Acute ischemic stroke treatment

Acute ischemic stroke treatment

In the complete absence of blood flowneuronal death occurs within 2–3 minutes from the exhaustion of energy stores. However, in most strokes, there is a salvageable penumbra (tissue at risk) that retains viability for a period of time through suboptimal perfusion from collaterals. Local cerebral edema from the stroke results in a compromise of these collaterals and progression of the ischemic penumbra to infarction if the flow is not restored and maintained. Prevention of this secondary neuronal injury drives the treatment of stroke and has led to the creation of designated Primary Stroke Centers that offer appropriate and timely triage and treatment of all potential stroke patients.

Time delays from initial CTA acquisition to neuroendovascular surgery (NES) team notification can prevent expedient treatment with endovascular thrombectomy (ET). Process improvements and automated stroke detection on imaging with automated notification of the NES team may ultimately improve the time to reperfusion 1).

American Heart Association Guidelines for the Early Management of Patients With Acute Ischemic Stroke

see Endovascular intervention for ischemic stroke treatment..

see Hypothermia for acute ischemic stroke treatment.

Brain ischemia and treatment are one of the important topics in neurological science. Free oxygen radicals and inflammation formed after ischemia are accepted as the most important causes of damage. Currently, there are studies on many chemopreventive agents to prevent cerebral ischemia damage. The aim of Aras et al is to research the preventive effect of the active ingredient in genistein There is currently no promising pharmacotherapy aside from intravenous or intra-arterial thrombolysis. Yet because of the narrow therapeutic time window involved, thrombolytic application is very restricted in clinical settings. Accumulating data suggest that non-pharmaceutical therapies for stroke might provide new opportunities for stroke treatment 2).

Progression of focal stroke symptoms still constitutes a serious clinical problem for which heparin has insufficient effectiveness in clinical practice. New therapies, ideally preventive, are needed 3).

Omega 3 fatty acid enhance cerebral angiogenesis and provide long-term protection after stroke 4).

After cerebral ischemia, revascularization in the ischemic boundary zone provides nutritive blood flow as well as various growth factors to promote the survival and activity of neurons and neural progenitor cells. Enhancement of angiogenesis and the resulting improvement of cerebral microcirculation are key restorative mechanisms and represent an important therapeutic strategy for ischemic stroke.

Improvements in acute ischemic stroke (AIS) outcomes have been achieved with intravenous thrombolytics (IVT) and intra-arterial thrombolytics vs supportive medical therapy. Given its ease of administration, noninvasiveness, and most validated efficacy, IVT is the standard of care in AIS patients without contraindications to systemic fibrinolysis. However, patients with large-vessel occlusions respond poorly to IVT. Recent trials designed to select this population for randomization to IVT vs IVT with adjunctive endovascular therapy have not shown improvement in clinical outcomes with endovascular therapy. This could be due to the lack of utilization of modern thrombectomy devices such as Penumbra aspiration devices, Solitaire stent-trievers, or Trevo stent-trievers, which have shown the best recanalization results. Continued improvement in the techniques with using these devices as well as randomized controlled trials using them is warranted 5).

With the emergence of new technologies in imaging, thrombolysis and endovascular intervention, the treatment modalities of acute ischemic stroke will enter a new era 6).

Within 3 h from symptom onset, the existence of FLAIR-positive lesions on pretreatment MRI is significantly associated with an increased bleeding risk due to systemic thrombolysis. Therefore, considering FLAIR-positive lesions on baseline MRI might guide treatment decisions in ischemic stroke 7).

see Acute ischemic stroke thrombolysis

see Blood Pressure Management


Yaeger KA, Rossitto CP, Marayati NF, Lara-Reyna J, Ladner T, Hardigan T, Shoirah H, Mocco J, Fifi JT. Time from image acquisition to endovascular team notification: a new target for enhancing acute stroke workflow. J Neurointerv Surg. 2021 Apr 8:neurintsurg-2021-017297. doi: 10.1136/neurintsurg-2021-017297. Epub ahead of print. PMID: 33832969.

