Lacunar syndrome

Small vessel/lacunar strokes have better short- and long-term (1-year) survival as compared to other stroke subtypes. In the NINDS trial of rt-PA within 3 hours of onset, patients classified as small vessel stroke on the basis of their clinical syndrome had a 50% chance of a normal NIHSS score at 3 months if they received placebo, increasing to 70% in the treatment group. In the Lausanne cohort, 95% were independent after their first event, as opposed to only 65% of the cardioembolic strokes and 49% with large vessel atherothrombotic infarctions. Eighty-two percent of patients with small vessel stroke were independent at 1 year. Even at the time of maximal deficit, between 38% and 64% of small vessel/lacunar patients were independent, with motor impairment and extent of white matter disease adversely affecting outcomes. " In TOAST, small vessel/lacunar stroke was the only subtype associated with a favorable outcome, independent of the NIHSS score. ... 

Lacunar infarcts are typically located in the basal ganglia, the deep white matter and in the brainstem (Fisher 1965a, 1998). Depending on their location and their size circumscribed neurological symptoms will occur. C. Miller Fisher described the four classical lacunar syndromes ... 

Fisher CM (1965c) The vascular lesion in lacunae. Trans Am Neurol Assoc 90 243-5 243-245 Fisher CM (1967) A lacunar stroke. The dysarthria-clumsy hand syndrome. Neurology 17 614-617 Fisher CM (1977) Bilateral occlusion of basilar arterybranches. 

While physicians may not recognize up to 80% of lacunes (Tuszynski et al. 1989), several clinical syndromes have been correlated with relevant lacunes detected at subsequent autopsy. Five of these are regarded as the classic lacunar syndromes pure motor hemiparesis, sensorimotor stroke, pure sensory hemiparesis, dysarthria clumsy hand syndrome, and ataxic hemiparesis (Donnan et al. 2002 Fisher 1982 Bamford 2001). Pure motor stroke is the commonest lacunar syndrome in clinical practice, while pure sensory stroke is encountered less frequently. The involvement of the face, arm and leg of one side is the characteristic feature of the first three syndromes while reductions of consciousness, cognitive or visual field defects are absent. Even though lacunar infarcts have been linked to lacunar syndromes, the latter are of course not specific for this stroke subtype and mimicked by cortical infarcts, intracerebral hematomas, and non-vascular causes (Bogousslavsky et al. 1988 Bamford 2001). 

With the use of DWI, small acute lesions lying in different vascular territories in addition to lacunar infarction provides evidence for the possibility of an embolic mechanism in a subset of classic lacunar syndromes (Gerraty et al. 2002 Ay et al. 

This was systematically studied with DWI in 62 consecutive patients who presented with a classic lacunar syndrome (Ay et al. 1999). DWI showed subsidiary acute lesion(s) in addition to the index lacunar lesion in ten patients (16%). The additional lesions were punctuate and lay within the leptomen-ingeal arterial territories in the majority. Patients with subsidiary infarction(s) more frequently harbored an embolic cause of stroke. This finding is critical because underlying embolic cause may give rise to recurrent strokes with more extensive brain injury. Identification of subsidiary infarctions on DWI should have an impact in prompting the physician to introduce the best effective treatment for secondary stroke prevention in a patient with lacunar infarction. 

DWI promises to have tremendous value in accurately localizing the subcortical or brainstem lesion(s). A summary of studies of DWI in patients with lacunar stroke is provided in Table 13.2. It is noteworthy that there is also a group of patients with lacunar infarction who harbor multiple chronic white matter lesions on the conventional MRI and present with non-specific syndromes that could not be attributed to a specific arterial territory. Such symptoms include worsening of a preexisting dysarthria, dysphagia or ataxia, sudden appearance of emotional incontinence or recent onset bowel or bladder problems. Excellent diagnostic performance of DWI in lacunar infarctions may help to prove ischemia as the cause of non-specific neurological symptoms in such patients. 

Ay et al. (1999b) 62 Clinical diagnosis of lacunar syndrome Almost one in six patients presenting with a classic lacunar syndrome has multiple lesions on DWI... 

Gerraty et al. (2002) 19 Clinical diagnosis of acute lacunar syndrome In 13 cases DWI and PI altered the final diagnosis of infarct pathogenesis from small perforating artery occlusion to large artery embolism... 

Bamford J (2001) Classical lacunar syndromes. In Bogousslavsky J, Caplan L (eds) Sreoke syndromes. Cambridge University Press, Cambridge, pp 583-589 Bamford J, Bogousslavsky J (eds) (2002) Subcortical stroke, 2nd edn. Oxford Medical Publications, Oxford, pp 27-34 Bamford J, Sandercock P, Jones L, Warlow C (1987) The natural history of lacunar infarction the Oxfordshire Community Stroke Project. Stroke 18 545-551 Benito-Leon J, Alvarez-Linera J, Porta-Etessam J (2001 Detec-tion of acute pontine infarction by diffusion-weighted MRI in capsular warning syndrome. Cerebrovasc Dis 11 350-351... 

Using only a few neurological findings the Oxfordshire Community Stroke Project (OCSP) classification allocates strokes to four subgroups, locating them either in the territory of the anterior (total anterior circulation infarct, TACI partial anterior circulation infarct, PACI lacunar infarct, LACI) and the posterior circulation, (posterior circulation infarct, POCI) (Bamford et al. 1991). The OCSP is a clinical syndromic classification, which... 

