The way of the lacune

Not a lacune but a lagoon

The terms lacune and lacunar are used at least 4 ways if not more:

  1. A lacunar syndrome – neurologic deficits pointing (not reliably) to small lesions (the most famous are pure motor stroke, pure sensory stroke, dysarthria-clumsy hand, ataxic hemiparesis and – perhaps the worst: sensorimotor stroke)
  2. A lacune as in small white matter lesion (e.g. < 1,5 cm, even < 1 cm sometimes)
  3. A lacune as in a small hole in the brain (either an old bleeding or an old lacune in the previous sense, this is the term implied by status lacunaris)
  4. A stroke with microangiopathic etiology (lacunar mechanism)

As for the geometry of interactions of these meanings:

  • not every lacunar syndrome is due to a small lesion (might be bigger), so 1 does not imply 2 – this is obviously different for each lacunar syndrome but worst for sensorimotor stroke
  • not every small lesion is due to microangiopathy (see below for more expansion on this)
  • not every microangiopathic lesion is small (e.g., anterior choroid artery strokes are often microangiopathic, but mostly big)
  • not every microangiopathic lesion or small lesions or small hole causes lacunar syndromes – you can even get aphasia from a small thalamic lesion

So I would suggest leaving out the term lacune altogether. Also you should cry out loud, throw yourself to the floor and start vomiting, whenever you hear it. If that doesn’t help, read on.

Tiny basal ganglia/capsula strokes are probably what we most associate with the above concepts – small, causing lacunar syndromes, often leaving holes in the brain. But they may be caused by at least three mechanisms:

  1. microangiopathy: this is what has been termed arteriolosclerosis or lipohyalinosis, pathologically not very well described
    Implication: treat hypertension, stop smoking, improve risk factors, give aspirine
  2. branch atheromatous disease: a plaque in the father vessel (MCA, BAS, PCA mostly) has either blocked the way to the branching endartery (hemodynamic) or lead to an embolus (arterioarterial embolism)
    Implication: treat large vessel disease aggressively (ASS + Clopidogrel for some time, high dose statins, treat risk factors, try to avoid stenting if possible)
  3. cardiac or carotid embolism (obviously, if the blood can find it’s way into the basal ganglia, so can emboli)

Now there is a peculiar tendency of small lesions to fluctuate aggressively (the fluctuating lacune, throw myself to the floor!). If they do, we used to generously infuse heparin at varying doses, never ever actually achieving the proper PTT, but this seems not to be hip anymore. I personally favor Aggrastat (Tirofiban) for this indication and have excellent experience; also I can use the SATIS study to justify it’s off label use. Others use eptifibatide. But – as always – someone should do a study on this.

Other treatments include: induced hypertension and Mg sulfate.

References:

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