Chen F, Qi Z, Luo Y, Hinchliffe T, Ding G, Xia Y, Ji X. Non-pharmaceutical therapies for stroke: Mechanisms and clinical implications. Prog Neurobiol. 2014 Jan 6. pii: S0301-0082(13)00147-0. doi: 10.1016/j.pneurobio.2013.12.007. [Epub ahead of print] PubMed PMID: 24407111.

Rödén-Jüllig A, Britton M. Effectiveness of heparin treatment for progressing ischaemic stroke: before and after study. J Intern Med. 2000 Oct;248(4):287-91. PubMed PMID: 11086638.

Wang J, Shi Y, Zhang L, Zhang F, Hu X, Zhang W, Leak RK, Gao Y, Chen L, Chen J. Omega-3 polyunsaturated fatty acids enhance cerebral angiogenesis and provide long-term protection after stroke. Neurobiol Dis. 2014 Apr 29. pii: S0969-9961(14)00103-X. doi: 10.1016/j.nbd.2014.04.014. [Epub ahead of print] PubMed PMID: 24794156.

Serrone JC, Jimenez L, Ringer AJ. The role of endovascular therapy in the treatment of acute ischemic stroke. Neurosurgery. 2014 Feb;74 Suppl 1:S133-41. doi: 10.1227/NEU.0000000000000224. PubMed PMID: 24402482.

Lu AY, Ansari SA, Nyström KV, Damisah EC, Amin HP, Matouk CC, Pashankar RD,Bulsara KR. Intra-arterial treatment of acute ischemic stroke: the continued evolution. Curr Treat Options Cardiovasc Med. 2014 Feb;16(2):281. doi:10.1007/s11936-013-0281-2. PubMed PMID: 24398801.

Hobohm C, Fritzsch D, Budig S, Classen J, Hoffmann KT, Michalski D. Predicting intracerebral hemorrhage by baseline magnetic resonance imaging in stroke patients undergoing systemic thrombolysis. Acta Neurol Scand. 2014 Jul 18. doi: 10.1111/ane.12272. [Epub ahead of print] PubMed PMID: 25040041.

Vacuum assisted delivery

Vacuum assisted delivery

Towner et al. stated that tThe rate of intracranial hemorrhage is higher among infants delivered by vacuum extraction, forceps, or cesarean section during labor than among infants delivered spontaneously, but the rate among infants delivered by cesarean section before labor is not higher, suggesting that the common risk factor for hemorrhage is abnormal labor 1)

While cranial birth injury in term infants are well recognized, to date, only small case series have been described. In an attempt to further define the spectrum of cranial birth injuries, Pollina et al. analyzed 41 consecutive cranial birth injuries over the period 1991-1998. The most common clinical presentations were apnea (39%) and seizures (37%). Average Apgar scores were 5.7 at 1 min and 7.3 at 5 min; 54% of infants had abnormally low Apgar scores at 1 min and 31% had abnormally low scores at 5 min. The most common intracranial lesion was subdural hematoma, present in 73% of infants; most had either a tentorial subdural hematoma (57%) and/or interhemispheric subdural hematoma (50%) location. Operative treatment was required in 5 infants (12%). Two of the 41 infants (4.8%) died. The study group was compared with a control group of 63 randomly selected births without cranial injury. Using a stepwise logistic regression model, independently significant variables included neonatal birth weight, Apgar scores at 1 and 5 min and mode of delivery. Compared with the controls, the study group had a significantly higher incidence of obstetrical forceps and/or vacuum deliveries. Combining vacuum, forceps and urgent cesarean section deliveries together as ‘urgent’ and elective cesarean and spontaneous vaginal deliveries as ‘nonurgent’, they could find no significant differences between these two groups. This data conflict with those of Towner et al. [N Engl J Med 1999;341:1709-1714], and suggest that the method of assisted delivery, rather than the urgency of the delivery or dysfunctional labor per se, is a more important variable in cranial birth injuries 2).

Birth brachial plexus injury.

Subgaleal hematoma most commonly occurs after vacuum assisted delivery, but may also be seen following head trauma.

