Lacunar stroke

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Lacunar stroke
CT of lacunar strokes.jpg
CT scan of two lacunar strokes.
Specialty Neurology

Lacunar stroke or lacunar cerebral infarct (LACI) is the most common type of ischemic stroke, resulting from the occlusion of small penetrating arteries that provide blood to the brain's deep structures. Patients who present with symptoms of a lacunar stroke, but who have not yet had diagnostic imaging performed, may be described as having lacunar stroke syndrome (LACS).

Contents

Much of the current knowledge of lacunar strokes comes from C. Miller Fisher's cadaver dissections of post-mortem stroke patients. He observed "lacunae" (empty spaces) in the deep brain structures after occlusion of 200–800 μm penetrating arteries and connected them with five classic syndromes. These syndromes are still noted today, though lacunar infarcts are diagnosed based on clinical judgment and radiologic imaging.

Signs and symptoms

Each of the five classical lacunar syndromes has a relatively distinct symptom complex. Symptoms may occur suddenly, progressively, or in a fluctuating (e.g., the capsular warning syndrome) manner. Occasionally, cortical infarcts and intracranial hemorrhages can mimic lacunar infarcts, but true cortical signs (aphasia, [1] visuospatial neglect, gaze deviation, and visual field defects) are always absent in lacunar strokes. The classic syndromes are as follows: [2] [3]

NameLocation of infarctPresentation
Pure motor stroke/hemiparesis (most common lacunar syndrome: 33–50%) posterior limb of the internal capsule, basilar part of pons, corona radiataIt is marked by hemiparesis or hemiplegia that typically affects the face, arm, or leg of the side of the body opposite the location of the infarct. Dysarthria, dysphagia, and transient sensory symptoms may also be present.
Ataxic hemiparesis (second most frequent lacunar syndrome) posterior limb of the internal capsule, basilar part of pons, and corona radiata, red nucleus, lentiform nucleus, superior cerebellar artery infarcts, anterior cerebral artery infarctsIt displays a combination of cerebellar and motor symptoms, including weakness and clumsiness, on the ipsilateral side of the body. [4] It usually affects the leg more than it does the arm; hence, it is known also as homolateral ataxia and crural paresis. The onset of symptoms is often over hours or days.
Dysarthria/clumsy hand (sometimes considered a variant of ataxic hemiparesis, but usually still is classified as a separate lacunar syndrome) basilar part of pons, anterior limb or genu of internal capsule, corona radiata, basal ganglia, thalamus, cerebral peduncleThe main symptoms are dysarthria and clumsiness (i.e., weakness) of the hand, which often are most prominent when the patient is writing; but dysarthria or involuntary movement can also be seen in legs. [5]
Pure sensory strokecontralateral thalamus (VPL), internal capsule, corona radiata, midbrainMarked by numbness (loss of sensation) on one side of the body; can later develop tingling, pain, burning, or another unpleasant sensation on one side of the body.
Mixed sensorimotor stroke thalamus and adjacent posterior internal capsule, lateral ponsThis lacunar syndrome involves hemiparesis or hemiplegia (weakness) with sensory impairment in the contralateral side. [6]

Silent lacunar infarction

Histopathology of a small lacunar infarct discovered incidentally on autopsy. Histopathology of a lacunar cerebral infarct.jpg
Histopathology of a small lacunar infarct discovered incidentally on autopsy.

A silent lacunar infarction (SLI) is one type of silent stroke which usually shows no identifiable outward symptoms, and is thus termed "silent." Because stroke is a clinical diagnosis (that is, it is defined by clinical symptoms), there is debate about whether SLI are considered to be strokes, even though the pathophysiology is presumably the same.[ citation needed ] Individuals who have a SLI are often completely unaware they have had a stroke. This type of stroke often causes lesions in the surrounding brain tissue that are visibly detected via neuroimaging techniques such as MRI and computed axial tomography (CT scan). Silent strokes, including silent lacunar infarctions, have been shown to be much more common than previously thought, with an estimated prevalence rate of eleven million per year in the United States. Approximately 10% of these silent strokes are silent lacunar infarctions. While dubbed "silent" due to the immediate lack of classic stroke symptoms, SLIs can cause damage to the surrounding brain tissue and can affect various aspects of a person's mood, personality, and cognitive functioning. A SLI or any type of silent stroke places an individual at greater risk for future major stroke. [7] [8]

Pathophysiology

Small arteries beneath brain. Arteries beneath brain Gray closer.jpg
Small arteries beneath brain.

