J F Soustiel

Western Galilee Hospital, Nahariya, Northern District, Israel

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Publications (47)83.32 Total impact

  • E Vlodavsky · E Palzur · J F Soustiel ·
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    ABSTRACT: Traumatic brain injuries represent the leading cause of death and morbidity in young adults in western countries, and are responsible for a major social and economical burden. For decades, the mainstay of neurotrauma management has been represented by control of post-traumatic edema. With the emergence of a better understanding of the underlying cellular mechanisms responsible for the generation of secondary brain damage, the hope for the "magic bullet" has prompted the development of novel drugs that have repeatedly failed to significantly improve outcome of head-injured patients. During the past decade, mitochondrial functional and structural impairment has emerged as a pivotal event in the pathway of cell to secondary death. Extensive research has identified a vast range of deleterious signals that are generated and integrated at the mitochondrial level resulting in impairment of major mitochondrial functions such as calcium homeostasis, free radicals generation and detoxification, energy production and neurosteroidogenesis. Mitochondria have therefore emerged as a potential therapeutic target. Within the spectrum of major mitochondrial structural components, the 18 kDa translocator protein has shown important and relevant functions such as steroid synthesis and modulation of the mitochondrial permeability transition that may substantially affect the fate of injured cells. This review summarizes the potential therapeutic implications of TSPO modulation in traumatic brain injury in the view of the current knowledge on this intriguing mitochondrial complex.
    CNS & neurological disorders drug targets 10/2013; · 2.63 Impact Factor
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    ABSTRACT: Of 1,949 successive acute severe head injuries (SHI) over a period of 11 years 1999-2009, 613 (31.5%) underwent evacuation of mass lesions. Mortality at 3 months of evacuated mass (EM) lesions was higher over 10 years compared with that of non-EM lesions (it was overall 22%). The reduction of mortality was significantly less in EM compared with that for non-surgical cases (14.4-9.4% recently) and for the cases that were operated but not for mass evacuation (18.1-12.1%). A few explanations are: first, more SDH (60.5% of the EM recently compared with 45.9% in the first few years); second, more severe cases and older patients with co-morbidities were treated surgically; third, advances in prehospital care brought more severe patients to operative care - the rate of referrals decreased from 61.5% to 52.8% recently; fourth, part of the significant shortening of the injury to NT admission time (163-141 min) vanished owing to the parallel elongation of admission to operation time (95-100 min), thus, the threshold recommendation of 4 h to mass evacuation was achieved in only 52%; fifth, introducing decompressive craniectomy was not associated with outcome improvement.
    Acta neurochirurgica. Supplement 01/2012; 114(114):301-4. DOI:10.1007/978-3-7091-0956-4_58
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    M Feinsod · J F Soustiel ·

    Journal of Neurology 04/2011; 258(9):1732-3. DOI:10.1007/s00415-011-6034-9 · 3.38 Impact Factor
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    A Rakier · J N Guilburd · J F Soustiel · M Zaaroor · M Feinsod ·
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    ABSTRACT: Two hundred and sixty-three consecutive head-injured patients aged over 65 years, admitted to a neurosurgical service, are reported. In contrast to younger age group the main cause was falls concomitant with a high rate of cardiovascular pre-existing disorders. The distribution of causes and grim results justify, in our opinion, regarding head injury in the elderly as a distinct entity requiring special surgical, medical, organizational and ethical considerations.
    Brain Injury 07/2009; 9(2):187-93. DOI:10.3109/02699059509008191 · 1.81 Impact Factor
  • J F Soustiel · H Hafner · AV Chistyakov · A Barzilai · M Feinsod ·
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    ABSTRACT: Forty patients who sustained minor head trauma were investigated by brainstem trigeminal and auditory evoked potentials (BTEP, BAEP) and middle-latency auditory evoked potentials (MLAEP). The patients were evaluated within the first 48 h following their admission and at 3 months after the injury. Outcome was scored at the follow-up examination according to six complaints: failure to resume previous professional activity, headache, memory disorders, dizziness and vertigo, behavioural and emotional disturbances, and other symptoms of a neurological nature. Post-concussion syndrome (PCS) was defined by the presence of four or more of the listed features. All three evoked potential modalities showed significantly increased latencies at the initial assessment, disclosing disseminated axonal damage. Unlike the BTEPs and the BAEPs, the MLAEPs proved to correlate to outcome at 3 months, especially in its psychocognitive aspects. These findings suggest that organic diencephalic-paraventricular primary damage may account for the occurrence of PCS.