Low and mid station vacuum assisted deliveries (VAD) are delicate manual procedures that entail a high degree of subjectivity from the operator and are associated with adverse neonatal outcome. Little has been done to improve the procedure, including the technical development, traction force and the possibility of objective documentation.

Romero et al. aimed to explore if a digital handle with instant haptic feedback on traction force would reduce the neonatal risk during low or mid station VAD.

A two centre, randomised superiority trial at Karolinska University HospitalSweden, 2016-2018. Cases were randomised bedside to either a conventional or a digital handle attached to a Bird metal cup (50 mm, 80 kPa). The digital handle measured applied force including an instant notification by vibration when high levels of traction force were predicted according to a predefined algorithm. Primary outcome was a composite of hypoxic ischaemic encephalopathy, intracranial haemorrhage, seizures, death and/or subgaleal hematoma. Three hundred eighty low and mid VAD in each group were estimated to decrease primary outcome from six to 2 %.

After 2 years, an interim analyse was undertaken. Meeting the inclusion criteria, 567 vacuum extractions were randomized to the use of a digital handle (n = 296) or a conventional handle (n = 271). Primary outcome did not differ between the two groups: (2.7% digital handle vs 2.6% conventional handle). The incidence of primary outcome differed significantly between the two delivery wards (4% vs 0.9%, p < 0.05). A recalculation of power revealed that 800 cases would be needed in each group to show a decrease in primary outcome from three to 1 %. This was not feasible, and the study therefore closed.

The incidence of primary outcome was lower than estimated and the study was underpowered. However, the difference between the two delivery wards might reflect varying degree of experience of the technical equipment. An objective documentation of the extraction procedure is an attractive alternative in respect to safety and clinical training. To demonstrate improved safety, a multicentre study is required to reach an adequate cohort. This was beyond the scope of the study.

Trial registration: NCT03071783 , March 1, 2017, retrospectively registered 3).

A newborn with a large, high parieto-frontally located mass after vacuum extraction. Imaging methods revealed a large subcutaneous collection of cerebrospinal fluid and hemorrhage. Traumatic dura lesions should be considered in neonates presenting with a large head lump after assisted delivery with vacuum extraction 4).

A child who was born by vacuum extraction delivery. Days after the birth, a frontal swelling, which was thought to be a caput succedaneum, enlarged. Imaging revealed an iatrogenic encephalocele with a large subcutaneous CSF collection. Surgical reconstruction was performed. A parasagittal dura defect was closed. There was no involvement of the superior sagittal sinus. Encephalocele is an infrequent complication of vacuum extraction delivery, rarely described in literature. The child had a good recovery after the operation, without neurologic deficits 5).

A newly-born infant with a congenital dural and bony defect and an associated short-segmented duplication of the superior sagittal sinus suffered from herniation and infarction of parietal brain tissue secondary to vacuum extraction. This ultimately led to the formation of a subgaleal cerebrospinal fluid (CSF) collection. Initial operative closure of the encephalocele was performed by attaching a galeal flap to the periostium surrounding the congenital defect. As the bony defect developed characteristics of a growing fracture later on, dural repair, transplantation of a split-bone flap and, finally, the insertion of a ventriculoperitoneal shunt became necessary. This case affirms that stringent indication and cautious usage of vacuum-assisted delivery is strongly recommended, especially in view of the possibility that undetected congenital cranial, vascular and/or cerebral alterations may be present 6).

Doward W, Sgouros S. Acute subdural haematomas following ventouse-assisted delivery. Pediatr Neurosurg. 2001 Dec;35(6):335. doi: 10.1159/000050448. PMID: 11786704.Doward W, Sgouros S. Acute subdural haematomas following ventouse-assisted delivery. Pediatr Neurosurg. 2001 Dec;35(6):335. doi: 10.1159/000050448. PMID: 11786704.


Towner D, Castro MA, Eby-Wilkens E, Gilbert WM. Effect of mode of delivery in nulliparous women on neonatal intracranial injury. N Engl J Med. 1999 Dec 2;341(23):1709-14. doi: 10.1056/NEJM199912023412301. PMID: 10580069.

