Cerebral Hemodynamics In Patients Research Articles

Improved hemodynamic parameters in middle cerebral artery infarction after decompressive craniectomy.

Decompressive craniectomy (DC) reduces mortality and improves functional outcome in patients with malignant middle cerebral artery infarction. However, little is known regarding the impact of DC on cerebral hemodynamics. Therefore, our goal was to study the hemodynamic changes that may occur in patients with malignant middle cerebral artery infarction after DC and to assess their relationship with outcomes. Twenty-seven patients with malignant middle cerebral artery infarction who were treated with DC were studied. The perfusion CT hemodynamic parameters, mean transit time, cerebral blood flow, and cerebral blood volume were evaluated preoperatively and within the first 24 hours after DC. There was a global trend toward improved cerebral hemodynamics after DC. Preoperative and postoperative absolute mean transit times were associated with mortality at 6 months, and the ratio of post- and preoperative cerebral blood flow was significantly higher in patients with favorable outcomes than those with unfavorable outcomes. Patients who underwent surgery 48 hours after stroke, those with midline brain shift>10 mm, and those who were >55 years showed no significant improvement in any perfusion CT parameters. DC improves cerebral hemodynamics in patients with malignant middle cerebral artery infarction, and the level of improvement is related to outcome. However, some patients did not seem to experience any additional hemodynamic benefit, suggesting that perfusion CT may play a role as a prognostic tool in patients undergoing DC after ischemic stroke.

Model-based physiomarkers of cerebral hemodynamics in patients with mild cognitive impairment

In our previous studies, we have introduced model-based “functional biomarkers” or “physiomarkers” of cerebral hemodynamics that hold promise for improved diagnosis of early-stage Alzheimer's disease (AD). The advocated methodology utilizes subject-specific data-based dynamic nonlinear models of cerebral hemodynamics to compute indices (serving as possible diagnostic physiomarkers) that quantify the state of cerebral blood flow autoregulation to pressure-changes (CFAP) and cerebral CO2 vasomotor reactivity (CVMR) in each subject. The model is estimated from beat-to-beat measurements of mean arterial blood pressure, mean cerebral blood flow velocity and end-tidal CO2, which can be made reliably and non-invasively under resting conditions. In a previous study, it was found that a CVMR index quantifying the impairment in CO2 vasomotor reactivity correlates with clinical indications of early AD, offering the prospect of a potentially useful diagnostic tool. In this paper, we explore the use of the same model-based indices for patients with amnestic Mild Cognitive Impairment (MCI), a preclinical stage of AD, relative to a control subjects and clinical cognitive assessments. It was found that the model-based CVMR values were lower for MCI patients relative to the control subjects.

CDP-choline (ceraxon) treatment with hypoxia in the newborn infant

CDP-choline (ceraxon) treatment with hypoxia in the newborn infant

Effect of Telmisartan on Cerebral and Systemic Haemodynamics in Patients with Recent Ischaemic Stroke: A Randomised Controlled Trial

High blood pressure (BP) is common in acute stroke and is independently associated with a poor outcome. Lowering BP might improve outcome if cerebral blood flow (CBF) is unaffected in the presence of dysfunctional autoregulation. We investigated the effect of telmisartan on systemic and cerebral haemodynamics in patients with recent stroke. Patients with ischaemic stroke (<5 days) were randomised to 90 days of telmisartan (80 mg) or placebo. CBF (primary outcome) was measured using xenon CT at baseline and 4 hours. BP and transcranial doppler (TCD) were performed at baseline, 4 hours after-treatment, and on days 4, 7, and 90. Cerebral perfusion pressure and zero filling pressure (ZFP) were calculated. Of a planned 24 patients, 17 were recruited. Telmisartan significantly accentuated the fall in systolic and diastolic BP over 90 days (treatment-time interactionp=0.047,p=0.003,resp.) but did not alter BP at 4 hours after treatment (171/99 versus 167/87 mmHg), CBF, or CBF velocity. ZFP was significantly lower in the treatment group(p=0.018). Impairment at 7 days and dependency at 90 days did not differ between the groups. In this underpowered study, telmisartan did not significantly alter BP or CBF after the first dose. Telmisartan reduced BP over the subsequent 90 days and significantly lowered ZFP. This trial is registered withISRCTN 41456162.