    Brain Injury 07/2009; 9(8):805-13. DOI:10.3109/02699059509008236 · 1.81 Impact Factor
  • M Zaaroor · J F Soustiel · B Brenner · Y Bar-Lavie · U Martinowitz · L Levi ·
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    ABSTRACT: Traumatic brain contusions may increase in size over time or may develop at a delay after injury. This may lead to neurological deterioration, long term morbidity or even death. Coagulation disorders after injury can contribute to progression of haemorrhage. Recombinant activated factor VII (rFVIIa) was used in 12 patients with a severe head injury who had no systemic coagulopathy but who were considered to be at risk of progression of their intracranial lesion. Twelve consecutive patients suffering from life-threatening acute head injuries from blunt (3 cases) and penetrating mechanisms were given with rFVIIa, either to prevent the expected development of brain contusion or to assist in bleeding control during surgery. In 11 patients, rFVIIa was given by the attending neurosurgeon. Two of the patients died of their severe penetrating injuries one of whom had severe vasospasm 2 days after administration of rFVIIa. The other 11 patients did not appear to suffer any treatment-related adverse effects. When the drug was given prophylactically to prevent brain resection (6 cases) or to limit the need for widening resection (5 cases), marked control was achieved in seven cases, and a lesser effect was observed in the other 4 cases. We conclude that, in a small and highly individually selected series of patients with severe head injury, the administration of rFVIIa did not lead to adverse effects. Although the majority of patients were considered to be at high risk of progression of their lesions, this occurred in only one. The early use of rFVIIa in head injured patients without systemic coagulopathy may reduce the occurrence of enlargement of contusions, the requirement of further operation, and adverse outcome. Prospective randomised controlled studies are required to investigate this.
    Acta Neurochirurgica 08/2008; 150(7):663-8. DOI:10.1007/s00701-008-1593-y · 1.77 Impact Factor
  • J F Soustiel · E Palzur · E Vlodavsky · L Veenman · M Gavish ·
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    ABSTRACT: Hyperbaric hyperoxia has been shown to reduce apoptosis in brain injury. As the 18-kDa translocator protein (TSPO), also known as peripheral-type benzodiazepine receptor, is closely associated with the mitochondrial transition pore and because of its role in mitochondrial respiration and apoptosis, we hypothesized that reduction of apoptosis by hyperoxia may involve the TSPO. TSPO and transferase-mediated dUTP nick end labelling (TUNEL) immunopositivity was first assessed in cortical contusion, created by dynamic cortical deformation, by immunohistochemistry in rats exposed to normoxia [(dynamic cortical deformation (DCD)], normobaric hyperoxia or hyperbaric hyperoxia [hyperbaric oxygen therapy (HBO)]. In a second step, transmembrane mitochondrial potential (Deltapsi(M)) and caspase 9 activity were assessed in the injured area in comparison with the noninjured hemisphere. Measurements were performed in DCD and HBO groups. A third group receiving both HBO and the TSPO ligand PK11195 was investigated as well. TSPO correlated quantitatively and regionally with TUNEL immunopositivity in the perilesional area. Hyperoxia reduced both the number of TSPO expressing and TUNEL positive cells in the perilesional area, and this effect proved to be pressure dependent. After contusion, we demonstrated a dissipation of Deltapsi(M) in isolated mitochondria and an elevation of caspase 9 activity in tissue homogenates from the contused area, both of which could be substantially reversed by hyperbaric hyperoxia. This protective effect of hyperoxia was reversed by PK11195. The present findings suggest that the protective effect of hyperoxia may be due to a negative regulation of the proapoptotic function of mitochondrial TSPO, including conservation of the mitochondrial membrane potential.
