Lacunar stroke

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"LACI" redirects here. LACI may also refer to the protein, lipoprotein-associated coagulation inhibitor (also
known as Tissue factor pathway inhibitor).
Lacunar stroke
Classification and external resources

Arteries beneath brain
ICD-10 G46.5-G46.7
ICD-9 434.91
DiseasesDB 31186
eMedicine pmr/63
MeSH D020520
Lacunar stroke or lacunar infarct (LACI) is a type of stroke that results from occlusion of one of the
penetrating arteries that provides 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 suffering
from Lacunar Stroke Syndrome (LACS).
Much of the current knowledge of lacunar strokes comes from C. M. Fisher's cadaverdissections of post-
mortem stroke patients. He observed "lacunes" (Latin for 'lake') of empty fluid left in the deep brain structures
after occlusion of 200-800 m penetrating arteries and connected them with 5 classic syndromes. These
syndromes are still noted today, though lacunar infarcts are diagnosed based on clinical judgment
and radiologic imaging.
Contents
[hide]
1 Epidemiology
2 Pathophysiology
3 Signs & Symptoms
4 Silent lacunar infarction
5 Treatment & Prognosis
6 References
7 External links
[edit]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.
[1]
They may be more frequent in men and in people of African, Mexican,
and Hong Kong Chinese descent.
[2]

[edit]Pathophysiology
Lacunes are caused by occlusion of a single deep penetrating artery that arises directly from the constituents of
the Circle of Willis,cerebellar arteries, and basilar artery. The corresponding lesions occur 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%). They occur less commonly in the deep cerebral white matter, the anterior limb of
the internal capsule, and the cerebellum.
The two proposed mechanisms are microatheroma and lipohyalinosis. 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 embolismor cardioembolism. In one recent series, 25% of
patients with clinical radiologically defined lacunes had a potential cardiac cause for their strokes.
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.
[edit]Signs & Symptoms
Each of the 5 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 infarct signs (such as
aphasia, neglect, and visual field defects) are always absent. The 5 classic syndromes are as follows:
Name Location of infarct Presentation
Pure motor
stroke/hemiparesis(most
common lacunar
syndrome: 33-50%)
posterior limb of the internal
capsule, or thebasis pontis
It is marked
by hemiparesis or hemiplegia that
typically affects the face, arm, or
leg of one
side. Dysarthria, dysphagia, and
transient sensory symptoms may
also be present.
Ataxic
hemiparesis (second most
frequent lacunar
syndrome)
posterior limb of the internal
capsule, basis pontis,
andcorona radiata.
It displays a combination of
cerebellar and motor symptoms,
including weakness and
clumsiness, on the ipsilateral side
of the body. 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
basis pontis
The main symptoms are dysarthria
and clumsiness (i.e., weakness) of
considered a variant of
ataxic hemiparesis, but
usually still is classified as
a separate lacunar
syndrome)
the hand, which often are most
prominent when the patient is
writing.
Pure sensory stroke contralateralthalamus (VPL)
Marked by persistent or transient
numbness, tingling, pain, burning,
or another unpleasant sensation on
one side of the body.
Mixed sensorimotor
stroke
thalamus and adjacent
posteriorinternal capsule
This lacunar syndrome involves
hemiparesis or hemiplegia with
ipsilateral sensory impairment
[edit]Silent lacunar infarction
A Silent lacunar infarction (SLI) is one type of silent stroke which usually shows no identifiable outward
symptoms thus the term "silent". Individuals who suffer a SLI are often completely unaware they have suffered
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 computerized axial tomography (CAT 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 (lesions) and can affect various aspects of a
persons mood, personality and cognitive functioning. A SLI or any type of silent stroke places an individual at
greater risk for future major stroke.
[3][4]

[edit]Treatment & Prognosis
Typically, tissue plasminogen activator may be administered within three 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. Blood thinners such as heparin and warfarin have
shown no benefit over aspirin with regards to five year survival.
[5]

Patients who suffer 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.
[6][7]

[edit]References
1. ^ Sacco S, Marini C, Totaro R, et al. A population-based study of the incidence and
prognosis of lacunar stroke. Neurology. May 9, 2006;66(9):1335-8.
2. ^ Mok VC, Wong A, Lam WW, et al. A case-controlled study of cognitive
progression in Chinese lacunar stroke patients. Clinical Neurology & Neurosurgery.
May 2, 2008
3. ^ Grau-Olivares M,et al. Neuropsychological abnormalities associated with lacunar
infarction. J Neurol Sci. 2007 Jun 15;257(1-2):160-5. Epub 2007 Feb 20. PMID
17316693
4. ^ Longstreth WT Jr, et al. Lacunar infarcts defined by magnetic resonance imaging
of 3660 elderly people: the Cardiovascular Health Study. Arch Neurol. 1998
Sep;55(9):1217-25. PMID 9740116
5. ^ Papamitsakis N. "Lacunar Syndromes" at
Emedicine;http://emedicine.medscape.com/article/1163029-overview
6. ^ Bamford J, Sandercock P, Jones L, et al. The natural history of lacunar infarction:
the Oxfordshire Community Stroke Project. Stroke. May-Jun 1987;18(3):545-51.
7. ^ Bejot Y, Catteau A, Caillier M, et al. Trends in incidence, risk factors, and survival
in symptomatic lacunar stroke in Dijon, France, from 1989 to 2006. A population-
based study. Stroke. Apr 24 2008.