The metabolism of monoamines in the central nervous system during compensated and decompensated heart failure

We found different associations between disturbances in the brain and heart during compensated and decompensated heart failure. Changes in the content of monoamines (MAs) in the brain at different stages of heart failure (HF) were related to different causes. The increased activity of MA-ergic systems during compensated HF was apparently associated with the functional load that is experienced by the structures of the brain during the development of cerebral processes of autonomic regulation of the compensatory function of the heart. Cerebral hemodynamics in patients with decompensated HF leads to a decrease in the activities of the dopaminergic and serotonergic systems and a permanent mismatch of the central and autonomic mechanisms of cardiac-activity regulation. A functional load test with the administration of dopamine and serotonin precursors revealed unequal MA-synthesizing capabilities of the brain in animals with compensated and decompensated HF. Reduced capacity of the MA-ergic systems during decompensated HF may lead to overwork of the central mechanisms of regulation and the gradual depletion and disruption of compensatory mechanisms, which aggravates the progression of heart failure.

Коррекция нарушений церебральной гемодинамики у больных с хроническими обструктивными заболеваниями легких

В статье представлены результаты исследования церебральной гемодинамики у пациентов с хроническими обструктивными заболеваниями легких. Проведено ультразвуковое исследование сосудистой системы головы. Выявлено снижение показателей артериального кровотока, цереброваскулярного резерва, затруднение венозного оттока из полости черепа, прогрессирующее с нарастанием стадии хронических обструктивных заболеваний легких. Сделан вывод о целесообразности применения препарата диосмина в составе комплексной терапии.

Effects of Indomethacin Test on Intracranial Pressure and Cerebral Hemodynamics in Patients With Refractory Intracranial Hypertension

Intracranial hypertension is the final pathway of many neurocritical entities, such as spontaneous intracerebral hemorrhage (sICH) and severe traumatic brain injury (sTBI). This study aimed to (1) determine alterations in intracranial pressure (ICP) and cerebral hemodynamics after an indomethacin (INDO) infusion test and the related association with survival in patients with refractory intracranial hypertension (RICH) secondary to sICH or sTBI and (2) assess the safety profile after INDO. INDO was administered in a loading dose (0.8 mg/kg/15 min), followed by a 2-hour continuous infusion (0.5 mg/kg/h) in RICH patients with ICP greater than 20 mm Hg who did not respond to first-line therapies. Changes in ICP, cerebral perfusion pressure (CPP), and cerebrovascular variables (assessed by transcranial Doppler and jugular bulb saturation) were observed. Clinical outcome was assessed at 1 and 6 months according to the Glasgow Outcome Scale and correlated with INDO infusion test response. Analysis of INDO safety profile was conducted. Thirteen sICH and 10 sTBI patients were studied. The median GCS score at admission was 6. Within 30 minutes of INDO infusion, ICP decreased (42.0 ± 13.5 vs 27.70 ± 12.7 mm Hg; Δ%: -48.4%; P < .001), and both CPP (57.7 ± 4.8 vs 71.9 ± 7.0 mm Hg; Δ%: +26.0%; P < .001) and middle cerebral artery velocity (35.2 ± 5.6 vs 42.0 ± 5.1 cm·s(-1); Δ%: +26.1%; P < .001) increased. The CPP response to a 2-hour INDO infusion test was correlated (R2 = 0.72, P < .001) with survival. No adverse events were observed after INDO. Our findings support the effectiveness and feasibility of an INDO test in decreasing ICP and improving cerebral hemodynamics in surviving RICH patients. Future studies to evaluate different doses, lengths of infusion, and longer term effects are needed.

Evaluation of cerebral hemodynamics of patients with chronic migraine

Evaluation of cerebral hemodynamics of patients with chronic migraine

Cerebral hemodynamics and baroreflex sensitivity after carotid artery stenting

The long-term hemodynamic effects of carotid angioplasty and stenting (CAS) are unclear. We performed a longitudinal study to investigate the variations in cerebral hemodynamics in patients undergoing CAS. We performed prospective evaluation of 63 symptomatic male patients (19 patients had transient ischemic attack and 44 had minor stroke; mean age: 77.3 ± 6.3 years [range: 51-86]). The mean blood flow velocities (MBFV) and pulsatility index (PI) of the middle cerebral arteries (MCA) on both sides were evaluated using transcranial color-coded Doppler (TCCD) ultrasonography. Cardiac autonomic activities were evaluated by measuring baroreflex sensitivity (BRS). All parameters were measured at baseline prior to CAS and at 1, 3, 6, and 12 months after CAS. The preoperative MBFV and PI of the ipsilateral MCA were significantly lower than those of the contralateral side. However, after CAS, MBFV in the ipsilateral MCA increased significantly until 2 weeks after stenting, after which the MBFV gradually decreased and remained stable for 1 year after CAS. Further, we observed a nonsignificant increase in MBFV in the contralateral MCA after CAS. In contrast to the MBFV, the BRS values decreased significantly 1 month after stenting and returned to baseline levels 6 months after CAS. Patients with CAS showed improved global cerebral hemodynamic status. However, the BRS did not normalize initially, and baseline value was achieved at 6 months after stenting.