    Neuropathology and Applied Neurobiology 11/2007; 34(4):412-23. DOI:10.1111/j.1365-2990.2007.00906.x · 3.93 Impact Factor
  • J F Soustiel · E Mahamid · A Chistyakov · V Shik · R Benenson · M Zaaroor ·
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    ABSTRACT: To compare the respective effects of established measures used for management of traumatic brain injury (TBI) patients on cerebral blood flow (CBF) and cerebral metabolic rates of oxygen (CMRO2), glucose (CMRGlc) and lactate (CMRLct). Thirty-six patients suffering from severe traumatic brain injury (TBI) were prospectively evaluated. In all patients baseline assessments were compared with that following moderate hyperventilation (reducing PaCO2 from 36 +/- 4 to 32 +/- 4 mmHg) and with that produced by administration of 0.5 gr/kg mannitol 20% intravenously. Intracranial and cerebral perfusion pressure (ICP, CPP), CBF and arterial jugular differences in oxygen, glucose and lactate contents were measured for calculation of CMRO2, CMRGlc and CMRLct. Following hyperventilation, CBF was significantly reduced (P < 0.0001). CBF remained most often above the ischemic range although values less than 30 ml x 100 gr(-1) x min(-1) were found in 27.8% of patients. CBF reduction was associated with concurrent decrease in CMRO2, anaerobic hyperglycolysis and subsequent lactate production. In contrast, mannitol resulted in significant albeit moderate improvement of cerebral perfusion. However, administration of mannitol had no ostensible effect either on oxidative or glucose metabolism and lactate balance remained mostly unaffected. Moderate hyperventilation may exacerbate pre-existing impairment of cerebral blood flow and metabolism in TBI patients and should be therefore carefully used under appropriate monitoring. Our findings rather support the use of mannitol for ICP control.
    Acta Neurochirurgica 09/2006; 148(8):845-51; discussion 851. DOI:10.1007/s00701-006-0792-7 · 1.77 Impact Factor
  • H. Hafner · B. Kaplan · J. Soustiel · M. Feinsod ·

    Clinical Neurophysiology 09/2006; 117:1-1. DOI:10.1016/j.clinph.2006.06.159 · 3.10 Impact Factor
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    G E Sviri · J F Soustiel · M Zaaroor ·
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    ABSTRACT: Brain natriuretic peptide (BNP) is a potent natriuretic and vasodilator factor which, by its systemic effects, can decrease cerebral blood flow (CBF). In aneurysmal subarchnoid hemorrhage (aSAH), BNP plasma concentrations were found to be associated with hyponatremia and were progressively elevated in patients who eventually developed delayed ischemic deficit secondary to vasospasm. The purpose of the present study was to evaluate trends in BNP plasma concentrations during the acute phase following severe (traumatic brain injury) TBI. BNP plasma concentration was evaluated in 30 patients with severe isolated head injury (GCS<8 on admission) in four time periods after the injury (period 1: days 1-2; period 2: days 4-5; period 3: days 7-8; period 4: days 10-11). All patients were monitored for ICP during the first week after the injury. The initial BNP plasma concentrations (42+/-36.9 pg/ml) were 7.3 fold (p<0.01) higher in TBI patients as compared to the control group (5.78+/-1.90 pg/ml). BNP plasma concentrations were progressively elevated through days 7-8 after the injury in patients with diffused SAH as compared to patients with mild or no SAH (p<0.001) and in patients with elevated ICP as compared to patients without elevated ICP (p<0.001). Furthermore, trends in BNP plasma concentrations were significantly and positively associated with poor outcome. BNP plasma concentrations are elevated shortly after head injury and are continuously elevated during the acute phase in patients with more extensive SAH and in those with elevated ICP, and correlate with poor outcomes. Further studies should be undertaken to evaluate the role of BNP in TBI pathophysiology.
    Acta Neurochirurgica 05/2006; 148(5):529-33; discussion 533. DOI:10.1007/s00701-005-0666-4 · 1.77 Impact Factor
  • E Vlodavsky · E Palzur · J F Soustiel ·
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    ABSTRACT: The acute inflammatory response plays an important role in secondary brain damage after traumatic brain injury (TBI). Neutrophils provide the main source of matrix metalloproteinases (MMPs) which also play a deleterious role in TBI. Numerous preclinical studies have suggested that hyperbaric oxygen therapy (HBOT) may by beneficial in various noncerebral and cerebral inflammatory diseases. The goal of this study was to evaluate the effects of HBOT on inflammatory infiltration and the expression of MMPs in correlation with secondary cell death in the rat model of dynamic cortical deformation (DCD). Twenty animals underwent DCD with subsequent HBOT (2.8 ATA, two sessions of 45 min each); 10 animals: DCD and normobaric oxygenation (1 ATA), 10 animals: not treated after DCD. Cell death was evaluated by TUNEL. Neutrophils were revealed by myeloperoxidase staining. Immunohistochemical staining for MMP-2 and -9 and tissue inhibitors of MMP-1 (TIMP-1) and -2 was also performed and the results were quantitatively evaluated by image analysis. In the animals treated by HBOT, a significant decrease in the number of TUNEL-positive cells and neutrophilic inflammatory infiltration was seen in comparison with nontreated animals and those treated by normobaric oxygen. The expression of MMP-9 was also significantly lower in the treated group. Staining for MMP-2 and TIMP-2 did not change significantly. Our results demonstrate that HBOT decreased the extent of secondary cell death and reactive neuroinflammation in the TBI model. The decline of MMP-9 expression after HBOT may also contribute to protection of brain tissue in the perilesional area. Further research should be centred on the evaluation of long-term functional and morphological results of HBOT.
