Aslan Lashkarivand

• Eide, Per Kristian; Lashkarivand, Aslan; Hernes, Susanne Miriam Sørensen; Ringstad, Geir Andre & Hovd, Markus (2026). Estimation of human brain fluid clearance using intrathecal imaging contrast agents. Fluids and Barriers of the CNS. 23(1). doi: 10.1186/s12987-026-00826-1. Fulltekst i vitenarkiv Vis sammendrag

  Background Extra-vascular brain fluid dynamics, including exchange through glymphatic and meningeal lymphatic pathways, has been proposed essential for waste clearance and solute transport in the central nervous system. Although animal studies provide evidence for these pathways’ role in clearing neurotoxic proteins and distributing solutes delivered to cerebrospinal fluid (CSF), translation to humans is limited. Quantitative, in vivo measures of inter-individual variability in brain fluid clearance in clinical populations are largely lacking. This study investigated the feasibility of estimating brain fluid clearance indices using intrathecal imaging contrast agents. Methods In a prospective and observational study, iodixanol (Visipaque, GE Healthcare, USA, 270 mg I/mL, 3 mL) was administered intrathecally as a CSF tracer and its clearance from CSF to blood was quantified using population pharmacokinetic modeling. Intracranial tracer enrichment in CSF was assessed by its radiodensity (Hounsfield units) within predefined regions of interest (cisterna magna, Sylvian fissure and vertex) on cranial computed tomography (CT) performed 2-, 4- and 24-hours post-injection. These results were compared with brain fluid clearance indices derived from a separate population pharmacokinetic model using intrathecal gadobutrol (Gadovist, Bayer AG, GE, 1.0 mmol/mL, 0.50 mL), with its enrichment in CSF defined as gadobutrol-induced T1 signal increase from baseline within corresponding subarachnoid spaces on magnetic resonance imaging (MRI). Results The study included 52 subjects receiving intrathecal iodixanol and 45 individuals receiving intrathecal gadobutrol. Marked inter-individual variability was observed in brain fluid clearance to blood for both contrast agents, as well as their distribution in CSF as assessed by CT and MRI. Brain fluid clearance from iodixanol and gadobutrol were significantly correlated. Notably, clearance indices showed stronger correlations with intracranial distribution in CSF for gadobutrol-derived MRI metrics than for iodixanol-derived CT metrics. Conclusions These findings demonstrate the feasibility of estimating brain fluid clearance in humans using intrathecal imaging contrast agents as CSF tracers. Brain fluid clearance capacity exhibits pronounced inter-individual variability and correlates with the degree of contrast enrichment in intracranial subarachnoid spaces, particularly when assessed by MRI. The results underscore the importance of individualized assessment of brain fluid clearance, with implications for studies on pathogenetic mechanisms of neurodegeneration and optimization of intrathecal drug delivery.

• Eide, Per Kristian; Undseth, Ragnhild Marie; Pripp, Are Hugo; Lashkarivand, Aslan; Nedregaard, Bård & Sletteberg, Ruth [Vis alle 10 forfattere av denne artikkelen] (2025). Impact of Subarachnoid Hemorrhage on Human Glymphatic Function: A Time-Evolution Magnetic Resonance Imaging Study. Stroke. ISSN 0039-2499. 56(3), s. 678–691. doi: 10.1161/STROKEAHA.124.047739. Fulltekst i vitenarkiv Vis sammendrag