According to Koffler et al., lacunes are derived from an "occlusion of a single deep penetrating artery that arises directly from the constituents of the circle of Willis, cerebellar arteries, and basilar artery". Other lesions that are associated with lacunes appear in the "deep nuclei of the brain (37% putamen, 14% thalamus, and 10% caudate) as well as the pons (16%) or the posterior limb of the internal capsule (10%)". These lesions are less common within other brain regions such as the cerebellum, cerebral white matter and anterior limb of the internal capsule. [9]

The two proposed mechanisms are microatheroma and lipohyalinosis . [10] At the beginning, lipohyalinosis was thought to be the main small vessel pathology, but 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). Alternatively, hypoperfusion is believed to be the mechanism when there is stenosis 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.

More recent advances have also suggested these mechanisms may play a combined role in the aetiology of lacunar infarction. The most current theory indicates endothelial dysfunction and increased permeability of the blood-brain barrier first allow leakage of blood contents, promoting gliosis and white matter hyper-intensities on magnetic resonance imaging. Moreover, focal narrowing of brain vessels and impairment of their ability to dilate in response to various stimuli may lead to a decreased cerebral blood flow and ultimately lacunar stroke. [11]

Advanced age, chronic hypertension, smoking and diabetes mellitus are risk factors. It is unclear whether there is an association with alcohol consumption, elevated cholesterol, or history of prior stroke. Lacunar strokes may result from carotid artery pathology or microemboli from the heart as in atrial fibrillation. Patients often recover well, but if there is enough white matter disease from lacunar pathology, one can see a subcortical dementia such as Binswanger disease.

Treatment and prognosis

Typically, tissue plasminogen activator may be administered within 3 to 4.5 hours of stroke onset if the patient is without contraindications (i.e. a bleeding diathesis such as recent major surgery or cancer with brain metastases). High dose aspirin can be given within 48 hours. For long term prevention of recurrence, medical regimens are typically aimed towards correcting the underlying risk factors for lacunar infarcts such as hypertension, diabetes mellitus and cigarette smoking. Anticoagulants such as heparin and warfarin have shown no benefit over aspirin with regards to five-year survival. [4]

Patients who have lacunar strokes have a greater chance of surviving beyond thirty days (96%) than those with other types of stroke (85%), and better survival beyond a year (87% versus 65-70%). Between 70% and 80% are functionally independent at 1 year, compared with fewer than 50% otherwise. [12] [13]

Occupational therapy and physical therapy interventions are used in the rehabilitation of lacunar stroke. A physiotherapy program will improve joint range of motion of the paretic limb using passive range of motion exercises. When increases in activity are tolerated, and stability improvements are made, patients will progress from rolling to side-lying, to standing (with progressions to prone, quadruped, bridging, long-sitting and kneeling for example) and learn to transfer safely (from their bed to a chair or from a wheel chair to a car for example). Assistance and ambulation aids are used as required as the patient begins walking and lessened as function increases. Furthermore, splints and braces can be used to support limbs and joints to prevent or treat complications such as contractures and spasticity. [14] The rehabilitation healthcare team should also educate the patient and their family on common stroke symptoms and how to manage an onset of stroke. Continuing follow-up with a physician is essential so that the physician may monitor medication dosage and risk factors. [14]

Epidemiology

It is estimated that lacunar infarcts account for 25% of all ischemic strokes, with an annual incidence of approximately 15 per 100,000 people. [15] They may be more frequent in men and in people of African, Mexican, and Hong Kong Chinese descent. [16]

Related Research Articles

A transient ischemic attack (TIA), commonly known as a mini-stroke, is a minor stroke whose noticeable symptoms usually end in less than an hour. TIA causes the same symptoms associated with strokes, such as weakness or numbness on one side of the body, sudden dimming or loss of vision, difficulty speaking or understanding language, slurred speech, or confusion.

