Brain hemorrhages
The
most frequent cause of cerebral hemorrhage is the "rupture" of a vessel due to
the damage caused by arterial hypertension; in this case the hemorrhage is
almost always localized in the typical place.
Other causes responsible for cerebral hemorrhage are:
-Very vascular malformations (aneurysms or arteriovenous malformations) (hemorrhage
in the subarachnoid space)
- primitive or metastatic brain tumors (intra-tumor hemorrhage)
- hemorrhagic transformation of an ischemic stroke
-complication in the use of anticoagulant drugs
- hemorrhagic diseases (leukemia, hemophilia, disseminated intravascular
coagulation, platelet diseases)
- deposition of amyloid substance in the arterial vessels (lobar hemorrhages)
- hematomas (blood stravases) between the meninge and the cranial case (so-called
extra dural hematomas) secondary to more or less relevant head injuries (exemplary
cases of the cyclist who falls, gets up and falls into a coma and the boxer
after a " normal "KO"
-ematomas between the outermost meningeal membrane (dura mater) and the
encephalic mass (so-called subdural hematomas)
Brain trauma
Head injury can result in:
Bone lesions (cranial fractures)
Parenchymal damages
Vascular lesions
From a temporal point of view, head injury can be divided into primary and
secondary:
They occur at the time of trauma, by direct impact, or sudden
acceleration-deceleration
They cause impact lesions, which cause extradural, subdural bleeding, contusions,
lacerations of the meningas and superficial damage of the nervous substance;
It may however be that the brain undergoes a backlash injury because the brain,
following the application of a force and sudden traumatism, undergoes sudden
acceleration and deceleration, essentially by brain tossing inside the skull. In
other cases, once a trauma has occurred, over time, damage can occur that is
clinically visible for hours or days.
From the spatial point of view they can instead be divided into focal or diffuse
lesions; focal points for ex. :
o Contact: cranial fractures, bruises and superficial lacerations, extradural
hematoma, intracranial hemorrhages
o From acceleration / deceleration: acute subdural haemorrhage
In the case of widespread lesions, we think of ischemic damage or widespread
axonal damage.The intraparenchymal traumatic damages are distinguished in:
- Concussions, term used clinically to describe a syndrome with loss of
consciousness and transitory paralysis, sometimes with convulsions, with
complete functional recovery (possible amnesia, but from the morphological point
of view no outcomes occur or are negligible), caused by a trauma in which the
movement of the skull is abruptly arrested. Symptomatology is thought to be
caused by damage to the reticular activation system or limited axonal damage
Contusions and encephalic lacerations
They are lesions with clear morphological evidence: they cause superficial
parenchymal hemorrhages caused by an impact trauma, where the brain comes into
contact with the skull box (or with points where the dura mater is reflected or
with the tentorium). They are more common on convexities (frontal poles, orbital
gyrations, temporal poles, occipital, posterior cerebellum). Contusive injuries
are very important in forensic medicine to clarify the dynamics of the accident
(in the image, for example, a lower trauma to the right could be hypothesized,
with stroke injuries - the preparation is observed from the front, with high
backlash injuries against the scythe and to the right).
o Usually the meninges are intact: if injured, we speak of lacerations
o They are subdivided into blow bruises and kickback contusions
o Herniations are possible (not direct, but mediated by increased pressure
caused by hemorrhage / edema)
o If the bruise heals, a depressed area with increased consistency and brownish
color (possible epileptogenic foci) is formed: yellow plaques, usually in the
sites of the backlash lesions
Widespread axonal damage
Responsible for most cases of post-traumatic dementia and one third of head
traumatic deaths; it can also be given by angular acceleration alone
or Macroscopically: few alterations, except in the most severe cases (hemorrhages
of the corpus callosum and of the dorsal areas of the encephalic trunk)
o Microscopically: acute, characteristic axonal swelling in the white matter
with so-called axonal spheroids, in addition to focal haemorrhagic lesions
After the trauma from the Iimmunohistochemical point of view we have positivity
for the amyloid precursor protein (APP) and α-SN. After a few weeks, increased
microglia, macrophages and astrocytosis, with degeneration of the stretches of
fibers involved.