  BACKGROUND: Subarachnoid hemorrhage (SAH) is associated with significant mortality and morbidity. The impact of SAH on human glymphatic function remains unknown. METHODS: This prospective, controlled study investigated whether human glymphatic function is altered after SAH, how it differs over time, and possible underlying mechanisms. Glymphatic enrichment was examined by intrathecal contrastenhanced magnetic resonance imaging (MRI, glymphatic MRI), utilizing the MRI contrast agent gadobutrol (Gadovist, Bayer AG, GE; 0.50 mmol) as a cerebrospinal fluid (CSF) tracer. The distribution of the tracer in the brain and the subarachnoid and ventricular CSF spaces was assessed using standardized multi-phase MRI T1 sequences, and between-group differences in percentage change of standardized T1 signal unit ratios over time were analyzed by linear mixed models. RESULTS: The study comprised 27 patients with SAH (19 female/8 male; 59.3±10.2 years) who were examined <3 months (n=5), 3 to 6 months (n=10), 6 to 12 months (n=5), or >12 months (n=7) after bleed. A sex- and age-matched control group of 22 individuals (15 female/7 male; 55.5±10.5 years) underwent the same glymphatic MRI protocol but had no neurological or CSF disease. The patients with SAH showed a marked impairment of glymphatic enrichment throughout the brain (particularly addressing the cerebral cortex and subcortical white matter), especially after 24 hours. The glymphatic impairment was accompanied by redistribution of CSF tracer from subarachnoid spaces toward ventricles. These alterations were most pronounced after 3 to 6 months and less after 12 months, though with interindividual variation. CSF tracer transport within perivascular subarachnoid spaces was impaired and coincided with impaired glymphatic enrichment. CONCLUSIONS: Human glymphatic function is severely impaired by SAH, particularly shortly after the event. Glymphatic failure is associated with redistribution of CSF from subarachnoid spaces toward ventricles. SAH-related impairment of fluid transport within perivascular subarachnoid spaces may contribute to reduced glymphatic influx. Since patient groups are small, care should be made when concluding about the impact of time on glymphatic function.

• Eide, Per Kristian; Hovd, Markus; Pripp, Are Hugo; Gjertsen, Øivind; Løvland, Grethe & Lashkarivand, Aslan [Vis alle 9 forfattere av denne artikkelen] (2025). Altered brain fluid dynamics in spontaneous intracranial hypotension. Fluids and Barriers of the CNS. 22. doi: 10.1186/s12987-025-00679-0. Fulltekst i vitenarkiv Vis sammendrag

  Background This prospective observational study explored alterations in brain fluid dynamics in patients with spontaneous intracranial hypotension (SIH) and confirmed spinal cerebrospinal fluid (CSF) leakage, specifically addressing CSF clearance to blood, glymphatic influx and measures of CSF flow. Methods A cohort of SIH patients with verified spinal CSF leaks was compared with an age- and sex-matched reference group having no CSF disturbance or neurological disorders. Prior to repair of CSF leakage, CSF clearance was quantified using population pharmacokinetics, glymphatic influx was assessed by intrathecal contrast-enhanced magnetic resonance imaging (MRI), and CSF flow patterns were measured using either phase-contrast MRI or multiphase analysis of CSF tracer transport within the subarachnoid spaces. Results The study included eight SIH cases and nine reference subjects. SIH was accompanied with a greater CSF clearance, severely reduced tracer enrichment in the subarachnoid spaces and impaired glymphatic influx throughout the brain, after the patients had been upright. However, with patients in the supine position during MRI scanning, times to first enrichment of tracer in cisterna magna or perivascular subarachnoid spaces were not affected, with no changes in CSF flow through the Sylvian aqueduct, indicating that ventricular CSF production remained unaffected. Conclusions SIH caused by spinal CSF leakage is accompanied with altered brain fluid dynamics, here illustrated by accelerated CSF clearance to blood and reduced glymphatic influx, likely due to reduced CSF volume load to the intracranial compartment in the upright position.

• Lashkarivand, Aslan; Ringstad, Geir & Wiedmann, Markus (2024). Empowering early career vascular neurosurgeons in the endovascular Era: Managing intraoperative aneurysm rupture through a systematic algorithmic approach. Journal of clinical neuroscience. ISSN 0967-5868. 120, s. 229–231. doi: 10.1016/j.jocn.2024.01.006. Fulltekst i vitenarkiv
• Sorteberg, Angelika; Lashkarivand, Aslan & Western, Elin (2024). Return to work after aneurysmal subarachnoid hemorrhage. Frontiers in Neurology. 15. doi: 10.3389/fneur.2024.1401493. Fulltekst i vitenarkiv Vis sammendrag

