Cerebral Embolism Formation

Hemorrhagic Conversion

In this example there is a gross parenchymatous hematoma with intraventricular extension,

midline shift, and herniation.

Ischemic infarction can be divided into "bland" infarction associated with secondary bleeding --
referred to as hemorrhagic conversion or transformation (HT) -- in ischemically infarcted areas
[Mohr JP and Sacco RL, 1992; Teal PA and Pessin MS, 1992; Pessin MS, In: Hacke et al (eds),
1991]. Bland infarction is characterized by bland widespread leukocyte infiltration and
macrophage invasion, with only scattered red cells being found. Hemorrhagic conversion may
take the form of infarction (HI) or, less commonly, parenchymatous infarction (PH). The
occurrence of hemorrhagic conversion is "predominantly a natural tissue consequence of
embolism" [Teal PA and Pessin MS, 1992].
An autopsy, HI may vary from patchy petechial bleeding to more confluent hemorrhages,
representing multifocal extravasation of blood from capillaries or venules [Teal PA and Pessin
MS, 1992]. HI and PH have different incidences, pathogenesis, and clinical outcome, but
distinguishing HI and PH on CT may be difficult [Teal PA and Pessin MS, 1992]. Although HI
and PH have often been grouped together, there are certain features on CT that help
characterize these two types of hemorrhagic transformation. On CT, HI appears as a
discontinuous heterogeneous mixture of high and low densities occurring within the vascular
territory of the infarct. In contrast, PH appears as a discrete, homogeneous collection of blood
that often exerts mass effect and may extend beyond the original infarct boundaries or even
into the ventricles.

HI occurs regularly in the natural evolution of acute

embolic stroke [Pessin MS, In: Hacke et al (eds),
1991]. In autopsy studies, the occurrence of HI has
ranged from 51% to 71% of recent embolic strokes
[Teal PA and Pessin MS, 1992]. However, CT studies
have shown a lower incidence, with studies of con-
coagulated patients who have predominantly embolic
infarcts indicating an overall incidence of 26% to
43%. According to another estimate, approximately
20% of patients with cardioembolic stroke have
hemorrhagic transformation in the infarcted zone,
usually occurring within 48 hours [Leonard AD,
Newburg S. J Neurosci Nurs. 1992;24:69].
Transformation of a bland embolic infarct to HT is rare
in the first 6 hours. Most HIs are asymptomatic, and
it is not uncommon to detect HI on CT patients who
are stable or improving. The pathogenesis of HT
appears to relate to reperfusion of bleeding from
recanalized but ischemically injured vessels by the
natural, dynamic dissolution of thrombi [Teal PA and
Pessin MS, 1992] -- i.e., an embolus that represents
all or part of a thrombus has a spontaneous tendency
to lyse and disperse. Reperfusion into the
ischemically injured vessels can therefore result in
varying degrees of blood extravasation through the
damaged blood-brain barrier.

As noted by Mohr and Sacco (1992), HI has been often explained as a result of reperfusion of
the vascular bed of the infarct, such as would occur
after fragmentation and distal migration of an
embolus or after early reopening of a large vessel
occlusion in the setting of a large infarction; the full
pressure of arterial blood into hypoxic capillaries
results in a diapedesis or red cells through their
hypoxic walls. The concept of restored lumen
patency is consistent with greater frequency of
hemorrhagic infarction in patients with
cardioembolic infarcts.

The occurrence of PH in areas of ischemic infarction

is less common that that of HI [Teal PA and Pessin
MS, 1992]. PH appears to be associated with
anticoagulation therapy, with a low incidence of
spontaneous PH in areas of ischemic infarction (on
the order of 2% to 9%) in patients no receiving
anticoagulation therapy. In contrast to HI, clinical
deterioration is often associated with PH. It has
been proposed that the pathogenesis of PH may involve "ischemic necrosis resulting in the
rupture of small penetrating vessels analogous to hypertensive hemorrhage, leading to
massive bleeding rather that the multifocal diapedesis of blood through capillary walls, as seen
in HI" [Teal PA and Pessin MS, 1992].

The observation that some hemorrhagic infarctions develop distal to the site of a persisting
occlusion suggests that reperfusion is not always a necessary condition. Investigators from
Japan examined the brains of 14 patients who died from herniation of the brain after
cardioembolic stroke with persistent occlusion of the internal carotid-middle arterial axis
[Ogata J, et al. Stroke. 1989;20:876-83]. The finding of hemorrhagic infarct in 7 of the
patients contradicts the concept that reopening a previously occluded vessel is the only
pathophysiologic mechanism for the development of hemorrhagic infarct. Analysis of blood
pressure after stroke has revealed on or more surges of arterial hypertension or rapid rise of
blood pressure in patients with hemorrhagic stroke without a reopening of the occluded artery;
it has been speculated that these blood pressure rises might explain hemorrhagic infarction in
many cases.

A relationship between hyperglycemia and hemorrhagic transformation has also been

suggested by he observation that occluding the middle cerebral artery of markedly
hyperglycemia cats was associated with 5-fold more frequent and 25-fold more extensive
hemorrhage into infarcts than in normoglycemic animals [de Courten-Myers GM, et al. 1992].
Compared with permanent occlusion, temporary restoration of blood flow after 4 hours caused
the most extensive hemorrhage into infarcts. It was concluded that hyperglycemia and
restoration of blood flow to ischemic territories were strong risk factors for hemorrhagic infarct
conversion. The evidence suggests that the marked tissue energy depletion accompanied by
acidosis damages brain vessels, causing leakage of edema fluid and red blood cells [de
Courten-Myers GM, et al, 1992]. Diffuse HI associated with marked hyperglycemia has been
reported in two patients [Broderick JP, et al, 1995].

In summary, HI occurs regularly in the natural evolution of acute embolic stroke and is usually
asymptomatic [Pessin MS, In: Hacke et al (eds), 1991]. PHs occur less frequently, but are
often symptomatic due to extension and mass effect beyond the original infarct territory.
Interest in these issues has been further generated by trials of thrombolytic therapy for acute
ischemic stroke.

Ventricles ( Lateral View )

Ventricles
Each lateral ventricle consists of several parts, pictured above. One part is called the anterior (frontal)
horn of the lateral ventricle, which is the front part of the lateral ventricle. The anterior horn is located in
the front section of the brain, known as the frontal lobe. The anterior horn is positioned in front of the
interventricular foramen, which connects the lateral ventricles to the third ventricle.

Above the anterior horn of the lateral ventricle is the corpus callosum (also pictured above). The
corpus callosum is a group of nerve fibers that connect both sides of the brain and allow them to
communicate. The anterior horns of the lateral ventricle are separated by two triangular-shaped
membranes known as the septum pellucidum. Directly below the anterior horn of the lateral ventricle is
the head of the caudate nucleus. The caudate nucleus is a paired group of nerve cells that play an
important role in body movements.

The back of the lateral ventricle is known as the posterior horn of the lateral ventricle. This is
sometimes referred to as the occipital horn of the lateral ventricle because it extends into a section of
the back part of the brain called the occipital lobe. More specifically, each posterior horn extends into
the white matter of the occipital lobe. White matter is a group of white nerve fibers that conduct nerve
impulses quickly. Like the anterior horn of the lateral ventricle, the corpus callosum is also above the
posterior horn.

The center part of the lateral ventricle is appropriately named the central part of the lateral ventricle.
The central part of the lateral ventricle is also known as the central body and the cella media. Above
the central part of the lateral ventricle is the corpus callosum (see above). The middle of the central
part of the lateral ventricle is formed by the back part of the septum pellucidum (see above).

Below the central part of the lateral ventricle are parts of the caudate nucleus (see above), parts of the
choroid plexus (the blood vessels in the lateral ventricle that produce cerebrospinal fluid), the
thalamus, and the fornix cerebri. The thalamus is a pair of large oval structures that sends out
messages regarding sensation. The fornix cerebri is an arch like body of nerve fibers that projects
outwards from the hippocampus (a structure in the lower part of the brain that is important for
memory).

The bottom of the lateral ventricle is known as the inferior horn of the lateral ventricle. This is
sometimes referred to as the temporal horn of the lateral ventricle because it is in an area of the brain
called the temporal lobe. Above the inferior horn is white matter of the brain. The middle of the inferior
horn is formed by the tail of the caudate nucleus (see above) and the stria terminalis. The stria
terminalis is a thin bundle of fibers that forms a pathway in the limbic system. The limbic system is an
area near the edge of the middle part of the brain that is important for producing emotions.

The amygdala bulges into the end of the inferior horn. The amygdala is a round mass of gray matter (a
gray appearing substance) in the temporal lobe. The temporal lobes are located on the sides of the
brain by the ears. The bottom and middle part of the internal horn is formed by the hippocampus (see
above), fimbria of the hippocampus, and collateral eminence. The fimbria of the hippocampus is a
band of fibers alongside the hippocampus. The collateral eminence is a bulging of white matter that is
found near the hippocampus.

WHAT ARE SOME OTHER DETAILS ABOUT THE LATERAL VENTRICLES

The lateral ventricles take on a curved shape that conforms to the shape of each half of the brain. The
lateral ventricles pass through all four lobes (sections) of the brain. As you can see from the pictures
above, the lateral ventricles are connected to the third ventricle. The area that connects the lateral
ventricles with the third ventricle is known as the interventricular foramen of Monro (also known as the
interventricular foramen and the foramen of Monro). The choroid plexus, which are the blood vessels
in the lateral ventricle that produce cerebrospinal fluid, are found in the central part of the lateral
ventral and the inferior horn, but not in the anterior or posterior horns.

WHAT ELSE ARE THE LATERAL VENTRICLES KNOWN AS

The lateral ventricle is also known as the ventriculus lateralis and the ventricle of cerebral hemisphere.

WHAT IS THE ORIGIN OF THE TERM, LATERAL VENTRICLES

Lateral ventricles comes from the Latin word "latus" meaning "side" and the Latin word "venter"
meaning "belly." Put the words together and you have "side belly."