Hemorrhagic stroke

notes by dr Claudio Italiano

Cerebral hemorrhage is an acute neurological syndrome due to the rupture of a cerebral arterial vessel and the consequent blood extravasation in the cerebral parenchyma.
We distinguish cerebral hemorrhages with a typical site, located in the deep structures (nuclei of the base, internal capsule, thalamus) and atypical site, which are localized in the parietal, frontal or occipital white matter. The subtentorial sites most frequently affected are the bridge and the toothed nucleus of the cerebellum.
Hemorrhage, due to the rupture of a blood vessel in the head, can be extra-axial, indicating that it occurs inside the skull but outside the brain, or intra-axial, which occurs inside the brain.

Extra-axial hemorrhages

Risultati immagini per arterie perforanti cerebrali They can be further divided into:
- epidural hematoma
- subdural hematoma and subarachnoid haemorrhage (depending on whether the bleeding occurs in the space between the skull and the cerebral membrane known as dura mater, between the latter and the arachnoid membrane or between the arachnoid and the pia mater respectively).

Intraxial bleeding

Unlike ischemic stroke, the hemorrhagic stroke depends on a hemorrhagic event, ie the spread of blood inside the brain parenchyma due to hemorrhage, which in turn generally depends on vascular malformations or due to the fact that the perforating arteries that rise at an angle rectum, are subject to micro-aneurysmal lesions. For example. lenticolostriate vessels are subject to these problems, usually related to hypertensive facts. Generally the symptoms that arise after a hemorrhagic stroke are more striking than those of a patient with ischemic stroke. The patient with haemorrhagic stroke can immediately present a state of severe numbness of the sensory, with psychomotor agitation or, in the most severe cases, also convulsions. Neck stiffness and hypertonicity of the limbs may be present. Hemorrhage can destroy the nuclei of the base and determine damage in the brain substance, until it penetrates into the ventricular space, determining the condition called "cerebral ventricular tamponade".

Bleeding can be:

1) a typical cerebral hemorrhage (capsular)
2) massive hemorrhage.

Etiology

Some causes responsible for cerebral hemorrhage are:

- Rupture of vascular malformations (aneurysms or arteriovenous malformations) (hemorrhage in the subarachnoid space)
- Primary 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)

Smptomatology

Malformazione vascolare cerebrale, artero-venosa o MAV

The haemorrhagic stroke is characterized by a severe stroke of abrupt or rapidly exacerbating stroke (mostly in subjects 50 and over), preceded or not by very short-lived prodromes (headache, vomit). Arteriovenous malformations (MAV) are vascular abnormalities characterized by a direct, pathological communication between arteries and veins that may be responsible for cerebral hemorrhage. Normally the blood passes from the arteries to the veins through the capillaries, microscopic vessels with very thin walls, at the level of which the exchanges of nutrients between blood and tissues are carried out. In the case of MAV, there are no capillaries and vessels located between the arterial circle and the veins undergo rupture and hemorrhage. A MAV is therefore made up of one or more afferent arteries (feeders), a nidus and drainage veins.
Hemiplegia, hemianesthesia, aphasia, often with early hypertonia, contralateral motor phenomena, intense vegetative disorders: facial cyanosis, breathing disorders (polypnea, bradypnea, Cheyne-Stokes breath) hyperthermia etc. Often there is a conjugate deviation of the head and eyes towards the side of the lesion or the opposite side. Hypertony in the plegic limbs is precocious, with mixed, pyramidal and extrapyramidal characters (due to direct or indirect lesion of the nuclei of the base and of the internal capsule).

One may have motor negativism or motor restlessness of the contralateral limbs of hemiplegia (by indirect compromise of the deep structures of the hemisphere base, due to displacement phenomena due to the hemorrhagic focus and edema of the injured hemisphere). A total flaccidity with bilateral Babinski has an unfortunate meaning. Neurological disorders are not easy to highlight when the patient is in a coma. It may be present at the examination of the papillary edema fundus on the side of the lesion. In 2/3 of the cases the evolution is unfavorable.
In 1/3 of the cases after the initial phase a stabilization and also the improvement of the disturbances of the conscience and of the neuro-vegetative sphere can occur; the pupillary and corneal reflexes reappear:

We distinguish
1) Deep intrasal hemorrhage typical:
- hemorrhage of the nuclei of the base
- thalamic haemorrhage: it is more localized, extending to the posterior arm of the internal capsule;
- lenticular nucleus hemorrhage (very rare).

