Online newspaper of professor Yasser Metwally

The author:Professor Yasser Metwally

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INTRODUCTION

Background: The lacunar hypothesis proposes that (1) symptomatic lacunes present with distinctive lacunar syndromes and (2) a lacune is due to occlusion of a single deep penetrating artery generated by a specific vascular pathology. This concept is controversial because different definitions of lacunes have been used. Lacunes may be confused with other empty spaces, such as enlarged perivascular (Virchow-Robbins) spaces, in which the specific small vessel pathology occasionally is absent. Originally, lacunes were defined pathologically, but lacunes now are diagnosed on clinical and radiological grounds. This problem is compounded by the present inability to image a single penetrating artery.

Lacunes may be defined as small subcortical infarcts (less than 15 mm in diameter) in the territory of the deep penetrating arteries and may present with specific lacunar syndromes or may be asymptomatic. Unfortunately, neither the 5 classical lacunar syndromes nor the radiological appearances are specific for lacunes. Lacunes occur most frequently in the basal ganglia and internal capsule, thalamus, corona radiata, and pons.

Pathophysiology: Lacunes are caused by occlusion of a single penetrating artery. The deep penetrating arteries are small nonbranching end arteries (usually smaller than 500 micrometers in diameter), which arise directly from much larger arteries (eg, the middle cerebral artery, anterior choroidal artery, anterior cerebral artery, posterior cerebral artery, posterior communicating artery, cerebellar arteries, basilar artery). Their small size and proximal position predispose them to the development of microatheroma and lipohyalinosis.

Initially, lipohyalinosis was thought to be the predominant small vessel pathology of lacunes; however, microatheroma now is thought to be the most common mechanism of arterial occlusion (or stenosis). Occasionally, atheroma in the parent artery blocks the orifice of the penetrating artery (luminal atheroma), or atheroma involves the origin of the penetrating artery (junctional atheroma).

A hemodynamic (hypoperfusion) mechanism is suggested when there is a stenosis (and not occlusion) of the penetrating artery. When no evidence of small vessel disease is found on histologic examination, an embolic cause is assumed, either artery-to-artery embolism or cardioembolism. In one recent series, 25% of patients with clinical radiologically defined lacunes had a potential cardiac cause for their strokes.

Frequency:

• In the US: In the US and other Western nations, lacunes make up 15-25% of all ischemic strokes. In 2 US community-based studies, the annual incidence rates of lacunar strokes were 13.4 and 19.5 cases per 100,000 population.

• Internationally: Two European community-based studies found higher annual incidence rates (31.7 and 53.0 cases per 100,000 population). This difference in incidence rates may be due in part to different definitions used in the studies.

Mortality/Morbidity: Lacunar strokes have a much more favorable prognosis than nonlacunar strokes.

• The early (less than 30 days) and late (at 1 year) survival rates are approximately 100%, with 85-90% for lacunar strokes and 85% and 65-70% for nonlacunar strokes, respectively.

• Between 70-80% of patients with lacunar strokes are functionally independent at 1 year, compared with fewer than 50% of patients with nonlacunar strokes.

Race: Some studies have found higher frequencies of lacunar strokes in African Americans, Mexican Americans, and Hong Kong Chinese.

Sex: Some studies have indicated a higher incidence of lacunar strokes in men.

Age: The incidence of lacunar strokes increases with age. The mean age of first lacunar stroke is approximately 65 years.

CLINICAL PICTURE

History: Symptoms may occur suddenly or may evolve in either a fluctuating (eg, the capsular warning syndrome) or a progressive manner.

Each of the 5 classical lacunar syndromes has a symptom complex that is relatively specific to it. Occasionally, cortical infarcts and intracranial hemorrhages can mimic a lacunar syndrome. Cortical symptoms (eg, aphasia, neglect) and visual field defects are absent.

• Pure motor stroke/hemiparesis

  • This is the most common (33-50%) lacunar syndrome. It consists of hemiparesis or hemiplegia that typically affects the face, arm, and leg equally; however, the face or leg can be involved to a lesser extent than other regions, and occasionally only arm or leg weakness is noted.

  • Transient sensory symptoms (but not signs) may be present.

  • Dysarthria and dysphagia also may be present.

  • The lacune is usually in the posterior limb of the internal capsule or the basis pontis.

• Ataxic hemiparesis

  • This is the second most frequent lacunar syndrome, consisting of weakness and clumsiness on one side of the body.

  • This lacunar syndrome usually affects the leg more than the arm; hence, it is known also as homolateral ataxia and crural paresis. The onset of symptoms is often over hours or days.

  • The most frequent sites of infarction are the posterior limb of the internal capsule, basis pontis, and corona radiata.

• Dysarthria/clumsy hand

  • Although now considered a variant of ataxic hemiparesis, this disorder usually still is classified as a separate lacunar syndrome.

  • The main symptoms are dysarthria and clumsiness (ie, weakness) of the hand, which often is most prominent when the patient is writing.

• Pure sensory stroke

  • This lacunar syndrome consists of persistent or transient numbness and/or tingling on one side of the body (eg, face, arm, leg, trunk).

  • Occasionally, the complaint is of pain, burning, or other unpleasant sensation. The infarct is usually in the thalamus.

• Mixed sensorimotor stroke

  • With this lacunar syndrome, hemiparesis or hemiplegia is noted with ipsilateral sensory impairment.

  • The infarct is usually in the thalamus and adjacent posterior internal capsule (seemingly, in both the carotid and vertebrobasilar territories).

Physical: Physical examination findings differ in each of the lacunar syndromes.

• Pure motor stroke/hemiparesis: Hemiparesis or hemiplegia is noted with hyperreflexia and Babinski sign, but no involvement of any other system is observed.

• Ataxic hemiparesis: A combination of pyramidal signs (eg, hemiparesis, hyperreflexia, Babinski sign) and cerebellar ataxia on the same side of the body often involves the leg more severely than other parts of the body. Nystagmus may be present.

• Dysarthria-clumsy hand: Unilateral lower facial weakness with dysarthric speech is noted. On protrusion, the tongue may deviate to the side of facial weakness. A mild ipsilateral hemiparesis usually is noted, but the arm is ataxic. Ipsilateral hyperreflexia and Babinski sign may be observed.

• Pure sensory stroke: Unilateral sensory loss is observed. Although the patient may complain of weakness, no weakness is found on examination.

• Mixed sensorimotor stroke: A combination of pyramidal signs (eg, hemiparesis, hyperreflexia, Babinski sign) are noted, as well as sensory loss in the absence of any cortical signs.

Table 1. Crossed brainstem lacunar syndromes (Click to download Table 1. in PDF format)

Causes: The cause of lacunar infarction is occlusion of a single small penetrating artery. This occlusion may be due to microatheroma and lipohyalinosis, which are associated with hypertension, smoking, and diabetes, or to microembolism from the heart or carotid arteries.

• Hypertension: Earlier studies have found that almost all patients with lacunes had hypertension; more recent studies have found hypertension in only 44-75% of patients. In the setting of chronic hypertension, the penetrating arteries, which usually are not affected by atherosclerosis, may develop microatheroma and lipohyalinosis.

• Diabetes mellitus is well recognized as a risk factor for development of small vessel disease throughout the body, including the penetrating arteries.

• Smoking is an established risk factor for lacunes.

• Embolism (either cardioembolism or artery-to-artery embolism) traditionally was considered a rare mechanism of lacunar stroke, but a potential embolic cause is not uncommon when lacunes are defined clinicoradiologically. A potential embolic cause may be a coincidental finding only. The following treatment modalities are discussed only in passing:

  • The role of anticoagulation or carotid endarterectomy in patients with lacunes has not been defined fully.

  • Although a recent study showed that the benefit of endarterectomy in patients with lacunes was smaller than in patients with nonlacunar strokes, the procedure is superior to medical therapy.

WORKUP

Lab Studies:

• Serum glucose to rule out hypoglycemia

• Prothrombin time/international normalized ratio (PT/INR) and activated partial prothrombin time (aPTT): Anticoagulant use with prolonged aPTT or PT (>15 sec) or INR greater than 1.7 are contraindications to thrombolysis.

• CBC: Thrombocytopenia is a contraindication for thrombolysis.

Imaging Studies:

• CT scan of the head: CT scan usually is negative in the acute stage; however, CT scanning is the imaging procedure of choice to rule out an intracerebral hemorrhage. It may show a large cortical stroke, an old lacune, or a space-occupying lesion.

• MRI of the head: MRI is more sensitive than a CT scan at identifying acute and old lacunes (particularly in the posterior fossa). MRI can help to identify acute hemorrhage, but there is a longer acquisition time than with CT scan. Magnetic resonance angiography (MRA) also should be performed, as occasionally lacunes are due to large vessel disease. If further anatomical details are needed, diffusion-weighted MRI may be indicated.

Other Tests:

• Electrocardiogram (ECG), Holter monitor study, carotid Doppler ultrasound, and echocardiogram may be required to identify a potential embolic cause for the lacune.

• Cerebral angiography is required if a severe (>70% occlusion) carotid stenosis is identified on noninvasive testing (carotid ultrasound or MRA) and if carotid endarterectomy is contemplated.

Histologic Findings: Lacunes are not examined histologically except at necropsy. Histologically, lacunes are no different from other brain infarcts. Cells undergoing necrosis initially are pyknotic, then their plasma and nuclear membranes break down. Polymorphonuclear cells appear followed by macrophages, and the necrotic tissue is removed by phagocytosis. A cavity surrounded by a zone of gliosis is the end result. Careful examination may reveal the underlying small vessel pathology.

Figure 1. Pontine lacunar infarction (Click to magnify figure)

Microatheroma causing occlusion or stenosis of a deep penetrating artery is the most common small vessel pathology, usually involving the artery in the first half of its course. Histologically, microatheroma is identical to large vessel atheroma with subintimal deposition of lipids and proliferation of fibroblasts, smooth muscle cells, and lipid-laden macrophages.

Lipohyalinosis is seen in the smaller penetrating arteries (<200 micrometers in diameter) and occurs almost exclusively in patients with hypertension. It has features of both atheroma formation and fibrinoid necrosis with lipid and eosinophilic fibrinoid deposition in the media.

Figure 2. A, lipohyalinosis, B, lacunar infarction. (Click to magnify figure)

MANAGEMENT

Rehabilitation Program:

• Physical Therapy: After initial assessment, a physical therapy program should begin with passive exercises, where the major joints of the paretic limb are moved through a full range of movement (ROM). As soon as patients are stable and can tolerate more active therapy, encourage them to sit up (initially in bed and later in a chair), to stand, and to transfer safely; then, they can commence ambulating with assistance and aids as required. The physical therapist can provide splints and braces to support joints and limbs, to treat and prevent complications (eg, shoulder-hand syndrome, spasticity), and to assist the patient in walking.

• Occupational Therapy: When the patient is stable, assess his or her ability to perform activities of daily living (ADL), such as dressing and undressing, bathing, personal grooming, toileting, preparing meals, and eating. The occupational therapist can advise on equipment that may allow the patient to be more independent. If the patient is returning home, an assessment of the residence identifies potential problems and necessary modifications (eg, handrails, moving a bed to a ground level room), thereby providing confidence to the patient and family.

• Speech Therapy: A speech-language therapist can assist with speech-language problems and swallowing disorders. Early assessment of a patient with swallowing problems may prevent dehydration and malnutrition from inadequate intake, as well as prevent aspiration and pneumonia. Cinefluoroscopy with barium swallow may be required in addition to the bedside assessment. Treatment may require a change in food consistency, a change in positioning or compensatory swallowing technique, or placement of a feeding tube. Patients with lacunes may be dysarthric (but not dysphasic), requiring treatment to improve functional communication.

• Recreational Therapy: Recreational therapy improves the functioning, independence, and self-confidence of patients following stroke through participation in individual and group recreational activities that they enjoyed before their strokes and through participation in new ones. The recreational therapist must assess the patient’s medical condition and physical capabilities, as well as the patient’s interests and hobbies. Then, the therapist must help the patient set realistic goals and make any necessary modifications to achieve these goals. Recreational therapy not only allows the stroke patient to practice motor skills but also allows the patient to remain socially active. Recreational therapy includes leisure activities, such as going for a walk, fishing, and gardening, as well as involvement in family and community activities, such as playing cards and going to a restaurant or church.

Medical Issues/Complications: Prevention of deep venous thrombosis (DVT), aspiration pneumonia, urinary tract infection, and decubitus ulcers are important considerations for any patient following stroke.

Surgical Intervention: Surgery (eg, gastrostomy/jejunostomy) rarely is required, but patients with severe dysphagia may require long-term tube feeding.

Consultations: A social worker should be consulted to assess personal and family resources, to inform the patient and family of government resources that are available, to facilitate discharge planning, and to coordinate community services.

MEDICATION

The medications used in the management of lacunes are not specific to this subtype of stroke.

FOLLOW-UP

Further Inpatient Care:

• If the patient is functionally independent and can return safely home and would benefit from intensive inpatient rehabilitation, transfer to a rehabilitation facility.

Further Outpatient Care:

• Outpatient physical, occupational, and/or speech therapy may be recommended.

• Medical follow-up is necessary to assess neurologic and functional improvement, to monitor and to treat risk factors, and to monitor drug compliance.

In/Out Patient Meds:

• Discharge on aspirin and ramipril.

• If the patient remains nonambulatory and is at high risk of deep vein thrombosis, continue subcutaneous heparin.

Transfer:

• Transfer may be required for further diagnostic evaluation and treatment, including rehabilitation.

Complications:

• Stroke progression or recurrent stroke

• Aspiration pneumonia

• Deep vein thrombosis and pulmonary embolism

• Urinary tract infection

• Depression

• Shoulder-hand syndrome

• Decubitus ulcers

Prognosis:

• Survival rates and rates of functional improvement for patients who have sustained lacunar strokes are better than for other subtypes of stroke (see Mortality/Morbidity).

• Risk of recurrent lacunar stroke is no higher (and possibly is lower) than in other subtypes of strokes, no more than 10% at 1 year.

Patient Education:

• The patient and family should know the common stroke symptoms. Inform them early about the importance of presentation, since TPA (which may be indicated) can be given only within 3 hours of stroke onset.

References

1. Adams HP Jr, Brott TG, Furlan AJ, et al: Guidelines for thrombolytic therapy for acute stroke: a supplement to the guidelines for the management of patients with acute ischemic stroke. A statement for healthcare professionals from a Special Writing Group of the Stroke Council, American Heart. Circulation 1996 Sep 1; 94(5): 1167-74.

2. Bamford JM, Warlow CP: Evolution and testing of the lacunar hypothesis. Stroke 1988 Sep; 19(9): 1074-82.
3. Gan R, Sacco RL, Kargman DE, et al: Testing the validity of the lacunar hypothesis: the Northern Manhattan Stroke Study experience. Neurology 1997 May; 48(5): 1204-11.
4. Inzitari D, Eliasziw M, Sharpe BL, et al: Risk factors and outcome of patients with carotid artery stenosis presenting with lacunar stroke. North American Symptomatic Carotid Endarterectomy Trial Group. Neurology 2000 Feb 8; 54(3): 660-6.
5. Post-stroke Rehabilitation Guideline Panel: Post-stroke rehabilitation – clinical practice guideline. Gaithersburg: Aspen Publishers; 1996.
6. Pullicino PM, Caplan LR, Hommel M: Cerebral small artery disease. In: Advances in Neurology. Vol 62. 1993.
7. The National Institute of Neurological Disorders and Stroke: Tissue plasminogen activator for acute ischemic stroke. The National Institute of Neurological Disorders and Stroke rt-PA Stroke Study Group. N Engl J Med 1995 Dec 14; 333(24): 1581-7.
8. Yusuf S, Sleight P, Pogue J, et al: Effects of an angiotensin-converting-enzyme inhibitor, ramipril, on cardiovascular events in high-risk patients. The Heart Outcomes Prevention Evaluation Study Investigators. N Engl J Med 2000 Jan 20; 342(3): 145-53.