with a brain CT and MRI. Since small perforating arteries are hard to visualize with CTA and MRA, the diagnosis is made by matching a patient’s clinical features with a small, noncortical infarct seen on CT/MRI. The initial CT/MRI is also useful in ruling out life-threatening conditions such as intracerebral hemorrhage or herniation.

MRIs have been shown to have a higher sensitivity and specificity than CT.[9] Diffusion-weighted imaging (DWI) is particularly important because it has higher sensitivity for acute infarcts when compared with T2 weighted MRI/FLAIR sequences.

In most cases, mapping a patient’s history of hypertension or diabetes and his/her clinical features with findings of acute ischemia on brain imaging is all that is needed for diagnosis of lacunar infarcts. However, if the patient is young and has no cerebral risk factors, further investigation may be required to determine if there is an embolic source. Vascular imaging and transcranial Doppler is warranted at the same time of initial CT/MRI to rule out large vessel ischemia.[10]

The acute treatment of lacunar infarctions is like that of acute ischemic strokes. Within 4.5 hours of symptom onset, patients should receive intravenous (IV) alteplase therapy. The contraindications to IV thrombolysis is the same as those for other types of acute ischemic strokes, some of which include ischemic stroke/head trauma in the past 3 months, previous intracranial hemorrhage, gastrointestinal (GI) malignancy or hemorrhage in the past 21 days, intracranial/spinal surgery in the past 3 months, and intra-axial intracranial neoplasm. For those patients not eligible for IV alteplase therapy, aspirin therapy is recommended. Otherwise, the acute treatment involves stabilization and early involvement of rehabilitation with speech and physical therapy.

The most important aspect of treatment for these patients is preventative. Aggressive blood pressure control, early high-dose statin therapy, and antiplatelet therapy are crucial. Anti-platelet therapy with aspirin, clopidogrel, and fixed-dose aspirin with dipyramidal are all acceptable medications. With the results of the CHANCE trial and the POINT trial, dual antiplatelet therapy for 3 weeks followed by single antiplatelet will provide the best scheme of therapy. More prolonged dual antiplatelet therapy (clopidogrel + aspirin) has not been shown to decrease the risk of recurrent strokes and resulted in a significantly increased risk of bleeding and death.[11] The present-day scheme of “aggressive medical therapy” with antiplatelet treatment, aggressive blood pressure control with a target of 120/80 mm Hg, high dose statin, good blood sugar control, stopping smoking, sodium reduction, and good weight control and lifestyle modification should be able to prevent at least 80% of strokes.[12] The LDL should be lowered to less than 100 with a high-intensity statin. Usually a high-intensity statin decreases LDL approximately 50% on an average. Strategies to reduce HbA1C less than 7 are also very important.  

The primary differential diagnoses that should be entertained are large vessel ischemic strokes (most commonly in the middle cerebral artery territory), intracranial hemorrhages (subarachnoid bleeds, subdural bleeds, intracerebral hemorrhage), seizures, and complicated migraine events.

As described earlier in the Evaluation section, large vessel ischemic strokes and intracranial hemorrhages are ruled out by brain imaging with CT and MRI. As described earlier, a large or giant lacune is pathophysiologically not a lacuna but rather, a striatocapsular infarct as described by Dr. Caplan resulting from atherothrombosis of the middle cerebral artery main-stem.  If an acute lacunar infarction is not visible on initial DWI, seizures and complicated migraines should be entertained as possible differential diagnoses.

Seizures will present with cortical signs in addition to focal neurologic deficits. Usually, neurologic deficits will also improve after 24 to 48 hours after the seizure event and post-ictal phase. Lastly, an EEG may be used to further rule out a seizure as the cause of the patient’s symptoms.

The main adverse event to be hypervigilant for in patients with acute lacunar infarctions is a hemorrhagic transformation or adverse bleeding events after IV alteplase therapy. Close monitoring with frequent neurologic exams and a high degree of suspicion can prevent these devastating events.

Preventative treatment is generally well tolerated. However, patients should be notified that there is an increased risk of bleeding on long-term antiplatelet therapy. Side effects of antihypertensive therapy, such as orthostatic hypotension and an increased risk of falls should also be explained to the patient. No data exists that lacunar infarct patients are at increased risk of statin myopathy over the general population. These medications should be prescribed at the lowest therapeutic dose.

The short-term prognosis of lacunar infarctions is better than other infarcts due to other stroke mechanisms. Multiple population-based epidemiological studies on lacunar infarcts have shown significantly better survival among patients who suffered from lacunar infarctions compared to those who suffered from non-lacunar infarcts.[5][13] These studies showed a case fatality of 0% to 3% within the first month and 3% to 9% within the first year, compared with 14% and 28%, respectively.

Though the short-term prognosis for patients with lacunar syndromes is better, there is not as stark a difference in the long-term prognosis when compared with non-lacunar events. Multiple studies have shown that the stroke recurrence rate and the risk of death between lacunar infarcts and non-lacunar infarcts are similar after 5 years. The main reason for the better 5-year survival rate in lacunar syndrome patients is attributed to the lower mortality within the first year of the ischemic event.[5][14]

As expected, patients that suffered from a lacunar infarction with worse initial neurologic deficits had a worse functional outcome. However, data does not exist comparing patient functional outcome and long-term prognosis between different mechanisms of lacunar infarction production.

After initial stabilization and neurology evaluation, many consultations are not required in the acute phase setting. Physical therapy (PT), speech therapy (ST), occupational therapy (OT), and rehabilitation services led by a Physical Medicine and Rehabilitation (PM and R) physician must be made immediately. Lacunar syndrome patients must be initially evaluated in the hospital as well as followed closely in the outpatient setting to ensure that the patient recovers as quickly as possible.

Furthermore, close contact between the patient’s neurologist, primary care physician, PM and R physician, and PT/ST/OT providers after hospital discharge further aids in the prevention of recurrent lacunar/ischemic strokes.

Patients must be educated on the importance of compliance with preventative medical therapy after he/she suffers from a lacunar syndrome. The pathophysiology of their syndrome/infarct should be explained, emphasizing that the most common cause of lacunar infarctions is chronic, uncontrolled hypertension.

This includes antihypertensive, statin, and diabetic medication compliance, following up regularly with their primary care physician, neurologist, and physical therapist, and doing regular exercises provided through physical therapy to regain neurologic function and improve the standard of living.

As mentioned earlier in the treatment and consultations sections, patients with lacunar infarctions must be managed and seen by a neurologist, a PM and R physician, and physical, occupational, and social therapists to get total care. In the outpatient setting, a neurologist may treat neurologic deficits like ataxic and motor hemiparesis with muscle relaxants like baclofen, tizanidine, and/or botox. More importantly, preventative measures with intense antihypertensive therapy, high dose statin therapy, and strict control of blood sugars must be initiated immediately after a lacunar ischemic event. Finally, outpatient rehabilitation therapy must be continued until a patient’s neurologic function can be returned to as close to his/her baseline prior to the infarction.