    Neuropathology and Applied Neurobiology 03/2006; 32(1):40-50. DOI:10.1111/j.1365-2990.2005.00698.x · 3.93 Impact Factor
  • Zaaroor Menashe · Bar-Lavie Y · Brenner B · Soustiel JF · Martinowitz U ·
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    ABSTRACT: Traumatic brain hemorrhagic lesions, such as brain contusions, may increase in size after the initial impact. Enlargement of the contusion or hematoma has been shown to correlate with a worse neurological outcome. Surgery is a poor option in this situation, because it may involve wide resection of brain tissue. Seven patients with no overt systemic coagulopathy suffering from blunt or penetrating severe head injuries, expected to lead to significant morbidity and possibly to mortality, were treated with rFVIIa in an attempt to control brain contusion and hemorrhage. In all seven patients, the use of rFVIIa seemed to control the evolving intracranial bleeding. Six of the seven patients recovered, while one died after developing severe vasospasm three days after administration of rFVIIa. These results are very encouraging and, therefore, a prospective trial evaluating the safety and efficacy of rFVIIa in head trauma and intracranial hemorrhage is warranted.
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    ABSTRACT: Numerous imaging techniques have been developed and applied to evaluate brain hemodynamics. Among these are: Positron Emission Tomography (PET), Single Photon Emission Computed Tomography (SPECT), Xenon-enhanced Computed Tomography (XeCT), Dynamic Perfusion-computed Tomography (PCT), Magnetic Resonance Imaging Dynamic Susceptibility Contrast (DSC), Arterial Spin-Labeling (ASL), and Doppler Ultrasound. These techniques give similar information about brain hemodynamics in the form of parameters such as cerebral blood flow (CBF) or volume (CBV). All of them are used to characterize the same types of pathological conditions. However, each technique has its own advantages and drawbacks. This article addresses the main imaging techniques dedicated to brain hemodynamics. It represents a comparative overview, established by consensus among specialists of the various techniques. For clinicians, this paper should offers a clearer picture of the pros and cons of currently available brain perfusion imaging techniques, and assist them in choosing the proper method in every specific clinical setting.
    Journal of Neuroradiology 01/2006; 32(5):294-314. DOI:10.1161/01.STR.0000177839.03321.25 · 1.75 Impact Factor
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    ABSTRACT: Summary Numerous imaging techniques have been developed and applied to evaluate brain hemodynamics. Among these are: Positron Emission Tomography (PET), Single Photon Emission Computed Tomography (SPECT), Xenon-enhanced Computed Tomography (XeCT), Dynamic Perfusion-computed Tomography (PCT), Magnetic Resonance Imaging Dynamic Susceptibility Contrast (DSC), Arterial Spin-Labeling (ASL), and Doppler Ultrasound. These techniques give similar information about brain hemodynamics in the form of parameters such as cerebral blood flow (CBF) or volume (CBV). All of them are used to characterize the same types of pathological conditions. However, each technique has its own advantages and drawbacks. This article addresses the main imaging techniques dedicated to brain hemodynamics. It represents a comparative overview, established by consensus among specialists of the various techniques. For clinicians, this paper should offers a clearer picture of the pros and cons of currently available brain perfusion imaging techniques, and assist them in choosing the proper method in every specific clinical setting.