  Introduction: Survivors of aneurysmal subarachnoid hemorrhage (aSAH) often recover without severe physical or cognitive deficits. However, strikingly low levels of engagement in productive employment have also been reported in aSAH patients with good or excellent outcomes. Knowledge about return to work (RTW) after aSAH and predictors of no RTW remain limited and controversial. The study aimed to delineate the return to maximum work capacity up to 5 years after the ictus in a larger number of consecutive aSAH patients from the entire aSAH severity spectrum and to identify demographic and medical predictors of no RTW. Methods: Data were acquired from a prospective institutional database. We included all 500 aSAH survivors aged > 18 years who were treated between January 2012 and March 2018. In addition to gathering data on work status and the type of work at ictus, we retrieved demographical data and assessed aSAH severity based on the quantification of subarachnoid, intraventricular, and intraparenchymal blood (ICH), as well as the World Federation of Neurological Societies (WFNS) grade. We registered the mode of aneurysm repair (endovascular or surgical) and recorded complications such as vasospasm, newly acquired cerebral infarctions, and chronic hydrocephalus. Results: Furthermore, work status and the grade of fatigue at follow-up were registered. RTW was assessed among 299 patients who were employed at ictus. Among them, 63.2% were women, and their age was 51.3 ± 9.4 (20–71) years. Return to gainful employment was 51.2%, with complete RTW accounting for 32.4%. The independent predictors of no RTW at ictus were age, the WFNS grade 3, and active smoking. The strongest independent predictor was the presence of clinically significant fatigue, which increased the risk of not returning to work by 5-fold. The chance to return to gainful employment significantly increased with the individual's years of education prior to their hemorrhage. The mode of aneurysm repair was not relevant with regard to RTW. Patients in the WFNS grades 1–2 more often returned to work than those in the WFNS grades 3–5, but our results indicate that neurological motor deficits are linked closer to no RTW than aSAH severity per se. Conclusion: Fatigue needs to be addressed as an important element on the path to return to work integration.

• Eide, Per Kristian; Lashkarivand, Aslan; Pripp, Are Hugo; Valnes, Lars Magnus; Hovd, Markus Herberg & Ringstad, Geir [Vis alle 8 forfattere av denne artikkelen] (2023). Plasma neurodegeneration biomarker concentrations associate with glymphatic and meningeal lymphatic measures in neurological disorders. Nature Communications. 14, s. 1–14. doi: 10.1038/s41467-023-37685-5. Fulltekst i vitenarkiv Vis sammendrag

  Clearance of neurotoxic brain proteins via cerebrospinal fluid (CSF) to blood has recently emerged to be crucial, and plasma biomarkers of neurodegen- eration were newly introduced to predict neurological disease. This study examines in 106 individuals with neurological disorders associations between plasma biomarkers [40 and 42 amino acid-long amyloid-β (Aβ40 and Aβ42), total-tau, glial fibrillary acidic protein (GFAP), and neurofilament light (NfL)] and magnetic resonance imaging measures of CSF-mediated clearance from brain via extra-vascular pathways (proxy of glymphatic function) and CSF-to- blood clearance variables from pharmacokinetic modeling (proxy of menin- geal lymphatic egress). We also examine how biomarkers vary during daytime and associate with subjective sleep quality. Plasma concentrations of neuro- degeneration markers associate with indices of glymphatic and meningeal lymphatic functions in individual- and disease-specific manners, vary during daytime, but are unaffected by sleep quality. The results suggest that plasma concentrations of neurodegeneration biomarkers associate with measures of glymphatic and meningeal lymphatic function.

• Sperre, Anette; Karsrud, Ina; Rodum, Anja; Lashkarivand, Aslan; Valnes, Lars Magnus & Ringstad, Geir [Vis alle 7 forfattere av denne artikkelen] (2023). Prospective Safety Study of Intrathecal Gadobutrol in Different Doses. American Journal of Neuroradiology. ISSN 0195-6108. 44(5), s. 511–516. doi: 10.3174/ajnr.A7841. Fulltekst i vitenarkiv
• Eide, Per Kristian; Lashkarivand, Aslan; Pripp, Are Hugo; Valnes, Lars Magnus; Hovd, Markus & Ringstad, Geir [Vis alle 8 forfattere av denne artikkelen] (2023). Mechanisms behind changes of neurodegeneration biomarkers in plasma induced by sleep deprivation. Brain Communications. 5(6). doi: 10.1093/braincomms/fcad343. Fulltekst i vitenarkiv Vis sammendrag