Effect of Combination Therapy with the Angiotensin Receptor Blocker Losartan plus Hydrochlorothiazide on Brain Perfusion in Patients with both Hypertension and Cerebral Hemodynamic Impairment due to Symptomatic Chronic Major Cerebral Artery Steno-Occlusive Disease: A SPECT Study

Background: While the combination of an angiotensin receptor blocker with thiazide diuretics produces a clinically beneficial reduction in blood pressure in patients who otherwise only partially respond to monotherapy with an angiotensin receptor blocker, blood pressure-lowering therapy with combination antihypertensive drug regimens in patients with cerebral hemodynamic impairment may adversely affect cerebral hemodynamics. The purpose of the present exploratory study was to determine whether blood pressure-lowering therapy with the combination of the angiotensin receptor blocker losartan plus hydrochlorothiazide (LPH) worsens brain perfusion in patients with both hypertension and cerebral hemodynamic impairment due to symptomatic chronic major cerebral artery steno-occlusive disease. Methods: Patients with losartan-resistant hypertension and reduced cerebrovascular reactivity (CVR) to acetazolamide due to symptomatic chronic internal carotid artery (ICA) or middle cerebral artery (MCA) steno-occlusive disease were prospectively entered into the present study and received 50 mg/day of losartan plus 12.5 mg/day of hydrochlorothiazideat 14 weeks after the last ischemic event. Cerebral blood flow (CBF) and CVR were measured before and 12 weeks after initiating LPH using N-isopropyl-p-[¹²³I]-iodoamphetamine single-photon emission computed tomography (SPECT). A region of interest (ROI) was automatically placed in the MCA territory on each SPECT image using a three-dimensional stereotactic ROI template. Results: None of the 18 patients who participated in the study experienced any new neurological symptoms or adverse effects related to antihypertensive drugs. Systolic (p < 0.001) and diastolic (p < 0.001) blood pressures were significantly reduced after the administration of LPH, with average reductions of 11 mm Hg in systolic blood pressure and 10 mm Hg in diastolic blood pressure. While in the affected hemisphere CBF did not differ between measurements taken before and after the administration of LPH, CVR was significantly higher after the administration of LPH than before (p = 0.007) and was significantly improved in 5 of 18 patients. In the contralateral hemisphere, CBF and CVR did not differ between measurements taken before and after the administration of LPH. There were no patients who experienced a significant deterioration in CBF or CVR in the affected or contralateral hemisphere after the administration of LPH. Conclusions: Although the present study was exploratory and its results were preliminary due to the small sample size, the current data suggest that blood pressure-lowering therapy with LPH apparently does not result in worsening of cerebral hemodynamics in patients with both hypertension and cerebral hemodynamic impairment due to symptomatic chronic ICA or MCA steno-occlusive disease.

Perfusion CT in Patients With Spontaneous Lobar Intracerebral Hemorrhage

The aim of the present study was to investigate cerebral hemodynamics in patients requiring surgical treatment for lobar intracerebral hemorrhage. Twenty patients who underwent surgery to remove a lobar spontaneous intracerebral hemorrhage were scanned before and after surgery using perfusion CT mapping. Mean transit time, time to peak of the residue function, cerebral blood volume, and cerebral blood flow were measured in 4 defined regions of interest. Preoperatively, time to peak of the residue function, cerebral blood volume, and cerebral blood flow were significantly impaired in the perihemorrhagic zone as compared with the ipsilateral and contralateral hemisphere. Perihematomal perfusion improved significantly after clot evacuation and there was no difference in time to peak of the residue function, cerebral blood flow, and cerebral blood volume values between the perihemorrhagic zone and ipsilateral as well as contralateral hemisphere after surgical treatment. Our findings illustrate distinct perihemorrhagic perfusion impairments in a selected patient population with lobar intracerebral hemorrhage as evident by impaired time to peak of the residue function, cerebral blood flow, and cerebral blood volume and their improvement after early surgical treatment. Whether these early improvements in hemodynamic measurements may influence secondary neuronal injury and ultimately clinical outcome, as opposed to the natural course of spontaneous intracerebral hemorrhage remains unclear.