  • Gill E Sviri · V Shik · B Raz · J F Soustiel ·
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    ABSTRACT: Brain natriuretic peptide (BNP) is a potent natriuretic factor responsible for hyponatremia observed in patients with SAH. Through its systemic effects (reduction of blood volume and blood pressure) BNP may augment cerebral blood flow reduction and ischemia secondary to vasospasm. The purpose of the present study was to evaluate the relationship between BNP plasma concentration during the first 12 days following SAH and the development of cerebral vasospasm (CVS). The authors propose a hypothesis for the role played by natriuretic peptides in the pathophysiology of cerebral vasospasm based on the present findings and review the literature. Thirty eight patients with spontaneous SAH were prospectively included in the present study. BNP plasma concentrations were assessed at four different time periods following SAH (day 1-3, 4-6, 7-9, 10-12). TCD evidence of CVS was found in 26 patients (68.5%), fourteen patients (36.8%) had delayed ischemic neurological deficits (DIND). Initial BNP plasma concentrations were significantly more elevated in patients who eventually did not develop DIND (95.07+/-107.65 pg/ml vs. 25.81+/-22.57 pg/ml, p=0.0053). However, in patients with DIND, the BNP plasma concentration increased by 3.69 ( p<0.05), 5.89 ( p<0.001) and 4.54 fold ( p<0.001) between days 1-3 to days 4-6, 7-9 and 10-12 respectively (day 1 was regarded as the day of hemorrhage). In patients without CVS or asymptomatic CVS the BNP plasma concentration decreased between days 1-3 to day 10-12. A similar trend in BNP plasma concentration was found in patients with severe SAH (Fisher's score 3-4) as compared with patients with non visible or moderate SAH (BNP concentration ratio day 7-9/1-3: 4.37 vs. 0.75, p=0.015; day 10-12/1-3: 3.37 vs. 0.3, p=0.0144). The trend in BNP plasma concentration between day 1-3 to day 7-9 was found to correlate with CVS severity with an average increase of 2.01, 3.8 and 5.44 fold for mild, moderate and severe VS respectively ( p<0.01, r=0.4174). These results suggest that BNP secretion in SAH patients is closely related to the bleeding intensity and vasospasm severity as well as to development of DIND with a progressive and marked increase during the clinical course in patients who eventually develop cerebral ischemia. Taken together the local and systemic effects of BNP on CBF suggest that BNP might play a role in the pathophysiology of CVS through its systemic effects on blood pressure and plasma volume BNP leading to an aggravation of brain ischemia secondary to vasospasm.
    Acta Neurochirurgica 10/2003; 145(10):851-60; discussion 860. DOI:10.1007/s00701-003-0101-7 · 1.77 Impact Factor
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    J.F. Soustiel · T.C. Glenn · P Vespa · B Rinsky · C Hanuscin · N.A. Martin ·
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    ABSTRACT: We sought to evaluate a new, angle-independent ultrasonic device for assessment of blood flow volume (BFV) in the internal carotid artery (ICA). Nineteen patients and 4 healthy volunteers were enrolled in a comparative study conducted in the Care Unit of the Division of Neurosurgery at UCLA Medical Center. All patients had been admitted because of severe brain injury: 15 patients with severe head trauma (Glasgow Coma Scale score< or =8) and 4 patients with subarachnoid hemorrhage due to aneurysm rupture. In all patients and subjects, cerebral blood flow (CBF) values obtained with the 133xenon-clearance technique were compared with BFV measurements in the ipsilateral ICA. Hemispheric CBF values showed a close and linear correlation with BFV measurements (r=0.76, P<0.0001). Global CBF values showed a higher correlation with the total BFV value obtained from both ICAs (r=0.84, P<0.0001). With 37 mL x min(-1) x 100 g(-1) as a cutoff value for the ischemic range, a BFV value of 220 mL/min would yield a positive predictive value of 91.7% and a negative predictive value of 82.6% (sensitivity 73.3%, specificity 95%). Conversely, BFV sensitivity and specificity were 60% and 96%, respectively, for the hyperemic range defined by a CBF value >55 mL x min(-1) x 100 g(-1) (positive predictive value of 85.7% and negative prediction value of 85.7%). BFV measurements with this new technology proved to accurately correlate with CBF values evaluated by the 133xenon-clearance technique. These results support the implementation of this technique for bedside assessment of cerebral hemodynamics in critically ill neurosurgical patients.