  Acute sleep deprivation has been shown to affect cerebrospinal fluid and plasma concentrations of biomarkers associated with neurodegeneration, though the mechanistic underpinnings remain unknown. This study compared individuals who, for one night, were either subject to total sleep deprivation or free sleep, (i) examining plasma concentrations of neurodegeneration biomarkers the morning after sleep deprivation or free sleep and (ii) determining how overnight changes in biomarkers plasma concentrations correlate with indices of meningeal lymphatic and glymphatic clearance functions. Plasma concentrations of amyloid-β 40 and 42, phosphorylated tau peptide 181, glial fibrillary acid protein and neurofilament light were measured longitudinally in subjects who from Day 1 to Day 2 either underwent total sleep deprivation (n = 7) or were allowed free sleep (n = 21). The magnetic resonance imaging contrast agent gadobutrol was injected intrathecally, serving as a cerebrospinal fluid tracer. Population pharmacokinetic model parameters of gadobutrol cerebrospinal fluid-to-blood clearance were utilized as a proxy of meningeal lymphatic clearance capacity and intrathecal contrast-enhanced magnetic resonance imaging as a proxy of glymphatic function. After one night of acute sleep deprivation, the plasma concentrations of amyloid-β 40 and 42 were reduced, but not the ratio, and concentrations of the other biomarkers were unchanged. The overnight change in amyloid-β 40 and 42 plasma concentrations in the sleep group correlated significantly with indices of meningeal lymphatic clearance capacity, while this was not seen for the other neurodegeneration biomarkers. However, overnight change in plasma concentrations of amyloid-β 40 and 42 did not correlate with the glymphatic marker. On the other hand, the overnight change in plasma concentration of phosphorylated tau peptide 181 correlated significantly with the marker of glymphatic function in the sleep deprivation group but not in the sleep group. The present data add to the evidence of the role of sleep and sleep deprivation on plasma neurodegeneration concentrations; however, the various neurodegeneration biomarkers respond differently with different mechanisms behind sleep-induced alterations in amyloid-β and tau plasma concentrations. Clearance capacity of meningeal lymphatics seems more important for sleep-induced changes in amyloid-β 40 and 42 plasma concentrations, while glymphatic function seems most important for change in plasma concentration of phosphorylated tau peptide 181 during sleep deprivation. Altogether, the present data highlight diverse mechanisms behind sleep-induced effects on concentrations of plasma neurodegeneration biomarkers.

• Lashkarivand, Aslan & Eide, Per Kristian (2023). Brain Sagging Dementia. Current Neurology and Neuroscience Reports. ISSN 1528-4042. 23(10), s. 593–605. doi: 10.1007/s11910-023-01297-9. Fulltekst i vitenarkiv Vis sammendrag

  Purpose of Review Brain sagging dementia (BSD) is a rare but devastating form of early-onset dementia characterized by intracranial hypotension and behavioral changes resembling behavioral variant frontotemporal dementia. This review aims to provide a comprehensive overview of BSD, highlighting its pathomechanism, diagnostic tools, and available treatment options. Recent Findings BSD exhibits a complex clinical manifestation with insidious onset and gradual progression of behavioral disinhibition, apathy, inertia, and speech alterations. Additionally, patients may exhibit brainstem and cerebellar signs such as hypersomnolence and gait disturbance. Although headaches are common, they may not always demonstrate typical orthostatic features. Recent radiological advances have improved the detection of CSF leaks, enabling targeted treatment and favorable outcomes. Summary Understanding the pathomechanism and available diagnostic tools for BSD is crucial for a systematic approach to timely diagnosis and treatment of this reversible form of early-onset dementia, as patients often endure a complex and lengthy clinical course.

• Lashkarivand, Aslan & Eide, Per Kristian (2022). Brain Sagging Dementia-Diagnosis, Treatment, and Outcome: A Review. Neurology. ISSN 0028-3878. 98(19), s. 798–805. doi: 10.1212/WNL.0000000000200511. Fulltekst i vitenarkiv
• Eide, Per Kristian; Lashkarivand, Aslan; Hagen-Kersten, Åsmund Aleksander; Gjertsen, Øivind; Nedregaard, Bård & Sletteberg, Ruth [Vis alle 11 forfattere av denne artikkelen] (2022). Intrathecal Contrast-Enhanced Magnetic Resonance Imaging of Cerebrospinal Fluid Dynamics and Glymphatic Enhancement in Idiopathic Normal Pressure Hydrocephalus. Frontiers in Neurology. 13, s. 1–21. doi: 10.3389/fneur.2022.857328. Fulltekst i vitenarkiv Vis sammendrag