<span class="mw-page-title-main">Cerebrovascular disease</span> Condition that affects the arteries that supply the brain

Cerebrovascular disease includes a variety of medical conditions that affect the blood vessels of the brain and the cerebral circulation. Arteries supplying oxygen and nutrients to the brain are often damaged or deformed in these disorders. The most common presentation of cerebrovascular disease is an ischemic stroke or mini-stroke and sometimes a hemorrhagic stroke. Hypertension is the most important contributing risk factor for stroke and cerebrovascular diseases as it can change the structure of blood vessels and result in atherosclerosis. Atherosclerosis narrows blood vessels in the brain, resulting in decreased cerebral perfusion. Other risk factors that contribute to stroke include smoking and diabetes. Narrowed cerebral arteries can lead to ischemic stroke, but continually elevated blood pressure can also cause tearing of vessels, leading to a hemorrhagic stroke.

<span class="mw-page-title-main">Caudate nucleus</span> Structure of the striatum in the basal ganglia of the brain

The caudate nucleus is one of the structures that make up the corpus striatum, which is a component of the basal ganglia in the human brain. While the caudate nucleus has long been associated with motor processes due to its role in Parkinson's disease, it plays important roles in various other nonmotor functions as well, including procedural learning, associative learning and inhibitory control of action, among other functions. The caudate is also one of the brain structures which compose the reward system and functions as part of the cortico–basal ganglia–thalamic loop.

<span class="mw-page-title-main">Ischemia</span> Restriction in blood supply to tissues

Ischemia or ischaemia is a restriction in blood supply to any tissue, muscle group, or organ of the body, causing a shortage of oxygen that is needed for cellular metabolism. Ischemia is generally caused by problems with blood vessels, with resultant damage to or dysfunction of tissue i.e. hypoxia and microvascular dysfunction. It also implies local hypoxia in a part of a body resulting from constriction. Ischemia causes not only insufficiency of oxygen, but also reduced availability of nutrients and inadequate removal of metabolic wastes. Ischemia can be partial or total blockage. The inadequate delivery of oxygenated blood to the organs must be resolved either by treating the cause of the inadequate delivery or reducing the oxygen demand of the system that needs it. For example, patients with myocardial ischemia have a decreased blood flow to the heart and are prescribed with medications that reduce chronotrophy and ionotrophy to meet the new level of blood delivery supplied by the stenosed vasculature so that it is adequate.

<span class="mw-page-title-main">Infarction</span> Tissue death due to inadequate blood supply

Infarction is tissue death (necrosis) due to inadequate blood supply to the affected area. It may be caused by artery blockages, rupture, mechanical compression, or vasoconstriction. The resulting lesion is referred to as an infarct (from the Latin infarctus, "stuffed into").

<span class="mw-page-title-main">Stroke</span> Death of a region of brain cells due to poor blood flow

Stroke is a medical condition in which poor blood flow to the brain causes cell death. There are two main types of stroke: ischemic, due to lack of blood flow, and hemorrhagic, due to bleeding. Both cause parts of the brain to stop functioning properly.

<span class="mw-page-title-main">Lateral medullary syndrome</span> Medical condition

Lateral medullary syndrome is a neurological disorder causing a range of symptoms due to ischemia in the lateral part of the medulla oblongata in the brainstem. The ischemia is a result of a blockage most commonly in the vertebral artery or the posterior inferior cerebellar artery. Lateral medullary syndrome is also called Wallenberg's syndrome, posterior inferior cerebellar artery (PICA) syndrome and vertebral artery syndrome.