    Stroke 09/2003; 34(8):1876-80. DOI:10.1161/01.STR.0000080942.32331.39 · 5.72 Impact Factor
  • J F Soustiel · V Shik · M Feinsod ·
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    ABSTRACT: Cerebral vasospasm has been commonly described following subarachnoid haemorrhage (SAH) though its impact on neurological outcome, especially in head trauma, has not been yet elucidated. The purpose of this study was to monitor and correlate neurological condition and flow velocities (FVs) in the arteries of the brain after SAH and more particularly to investigate the influence of basilar artery (BA) vasospasm on neurological outcome. Daily transcranial Doppler (TCD) evaluations were conducted in 116 consecutive patients with subarachnoid haemorrhage. SAH was of traumatic origin (tSAH) in 59 patients and spontaneous (sSAH) in 57 patients. Vasospasm in the MCA and ACA was defined by a mean FV exceeding 120 cm/s and three times the mean FV of the ipsilateral ICA. Basilar artery (BA) vasospasm was defined as moderate whenever the FV was higher than 60 cm/s and severe above 85 cm/s. Sixty-two patients (53.4%) had elevated FVs in the BA, among these 34 (29.3%) had FVs above 85 cm/s. Basilar vasospasm was significantly more common in tSAH (59.7%) than in sSAH (40.3%, P=0.041). In patients with moderate and severe BA vasospasm, FVs in the BA increased on the third day after admission and remained elevated for a week before returning to normal value by the end of the second week. This elevation in BA FVs in patients with BA vasospasm was followed by a significant and progressive worsening in the neurological condition at the end of the first week. Permanent neurological deficit was associated with elevated BA FVs consistent with moderate BA vasospasm whereas patients who remained in persistent vegetative state, had FVs consistent with severe BA vasospasm (P=0.00019). The present results further support that BA vasospasm may act as an independent factor of ischaemic brain damage following SAH, especially in head trauma.
    Acta Neurochirurgica 03/2002; 144(2):137-44; discussion 144. DOI:10.1007/s007010200016 · 1.77 Impact Factor
  • A Lev · Z Kotler · B Sfez · J Soustiel · M Feinsod ·
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    ABSTRACT: We present a new imaging technology that will allow to obtain three-dimensional maps of oxygen saturation in the brain tissues. This technology is not invasive and not ionizing, and can lead to small, portable device that can be brought to bedside. The technology uses a combination of near-infrared laser light and ultrasound. Like for other near-infrared spectroscopy techniques, light gives the information on the hemoglobin species present in the tissues. However, since tissues are turbid media, light alone cannot give precise local information. In the technique that we demonstrate, localization is obtained using a focussed ultrasound that locally shifts the laser wavelength, similarly to laser doppler techniques. The frequency-shifted light can be precisely detected and attributed without ambiguities to a specific location. By scanning the ultrasound focus, we can obtain a mapping of the oxygen saturation. We present preliminary results on a phantom showing the detection of an absorbing object buried more than two centimeters within the phantom. Scanning the ultrasound on the phantom allows to determine precisely the object position and absorption. Scattering and absorption parameters of the phantom are similar to the brain's. The probe works in the reflection mode, meaning that no transillumination is needed. The ultrasound frequency is 1.25 MHz, ensuring relatively good ultrasound penetration within the skull. The method is very promising for brain imaging of trauma or tumors. It is particularly suited for monitoring, since the use of the ultrasound removes the well-recognized problem of light propagation in the CSF.
    Acta neurochirurgica. Supplement 02/2002; 81:295-7.
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    AV Chistyakov · J F Soustiel · H Hafner · M Trubnik · G Levy · M Feinsod ·
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    ABSTRACT: The changes in excitatory and inhibitory responses to transcranial magnetic stimulation (TMS), as attested by motor evoked potential (MEP) and silent period (SP) parameters, were compared in patients who sustained minor to moderate head injury. A total of 38 patients with brain concussion, and diffuse, focal, and combined brain injury and 20 healthy volunteers were examined. The MEPs and SPs were recorded from the abductor pollicis brevis muscle after single pulse TMS 2 weeks after head trauma. The parameters assessed were the MEP resting threshold, the MEP/M wave amplitude ratio, the central motor conduction time (CMCT), the SP threshold, the interthreshold difference (ITD), and the SP duration (SPD). The main finding was an increase in the ITD in patients with mild and moderate head injury due to the relatively greater augmentation of the MEP threshold. This was associated with a reduction of the MEP/M wave amplitude ratio. The degree of MEP and SP changes depended on severity of head injury and was not related to the type of brain lesions. The SPD did not differ significantly in brain concussion, or diffuse, focal and combined brain injury groups compared with the control group. The CMCT was prolonged in patients with diffuse and combined brain lesions. Among subjective complaints only fatigue was significantly related to ITD, MEP, and SP threshold abnormalities. The results suggest that mechanisms involved in MEP and SP generation are differently affected in head injury, the first being impaired more severely. The increase of the ITD accompanied by reduction of the MEP/M wave amplitude ratio may reflect a dissociated impairment of inhibitory and excitatory components of central motor control in head trauma.
