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middle_cerebral_artery_occlusion

Middle cerebral artery occlusion

Middle cerebral artery stenosis may lead to a middle cerebral artery stroke via three mechanisms:

(1) deep lacunar infarcts that develop when the exiting branch of the lenticulostriate artery is trapped within the thromboatheroma

(2) development of atheromatous ulceration with thrombosis and subsequent distal embolization

(3) hemispheric hypoperfusion caused by significant MCA obstruction and inadequate collateralization

Complications

Clinical presentation

In these patients the clinical presentation usually starts with focal signs and progresses with a decline of consciousness until brainstem dysfunction is evident.

A shift of the ischemic tissue rather than intracranial hypertension is the most likely responsible for the initial decrease in consciousness 1) 2).

Several other satellite reactions are involved in an inexorable pathogenetic cascade, including disturbances of microvascular tone, endothelial cell swelling, and activation of platelets, leucocytes, and coagulation 3).

Diagnosis

Imaging studies are the mainstay for identification of people at higher risk for malignant infarction among the ischemic stroke population.

Perfusion computed tomography of the brain is routinely performed for first and later controls. The earliest warning signs for developing malignant infarction include involvement of an area larger than 50% of the MCA territory and an infarct extending also to the anterior or posterior cerebral artery territories. A midline shift >10 mm, effacement of subarachnoid spaces, and attenuation of corticomedullary differentiation are also related to higher risk of severe deterioration 4), but they usually occur later, when a malignant syndrome is already in progress. The intravenous injection of contrast medium with elaboration of its distribution (perfusion-CT) entails higher diagnostic accuracy of ischemic areas and an even earlier detection of patients at higher risk. A drop in cerebral perfusion of more 66% is related to a likely malignant evolution 5)

Magnetic resonance imaging is another helpful exam, which in ischemic stroke can be used for prognostic purposes within few hours of clinical onset. Its sensitivity is higher than CT and it is more likely to show changes at earlier time points than CT scan. On diffusion weighted images (DWI) an ischemic area of at least 145 mL strongly predicts a massive cerebral infarction 6) 7).

It is straightforward that at final stages the pressure inside the skull of patients with large cerebral infarction is probably high. Anyway, a pressure increase limited to the infarcted and immediately adjacent areas could happen, leading to neurological worsening and even death despite no spread of intracranial hypertension 8).

Undisputed poor prognosis predictors as CT uncal herniation and anisocoria sometimes occur without an overall ICP raise is detected 9).

The measurement may also be influenced by the device used (solid-state or fluid-filled) as well as by its location (subdural, intraparenchymal, intraventricular; ipsilateral or contralateral to ischemia) 10).

Treatment

Osmotherapy, buffers, sedation, mannitol, hyperventilation 11) 12) , and more recently hypothermia 13) 14) 15) are the intensive care treatments which can be applied in patients with clinical worsening due to ischemic tissue swelling. Unfortunately, they represent only short-lived interventions and temporizing measures which just slow the inexorable development of further deterioration from tissue displacement and brain stem shift 16) 17) 18) 19).

Surgery conversely can be very effective with adequate indications; the reasonable operative treatment in massive cerebral infarction is decompressive hemicraniectomy. The goal of such removing of a part of the cranial vault is to reduce the pressure of the swollen ischemic tissue and to save the brain that is still viable. Several animal studies demonstrated the biological effects of this surgical procedure, as the improvement of the overall cortical perfusion 20) 21) and the reduction of apoptosis in the ischemic border zone 22). To not consider the surgical option leads to missed opportunities of successful treatment 23) , but on the other hand not all the patients with the above requisite may really benefit from the intervention.

Decompressive hemicraniectomy should be performed within 48 h of stroke 24) 25) before brainstem dysfunction is patent. The requisite for the surgical indication is an even initial worsening in patients with verified massive cerebral infarction, and clinical trials failed to demonstrate benefits by prophylactic ultra-early surgery as no differences were found between patients treated at 24 and 48 hours from stroke onset 26) 27) 28). Anyway the possible occurrence of a radiological worsening despite a stable clinical status keeps being an unresolved issue for indication to decompress.

The second factor that the neurosurgeon has to consider is the patient prestroke condition, which is a good predictor of the chance of survive and mostly of the quality of life in case of surgical intervention 29) 30). In the available clinical trials the patient age resulted in one of the most reliable outcome indicators. Generally, patients older than 60 years are not ideal candidates for surgical decompression 31) 32), as they possess a lower neuronal plasticity and also frequently have more vascular risk factors and comorbidities. Even in young patients with severe hypertension, cardiac failure, pulmonary embolism, and other analogous unfavorable diseases the hemicraniectomy might result highly risky and less effective. Conversely also in older patients with a good antecedent condition hemicraniectomy seems somehow to improve the prognosis 33). As not univocal data result from literature it is suggested to not routinely perform surgical decompression in stroke patients older than 60 years at least in really well-selected cases. The effects of hemicraniectomy in patients aged over 65 years will be anyway assessed in the ongoing Destiny II trial.

Surgery can be safely performed even after intravenous tissue plasminogen activator administration for thrombolysis 34) 35). The side of the stroke does not seem to affect the vital status after surgical decompression, so it should not influence the choice to operate 36) 37). However, the family should be informed about the likely chance for the patient to survive but with severe speech disturbances. Family in turn may provide useful information concerning the patient's wishes 38).

The skin incision can be made as a big question mark or a midline leaf-spring. Some surgeons advocate resection of the temporal muscle and fascia to allow a maximum decompression 39) , but this is not commonly performed. The craniotomy should include the frontal, parietal, and temporal bones and its anteroposterior length should not be inferior to 12 cm; larger openings up to 14 cm or more are thought to allow an even better pressure relieve 40). Particular attention has to be paid to decompression of the basal temporal area, as it represents a critical compartment with close relationship with the brainstem. In order to gain additional room, the dura mater is commonly opened as well. It can then be enlarged with a biological or synthetic substitute or left patent, just covered by hemostatic material for a faster closure 41). The cerebral tissue itself should be completely preserved at surgery for recovery of the not deadly damaged areas, which may be not distinguishable from the infarction itself.

The bone flap can be preserved in a subcutaneous pocket overlying the abdomen, but this leads to partial reabsorption in the following weeks, longer operation times, and additional risks related to the additional wound. A valid and currently prevailing alternative is to store the bone frozen (−80°C) in a sterile box. The possible complications of decompressive craniectomy are surgical site infections, hemorrhagic troubles and extra-axial fluid collections, hydrocephalus, and the so-called sinking flap syndrome 42)

Cranioplasty

It is not exceptional that after cranioplasty the patients show some clinical improvement 43) 44). The need to primarily use different materials than the autologous bone to cover the skull defect is uncommon in patients decompressed for ischemic stroke. The perfect timing for cranioplasty after hemicraniectomy is debated, and in the literature do articles specific for patients who underwent surgery for malignant cerebral infarction not exist. It can anyway be deduced from more general studies that the bone flap can be usually repositioned within 5 to 12 weeks 45) 46) 47) 48).

Outcome

Malignant evolution is more common in younger patients 49).

Despite optimal medical management this condition may lead to death in 70–80% of cases 50) 51).

The criteria for surgical indication mean a selection of patients who likely will have less postoperative disabilities. Living with a severe neurological impairment may appear more acceptable in some cultures, and inhumane in others. A recent review anyway concluded that the vast majority of operated patients do not regret having undergone surgery 52).

The natural history of middle cerebral artery occlusion MCA occlusion has become increasingly important since the surgical option of EC/IC bypass surgery has been available.

The clinical course of 24 patients with angiographically-demonstrated occlusion of the MCA artery was reviewed. Eight patients presented with a major disabling stroke and five of these died during the acute phase of this ischemic event. The remaining 19 patients were followed for a mean of 54.2 months. There were five deaths in follow-up and two of these were due to subsequent strokes. Fourteen patients manifested a benign course: one of these had a further minor stroke and four had TIAs. Altogether, 3 strokes occurred during the follow-up period (2 fatal, 1 minor) and all were in the territory of the artery known to be occluded. Of those patients who survived their presenting ischemic event, 12 (63%) remained completely functional in terms of activities of daily living. MCA occlusion does not necessarily carry a poor prognosis with medial therapy alone and the role of bypass surgery hopefully will be clarified by the ongoing clinically randomized trial 53).

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middle_cerebral_artery_occlusion.txt · Last modified: 2016/12/15 23:31 (external edit)