  Idiopathic normal pressure hydrocephalus (iNPH) is a neurodegenerative disease, characterized by cerebrospinal fluid (CSF) flow disturbance. Today, the only available treatment is CSF diversion surgery (shunt surgery). While traditional imaging biomarkers typically assess CSF space anatomy, recently introduced imaging biomarkers of CSF dynamics and glymphatic enhancement, provide imaging of CSF dynamics and thereby more specifically reveal elements of the underlying pathophysiology. The biomarkers address CSF ventricular reflux grade as well as glymphatic enhancement and derive from intrathecal contrast-enhanced MRI. However, the contrast agent serving as CSF tracer is administered off-label. In medicine, the introduction of new diagnostic or therapeutic methods must consider the balance between risk and benefit. To this end, we performed a prospective observational study of 95 patients with iNPH, comparing different intrathecal doses of the MRI contrast agent gadobutrol (0.10, 0.25, and 0.50 mmol, respectively), aiming at the lowest reasonable dose needed to retrieve diagnostic information about the novel MRI biomarkers. The present observations disclosed a dose-dependent enrichment of subarachnoid CSF spaces (cisterna magna, vertex, and velum interpositum) with dose-dependent ventricular reflux of tracer in iNPH, as well as dose-dependent glymphatic tracer enrichment. The association between tracer enrichment in CSF and parenchymal compartments were as well dose-related. Intrathecal gadobutrol in a dose of 0.25 mmol, but not 0.10 mmol, was at 1.5T MRI considered sufficient for imaging altered CSF dynamics and glymphatic enhancement in iNPH, even though 3T MRI provided better sensitivity. Tracer enrichment in CSF at the vertex and within the cerebral cortex and subcortical white matter was deemed too low for maintaining diagnostic information from a dose of 0.10 mmol. We conclude that reducing the intrathecal dose of gadobutrol from 0.50 to 0.25 mmol gadobutrol improves the safety margin while maintaining the necessary diagnostic information about disturbed CSF homeostasis and glymphatic failure in iNPH.

• Hovd, Markus Herberg; Mariussen, Espen; Uggerud, Hilde Thelle; Lashkarivand, Aslan; Christensen, Hege & Ringstad, Geir [Vis alle 7 forfattere av denne artikkelen] (2022). Population pharmacokinetic modeling of CSF to blood clearance: prospective tracer study of 161 patients under work-up for CSF disorders. Fluids and Barriers of the CNS. 19(1). doi: 10.1186/s12987-022-00352-w. Fulltekst i vitenarkiv Vis sammendrag

  Background Quantitative measurements of cerebrospinal fluid to blood clearance has previously not been established for neurological diseases. Possibly, variability in cerebrospinal fluid clearance may affect the underlying disease process and may possibly be a source of under- or over-dosage of intrathecally administered drugs. The aim of this study was to characterize the cerebrospinal fluid to blood clearance of the intrathecally administered magnetic resonance imaging contrast agent gadobutrol (Gadovist, Bayer Pharma AG, GE). For this, we established a population pharmacokinetic model, hypothesizing that cerebrospinal fluid to blood clearance differs between cerebrospinal fluid diseases. Methods Gadobutrol served as a surrogate tracer for extra-vascular pathways taken by several brain metabolites and drugs in cerebrospinal fluid. We estimated cerebrospinal fluid to blood clearance in patients with different cerebrospinal fluid disorders, i.e. symptomatic pineal and arachnoid cysts, as well as tentative spontaneous intracranial hypotension due to cerebrospinal fluid leakage, idiopathic intracranial hypertension, or different types of hydrocephalus (idiopathic normal pressure hydrocephalus, communicating- and non-communicating hydrocephalus). Individuals with no verified cerebrospinal fluid disturbance at clinical work-up were denoted references. Results Population pharmacokinetic modelling based on 1,140 blood samples from 161 individuals revealed marked inter-individual variability in pharmacokinetic profiles, including differences in absorption half-life (time to 50% of tracer absorbed from cerebrospinal fluid to blood), time to maximum concentration in blood and the maximum concentration in blood as well as the area under the plasma concentration time curve from zero to infinity. In addition, the different disease categories of cerebrospinal fluid diseases demonstrated different profiles. Conclusions The present observations of considerable variation in cerebrospinal fluid to blood clearance between individuals in general and across neurological diseases, may suggest that defining cerebrospinal fluid to blood clearance can become a useful diagnostic adjunct for work-up of cerebrospinal fluid disorders. We also suggest that it may become useful for assessing clearance capacity of endogenous brain metabolites from cerebrospinal fluid, as well as measuring individual cerebrospinal fluid to blood clearance of intrathecal drugs.

