Flow Diversion for the Treatment of Basilar Bifurcation Aneurysm

Flow diversion for basilar apex aneurysms has rarely been reported.

A retrospective review of prospectively maintained databases at 8 academic institutions (St. Michael’s Hospital, Toronto, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts.Toronto Western Hospital, University of Alabama at Birmingham, State University of New York at Buffalo, University of Florence, Italy. Toulouse University Hospital, Yale School of Medicine, New Haven), was performed from 2009 to 2016 to identify patients with basilar apex aneurysms treated with flow diversion. Clinical and radiographic data were analyzed.

Sixteen consecutive patients (median age 54.5 yr) underwent 18 procedures to treat 16 basilar apex aneurysms with either the Pipeline Embolization Device (Medtronic) or Flow Redirection Endoluminal Device (Microvention). Five aneurysms (31.3%) were treated in the setting of subarachnoid hemorrhage. Seven aneurysms (43.8%) were treated with flow diversion alone, while 9 (56.2%) underwent flow diversion and adjunctive coiling. At a median follow-up of 6 mo, complete (100%) and near-complete (90%-99%) occlusion was noted in 11 (68.8%) aneurysms. Incomplete occlusion occurred more commonly in patients treated with flow diversion alone compared to those with adjunctive coiling. Patients with partial occlusion were significantly younger. Retreatment with an additional flow diverter and adjunctive coiling occurred in 2 wide necked aneurysms. There was 1 mortality in a patient (6.3%) who experienced posterior cerebral artery and cerebellar strokes as well as subarachnoid hemorrhage after the placement of a flow diverter. Minor complications occurred in 2 patients (12.5%).

Flow diversion for the treatment of basilar apex aneurysms results in acceptable occlusion rates in highly selected cases. Both primary flow diversion and rescue after failed clipping or coiling resulted in a modified Rankin Scale score that was either equal or better than at presentation and the technology represents a viable alternative or adjunctive option 1).


Da Ros et al., retrospectively analyzed data from all consecutive patients treated with flow-diverter stents between January 2011 and January 2015. Patients with large basilar apex aneurysms treated with a flow-diverter stent were included in the study. Clinical presentations, technical details, intra- and perioperative complications, and clinical and angiographic outcomes were recorded, with a midterm follow-up.

Of the 175 aneurysms treated with flow-diverter stents, 5 patients (2 women and 3 men; age range, 44-58 years) received flow-diverter stent for basilar apex aneurysms. The mean follow-up after stent deployment was 21 months (range, 15-24 months). One patient died on day 31 from an early postprocedural midbrain hemorrhage. One patient had a right cerebellar hemispheric ischemic lesion with a transient cerebellar syndrome resolved within 24 hours without neurologic sequelae at the latest follow-up. The mRS was 0 in 4 patients and 6 in 1 patient at last follow-up.

Flow diversion is a feasible technique with an efficacy demonstrated at a midterm follow-up, especially in the case of basilar apex aneurysm recurrences after previous endovascular treatments. Concern about its safety profile still exists 2).


A 73-year-old male was previously treated for an unruptured 11-mm basilar apex aneurysm with stent-assisted coiling using a Neuroform stent. The aneurysm was retreated twice with repeat coiling. After the third recurrence and persistent aneurysm growth into a giant, symptomatic lesion, we decided to proceed with flow diversion. We performed Y-stenting of the basilar bifurcation using three PFEDs, and was recoiled the aneurysm sac. Due to the low porosity of the flow diverters, a side-by-side double-barrel configuration was necessary in the basilar artery. Without the PFED’s resheathable capability, it would not have been possible to perform Y-stenting with flow diverters 3).

References

1)

Dmytriw AA, Adeeb N, Kumar A, Griessenauer CJ, Phan K, Ogilvy CS, Foreman PM, Shallwani H, Limbucci N, Mangiafico S, Michelozzi C, Krings T, Pereira VM, Matouk CC, Zhang Y, Harrigan MR, Shakir HJ, Siddiqui AH, Levy EI, Renieri L, Cognard C, Thomas AJ, Marotta TR. Flow Diversion for the Treatment of Basilar Apex Aneurysms. Neurosurgery. 2018 Dec 1;83(6):1298-1305. doi: 10.1093/neuros/nyx628. PubMed PMID: 29529233.
2)

Da Ros V, Caroff J, Rouchaud A, Mihalea C, Ikka L, Moret J, Spelle L. Large Basilar Apex Aneurysms Treated with Flow-Diverter Stents. AJNR Am J Neuroradiol. 2017 Jun;38(6):1156-1162. doi: 10.3174/ajnr.A5167. Epub 2017 Apr 27. PubMed PMID: 28450438.
3)

Ding D, Starke RM, McGuinness B, Brew S. Double-barrel Y-configuration Stenting for Flow Diversion of a Giant Recurrent Basilar Apex Aneurysm with the Pipeline Flex Embolization Device. J Neurosci Rural Pract. 2016 Dec;7(Suppl 1):S99-S102. doi: 10.4103/0976-3147.196439. PubMed PMID: 28163518; PubMed Central PMCID: PMC5244076.