Quantification of cerebral hemodynamics in patients with multiple sclerosis: dynamic contrast-enhanced MRI in 3D at 3T

The quantification of cerebral hemodynamics, comprised of cerebral blood flow (CBF), cerebral blood volume (CBV) and permeability-surface area product (PS) as a measure of blood-brain barrier permeability in MS lesions in the brain is challenging. With conventional dynamic susceptibility weighted MRI, several issues with quantification arise, in particular in areas with blood-brain barrier disruption. In this study, we investigate the feasibility of a rapid 3D T1-weighted dynamic contrast-enhanced (DCE) MRI measurement, providing coverage of the entire neurocranium, in combination with a two-compartment modelling approach for the quantification of CBF, CBV and PS as a measure of blood-brain barrier leakage in contrast-enhancing (CE) lesions and in normal-appearing white matter (NAWM) in patients with multiple sclerosis (MS).

Leptomeningeal collateral and cerebral hemodynamics in patients with ICA and MCA steno-occlusion

<title/>Objectives: The purpose of our study was to evaluate the correlation between fluid-attenuated inversion recovery (FLAIR) images of hyperintense vessel (HV), a representative of leptomeningeal vessels (LMVs), and cerebral vascular hemodynamic status in patients with steno-occlusive disease of the internal carotid artery (ICA) and middle cerebral artery (MCA).Methods: Sixty-eight patients with unilateral ICA or MCA stenosis or occlusion were enrolled. Correlations between hyperintense vessel (HV) on FLAIR images and hemodynamic status measured by quantitative single-photon emission computed tomography data were evaluated in four groups: affected (A) and non-affected (B) hemispheres in HV-positive patients, and affected (C) and non-affected (D) hemispheres in HV-negative patients.Results: The presence of HV was most frequently seen on affected hemispheres in patients with MCA and ICA occlusions. HV was significantly higher in the anterior communicating artery (AcomA) (−), posterior communicating artery (PcomA) (−) group than in other groups, which included either or both AcomA and PcomA (P = 0·008). The presence of HV had a significant correlation with transdural anastomosis (P = 0·046) and LMV (P = 1·64×10−9). No significant difference was observed in resting regional cerebral blood flow among the four groups. Vascular reserve in group A was significantly less compared to other groups (P = 0·021).Conclusions: HV is related to the hemisphere with severe ICA and MCA steno-occlusion when the circle of Willis is insufficient. The HV-positive hemisphere on the steno-occlusive side shows a lower vascular reserve than that in the contralateral hemisphere or HV-negative hemispheres.

Stellate ganglion block for treatment of cerebral vasospasm in patients with aneurysmal subarachnoid hemorrhage - A preliminary study

Background:Stellate ganglion block improves cerebral perfusion by decreasing the cerebral vascular tone. Its effects on cerebral vasospasm to relieve neurological deficits have not been evaluated. This prospective observational study was carried out to evaluate the effect of stellate ganglion block on cerebral hemodynamics in patients with symptomatic cerebral vasospasm following aneurysmal subarachnoid hemorrhage.Materials and Methods:Fifteen patients of either sex, aged 18-75 years, who underwent surgical clipping of aneurysm and developed refractory cerebral vasospasm were included. Stellate ganglion block was performed using 10 ml of bupivacaine 0.5% on the side with maximum cerebral blood flow velocity. Neurological status, cerebral blood flow velocity and pulsatility index were assessed before and 10 minutes, 30 minutes, 2 hours, 6 hours, 12 hours and 24 hours after stellate ganglion block.Results:Improved Glasgow coma score was observed 30 minutes after stellate ganglion block. Neurological deficits reduced in 11 patients. Ipsilateral middle cerebral artery mean flow velocity decreased from 133.66 cm/sec before stellate ganglion block to 110.53 cm/sec at 6 hours (P<0.001) and 121.62 cm/sec at 24 hours (P<0.001) after stellate ganglion block. There was a decrease in ipsilateral anterior cerebral artery mean flow velocity after stellate ganglion block (P<0.001), which persisted for 12 hours. A decline in flow velocities was observed in contralateral middle cerebral artery (P=0.008) and anterior cerebral artery (P=0.041) for 12 hours.Conclusion:This study suggests stellate ganglion block to be an effective modality of treatment for refractory cerebral vasospasm after aneurysmal subarachnoid hemorrhage.