Pollina J, Dias MS, Li V, Kachurek D, Arbesman M. Cranial birth injuries in term newborn infants. Pediatr Neurosurg. 2001 Sep;35(3):113-9. doi: 10.1159/000050403. PMID: 11641618.

Romero S, Pettersson K, Yousaf K, Westgren M, Ajne G. Perinatal outcome after vacuum assisted delivery with digital feedback on traction force; a randomised controlled study. BMC Pregnancy Childbirth. 2021 Feb 26;21(1):165. doi: 10.1186/s12884-021-03604-z. PMID: 33637058; PMCID: PMC7913459.

Poryo M, Yilmaz U, Linsler S, Gortner L, Meyer S. A newborn with a large mass: vacuum extraction-caused dura lesion. Clin Case Rep. 2015 Dec 6;4(1):101-2. doi: 10.1002/ccr3.428. PMID: 26783449; PMCID: PMC4706397.

Jeltema HR, Hoving EW. Iatrogenic encephalocele: a rare complication of vacuum extraction delivery. Childs Nerv Syst. 2011 Dec;27(12):2193-5. doi: 10.1007/s00381-011-1600-0. Epub 2011 Oct 11. PMID: 21987344; PMCID: PMC3217141.

Neumann JO, Herweh C, Halatsch ME. Congenital duplication of the superior sagittal sinus and parietal encephalocele after vacuum extraction delivery. Acta Neurochir (Wien). 2010 Apr;152(4):713-6. doi: 10.1007/s00701-009-0470-7. Epub 2009 Jul 29. PMID: 19639246.

Delayed cerebral ischemia diagnosis

Delayed cerebral ischemia diagnosis

Local intraparenchymal neuromonitoring in the anterior cerebral artery/middle cerebral artery watershed area might detect the vast majority of delayed cerebral ischemias for all intracranial aneurysm locations, except for basilar artery aneurysms. In ACA and AcomA aneurysms, bilateral DCI of the ACA territory was common, and bilateral probe positioning might be considered for monitoring high-risk patients. Non-focal monitoring methods might be preferably used after BA aneurysm rupture 1).

Evaluating the proportion of the brain with critical hypoperfusion after SAH may better capture the extent of DCI than averaging CBF across heterogenous brain regions 2).

Early low CBF measurements and a high lactate and lactate to pyruvate ratio may be early warning signs of the risk of developing Delayed cerebral ischemia (DCI). The clinical value of these findings needs to be confirmed in larger studies 3).

Transcranial Doppler (TCD) and transcranial color-coded duplex sonography (TCCS) are noninvasive modalities that can be used to assess vasospasm. However, high flow velocity does not always reflect DCI.

Significant literature shows that perfusion computed tomography (CTP) can provide sufficient information on cerebral hemodynamics and effectively indicate delayed cerebral ischemia (DCI) before the development of infarction. Sun et al. aimed at performing a meta-analysis to provide a more full and accurate evaluation of CTP and CTP parameters in detecting DCI in patients with aneurysmal subarachnoid hemorrhage.

In the PubMed, MedLine, Embase and Cochrane databases analysis published from February 2005 to February 2013. The extraction of CTP parameters, including cerebral blood volume (CBV), cerebral blood flow (CBF), mean transit time (MTT), time to peak (TTP), interhemispheric ratios for CBV and CBF and interhemispheric differences for MTT and TTP. Pooled estimates of sensitivity, specificity, positive likelihood ratio (PLR), negative likelihood ratio (NLR), diagnostic odds ratio (DOR) and the summary receiver-operating characteristic curve were determined.

Four research studies are met the inclusion criteria for the analysis. The pooled sensitivity, specificity, PLR, NLR and DOR of CTP for detecting the DCI were 82%, 82%, 4.56, 0.22 and 20.96, respectively. Through the evaluation of absolute CTP parameters, CBF and MTT showed diagnostic value for DCI, but CBF and TTP did not. Moreover, CBF ratio, MTT difference and TTP difference showed more diagnostic value than CBV ratio in DCI detection by the assessment of relative CTP parameters.