    Journal of Neurology Neurosurgery & Psychiatry 06/2001; 70(5):580-7. DOI:10.1136/jnnp.70.5.580 · 6.81 Impact Factor
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    J F Soustiel · E Levy · R Bibi · S Lukaschuk · D Manor ·
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    ABSTRACT: Hemodynamics of cerebral vasospasm after subarachnoid hemorrhage remain unclear, and the discrepancy between ultrasonographic or angiographic evidence of arterial narrowing and neurological ischemic deficit is still debated. Most blood flow studies have been involved with large arteries, and thus, very little is known regarding the hemodynamic behavior of small perforating vessels. Patients with symptomatic vasospasm, however, often present with neurological signs suggesting involvement of deep-sited areas of the brain supplied by perforating arteries. A pulsatile pump was set to provide an outflow of 350 mL/min through a 10-mm-diameter C-flex tube at a perfusion pressure of 130/80 mm Hg. The perfusion fluid used was prepared to approximate blood viscosity. Perforating arteries were simulated by a 1-mm tube connected to the parent tube at a 90 degrees angle. Cylindrical stenotic devices of decreasing diameters were then introduced into the parent tube at the level of the aperture of the secondary tube and 1.5 diameters upstream of it. Velocity profiles both proximal and distal to the stenosis in the parent tube were obtained with a newly developed ultrasonographic flowmeter that allows for high spatial resolution. Increasing stenosis resulted in decreased outflow in the main tube, although it was significant only with severe stenosis. Whenever the simulated stenosis was placed upstream of the secondary tube, flow reduction was associated with a progressive change in the velocity profile, which gradually changed from laminar conditions to a jet stream limited to the center of the lumen. Further diameter reduction was responsible for the occurrence of flow separation with retrograde flow velocities in the periphery of the lumen. In the secondary tube, flow reduction was much more pronounced and began at a lesser degree of stenosis. Increasing fluid viscosity and decreasing perfusion pressure enhanced flow separation and prominently affected the outflow in the secondary tube. Conversely, whenever the simulated stenosis involved the branching area of the secondary tube, there was a slightly progressive decrease in the relative flow in the main tube as the stenosis became tighter. When the stenosis equaled the diameter of the secondary tube, the relative contribution of the secondary tube increased markedly at the expense of the main tube outflow. The present results show that local cerebral vasospasm induces changes in postvasospastic velocity profile affecting the shear rate and may eventually lead to flow separation. This phenomenon may, in turn, result in a venturi-like effect over the aperture of perforating arteries branching out of the postvasospastic portion of the affected parent artery. These alterations of cerebral hemodynamics may account for at least part of the vasospasm symptomatology, especially in the vertebrobasilar system, where vasospasm is commonly focal rather than diffuse. Furthermore, these changes proved to be affected significantly by manipulations of pressure and viscosity, supporting the use of hyperdynamic therapy in the management of cerebral vasospasm.
    Stroke 04/2001; 32(3):629-35. DOI:10.1161/01.STR.32.3.629 · 5.72 Impact Factor

Publication Stats

802 Citations
83.32 Total Impact Points


  • 2013
    • Western Galilee Hospital
      Nahariya, Northern District, Israel
  • 1988-2012
    • Rambam Medical Center
      • Department of Neurosurgery
      H̱efa, Haifa, Israel
  • 1996-2011
    • Technion - Israel Institute of Technology
      • • Rambam Medical Center
      • • Ruth and Bruce Rappaport Faculty of Medicine
      • • Electrical Engineering Group
      H̱efa, Haifa District, Israel

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