Subcortical white matter infarcts may mimic a superficial MCA infarct causing a partial anterior circulation syndrome or present as a lacunar syndrome (pure motor, ataxic hemiparesis or sensori motor stroke). Superficial perforating artery infarcts (medullary branches) are often accompanied by cortical spotty lesions. Borderzone and white matter medullary branches infarctions are usually caused by hypoperfusion due lo large vessel occlusion or stenosis (Bogousslavsky 1993 Donnan and Yasaka 1998), but white matter medullary branches infarction can also be caused by cardioembolism (Lee et al. 2003). 

DWI can demonstrate scattered lesions in acute stroke patients with initial negative CT (Koennecke et al. 2001) associated with an embolic etiology. In patients presenting with classical lacunar syndromes, DWI can demonstrate lesions not apparent in CT or conventional MR in addition to the lesion in the territory of a single perforator. The most common associated lesions are punctuate subsidiary lesions in the territory of the leptomeningeal arteries (Ay et al. 1990). 

Samuelsson M, Lindell D, Norrving B (1996). Presumed pathogenetic mechanisms of recurrent stroke after lacunar infarction. Cerebrovascular Diseases 6 128-136 Sanna G, Bertolaccini ML, Hughes GR (2005). Hughes syndrome the antiphosphoUpid syndrome a new chapter in neurology. Annals of the New York Academy of Sciences 1051 465-486... 

It may be difficult to distinguish between some partial anterior circulation syndromes and a lacunar stroke. 

Some anterior circulation syndromes, usually classified as partial anterior circulation syndromes, are caused by boundary zone infarcts. The rare anterior choroidal artery distribution infarcts, which can be defined only by the CT or MRI pattern, are probably caused by microvascular disease as well as embolism, and they can lead to a partial anterior circulation syndrome or lacunar syndrome (Hupperts et al. 1994). 

Lacunar syndromes are defined clinically. They are highly predictive of small, deep lesions affecting the motor and/or sensory pathways in the corona radiata, internal capsule, thalamus, cerebral peduncle or pons. Although a few patients have a partial anterior circulation infarct (Bamford et al. 1987 Anzalone and Landi 1989 Arboix et al. 2007), the great majority have small iirfarcts, which are sometimes visible on CT, more often on MRI. These are caused by presumed occlusion of a small perforating artery affected by intracranial small vessel disease (see Fig. 10.2). There is no visual field defect, no new cortical... 

Pure motor stroke constitutes about 50% of lacunar cases. It consists of a unilateral motor deficit involving two or three areas, the face, upper arm and/or leg, including the whole of each area that is affected. There are often sensory symptoms but no sensory signs. The lesion occurs at locations where the motor pathways are closely packed together and separate from other pathways usually in the internal capsule or pons, sometimes the corona radiata or cerebral peduncle, and rarely in the medullary pyramid. There may be a flurry of immediately preceding TIAs, the so-called capsular warning syndrome (Donnan et al. 1996). 

Ataxic hemiparesis constitutes about 10% of cases. It is the combination of corticospinal and ipsilateral cerebellar-like dysfunction affecting the arm and/or leg. It includes a syndrome in which there is little more than dysarthria and one clumsy hand. The lesion is usually in the pons, internal capsule or cerebral peduncle. Dysarthria, with or without upper motor neuron facial weakness, may also be a lacunar syndrome with similar lesion localization as ataxic hemiparesis, but there are other localizing possibilities as well. 

Small deep infarcts in the subcortical white matter of the corona radiata may result from small vessel disease affecting the long medullary perforating arteries extending down from cortical branches of the middle cerebral artery or from embolism. Such centrum semiovale infarcts present as either a lacunar syndrome or, occasionally, as a partial anterior cirulation syndrome with cortical features (Read et al. 1998 Lammie and Wardlaw 1999). They are not, however, easy to classify or to distinguish from border zone infarcts deeper in the white matter lying between the arterial territories of the deep perforators from the first part of the middle cerebral artery and the superficial medullary perforators. 

Various other lacunar syndromes have been described with rather poor clinical-pathological-anatomical correlation for example, chorea or hemiballismus usually appears to he caused by a lesion in the contralateral subthalamic nucleus or elsewhere in the basal ganglia and tends to get better (Ghika and Bogousslavsky 2001). 

Headache is not uncommon around the time of stroke onset. It is more often severe in primary intracerebral hemorrhage than ischemic stroke, and more often severe with posterior than anterior circulation strokes. If the headache is localized at all, it tends to be over the site of the lesion. Headache is more common in cortical and posterior circulation than lacunar infarcts (Kumral et al. 1995). Severe unilateral neck, orbital or scalp pain suggests internal carotid artery dissection, particularly if there is an ipsilateral Horner s syndrome. Severe occipital headache can occur with vertebral artery dissection. Headache is also a particular feature of venous infarcts. Unusual headache in the days before stroke would suggest giant cell arteritis or perhaps a mass lesion rather than a stroke. 

Bamford J, Sandercock PAG, Jones L et al. (1987). The natural history of lacunar infarction the Oxfordshire Community Stroke Project. Stroke 18 545-551 Bamford J, Sandercock P, Dennis M et al. (1991). Classification and natural history of clinically identifiable subtypes of cerebral infarction. Lancet 337 1521-1526 Bassetti C, Bogousslavsky J, Regh F (1993). Sensory syndromes in parietal stroke. Neurology 43 1942-1949 Bassetti C, Bogousslavsky J, Barth A, Regli F... 

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