<span class="mw-page-title-main">Cerebral hypoxia</span> Oxygen shortage of the brain

Cerebral hypoxia is a form of hypoxia, specifically involving the brain; when the brain is completely deprived of oxygen, it is called cerebral anoxia. There are four categories of cerebral hypoxia; they are, in order of increasing severity: diffuse cerebral hypoxia (DCH), focal cerebral ischemia, cerebral infarction, and global cerebral ischemia. Prolonged hypoxia induces neuronal cell death via apoptosis, resulting in a hypoxic brain injury.

<span class="mw-page-title-main">Perivascular space</span>

A perivascular space, also known as a Virchow–Robin space, is a fluid-filled space surrounding certain blood vessels in several organs, including the brain, potentially having an immunological function, but more broadly a dispersive role for neural and blood-derived messengers. The brain pia mater is reflected from the surface of the brain onto the surface of blood vessels in the subarachnoid space. In the brain, perivascular cuffs are regions of leukocyte aggregation in the perivascular spaces, usually found in patients with viral encephalitis.

<span class="mw-page-title-main">Cerebral infarction</span> Medical condition

Cerebral infarction is the pathologic process that results in an area of necrotic tissue in the brain. It is caused by disrupted blood supply (ischemia) and restricted oxygen supply (hypoxia), most commonly due to thromboembolism, and manifests clinically as ischemic stroke. In response to ischemia, the brain degenerates by the process of liquefactive necrosis.

<span class="mw-page-title-main">Anterior inferior cerebellar artery</span> Major blood supply to the cerebellum

The anterior inferior cerebellar artery (AICA) is one of three pairs of arteries that supplies blood to the cerebellum.

<span class="mw-page-title-main">Watershed stroke</span> Medical condition

A watershed stroke is defined as a brain ischemia that is localized to the vulnerable border zones between the tissues supplied by the anterior, posterior and middle cerebral arteries. The actual blood stream blockage/restriction site can be located far away from the infarcts. Watershed locations are those border-zone regions in the brain supplied by the major cerebral arteries where blood supply is decreased. Watershed strokes are a concern because they comprise approximately 10% of all ischemic stroke cases. The watershed zones themselves are particularly susceptible to infarction from global ischemia as the distal nature of the vasculature predisposes these areas to be most sensitive to profound hypoperfusion.

<span class="mw-page-title-main">Carotid artery dissection</span> Human disease

Carotid artery dissection is a separation of the layers of the artery wall in the carotid arteries supplying oxygen-bearing blood to the head. It is the most common cause of stroke in younger adults.The term 'cervical artery dissection should also be considered in the context of this article.

<span class="mw-page-title-main">Anterior cerebral artery syndrome</span> Medical condition

Anterior cerebral artery syndrome is a condition whereby the blood supply from the anterior cerebral artery (ACA) is restricted, leading to a reduction of the function of the portions of the brain supplied by that vessel: the medial aspects of the frontal and parietal lobes, basal ganglia, anterior fornix and anterior corpus callosum.

Benedikt syndrome, also called Benedikt's syndrome or paramedian midbrain syndrome, is a rare type of posterior circulation stroke of the brain, with a range of neurological symptoms affecting the midbrain, cerebellum and other related structures.

Lipohyalinosis is a cerebral small vessel disease affecting the small arteries, arterioles or capillaries in the brain. Originally defined by C. Miller Fisher as 'segmental arteriolar wall disorganisation', it is characterized by vessel wall thickening and a resultant reduction in luminal diameter. Fisher considered this small vessel disease to be the result of hypertension, induced in the acute stage by fibrinoid necrosis that would lead to occlusion and hence lacunar stroke. However, recent evidence suggests that endothelial dysfunction as a result of inflammation is a more likely cause for it. This may occur subsequent to blood–brain barrier failure, and lead to extravasation of serum components into the brain that are potentially toxic. Lacunar infarction could thus occur in this way, and the narrowing – the hallmark feature of lipohyalinosis – may merely be a feature of the swelling occurring around it that squeezes on the structure.