As a non-invasive and short time consuming screening method, CTP own a high diagnostic value for the detection of DCI after aneurysm rupture 4).

CTP maps were calculated with tracer delay-sensitive and tracer delay-insensitive algorithms and were visually assessed for the presence of perfusion deficits by two independent observers with different levels of experience. The diagnostic value of both algorithms was calculated for both observers.

Seventy-one patients were included. For the experienced observer, the positive predictive values (PPVs) were 0.67 for the delay-sensitive and 0.66 for the delay-insensitive algorithm, and the negative predictive values (NPVs) were 0.73 and 0.74. For the less experienced observer, PPVs were 0.60 for both algorithms, and NPVs were 0.66 for the delay-sensitive and 0.63 for the delay-insensitive algorithm.

Test characteristics are comparable for tracer delay-sensitive and tracer delay-insensitive algorithms for the visual assessment of CTP in diagnosing DCI. This indicates that both algorithms can be used for this purpose 5).

Whole-brain CT Perfusion (CTP) on Day 3 after aneurysmal subarachnoid hemorrhage (aSAH) allows early and reliable identification of patients at risk for delayed ischemic neurological deficits (DIND) and tissue at risk for delayed cerebral infarction (DCI) 6).

The association between alpha-delta ratio (ADR) on quantitative electroencephalography (EEG) and DCI has been reported in several previous studies, but their results are conflicting 7).


Hurth H, Steiner J, Birkenhauer U, Roder C, Hauser TK, Ernemann U, Tatagiba M, Ebner FH. Relationship of the vascular territory affected by delayed cerebral ischemia and the location of the ruptured aneurysm in patients with aneurysmal subarachnoid hemorrhage. Neurosurg Rev. 2021 Mar 29. doi: 10.1007/s10143-021-01522-4. Epub ahead of print. PMID: 33782797.

Jafri H, Diringer MN, Allen M, Zazulia AR, Zipfel GJ, Dhar R. Burden of cerebral hypoperfusion in patients with delayed cerebral ischemia after subarachnoid hemorrhage. J Neurosurg. 2019 May 31:1-8. doi: 10.3171/2019.3.JNS183041. [Epub ahead of print] PubMed PMID: 31151110.

Rostami E, Engquist H, Howells T, Johnson U, Ronne-Engström E, Nilsson P, Hillered L, Lewén A, Enblad P. Early low cerebral blood flow and high cerebral lactate: prediction of delayed cerebral ischemia in subarachnoid hemorrhage. J Neurosurg. 2017 Jun 2:1-9. doi: 10.3171/2016.11.JNS161140. [Epub ahead of print] PubMed PMID: 28574309.

Sun H, Zhang H, Ma J, Liu Y, Wang K, You C. Accuracy of computed tomography perfusion in detecting delayed cerebral ischemia following aneurysmal subarachnoid hemorrhage: a meta-analysis. Neurol India. 2013 Sep-Oct;61(5):507-12. doi: 10.4103/0028-3886.121922. PubMed PMID: 24262454.

Cremers CH, Dankbaar JW, Vergouwen MD, Vos PC, Bennink E, Rinkel GJ, Velthuis BK, van der Schaaf IC. Different CT perfusion algorithms in the detection of delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage. Neuroradiology. 2015 Jan 23. [Epub ahead of print] PubMed PMID: 25614332.

Malinova V, Dolatowski K, Schramm P, Moerer O, Rohde V, Mielke D. Early whole-brain CT perfusion for detection of patients at risk for delayed cerebral ischemia after subarachnoid hemorrhage. J Neurosurg. 2015 Dec 18:1-9. [Epub ahead of print] PubMed PMID: 26684786.

Yu Z, Wen D, Zheng J, Guo R, Li H, You C, Ma L. The predictive accuracy of alpha-delta ratio on quantitative electroencephalography for delayed cerebral ischemia in patients with aneurysmal subarachnoid hemorrhage: a meta-analysis. World Neurosurg. 2019 Feb 27. pii: S1878-8750(19)30493-0. doi: 10.1016/j.wneu.2019.02.082. [Epub ahead of print] PubMed PMID: 30825635.
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