PARKIN Mutation

Mutations in the parkin gene (PARK2;OMIM #600116) 1) 2), are the most common genetic risk factors for early-onset Parkinson’s disease (EOPD) 3) 4) 5) 6) 7) 8) 9) 10) 11) 12) 13).

Kunath et al., propose that Parkinson’s patients with PARKIN mutations may benefit most from a cell replacement therapy because (i) they often lack synucleinopathy, and (ii) their neurodegeneration is often confined to the nigrostriatal pathway. While patients with PARKIN mutations exhibit clinical signs of Parkinson’s, post-mortem studies to date indicate the majority lack Lewy bodies suggesting the nigral dopaminergic neurons are lost in a cell autonomous manner independent of α-synuclein mechanisms. Furthermore, these patients are usually younger, slow-progressing, and typically do not suffer from complex non-nigral symptoms that are unlikely to be ameliorated by a cell replacement therapy. Transplantation of dopaminergic cells into the putamen of these patients will provide neurons with wild-type PARKIN expression to re-innervate the striatum. The focal nature of PARKIN-mediated neurodegeneration and lack of active synucleinopathy in most young-onset cases makes these patients ideal candidates for a dopaminergic cell replacement therapy. Strategies to improve the outcome of cell replacement therapies for sporadic Parkinson’s include the use of adjunct therapeutics that target α-synuclein spreading and the use of genetically engineered grafts that are resistant to synucleinopathy 14).

References

1)

Kitada T, Asakawa S, Hattori N, et al. Mutations in the parkin gene cause autosomal recessive juvenile parkinsonism. Nature. 1998 Apr 9;392(6676):605–608.
2)

Hedrich K, Eskelson C, Wilmot B, et al. Distribution, type, and origin of Parkin mutations: Review and case studies. Mov Disord. 2004 Oct;19(10):1146–1157.
3)

Lucking CB, Durr A, Bonifati V, et al. Association between early-onset Parkinson’s disease and mutations in the parkin gene. French Parkinson’s Disease Genetics Study Group. N Engl J Med. 2000 May 25;342(21):1560–1567.
4)

Hedrich K, Marder K, Harris J, et al. Evaluation of 50 probands with early-onset Parkinson’s disease for Parkin mutations. Neurology. 2002 Apr 23;58(8):1239–1246.
5)

Abbas N, Lucking CB, Ricard S, et al. A wide variety of mutations in the parkin gene are responsible for autosomal recessive parkinsonism in Europe. French Parkinson’s Disease Genetics Study Group and the European Consortium on Genetic Susceptibility in Parkinson’s Disease. Hum Mol Genet. 1999 Apr;8(4):567–574.
6)

Periquet M, Latouche M, Lohmann E, et al. Parkin mutations are frequent in patients with isolated early-onset parkinsonism. Brain. 2003 Jun;126(Pt 6):1271–1278.
7)

Lohmann E, Periquet M, Bonifati V, et al. How much phenotypic variation can be attributed to parkin genotype? Ann Neurol. 2003 Aug;54(2):176–185.
8)

Camargos ST, Dornas LO, Momeni P, et al. Familial Parkinsonism and early onset Parkinson’s disease in a Brazilian movement disorders clinic: phenotypic characterization and frequency of SNCA, PRKN, PINK1, and LRRK2 mutations. Mov Disord. 2009 Apr 15;24(5):662–666.
9)

Macedo MG, Verbaan D, Fang Y, et al. Genotypic and phenotypic characteristics of Dutch patients with early onset Parkinson’s disease. Mov Disord. 2009 Jan 30;24(2):196–203.
10)

Hertz JM, Ostergaard K, Juncker I, et al. Low frequency of Parkin, Tyrosine Hydroxylase, and GTP Cyclohydrolase I gene mutations in a Danish population of early-onset Parkinson’s Disease. Eur J Neurol. 2006 Apr;13(4):385–390.
11)

Chung EJ, Ki CS, Lee WY, Kim IS, Kim JY. Clinical features and gene analysis in Korean patients with early-onset Parkinson disease. Arch Neurol. 2006 Aug;63(8):1170–1174.
12)

