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First off, when learning about these two diseases, they are similar in so many ways.

Pathoma says focal infarcts are from benign htn (the pathologic feature of Hyaline arterioscelerosis) and charcot bouchard are from chronic or malignant htn (so I'm assuming the path is hyperplastic arterioscelerosis or onion skinning + fibrinoid necrosis - features of chronic htn)...BUT uworld says BOTH charcot bouchard and focal infarcts are from chronic HTN...what is correct?

So first off with with the similarities, they BOTH affect lenticulostriate arteries feeding the basal ganglia and are due to hypertension? If UWorld is correct, then I assume both are from chronic hypertension- another similarity. As far as differences, UWorld mentions the size of lesion, the ability to diagnose the hemorrhagic lesion in charcot-bouchard early but not the initial pale ischemic infarct leading to a cavitary lesion (which weeks later can be diagnosed) of the focal infarct...but my question is ultimately once again is the pathological process origin chronic HTN?

So am i missing something, because it would then seem from a pathological standpoint, pretty much if the lenticulostriate artery under chronic HTN purely causes ischema OR weakens the vessel wall enough to rupture it the point of divergence leading two two different diagnosis
 

Morsetlis

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The Charcot-Bouchard aneurysms are due to intraparenchymal hypertension in the basal ganglia like you said.

The lacunar infarcts are ischemic strokes, not hemorrhagic strokes. They are lacunar because of the liquefactive necrosis pools they leave behind. Microatheroma is now thought to be the most common etiology.
 

calvnandhobbs68

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First off, when learning about these two diseases, they are similar in so many ways.

Pathoma says focal infarcts are from benign htn (the pathologic feature of Hyaline arterioscelerosis) and charcot bouchard are from chronic or malignant htn (so I'm assuming the path is hyperplastic arterioscelerosis or onion skinning + fibrinoid necrosis - features of chronic htn)...BUT uworld says BOTH charcot bouchard and focal infarcts are from chronic HTN...what is correct?

So first off with with the similarities, they BOTH affect lenticulostriate arteries feeding the basal ganglia and are due to hypertension? If UWorld is correct, then I assume both are from chronic hypertension- another similarity. As far as differences, UWorld mentions the size of lesion, the ability to diagnose the hemorrhagic lesion in charcot-bouchard early but not the initial pale ischemic infarct leading to a cavitary lesion (which weeks later can be diagnosed) of the focal infarct...but my question is ultimately once again is the pathological process origin chronic HTN?

So am i missing something, because it would then seem from a pathological standpoint, pretty much if the lenticulostriate artery under chronic HTN purely causes ischema OR weakens the vessel wall enough to rupture it the point of divergence leading two two different diagnosis

Just had this question too...was slightly pissed that they expected me to know what was considered a small vs large lesion lol.
 
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Charles_Carmichael

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The way I've understood it, long-standing HTN can cause both Charcot-Bouchard aneurysms and hyaline arteriolosclerosis (not hyperplastic) in the lenticulostriate arteries.

If the hyaline arteriolosclerosis is predominant and you get ischemia (ex. as a consequence of hypotension + the hyaline arteriolosclerosis), you'll get a lacunae infarct.

If there's formation of Charcot-Bouchard aneurysms and one of them ruptures, you're going to get intracerebral hemorrhage into the deep structures of the brain -- basically, a hemorrhagic infarct.

So, long-standing HTN can cause both things. What type of infarct you end up with depends on whether you have severe hyaline arteriolosclerosis vs. whether you've weakened the vessel wall enough to cause aneurysms and increase the risk of rupture.

At least, that's how I work down the algorithm in my head. Others can feel free to correct me if I'm wrong.
 

Myxedema

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From Robbins Pathologic Basis of Disease, 8th Edition, Chapter 28 - "The Central Nervous System":
HYPERTENSIVE CEREBROVASCULAR DISEASE
The most important effects of hypertension on the brain include lacunar infarcts, slit hemorrhages, and hypertensive encephalopathy, as well as massive hypertensive intracerebral hemorrhage. The incidence of these disorders is likely to decline with increased screening for hypertension and aggressive management of blood pressure

Lacunar Infarcts
Hypertension affects the deep penetrating arteries and arterioles that supply the basal ganglia and hemispheric white matter as well as the brainstem. These cerebral vessels develop arteriolar sclerosis and may become occluded; the structural changes are similar to those described in the systemic vessels of individuals with hypertension (Chapter 11). An important clinical and pathologic consequence of CNS arterial lesions is the development of single or multiple, small, cavitary infarcts known as lacunae (Fig. 28-17). These are lake-like spaces, less than 15 mm wide, which occur in the lenticular nucleus, thalamus, internal capsule, deep white matter, caudate nucleus, and pons, in descending order of frequency. On microscopic examination they consist of areas of tissue loss with scattered lipid-laden macrophages and surrounding gliosis. Depending on their location in the CNS, lacunae can either be clinically silent or cause severe neurologic impairment. Affected vessels may also be associated with widening of the perivascular spaces but without tissue infarction (état criblé).
INTRACRANIAL HEMORRHAGE
...
Intracerebral (Intraparenchymal) Hemorrhage
Hypertension is the most common underlying cause of primary brain parenchymal hemorrhage, accounting for more than 50% of clinically significant hemorrhages and for roughly 15% of deaths among individuals with chronic hypertension. Hypertension causes a number of abnormalities in vessel walls, including accelerated atherosclerosis in larger arteries; hyaline arteriolosclerosis in smaller vessels; and, in severe cases, proliferative changes and frank necrosis of arterioles. Arteriolar walls affected by hyaline change are presumably weaker than are normal vessels and are therefore more vulnerable to rupture. In some instances chronic hypertension is associated with the development of minute aneurysms, termed Charcot-Bouchard microaneurysms, which may be the site of rupture. Charcot-Bouchard aneurysms, not to be confused with saccular aneurysms of larger intracranial vessels, occur in vessels that are less than 300 μm in diameter, most commonly within the basal ganglia.

In summary, both Charcot-Bouchard microaneurysms and lacunar infarcts occur as a result of hypertension:
  • Charcot-Bouchard microaneurysms: Chronic hypertension --> Formation of small aneurysms --> Rupture of aneurysms --> Intracerebral hemorrhage, most commonly located in basal ganglia and thalamus (Hemorrhage itself is not necessarily small; what is small here is the size of the aneurysm). Clinical presentation of intracerebral hemorrhage is associated with increased intracranial pressure: Headache, altered mental status, seizures, brain herniations, coma, and death.
  • Lacunar infarcts:: Chronic hypertension --> Arteriolar sclerosis --> Occlusion of sclerotic artery --> A small sized infarct occurs, most commonly located in basal ganglia and brainstem (Here, the infarct itself is small, not the arteriolar sclerosis). Clinical presentation is pure sensory and motor loss.
 
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