Diagnosis and Treatment of Lacunar Infarcts

Diagnosis and Treatment of Lacunar Infarcts

By Dr.Ravindra Patil

Introduction

Stroke is one of the most common illnesses causing paralysis and loss of sensation. Often one side of the body is paralysed when a major part of the brain is deprived of blood either by a blood clot or cerebral haemorrhage. However there is another type of stroke on a much smaller scale. It is called Lacunar strokes, a type of stroke caused by the occlusion of small deep penetrating branches of the main brain arteries. They include branches from all the cerebral arteries. Most lacunar strokes involve the non-cortical areas and remain asymptomatic because only small parts of the brain are affected. However, if many small parts of the brain suffer ischaemia [a condition where a body part suffers lack of blood supply and dies, which is known as an infarct], the multiple small lacunar infarcts can lead to significant movement, sensory and functional disabilities.

Table of Contents

Causes of Lacunar Infarcts

In lacunar infarction, the small penetrating cerebral vessels supplying the subcortical areas are occluded due to various vascular disease conditions.

In some cases, small pieces of blood clots called embolic fragments from a distant part can travel the small arteries of the brain and cause deep penetrating artery occlusion, ischemia and infarction.

Lacunar infarcts and strokes are in turn caused by hypertension, diabetes, smoking, high LDL levels, carotid artery atherosclerosis, peripheral artery disease, TIA, and hyperhomocysteinemia.

 

Certain genetic factors also increase the risk of developing small vessel disease. 

Pathophysiology

Occlusion or blockage of the small penetrating arteries causes small lacunar strokes. Their size varies from 3 mm to 20 mm in dimension. However, only 17% of lacunar strokes are less than 10 mm in size.

Small arterial occlusions are caused by lipohyalinosis and micro-atheroma formation.

History and Physical Examination

As with ischemic strokes, lacunar infarcts usually present with sudden onset of neurological deficits. However, some lacunar infarctions may present in a stepwise pattern and are known to worsen in a short time.

Lacunar infarcts are common in the thalamus, basal ganglia, pons, and white matter of the internal capsule.

Lacunar infarcts can be asymptomatic.

Clinical presentation depends on the area of brain involvement.

Certain lacunar infarcts, like in the posterior limb of the internal capsule or the pons, can present with severe hemiplegia.

Lacunar strokes seldom affect memory, language, and judgment.

Types of lacunar Infarcts

Pure motor hemiparesis – contralateral hemiparesis of the face, arm, and leg. [45%].

Ataxic hemiparesis comprises 10 to 18% of cases. It causes hemiparesis of the contralateral face and leg and ataxia of the contralateral limb. Lack of coordination is the prominent feature of this stroke.

Pure sensory stroke involves the thalamus or corona radiata; it presents with the absent or abnormal sensation of the contralateral of the face, arm, and leg. It accounts for 7% of cases of lacunar strokes.

Dysarthria: clumsy hand syndrome and problems pronouncing words due to voice box muscle weakness

A sensory: motor stroke is the second most common type of lacunar strokes. They account for 20% of cases.

Evaluation

Sudden onset of neurological deficit requires a plain head CT scan and CT angiogram of the head and neck. MRI is a superior imaging method. Carotid ultrasound also helps diagnose an atherosclerotic narrowing of the extracranial carotid artery.

Treatment

The initial goal of acute-stage treatment is ensuring medical stability and determining if the patient is fit for thrombolysis. Treatment with ‘tissue plasminogen activator’ (TPA) improves outcomes for ischemic stroke patients if TPA is administered within 4.5 hours of the first symptoms. But cerebral haemorrhage must be ruled out before TPA treatment. An acute lacunar infarct is efficiently treated with TPA.

After 4.5 hours, dual antiplatelet therapy [DAPT] with aspirin and clopidogrel within 24 hours of symptom onset is begun and continued for 21 days. DAPT in the acute phase effectively lowers recurrent ischemic stroke for 90 days from symptom onset.

Management of blood pressure if present, is done allowing for permissive hypertension. This means, if the BP is lowered to normal levels, the brain may be starved of oxygen. Lowering the blood pressure below185/110 mmHg is ideal. Blood sugar management is done to maintain normal blood glucose levels at 60–180 mg/dL. Blood volume is corrected by giving isotonic saline and oxygen saturation must be above 90%. Statin therapy to reduce LDL is begun if LDL is high.

Stroke Prevention

A lacunar infarct patient is likely to suffer stroke. Hence primary and secondary stroke prevention remains an essential part of the treatment plan. Primary prevention includes the prevention of the first episode of stroke, and secondary prevention includes the prevention of recurrence.

Antihypertensive medications, diabetes control, cholesterol-lowering agents, smoking cessation, dietary intervention, weight loss, and exercise as appropriate are done for primary prevention.

Secondary prevention is done to prevent recurrence of stroke. It includes antithrombotic agents like aspirin, clopidogrel, extended-release dipyridamole, and ticlopidine and managing underlying risk factors. Antiplatelet agents reduce the risk of recurrence in patients with lacunar strokes.

Differential Diagnosis

Differential diagnoses of lacunar infarcts include the following:

  • Ischemic stroke in the middle cerebral artery territory
  • Intracranial haemorrhages
  • Seizures
  • Complicated migraine
  • Brain tumours
  • Multiple sclerosis (MS)

Prognosis

Earlier studies suggested that lacunar stroke has a better prognosis compared to other strokes. It has a high survival rate, a low recurrence rate, and a relatively good functional recovery. But there is an increased risk of death, mainly from cardiovascular causes.

Complications

Lacunar strokes are thought to be the leading cause of vascular dementia and cognitive impairment. Accumulated lacunar infarcts can lead to other disease-related complications due to physical disability, including, but not limited to, aspiration pneumonia, deep vein thrombosis, pulmonary embolism, urinary tract infection, depression, and decubitus ulcers.

Rehabilitation

Physical therapy and rehabilitation are essential steps for lacunar stroke patients with physical disabilities. Speech therapy, occupational therapy may be needed after hospital care to regain strength and functions. The goal of rehabilitation is to optimize functional recovery.

How to prevent Stroke

People need to be aware of risk factors of stroke. Take medicines regularly for diabetes, BP, antithrombotic agents etc… Maintain a healthy diet, exercise regularly, avoid smoking, and avoid excessive alcohol use. Correct lipid disorders with medicines.

The timeline of recovery from a lacunar stroke is different for everyone. Home safety is essential. Fall risk due to physical disability is common. Depression is common in people who have experienced a stroke and should be addressed if present. Cognitive impairment due to multiple subcortical strokes can progress to vascular dementia and should be monitored.

Enhancing Healthcare Team Outcomes

Patients with lacunar infarctions must be managed by a neurologist, family clinicians, nursing staff, and physical, occupational, and social therapists, all operating as an interprofessional team, to receive comprehensive care. Samarth Neuro and Super Speciality Hospital has all the facilities and specialist doctors to mange acute Lacunar Stroke.

Rehabilitation therapy must be continued to maximize the patient’s neurologic function to bring them close to their baseline before the infarction.

Long-term care coordination is the responsibility of the Family Physicians. Emphasis on managing stroke risk factors includes intense antihypertensive therapy, lipid management, and strict control of blood sugars are essential after the lacunar ischemic event.