Lacunar syndrome refers to a group of neurological disorders that result from small subcortical infarcts affecting the white matter and deep gray matter of the brain. Lacunar infarcts are small (less than 15 mm in diameter) lesions that occur within the territory of perforating arterioles that supply the deep structures of the brain.
What causes lacunar syndrome?
Lacunar infarcts are most commonly caused by small vessel disease leading to occlusion of the perforating arterioles. The most frequent cause is hypertensive arteriopathy, in which chronic high blood pressure damages the small penetrating arteries that supply deep brain structures. Other causes include embolism from the heart in atrial fibrillation, congophilic angiopathy (blood vessel changes seen in Alzheimer’s disease), vasculitis, CADASIL, Fabry disease, and mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes (MELAS).
Risk factors for lacunar stroke include:
- Hypertension
- Diabetes
- Dyslipidemia
- Smoking
- Older age
- African American ethnicity
What are the symptoms of lacunar syndrome?
There are several classic lacunar syndromes that correspond to the location of the infarction in the brain:
Pure motor stroke
This is the most common lacunar syndrome, accounting for about a third of cases. It occurs due to infarction of the posterior limb of the internal capsule, basis pons, or cerebral peduncle. Symptoms include:
- Ipsilateral paralysis and/or weakness of face, arm, and leg
- In severe cases, paralysis of entire one side of the body (hemiplegia)
- Face and arm more affected than leg
- No sensory loss
Pure sensory stroke
Results from lesion in the ventral posterolateral nucleus of the thalamus. Characterized by:
- Contralateral loss of sensation in face, arm, leg and trunk
- Pseudoathetosis (involuntary writhing movements of fingers) – rare
Ataxic hemiparesis
Caused by infarct of basis pons on side opposite symptoms. Features:
- Ipsilateral weakness of arm and leg
- Ipsilateral cerebellar-like ataxia (incoordination)
- Dysarthria (slurred speech)
- Nausea, vomiting, nystagmus common in acute phase
Dysarthria-clumsy hand syndrome
Results from infarction in the basis pons. Characterized by:
- Ipsilateral weakness and poor coordination of hand
- Dysarthria (slurred speech)
- Usually face and leg strength preserved
Mixed lacunar syndromes
May have overlapping features of pure motor, pure sensory, ataxic hemiparesis, or dysarthria-clumsy hand syndromes. For example:
- Sensorimotor stroke – Both motor and sensory deficits
- Ataxic hemiparesis with facial paresis – Ataxia plus facial droop on same side
How is lacunar syndrome diagnosed?
Diagnosis of lacunar syndrome involves:
- Neurological exam to identify deficits
- Brain imaging (CT or MRI) to identify small deep infarct
- Vascular imaging like CTA or MRA to evaluate blood vessels
- Cardiac imaging like echocardiogram to rule out embolic sources
- Lab tests for vascular risk factors and causes (diabetes, lipids, etc)
MRI is the most sensitive for identifying small lacunes. The location of the infarct seen on imaging can help determine the affected vessel and confirm the lacunar syndrome.
How is lacunar syndrome treated?
Treatment of acute lacunar stroke is similar to other strokes and aims to limit damage by restoring blood flow. This includes:
- Intravenous thrombolysis (tPA) – clot busting drug
- Endovascular thrombectomy – mechanical clot removal
- Supportive care – blood pressure management, hydration, etc.
Preventing future strokes involves controlling vascular risk factors through lifestyle changes and medications:
- Blood pressure control – antihypertensive medications
- Glucose control in diabetes
- Dyslipidemia treatment with statins
- Smoking cessation
- Antiplatelet therapy – aspirin, Plavix
Rehabilitation services like physical, occupational and speech therapy help maximize recovery from neurological deficits.
What is the prognosis for lacunar syndrome?
Compared to other strokes, lacunar infarcts tend to cause milder initial symptoms but have a higher risk of recurrence. Overall prognosis depends on:
- Size and location of the infarct
- Presence of additional small vessel disease in the brain
- Degree of neurological deficits
- Control of vascular risk factors
Patients with isolated small lacunes and few risk factors have better outcomes. Large lacunes or confluent white matter disease related to extensive small vessel disease have poorer prognosis.
While initial lacunar strokes may be less severe, up to 50% of patients develop additional silent lacunes over 5 years. Recurrent strokes and accumulating neurological injury leads to increased disability and dementia.
Epidemiology of lacunar infarcts
Some key epidemiological statistics on lacunar infarcts:
- Represent about 25% of all ischemic strokes
- More common in African Americans
- Incidence increases with age
- Men affected slightly more than women
- Hypertensive patients have a 7-fold increased risk
- Diabetics have a 3-fold increased risk
The table below shows incidence of lacunar stroke per 100,000 people by age and race/ethnicity in the United States:
| Age | White | Black | Hispanic |
|---|---|---|---|
| 45-54 years | 6 | 55 | 16 |
| 55-64 years | 43 | 128 | 47 |
| 65-74 years | 92 | 256 | 125 |
| 75-84 years | 224 | 444 | 266 |
This shows the sharp increase in incidence of lacunar stroke with age, especially in African American populations.
Conclusion
In summary, lacunar syndrome refers to the clinical manifestation of small deep infarctions in the brain resulting from occlusion of penetrating arterioles. It frequently manifests as pure motor, pure sensory, sensorimotor, ataxic or dysarthric syndromes depending on the location. Diagnosis is made by brain imaging showing characteristic small deep lesions. Treatment acutely involves restoring blood flow and preventing early recurrence. Long term management focuses on controlling vascular risk factors. Prognosis depends on the extent of small vessel disease and preventing recurrent strokes through risk factor modification.