• Mannerak, Mari Aaroe; Lashkarivand, Aslan & Eide, Per Kristian (2021). Trigeminal neuralgia and genetics: A systematic review. Molecular Pain. 17. doi: 10.1177/17448069211016139. Fulltekst i vitenarkiv Vis sammendrag

  Trigeminal neuralgia (TN) is a severe facial pain disease of unknown cause and unclear genetic background. To examine the existing knowledge about genetics in TN, we performed a systematic study asking about the prevalence of familial trigeminal neuralgia, and which genes that have been identified in human TN studies and in animal models of trigeminal pain. MedLine, Embase, Cochrane Library and Web of Science were searched from inception to January 2021. 71 studies were included in the systematic review. Currently, few studies provide information about the prevalence of familial TN; the available evidence indicates that about 1–2% of TN cases have the familial form. The available human studies propose the following genes to be possible contributors to development of TN: CACNA1A, CACNA1H, CACNA1F, KCNK1, TRAK1, SCN9A, SCN8A, SCN3A, SCN10A, SCN5A, NTRK1, GABRG1, MPZ gene, MAOA gene and SLC6A4. Their role in familial TN still needs to be addressed. The experimental animal studies suggest an emerging role of genetics in trigeminal pain, though the animal models may be more relevant for trigeminal neuropathic pain than TN per se. In summary, this systematic review suggests a more important role of genetic factors in TN pathogenesis than previously assumed.

• Eide, Per Kristian; Mariussen, Espen; Uggerud, Hilde Thelle; Pripp, Are Hugo; Lashkarivand, Aslan & Hassel, Bjørnar [Vis alle 9 forfattere av denne artikkelen] (2021). Clinical application of intrathecal gadobutrol for assessment of cerebrospinal fluid tracer clearance to blood. JCI Insight. 6(9), s. 1–13. doi: 10.1172/jci.insight.147063. Fulltekst i vitenarkiv Vis sammendrag

  BACKGROUND. Methodology for estimation of cerebrospinal fluid (CSF) tracer clearance could have wide clinical application in predicting excretion of intrathecal drugs and metabolic solutes from brain metabolism and for diagnostic workup of CSF disturbances. METHODS. The MRI contrast agent gadobutrol (Gadovist) was used as a CSF tracer and injected into the lumbar CSF. Gadobutrol is contained outside blood vessels of the CNS and is eliminated along extravascular pathways, analogous to many CNS metabolites and intrathecal drugs. Tracer enrichment was verified and assessed in CSF by MRI at the level of the cisterna magna in parallel with obtaining blood samples through 48 hours. RESULTS. In a reference patient cohort (n = 29), both enrichment within CSF and blood coincided in time. Blood concentration profiles of gadobutrol through 48 hours varied between patients diagnosed with CSF leakage (n = 4), idiopathic normal pressure hydrocephalus dementia (n = 7), pineal cysts (n = 8), and idiopathic intracranial hypertension (n = 4). CONCLUSION. Assessment of CSF tracer clearance is clinically feasible and may provide a way to predict extravascular clearance of intrathecal drugs and endogenous metabolites from the CNS. The peak concentration in blood (at about 10 hours) was preceded by far peak tracer enhancement at MRI in extracranial lymphatic structures (at about 24 hours), as shown in previous studies, indicating a major role of the spinal canal in CSF clearance capacity. FUNDING. The work was supported by the Department of Neurosurgery, Oslo University Hospital; the Norwegian Institute for Air Research; and the University of Oslo.