<span class="mw-page-title-main">C. Miller Fisher</span> Canadian doctor, neurologist, pathologist

Charles Miller Fisher was a Canadian neurologist whose notable contributions include the first detailed descriptions of lacunar strokes, the identification of transient ischemic attacks as stroke precursors, the identification of the link between carotid atherosclerosis and stroke, and the description of a variant form of Guillain–Barré syndrome which bears his name.

A silent stroke is a stroke that does not have any outward symptoms associated with stroke, and the patient is typically unaware they have suffered a stroke. Despite not causing identifiable symptoms, a silent stroke still causes damage to the brain and places the patient at increased risk for both transient ischemic attack and major stroke in the future. In a broad study in 1998, more than 11 million people were estimated to have experienced a stroke in the United States. Approximately 770,000 of these strokes were symptomatic and 11 million were first-ever silent MRI infarcts or hemorrhages. Silent strokes typically cause lesions which are detected via the use of neuroimaging such as MRI. The risk of silent stroke increases with age but may also affect younger adults. Women appear to be at increased risk for silent stroke, with hypertension and current cigarette smoking being amongst the predisposing factors.

<span class="mw-page-title-main">Cerebral autosomal recessive arteriopathy with subcortical infarcts and leukoencephalopathy</span> Medical condition

Cerebral autosomal recessive arteriopathy with subcortical infarcts and leukoencephalopathy (CARASIL) is disease of the arteries in the brain, which causes tissue loss in the subcortical region of the brain and the destruction of myelin in the CNS. CARASIL is characterized by symptoms such as gait disturbances, hair loss, low back pain, dementia, and stroke. CARASIL is a rare disease, having only been diagnosed in about 50 patients, of which ten have been genetically confirmed. Most cases have been reported in Japan, but Chinese and caucasian individuals have also been diagnosed with the disease. CARASIL is inherited in an autosomal recessive pattern. There is currently no cure for CARASIL. Other names for CARASIL include familial young-adult-onset arteriosclerotic leukoencephalopathy with alopecia and lumbago without arterial hypertension, Nemoto disease and Maeda syndrome.

<span class="mw-page-title-main">Arterial occlusion</span>

Arterial occlusion is a condition involving partial or complete blockage of blood flow through an artery. Arteries are blood vessels that carry oxygenated blood to body tissues. An occlusion of arteries disrupts oxygen and blood supply to tissues, leading to ischemia. Depending on the extent of ischemia, symptoms of arterial occlusion range from simple soreness and pain that can be relieved with rest, to a lack of sensation or paralysis that could require amputation.

