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.


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