P35-7 Cerebral hemodynamics in patients with moyamoya syndrome associated with atherosclerotic occlusion of the middle cerebral arteries

P35-7 Cerebral hemodynamics in patients with moyamoya syndrome associated with atherosclerotic occlusion of the middle cerebral arteries

Relative Hypotension in the Beach-Chair Position: Effects on Middle Cerebral Artery Blood Velocity

When anaesthetising patients for arthroscopic shoulder surgery, it is common practice to sit the patient in the beachchair position and to optimise arthroscopy by allowing relative hypotension. There is little published information regarding the cerebral haemodynamic effects of hypotension in the sitting position during general anaesthesia. In this study, 19 patients scheduled for shoulder surgery were anaesthetised with desflurane. Phenylephrine and/or remifentanil were used to control blood pressure. Cerebral haemodynamics were assessed by monitoring middle cerebral artery blood velocity with transcranial Doppler, and by invasive arterial pressure monitoring with the transducer kept level with the external auditory meatus. Pressure and velocity waveforms were analysed to calculate apparent zero flow pressure and resistance area product. Cerebral haemodynamics in patients anaesthetised supine at the pre-induction blood pressure were compared with haemodynamics while seated at 45 degrees with hypotension. According to our routine practice, blood pressure management was guided by non-invasive measurement of systolic pressure using an arm cuff Changing from supine/normotensive to sitting/hypotensive caused mean arterial pressure at the auditory meatus to decrease 47 +/- 7% and middle cerebral artery blood velocity to decrease 22 +/- 7%. In the beach-chair position, systolic pressure was 96 +/- 10 mmHg in the arm and 76 +/- 10 mmHg at the auditory meatus (P < 0.0001). Both resistance area product and apparent zero flow pressure decreased, suggesting decreases in cerebrovascular resistance and critical closing pressure. Although there was some evidence of an autoregulatory response, middle cerebral artery blood velocity decreased when relative hypotension was induced in patients anaesthetised with desflurane in the beach-chair position.

Blood Pressure Lowering with Valsartan Is Associated with Maintenance of Cerebral Blood Flow and Cerebral Perfusion Reserve in Hypertensive Patients with Cerebral Small Vessel Disease

The purpose of this study was to determine the effect of systemic blood pressure-lowering treatment with an angiotensin II receptor blocker, valsartan, on cerebral hemodynamics in patients with hypertension and evidence of cerebral small vessel disease. We used positron emission tomography and acetazolamide challenge tests to measure cerebral blood flow (CBF) and cerebrovascular reserve (CVR) in 8 patients with hypertension (mean age 70.8 years) with lacunar infarcts and white matter lesions before and after valsartan therapy. Systemic blood pressure was significantly decreased from baseline after treatment with valsartan. The baseline global CBFs before and after treatment were 38.2 +/- 5.6 mL/min/100 g and 39.9 +/- 9.0 mL/min/100 g, respectively. The CVRs before and after treatment were 52.2 +/- 18.4% and 39.7 +/- 18.9%, respectively. Differences in these parameters were not significant. Both regional CBF and CVR in the corona radiata with moderate or severe white matter lesions were also preserved after valsartan therapy compared with those before treatment. Cerebral hemodynamics were preserved after blood pressure lowering with valsartan therapy. Valsartan could be a feasible antihypertensive regimen in terms of cerebral circulation in patients with cerebral small vessel disease.

Nocturnal Cerebral Hemodynamics in Snorers and in Patients with Obstructive Sleep Apnea: A Near-Infrared Spectroscopy Study

Sleep disordered breathing (SDB) of the obstructive type causes hemodynamic consequences, leading to an increased cerebrovascular risk. The severity of SDB at which detrimental circulatory consequences appear is matter of controversy. Aim of the present study is the investigation of cerebral hemodynamics in patients with SDB of variable severity using near-infrared spectroscopy (NIRS). N/A. Sleep laboratory. Nineteen patients with SDB. N/A. Patients underwent nocturnal videopolysomnography (VPSG) coupled with cerebral NIRS. NIRS data were averaged for each patient, and a new method (integral) was applied to quantify cerebral hemodynamic alterations. Nocturnal VPSG disclosed various severities of SDB: snoring (7 patients, apnea-hypopnea index [AHI] = 2 +/- 2/h, range: 0.5-4.5); mild SDB (7 patients, AHI = 14 +/- 8/h, range: 6.3-28.6); and severe obstructive sleep apnea syndrome (5 patients, AHI = 79 +/- 20/h, range: 39.6-92.9). Relative changes of NIRS parameters were significantly larger during obstructive apneas (compared with hypopneas; mean deoxygenated hemoglobin [HHb] change of 0.72 +/- 0.23 and 0.13 +/- 0.08 micromol/L per sec, p value = 0.048) and in patients with severe SDB (as compared with patients with mild SDB and simple snorers; mean HHb change of 0.84 +/- 0.24, 0.02 +/- 0.09, and 0.2 +/- 0.08 micromol/L per sec, respectively, p value = 0.020). In this group, NIRS and concomitant changes in peripheral oxygen saturation correlated. The results of this study suggest that acute cerebral hemodynamic consequences of SDB lead to a failure of autoregulatory mechanisms with brain hypoxia only in the presence of frequent apneas (AHI > 30) and obstructive events.