• Lashkarivand, Aslan; Sorteberg, Wilhelm; Rosseland, Leiv Arne & Sorteberg, Angelika (2020). Survival and outcome in patients with aneurysmal subarachnoid hemorrhage in Glasgow coma score 3–5. Acta Neurochirurgica. ISSN 0001-6268. 162(3), s. 533–544. doi: 10.1007/s00701-019-04190-y. Fulltekst i vitenarkiv Vis sammendrag

  Background Outcome of early, aggressive management of aneurysmal subarachnoid hemorrhage (aSAH) in patients with Hunt and Hess grade V is hitherto limited, and we therefore present our results. Methods Retrospective study analyzing the medical data of 228 aSAH patients in Glasgow Coma Score 3–5 admitted to our hospital during the years 2002–2012. Background and treatment variables were registered. Outcome was evaluated after 3 and 12 months. Results We intended to treat 176 (77.2%) patients, but only 146 went on to aneurysm repair. Of 52 patients managed conservatively, 27 had abolished cerebral circulation around arrival and 25 were deemed unsalvageable. One-year overall mortality was 65.8% and most (84.7%) of the fatalities occurred within 30 days. One-year mortality was higher in patients > 70 years. Without aneurysm repair, mortality was 100%. After 1 year, 21.9% of all patients lived independently and 4.8% lived permanently in an institution. Outcome in the 78 survivors (34.2%) was favorable in 64.1% in terms of modified Rankin Scale score 0–2, and 85.9% of survivors were able to live at home. Return to work was low for all 228 patients with 14.0% of those employed prior to the hemorrhage having returned to paid work, and respectively, 26.3% in the subgroup of survivors. Conclusions Even with aggressive, early treatment, 1-year mortality is high in comatose aSAH patients with 65.8%. A substantial portion of the survivors have a favorable outcome at 1 year (64.1%, corresponding to 21.9% of all patients admitted) and 85.9% of the survivors could live at home alone or aided.

• Lashkarivand, Aslan; Ringstad, Geir & Eide, Per Kristian (2019). Surgery for Brainstem Cavernous Malformations: Association between Preoperative Grade and Postoperative Quality of Life. Operative Neurosurgery. ISSN 2332-4252. 18(6), s. 590–598. doi: 10.1093/ons/opz337. Fulltekst i vitenarkiv

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• Lashkarivand, Aslan & Eide, Per Kristian (2024). Dementia in spontaneous intracranial hypotension: a call for accurate terminology. Neuroradiology. ISSN 0028-3940. doi: 10.1007/s00234-024-03530-9. Fulltekst i vitenarkiv
• Hovd, Markus Herberg; Mariussen, Espen; Uggerud, Hilde Thelle; Lashkarivand, Aslan; Christensen, Hege & Ringstad, Geir [Vis alle 7 forfattere av denne artikkelen] (2023). CSF to blood clearance differs substantially across individuals and patients with CSF disorders. Fluids and Barriers of the CNS. 19. doi: 10.1186/s12987-022-00397-x. Fulltekst i vitenarkiv
• Wiedmann, Markus; Olesrud, Ida; Lashkarivand, Aslan; Dheyauldeen, Sinan Ahmed Dheyauldeen; Heck, Ansgar & Berg-Johnsen, Jon [Vis alle 7 forfattere av denne artikkelen] (2023). Endoskopisk firehåndsteknikk ved hypofysesvulster. 143(9). doi: 10.4045/tidsskr.22.0693. Fulltekst i vitenarkiv
• Lashkarivand, Aslan & Eide, Per Kristian (2022). The first report on brain sagging dementia caused by a cranial leak: A case report. Frontiers in Neurology. 13, s. 1–6. doi: 10.3389/fneur.2022.1006060. Fulltekst i vitenarkiv Vis sammendrag

  Objective Brain Sagging Dementia (BSD) is an increasingly recognized syndrome for which diagnostic criteria recently were proposed. There have been no reports on BSD caused by a cranial leak. Here we present the first report on a patient with BSD caused by a cranial leak. Case description A 60-year old male patient was admitted with a 2-year history of orthostatic headache and gradually progressive cognitive and behavioral changes. Traditional treatments for spontaneous intracranial hypotension, including repeated epidural blood patches, failed. Brain imaging showed severe brain sagging, and intracranial pressure monitoring demonstrated intracranial hypotension. No leakage site was found. His past medical history revealed an accident where a ski pole struck his head at age ten. Due to progressive clinical decline, surgery was pursued. A cranial defect with an accompanying cerebrospinal fluid leak site representing the trauma from his childhood was found and repaired. He also was in need of a ventriculoperitoneal shunt. Following surgery, he improved and recovered completely. Discussion This case report illustrates that a cranial leak may cause BSD, even with a “lucid interval” between trauma and symptom debut spanning many years. Moreover, this report validates well the recently proposed BSD diagnostic criteria.

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