TAC encefalo: emorragia cerebrale da MAV intraparenchimale, che alla tac si evidenzia come area bianca

Brain CT scan: cerebral hemorrhage from intraparenchymal MAV, which at tac is shown as a white area

2) intracerebral hematoma or atypical hemorrhage.
It is a blood collection, even of considerable size, at the level of the cerebral white matter.
The symptomatology can begin abruptly or proceeded by headache and epileptic seizures.
The symptoms of a brain lesion at the outbreak, which can sometimes lead to a diagnosis of site (frontal, parietal, temporal or occipital lobe), are associated with those of intracranial hypertension (vomiting, headache, progressive obfuscation of consciousness); the disproportion between the modest signs of an outbreak and the intensity of the signs of intracranial hypertension is characteristic. It is important to arrive at an early diagnosis, as surgery is often indicated: the brain arteriography and above all the CT scan are decisive;

3) cerebro-meningeal haemorrhage due to rupture of an angioma or an aneurysm with blood diffusion. A profound cerebral hemorrhage may occur which makes its way into a ventricular cavity or a superficial cerebral hemorrhage that invades the subarachnoid space. In superficial cerebral haemorrhages the onset is often characterized by partial and / or generalized seizures, with focal neurological deficits and signs of meningeal irritation. In the subarachnoid hemorrhage (angiomas, aneurysms, hypertension, hemorrhagic diseases, cranial traumas) the hemorrhagic effusion is collected between the two sheets (pia and arachnoid) of the leptomeninges; the symptoms are those of a meningeal syndrome with usually sudden onset.

Diagnostic-differential considerations between hemorrhage and softening

For a differential diagnosis between haemorrhage and cerebral softening it is necessary to carefully evaluate the anamnestic data and the objective neurological finding and possibly the use of complementary examinations. It must be taken into account that: the paradigmatic frameworks are rather exceptional and the atypical pictures are very frequent, that the softening apoplexy is more frequent than the one from haemorrhage (3 to 2) and the age of onset is earlier in the haemorrhage. The previous history of TIA is much more frequent in softening; this, moreover it rises more frequently during the sleep, while the hemorrhage during the activity. Both the haemorrhage and the softening can arise abruptly or gradually, but an abrupt episode followed by a progressive improvement or a gradual onset with modest alterations of the conscience make it susceptible to softening and so if the onset has been preceded by recent, repeated episodes of TIA. The onset with headache and vomiting is slightly more frequent in the bleeding. Loss of consciousness at the onset of stroke is more common in hemorrhage than softening. Early hypertonia (in the first 24 hours) is more characteristic of hemorrhage and so is also the nuchal rigidity and early hypertonia of the paretic limbs. An ipsilateral mydriasis is more common in hemorrhage. The presence of blood in the liquor is typical, but not constant, of cerebral hemorrhage; the increase of some enzymatic activities (transaminases, glutamic-oxaloacetic, lactic acid-dihydrogen), proteins and cellular elements in the liquor is in favor of softening. Among other causes of apoplexy the cerebral embolisms must be remembered. In this case the onset is sudden, with short-lived coma, inconstant and non-evolutionary motor deficit, with rapid regression (for better collateral circulation efficiency). It will be thought of embolism, in the presence of morbid conditions that can give emboli in the cerebral area: carotid thrombosis, myocardial thrombus of infarction, bacterial endocarditis, atrial fibrillation, pulmonary diseases; emboli can detach from atheromatous plaques of cerebral arteries. The coexistence of a retinal embolism is in favor of the embolic event. A neurological syndrome due to a decrease in cerebral blood flow following myocardial infarction, makes Chini's coronary-cerebral syndrome. From a few hours to three days after myocardial infarction, in fact, focal manifestations may arise, such as hemiparesis or Jacksonian seizures, by cerebral localization of emboli coming from cardiac parietal thrombus. Already in the onset of myocardial infarction, a decrease in cerebral blood flow can also occur due to a decrease in cardiac output, which results in general manifestations (epileptic accesses, psychomotor agitation, psychic torpor, coma).

cfr index of neurology