References

  1. ↑ Kohlhase, K.; Schaefer, J. H.; Lapa, S.; Jurcoane, A.; Wagner, M.; Hok, P.; Kell, C. A. (2021). "Aphasia associated with lacunar infarctions". Der Nervenarzt. 92 (8): 802–808. doi:10.1007/s00115-021-01072-6. PMC   8342334 . PMID   33591414.
  2. ↑ Giacomozzi, S.; Caso, V.; Agnelli, G.; Acciarresi, M.; Alberti, A.; Venti, M.; Mosconi, M. G.; Paciaroni, M. (2020). "Lacunar stroke syndromes as predictors of lacunar and non-lacunar infarcts on neuroimaging: A hospital-based study". Internal and Emergency Medicine. 15 (3): 429–436. doi:10.1007/s11739-019-02193-2. PMID   31535289. S2CID   202641797.
  3. ↑ Arboix, Adria; Alioc, Josefina (2010). "Cardioembolic Stroke: Clinical Features, Specific Cardiac Disorders and Prognosis". Current Cardiology Reviews. 6 (3): 150–161. doi:10.2174/157340310791658730. PMC   2994107 . PMID   21804774.
  4. 1 2 Lacunar Syndrome at eMedicine
  5. ↑ Tuo, H.; Tian, Z.; Ma, X.; Cui, Y.; Xue, Y.; Che, J.; Xu, C.; Chen, K.; Zhang, Y.; Zhang, L.; Bi, H.; Le, W.; Ondo, W. (2019). "Clinical and radiological characteristics of restless legs syndrome following acute lacunar infarction". Sleep Medicine. 53: 81–87. doi:10.1016/j.sleep.2018.06.004. PMID   30458382. S2CID   53713034.
  6. ↑ Micheli, Sara; Corea, Francesco (2012). "Lacunar versus non-lacunar syndromes". Frontiers of Neurology and Neuroscience. 30: 94–98. doi:10.1159/000333426. ISBN   978-3-8055-9911-5. PMID   22377873.
  7. ↑ Grau-Olivares, Marta; Arboix, Adrià; Bartrés-Faz, David; Junqué, Carme (2007). "Neuropsychological abnormalities associated with lacunar infarction". Journal of the Neurological Sciences. 257 (1–2): 160–5. doi:10.1016/j.jns.2007.01.022. PMID   17316693. S2CID   2768316.
  8. ↑ Longstreth Jr, W. T.; Bernick, C; Manolio, T. A.; Bryan, N; Jungreis, C. A.; Price, T. R. (1998). "Lacunar infarcts defined by magnetic resonance imaging of 3660 elderly people: The Cardiovascular Health Study". Archives of Neurology. 55 (9): 1217–25. doi:10.1001/archneur.55.9.1217. PMID   9740116.
  9. ↑ Neuropsychology : a review of science and practice, volume III. Koffler, Sandra,, Mahone, E. (E. Mark),, Marcopulos, Bernice A.,, Johnson-Greene, Douglas Eric, 1962-, Smith, Glenn E. New York, NY. 2018-12-17. ISBN   978-0-19-065256-2. OCLC   1078637067.{{cite book}}: CS1 maint: location missing publisher (link) CS1 maint: others (link)
  10. ↑ Caplan, Louis R (2015). "Lacunar Infarction and Small Vessel Disease: Pathology and Pathophysiology". Journal of Stroke. 17 (1): 2–6. doi:10.5853/jos.2015.17.1.2. PMC   4325635 . PMID   25692102.
  11. ↑ Regenhardt, Robert W.; Das, Alvin S.; Lo, Eng H.; Caplan, Louis R. (2018-10-01). "Advances in Understanding the Pathophysiology of Lacunar Stroke: A Review". JAMA Neurology. 75 (10): 1273–1281. doi:10.1001/jamaneurol.2018.1073. PMC   7426021 . PMID   30167649.
  12. ↑ Bamford, J.; Sandercock, P.; Jones, L.; Warlow, C. (1987). "The natural history of lacunar infarction: The Oxfordshire Community Stroke Project". Stroke. 18 (3): 545–51. doi: 10.1161/01.STR.18.3.545 . PMID   3590244.
  13. ↑ Bejot, Y.; Catteau, A.; Caillier, M.; Rouaud, O.; Durier, J.; Marie, C.; Di Carlo, A.; Osseby, G.-V.; Moreau, T.; Giroud, M. (2008). "Trends in Incidence, Risk Factors, and Survival in Symptomatic Lacunar Stroke in Dijon, France, from 1989 to 2006: A Population-Based Study". Stroke. 39 (7): 1945–51. doi: 10.1161/STROKEAHA.107.510933 . PMID   18436869.
  14. 1 2 Lacunar Stroke at eMedicine
  15. ↑ Sacco, S.; Marini, C.; Totaro, R.; Russo, T.; Cerone, D.; Carolei, A. (2006). "A population-based study of the incidence and prognosis of lacunar stroke". Neurology. 66 (9): 1335–8. doi:10.1212/01.wnl.0000210457.89798.0e. PMID   16682663. S2CID   494869.
  16. ↑ Mok, Vincent C.; Wong, Adrian; Lam, Wynnie W.; Baum, Lawrence W.; Ng, Ho Keung; Wong, Lawrence (2008). "A case-controlled study of cognitive progression in Chinese lacunar stroke patients". Clinical Neurology and Neurosurgery. 110 (7): 649–56. doi:10.1016/j.clineuro.2008.03.013. PMID   18456396. S2CID   33602657.
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