Bras J, Guerreiro R, Ribeiro M, et al. Analysis of Parkinson disease patients from Portugal for mutations in SNCA, PRKN, PINK1 and LRRK2. BMC Neurol. 2008;8:1.
13)

Vinish M, Prabhakar S, Khullar M, Verma I, Anand A. Genetic screening reveals high frequency of PARK2 mutations and reduced Parkin expression conferring risk for Parkinsonism in North West India. J Neurol Neurosurg Psychiatry. 2009 Sep 3;
14)

Kunath T, Natalwala A, Chan C, Chen Y, Stecher B, Taylor M, Khan S, Muqit MMK. Are PARKIN patients ideal candidates for dopaminergic cell replacement therapies? Eur J Neurosci. 2018 Dec 26. doi: 10.1111/ejn.14314. [Epub ahead of print] PubMed PMID: 30586214.

Repetitive transcranial magnetic stimulation for stroke

Repetitive transcranial magnetic stimulation (rTMS) combined with treadmill training has been suggested to modulate corticomotor activity and improve gait performance in people with Parkinson’s disease.

It is unclear whether this combination therapy has a similar effect in people with stroke.

Review

Studies included in a review were identified by searching PubMed and ISI Web of Science. The search terms were (rTMS OR “repetitive transcranial magnetic stimulation”) AND (stroke OR “cerebrovascular accident” OR CVA) AND (rehab OR rehabilitation OR recover*). The retrieved records were assessed for eligibility and the most relevant features extracted to a summary table.

Seventy out of 691 records were deemed eligible, according to the selection criteria. The majority of the articles report rTMS showing potential in improving motor function, although some negative reports, all from randomized controlled trials, contradict this claim. Future studies are needed because there is a possibility that a bias for non-publication of negative results may be present.

rTMS has been shown to be a promising tool for stroke rehabilitation, in spite of the lack of standard operational procedures and harmonization. Efforts should be devoted to provide a greater understanding of the underlying mechanisms and protocol standardization 1).

Case series

A study of Wang et al., from the Taipei Veterans General Hospital aimed to investigate whether high-frequency rTMS enhances the effects of subsequent treadmill training in individuals with chronic stroke.

Fourteen participants meeting the selection criteria were randomly assigned to either the experimental (n = 8) or control (n = 6) group. The experimental group received 5 Hz rTMS prior to treadmill training three times per week for 3 weeks. The control group received sham rTMS before treadmill training. Walking speed, gait symmetry, corticomotor excitability, motor function of the lower extremities, and muscle activity during walking were measured before intervention, after intervention, and at 1-month follow-up.

The walking speed, spatial asymmetry of gait, and motor function of the lower extremities improved significantly in the experimental group, and these improvements exhibited significant differences in between-group comparisons. However, there was no significant difference in corticomotor excitability or brain asymmetry ratio after the intervention in each group.

The current results revealed that applying 5 Hz high-frequency rTMS over the leg motor cortex in the affected hemisphere enhanced the effects of subsequent treadmill training on gait speed and spatial asymmetry in individuals with chronic stroke. Improvement in gait speed persisted for at least 1 month in individuals with chronic stroke 2).


Bates and Rodger, used it in motor functional recovery from cerebral ischemic stroke to illustrate the difficulties in interpreting and assessing the therapeutic potential of rTMS for neurotrauma in terms of the presumed mechanisms of action of rTMS 3).

References

1)

Dionísio A, Duarte IC, Patrício M, Castelo-Branco M. The Use of Repetitive Transcranial Magnetic Stimulation for Stroke Rehabilitation: A Systematic Review. J Stroke Cerebrovasc Dis. 2018 Jan;27(1):1-31. doi: 10.1016/j.jstrokecerebrovasdis.2017.09.008. Epub 2017 Oct 27. Review. PubMed PMID: 29111342.
2)

Wang RY, Wang FY, Huang SF, Yang YR. High-frequency repetitive transcranial magnetic stimulation enhanced treadmill training effects on gait performance in individuals with chronic stroke: A double-blinded randomized controlled pilot trial. Gait Posture. 2018 Dec 18;68:382-387. doi: 10.1016/j.gaitpost.2018.12.023. [Epub ahead of print] PubMed PMID: 30586670.
3)

Bates KA, Rodger J. Repetitive transcranial magnetic stimulation for stroke rehabilitation-potential therapy or misplaced hope? Restor Neurol Neurosci. 2015;33(4):557-69. doi: 10.3233/RNN-130359. Review. PubMed PMID: 24595227
× How can I help you?
WhatsApp WhatsApp us
%d bloggers like this: