Classically, the Arteriovenous Malformations Can Be Classified As

Classically, the arteriovenous malformations can be classified as:

-True arteriovenous malformation

-Cavernoma

-Venous malformation

-Telangiectasia

Currently there is a tendency to add to this classification the arteriovenous fistulas and to rename the venous malformations into incidental venous developing anomaly since they have no pathological meaning and are more frequently observed due to the widespread of the MRI usage. The same goes for the cerebral telangiectasia since they also are without any pathological significance and have no therapeutic indication except the case when they represent an epileptogenic foci.

Of great importance is the cavernoma (cavernous malformation) whichrepresents a blackberry like vascular malformation of variable dimension, surrounded by brain parenchyma, composed of dilated vascular canals with a single endothelial layer. The cavernoma usually connects slow flow vessels thus they are usually angiographically occultlessions(they don’t appear on the endovascular angiogram). They are very well visualized on the MRI. They usually manifest by rupturing (intracerebralhemathoma) or epileptic seizures, in which case surgical resection is required. Incidental discovered cavernomas (MRI taken for another reason) are surgically treated based on the operative estimated risk depending on the location (superficial vs deep seated; eloquent area of not, brainsteam location, etc) risk of rupture, age of patient, etc.

True arteriovenous malformations are staged into 5 grades based on the possibility of surgical resection. (Spetzler scale, 1986) This grades represent the sum of points accorded based on three criteria: dimension, position in an eloquent area and venous drainage

The clinical manifestation of arteriovenous malformations could be classified into 3 syndromes: hemorrhagic (subarachnoid hemorrhage, intracerebral hematoma), epileptic and pseudotumoral.

The therapeutic possibilities consist of one or more of the following: microsurgical resection (coagulation or clipping of the arterial pedicles with dissection around the nidus followed up by the coagulation of the venous pedicles and resection of the malformation), radiosurgery, and embolization.

Medical protocols in the case of subarachnoid hemorrhage.

Subarachnoid hemorrhage (SAH) which in 80% of the cases is because of an ruptured aneurysm, can present different clinical stages based on the gravity of the case ( sudden death, coma, neurological deficit, confusional syndrome, meningeal syndrome, or just a simple headache with sudden onset) The association with a intracerebral hematoma can diversify even more the clinical presentation.

60% of the patients presenting to the hospital have a medium or moderate SAH (score II or III). The clinical steps that these patients need to follow are:

-CT scan as fast as possible to document the SAH and make the diagnostic, and try to localize the origin of rupture (locating the aneurysm)

-CT angiography to highlight the aneurysm. In 20% of the cases the image is negative or a more specific search is needed in order to find the aneurysm (or multiple aneurysms)

-Every time it is possible to find the ruptured aneurysm, it is important to exclude it from circulation and prevent a new rupture. Currently there are two main techniques to do so: microsurgical clipping and endovascular embolization.There is somewhat of a competition in practice on which technique is better. In some types of aneurysm there is a clear indication on which technique is better. In a lot of cases instead, either techniques can be used with the same risks and benefits. Sometimes these procedures are complementary and represent an alternative, as a backup plan in case of the failure of the first choice.

-The surgical intervention to clip an aneurysm is made for patients that have a distal positioned aneurysm more harder to reach with a catheter; broad base neck aneurysm; giant aneurysms; partially thrombosed aneurysms, fragile aneurysm that have a high risk of rupturing on embolization, aneurysm that present collateral arteries for which the permeability needs to be kept, or the case of failed embolization. Early surgery (within the first 24-72h) is applied to patients in acceptable clinical state with low anesthesiological and surgical risk. This attitude prevents a new rupture from occurring and allows the induction of controlled hypertension to prevent the effects of cerebral vasospasm. The role of evacuating the blood clots from the subarachnoid space may be also benefic.

-Patients in bad clinical health, with high anesthesiological and surgical risk could get worse under an early intervention due to secondary cerebral lessions and also due to vegetative and systemic complications. These group of patients are treated in a conservative manner (even with the risk of a second rupture) in order to first stabilize the vegetative and systemic deficits. The surgery is performed either immediately the state of the patients allows it, or after the passing of the first 14-21 days ( the risk of cerebral vasospasm is greater)

-Patients with normal angiographic findings on which no other cause of SAH can be found (hemorrhagic disorders, hemorrhagic meningitis, tumor etc) must be further investigated by an MRI ( revealing and angiographic occult lesion ) and reevaluated angiographicaly after 1-3 months ( there is the chance of an aneurysm to be “masked” by the vasospasm or a temporary thrombus)

-If SAH is associated with an intracerebral hematoma with mass effect, the hematoma must be first evacuated and then the clip can be placed (usually during the same surgery)

-The association with hydrocephalus requires usually an external ventricular drain to be placed

-Intensive care, conservator and adequate treatment to reduce the risk of a new rupturing from occurring and vasospasm prophylaxis are initiated from the beginning and are adapted every step of the way.

In order to put to practice this protocol, the following equipment is needed:

-ER dedicated CT scanner

-Angiographic lab capable of digital subtraction angiography via Seldinger technique

-The possibility of endovascular embolization with a dedicated and specialized team

-Neurosurgical unit specialized in vascular microsurgery and an OR equipped accordingly

-Adequate neuroanesthesia and intensive neurotherapy

The possibility of perfectioning the noninvasive angiographic studying (MRA or CTA) could present some changes to the presented protocol.

The sever forms of SAH (grade IV and V) are included in the management of sever cerebral vascular injuries. The problems in treating a neurologic coma are similar in some way with the treatment of severe traumatic injuries. In the absence of a clear clinical history, the difference between a severe traumatic injury and a vascular injury with a minor secondary traumatic injury due to falling is hard to make until further investigation. The same treatment for maintaining vital signs and preventing secondary cerebral injuries is applied. In case of improvement and if the patients state allows it, angio is performed and the aneurysm is treated.

Primary intracerebral hematoma

Besides the traumatic intracerebral hematoma which was already discussed, there can also be described spontaneous hematomas due to vascular hemorrhage. Spontaneous intracerebral hematomas can occur secondary to the rupturing of a vascular formation: aneurysm, true arteriovenous malformation, cavernoma or they can appear due to the rupture of a tumoral vessel (hemorrhagic tumors: melanoma metastasis,glioblastoma)

In case the intracerebral hematoma is neither traumatic nor secondary to a hemorrhagic formation, it is called primary hematoma. Currently they are called spontaneous intracerebral hematoma. This category includes:

-Hypertensive hemathoma, representing the rupture of a modified arteriol with hialinosys. Chronic hypertension induces hialinosysto arteries and a subsequent hypertensive episode can rupture it. These changes occur more frequently in small diameter arteries, such as those found in the center of brain.

-Amiloid hematoma: located more frequently subcortical and multilocular in elderly patients with vessels that suffered amyloid degeneration.

-Hematoma due to hemostasis deficits, more frequently in patients with anticoagulation therapy

The hematoma usually presents as an acute installed focal neurologic deficit (hemiplegia usually) with altered level of consciousness and increased intracranian pressure.

The diagnosis is made based on a CT scan witch also helps us on deciding the treatment:

-Conservator treatment and watchful waiting till the resorption of the hematoma ( usually for small of medium hematomas with good clinical evolution)

-Surgical evacuation or stereotactic puncture ( for compressive hematomas in accessible positions)

-Intensive care for patients with thalamic hematomas (the thalamic destructionleads to neurovegetative disorders and a severe altered level of consciousness)

Putaminal hematomas represent a location on which surgical evacuation can be performed, especially if the hematoma has a lobar extension, but the outcome is less favorable than in pure lobar hematoma.

Medical protocol for primary intracerebral hematoma

Initial emergency measures to maintain vital signs are similar. Because of the fact that most of the hematomas are of hypertensive origin, medication to lower blood pressure is initiated from the beginning. Care must be taken in order not to lower to much the pressure in order to keep the cerebral perfusion normal. Once admitted to the hospital, the patients is guided through the next steps:

-Evaluation of the severity: progressive aggravation, severe state from the beginning, partial amelioration, unstable evolution etc…

-Emergency CT scan: gives us important details regarding the positioning of the hematoma and the clinical treatment. Superficial location (lobar) represents a criteria for surgical treatment while deep seated lesions (internal capsule, basal nuclei) or in the brainsteam are rarely treated surgically.

A series of clinical and imagistic criteria are used to evaluate and treat the patient. One contradiction that appears in some cases is the question of wheatear the severe clinical state is due to the primary cerebral lesion or is it due to the expansive nature of the hematoma and intracranial pressure. If the first is true, then the surgical treatment would worsen the situation because of additional cerebral injury and the potential to rebleed. If the second is true, then the lack of surgical intervention would lead to death due to the increased intracranial pressure (herniation and low blood perfusion). Since both mechanisms are somewhat related in the majority of cases, the final verdict is given by the experience and rationale of the neurosurgical unit.

-Surgical intervention in order to evacuate the hematoma can be made immediately after presenting to the hospital (mass effect is certain, hematoma or important component of it in lobar position) after a period of watchful waiting for severe cases with unstable evolution (in order for the hematoma to become chronic and facilitate a spontaneous hemostasis) and immediately after deterioration in patients with secondary aggravation.

-Intensive care with or without surgical evacuation of the hematoma for thalamic hematomas or severe vegetative disorders, and in cases where the surgical intervention could worsen the status of the patient. Also represents the choice of treatment for small, well tolerated, without mass effect hematomas.

-Since during the clinical evolution of a intracerebral hematoma there is the possibility that at any moment a rebleeding can occur, it is important to watch and observe the patient even if he is clinically healthy and also have available the OR for a case of emergency.

-After the acute phase, the medical treatment of associated pathologies is continued and neuromotoric rehabilitation is initiated.

In order to ensure the standard treatment for a hemorrhagic vascular accident such as anintracerebral hematoma, the following equipment is needed:

-Ambulance

-Neurointensive care unit and neuroanesteshia

-CT scanner ready for emergency scans

-OR available and acces to minimal invasive techniques such as : microsurgery, endoscopy, stereotaxic puncture, ultrasonic aspiration

-Access to neuromotoric rehabilitation

-Access to further imagistic investigation such as MRI or angio

Neurosurgical possibilities in the profilaxis and therapy of ischemic vascular injury

Conservative treatment with anticoagulants and fibrinolitics has ameliorated the prognostic for ischemic vascular injuries, which in most of the cases represent a subject for neurology.

The surgical possibility of revascularization of an ischemic segment has led to the development of a new and various techniques such as: thromboarterectomy, exo-endo vascular anastomosis and so on. The usefulness of this techniques has been questioned lately since they don’t offer sufficient blood irrigation in the ischemic segment in order to prevent necrotic lesions, and revascularization can spontaneously appear without intervention. Even more, there is the risk of transforming an ischemic injury into a hemorrhagic injury. Currently, the technique of injecting locally endovascular fibrinolitics nearthe thrombus or endovascular extraction of the thrombus has evolved very much. Thrombolysis can be practiced only in the first 3 hours since debut. It is known that a nerve cell can resist to anoxia for about 3-5 minutes. In the middle of the infarcted zone it is instead considered that the necrosis area is surrounded by an area with diminished irrigation and metabolic rated called penumbra area. In this area the neurons are surviving in a parabiotic state for an amount of time variable of the collateral blood circulation and subpial anastomosis.

In the cerebral infarct with pseudotumoral or edematogeneffect, one of the surgical techniques to prevent intracranial hypertension is called decompresivecraniectomy. The results are currently under discussion.

In selected patients with cerebral hypoperfusion(hemodynamic circulatory insufficiency) the stenosis can be treated by endarterectomy or stenting, or even new vascular anastomosis can be made to supplement the hypoperfused area. One of the most used anastomosis is between the carotid artery and the middle cerebral artery.

Carotid endarterectomy

It is used in neurosurgery to desobstruct large vessels of the neck with stenosis, the most frequent location being the carotid artery. At the level of the carotid bifurcation, turbinaryhemodinamyc factors favor atherosclerosis. The narrowing of the diameter and the ulceration of the plaque are further favoring factors for thrombus formation which can easily detach and become cerebral emboli. About 30% of ischemic vascular injuries occur in such a manner. Screening of high risk patients for such modifications can reveal the atherosclerotic plaque in an asymptomatic patient. The methods used for such screening can be clinical (carotid auscultation) echo-doppler (carotid stenosis) and angiographic studies (measuring the exact level of stenosis and extension)

The clinical symptomatology which can result from these cerebral emboli which represent the carotid etiology of ischemic vascular injuries may be classified as follows:

-Transitory ischemic accident (sudden onset with focal neurological deficit which resolves within the first hour)

-Constituted ischemic vascular injury which can be further described as being either stable, remitting, of in evolution. It is usually followed by hemiparesis, hemiplegia, aphasia, etc, or even decease.

Conservator treatment is related to igieno-dietetic diet, hypertensive and dyslipidemic medication, management of the ischemic accident itself and initiation of antiplatelet therapy. These measures don’t offer a full protection against a new accident. Removal of the carotid stenosis is important and it can be made either surgically or endovascular by placing a stent. The surgical operation (endarterectomy) consists of temporarily clipping the three major adjacent vessels from the carotid bifurcation, incision of the carotid artery, removal of the atherosclerotic plaque and close suture of the artery with removal of the temporary clipps. In order to prevent ischemia of the brain during the intervention, a shunt can be placed between the carotid artery and internal carotid artery. Both techniques (surgical and endovascular) are invasive measures with high risk. This high risk for a prophylactic measure is related to the fact the patients are usually elderly, with associated coronary and cerebral atherosclerosis. Comparative studies between the natural evolution of the atherosclerosis and the risk of the intervention have led to consider that patients who have a stenosis greater than 70% and are young are suitable candidates for surgery