Cerebral haemodynamics in patients with glutaryl-coenzyme A dehydrogenase deficiency

In glutaric aciduria type 1, glutaryl-coenzyme A and its derivatives are produced from intracerebral lysine and entrapped at high concentrations within the brain, where they interfere with energy metabolism. Biochemical toxicity is thought to trigger stroke-like striatal degeneration in susceptible children under 2 years of age. Here, we explore vascular derangements that might also contribute to brain damage. We studied injured and non-injured Amish glutaric aciduria type 1 patients using magnetic resonance imaging (n = 26), transcranial Doppler ultrasound (n = 35) and perfusion computed tomography (n = 6). All glutaric aciduria type 1 patients had wide middle cerebral, internal carotid and basilar arteries. In non-injured patients, middle cerebral artery velocities were 18-26% below control values throughout late infancy and early childhood, whereas brain-injured children had an early velocity peak (18 months) and low values thereafter. Perfusion scans from six patients showed that tissue blood flow did not undergo a normal developmental surge. We observed four different perfusion patterns. (i) Three children (two non-injured) had low cerebral blood flow, prolonged mean transit time, elevated cerebral blood volume and high mean transit time/cerebral blood flow and cerebral blood volume/cerebral blood flow ratios. This pattern optimizes substrate extraction at any given flow rate but indicates low perfusion pressure and limited autoregulatory reserve. (ii) Ten hours after the onset of striatal necrosis in an 8-month-old infant, mean transit time and cerebral blood volume were low relative to cerebral blood flow, which varied markedly from region to region. This pattern indicates disturbed autoregulation, regional perfusion pressure gradients, or redistribution of flow from functional capillaries to non-exchanging vessels. (iii) In an infant with atrophic putaminal lesions, striatal flow was normal but mean transit time and cerebral blood volume were low, consistent with perfusion in excess of metabolic demand. (iv) Finally, a brain-injured adult with glutaric aciduria type 1 had regional perfusion values within the normal range, but the putamina, which normally have the highest regional perfusion, had cerebral blood flow values 24% below cortical grey matter. Although metabolic toxicity appears central to the pathophysiology of striatal necrosis, cerebrovascular changes probably also contribute to the process. These changes may be the primary cause of expanded cerebrospinal fluid volume in newborns, intracranial and retinal haemorrhages in infants and interstitial white matter oedema in children and adults. This pilot study suggests important new areas for clinical investigation.

The effect of levodopa treatment on cerebral hemodynamics in patients with Parkinson's disease: Serial transcranial Doppler studies

Levodopa treatment in patients with Parkinson's disease (PD) is known to cause elevation in serum homocysteine levels. We investigated whether this increase in homocysteine level influences cerebral vascular flow velocity and resistance using transcranial Doppler (TCD). This study included 17 patients with de novo PD. Homocysteine levels and TCD parameters at middle cerebral artery were investigated before and after 3 months of levodopa treatment. Correlation analyses were done between changes in homocysteine levels and TCD parameters. After 3 months of levodopa treatment, homocysteine level increased significantly from 13.3mg/dL to 17.0 mg/dL ( p < 0.001), but there were no meaningful changes in mean velocity (MV) and pulsatility index (PI). Correlation analysis revealed that the changes in homocysteine level had negative correlation with MV ( r = −0.53, p = 0.027) and positive correlation with PI ( r = 0.55, p = 0.028). Our study infer that although short-term treatment of levodopa itself does not cause overall alteration of cerebral blood flow velocities and resistances, patients who has greater degree of increased homocysteine level may still be at a risk of developing cerebral vascular stiffness.