Intracerebral hemorrhage: non-hypertensive causes.

Abstract

SPONTANEOUS, non-traumatic intracerebral hemorrhage (ICH) in the adult is most commonly secondary to hypertensive cerebrovascular disease. In 70-90% of cases of spontaneous ICH, arterial hypertension is the presumed cause.1 These hypertensive hemorrhages show a predilection for certain anatomic locations: the basal ganglia (the putamen in particular), the subcortical white matter, and the thalamus account for 35%, 25%, and 20% of ICHs, respectively, whereas the posterior fossa locations, the cerebellum and pons, are responsible for only 10% and 5% of the cases.2 Irrespective of their anatomic locations, the common pathogenesis in these hemorrhages involves the hypertension-induced degeneration of the media of small (50-200 micra) arteries called "lypo-hyalinosis," 3 and/ or the formation of "microaneurysms", both of which occur preferentially in perforating or small sub-cortical arteries, thus resulting in the characteristic anatomic distribution of hypertensive ICH.A significant number of cases of ICH are due to causes other than hypertension. The frequency of such cases varies from 25% to 50% among series, and depends on the anatomic type of ICH being considered: non-hypertensive mechanisms may account for as many as 55% of "lobar" ICH cases, 4 ' 3 while pontine hemorrhage is virtually always (90%) hypertensive, and the deep ganglionic (putaminal, thalamic) and cerebellar varieties occupy an intermediate position (35%, 25%, and 38% being of non-hypertensive mechanism, respectively). Among the many possible mechanisms of ICH not primarily related to hypertension, there are several that occur with high enough frequency to warrant separate discussion. These causes of ICH are related to special types of arterial pathology, to the presence of brain tumors, or to the use of medications, and include: cerebral amyloid angiopathy, small vascular malformations, primary or metastatic brain tumors, oral anticoagulants, and amphetamines and a variety of other sympathomimetic drugs. Cerebral Amyloid AngiopathyThis condition is a unique form of angiopathy due to deposits of amyloid in the media and adventitia of

Intracerebral hematomas during anticoagulant treatment.

“…38 Unfortunately, there are no prospective studies on which to base the degree of anticoagulation required to avoid or treat arterial thromboembolism. 39 ' 40 However, our conclusion, that the use of anticoagulants increases the risk of ICH but that this risk is not directly dependent on the degree of anticoagulation, suggests an all-or-nothing phenomenon with a low threshold.…”

In Vitro Characterization of Ephedrine-Related Stereoisomers at Biogenic Amine Transporters and the Receptorome Reveals Selective Actions as Norepinephrine Transporter Substrates

“…Our data indicate that (Ϫ)-phenylpropanolamine and (ϩ)-phenylpropanolamine [(Ϫ)-norephedrine and (ϩ)-norephedrine) and (Ϫ)-ephedrine and (ϩ)-ephedrine] have similar activity at the biogenic amine transporters. This suggests that the potential for hemorrhagic stroke may not arise as a direct result of the pharmacological mechanism of action, NE release, but rather from idiosyncratic vasculitis (Kase, 1986;Glick et al, 1987).…”

Clinical and Radiographic Features of Lobar Cerebral Hemorrhage: Hypertensive Versus Non-hypertensive Cases

“…Indeed, lobar ICH is the result of other heterogeneous causes, including arteriovenous malformation, cavernous angioma, aneurysm, brain tumors, especially those of metastatic origin (2,3), the use of anticoagulant or fibrinolytic agents, cerebral amyloid angiopathy and vasculitis (2). Furthermore, the frequency of lobar ICH complicated by amphetamines (4), pseudoephedrine (5), and cocaine (6) has increased recently.…”