Traumatic intracerebral hemorrhages
Epidural (or extradural) hemorrhages
Hemorrhages are usually caused by rupture of the medial meningeal artery,
usually associated with bone fracture (being an artery, the expansion can be
very rapid): compresses the dura and the cerebral parenchyma
Radiologically, it takes on a "biconcave lens" appearance
The time that elapses between the onset of hemorrhage and the onset of
compression symptoms (caused by the hematoma) is defined as "lucid interval":
this is because the dura mater initially opposes the compression of the
parenchyma (then the blood rises too much)
These haemorrhages are often associated with cerebral edema and herniations,
bruises, etc. are possible
Subdural haemorrhages
They are characterized by the collection of blood between the internal surface
of the dura mater and the arachnoid. In most cases there are tear lesions of
connecting veins (bridge veins, bridging) caused by acceleration or deceleration
at high speed. The bridge veins can be more easily torn in children (very thin
vessel wall) and in the elderly (the bridge veins are "stretched" by cerebral
atrophy: even a trauma without bone fracture can give hematoma). In general,
lesions appear, with varying severity, on the convexity. Treatment is the
removal of blood and connective tissue.
- Acute phenomena present with red blood, semiliquid or more often coagulated.
It is usually evident the association with a trauma (often associated with other
trauma injuries, edema, compressions, herniations)
- Chronic phenomena present us with dark, turbid liquid, delimited by connective
connective tissue neomembrane,
often associated with atrophy. The association
with a trauma is often not evident (slow evolution, differential diagnosis with
dementia)
subarachnoid
They occur mainly due to a primary disease (laceration) of the cerebral vessels.
The traumatic cause is rarer.
These are dangerous events, burdened by a high mortality rate (especially those
caused by rupture of aneurysms).
In general, the most frequent causes are:
- Aneurysms
- Saccular aneurysms (berry aneurism): also called berry aneurysms, mainly
involve the vessels of the cranial base (as the circle of Willis before entering
the brain parenchyma). These are events with a prevalence of 2-5% (prevalence
increases with age), probably congenital in nature, not identifiable at birth,
which develop at a certain age. They usually have dimensions smaller than cm
(and circular shape because due to focal weakening of the wall) but can reach
even 2-3 cm. 25-50% of the
patients die at the first episode of rupture (also because they do not show
prodromal symptoms)
- Fusiform aneurysms: they occur mainly in the case of hypertension (atherosclerotic
aneurysms) and have a tapered shape (because the pressure is distributed over
the entire wall). They are mainly dependent on the basic artery.
- Infectious (septic) aneurysms
- Dissection (also from aortic dissection that goes back along the carotids)
- Trauma
- Extension of intraparenchymal hemorrhage
- Vascular malformations
- Arteriovenous malformations (MAV)
- Cavernous angiomas
- Capillary telangiectasia
Intraparenchymal hemorrhages
They occur mainly due to hypertension (the most frequent cause in all cases) or
a primary disease of the cerebral vessels. The traumatic cause is rarer. The
areas most affected are "deep gray areas" such as putamen and thalamus, or
cerebral lobes, bridge, cerebellar hemispheres. The causes of include:
- Hypertension: systemic hypertension causes atherosclerotic lesions that may
lead to the development of fusiform aneurysms at risk of rupture. Hypertension
can also lead to the formation of very small aneurysms, called Charcot-Bouchard
microaneurysms, on small vessels, below 300 μm. These microaneurisms can break
and give rise to serious bleeding.
- Coagulation diseases
- Neoplasms
- Amyloidotic angiopathy (from Aβ40, with arteriolar and capillary deposits)
- Vasculitis
- Vascular malformations
Diffuse cerebral edema (swelling)
Cerebral edema appears as a swelling of the cerebral gyrus and a thinning of the
furrows (the opposite of the atrophic situation, in which the fissures are wider
and the gyrations are less pronounced). It is not specific to any type of
disease (it has many etiologic agents) and can cause hernias.
Subdural hematoma is a phenomenon that occurs less rapidly than epidural.
neurology index