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Biomedical subjects

D Georgiadis

Publications and source records attributed to D Georgiadis.

At least 37 records · Page 2Linked to original sources
PubMed2003

Ischemic infarct involving all arterial territories of the thalamus.

Ischemic infarcts of the thalamus involve one or two of its four arterial territories that are usually supplied by the posterior cerebral (PCA) and the posterior communicating (PCoA) arteries. We report a patient who suffered ischemic infarcts in all arterial territories of the right thalamus. Magnetic resonance (MR) angiography showed an occlusion of the right PCA and failed to visualize a PCoA. We assume that the absence of a relevant thalamic blood supply deriving from the PCoA enabled PCA occlusion to cause infarcts in all thalamic territories.

Arteries↗
PubMed2003

Recanalisation of cerebral venous thrombosis.

OBJECTIVE: To investigate recanalisation in the first 12 months after cerebral venous thrombosis. METHODS: 33 consecutive patients presenting with cerebral venous thrombosis were enrolled in the study. Diagnosis was made by magnetic resonance imaging (MRI) and magnetic resonance venography (MRV) or catheter angiography. Patients were initially treated with intravenous heparin. Warfarin was given for at least four months. Cerebral MRI and MRV were done at four months and repeated after 12 months if venous thrombosis persisted. Outcome was evaluated by the Rankin scale at 12 months. RESULTS: Outcome at 12 months was good, with a median modified Rankin scale score of 0 (range 0 to 2); 27 patients (82%) had no residual deficits. No patient suffered recurrent cerebral venous thrombosis, deep vein thrombosis, or pulmonary embolism during follow up. After four months, all deep cerebral veins and cavernous sinuses, 94% of superior sagittal sinuses, 80% of straight sinuses, 73% of jugular veins, 58% of transverse sinuses, and 41% of sigmoid sinuses had recanalised. No further recanalisation was observed thereafter. CONCLUSIONS: The results suggest that recanalisation only occurs within the first four months following cerebral venous thrombosis and not thereafter, irrespective of oral anticoagulation.

Adult↗
PubMed2002

[Clinical relevance of detection of microembolism signals with transcranial Doppler ultrasound diagnosis].

Detection of microembolic signals (MES) has been described in several patients groups. A potential clinical relevance of this technique has been established (1) during the first hours following carotid endarterectomy and (2) for patients with asymptomatic ICA stenosis or various autoimmune disorders. Intraoperative monitoring in patients undergoing cardiac or carotid surgery can be used to improve the surgical technique but provides no prognostic information for individual patients. Microembolic signals in patients with prosthetic heart valves cannot be used as markers for stroke risk; their potential significance as markers for neuropsychological deficits remains unclear. Recent reports suggest that MES can be used as surrogate markers for assessing the efficacy of antiplatelet agents. The fact that automated MES detection is not feasible greatly reduces the technique's applicability. On the whole, MES detection--with the exception of the patient groups listed above--provides pathophysiological rather than clinically relevant information.

Feasibility Studies↗
PubMed2002

[Current concepts of intensive care of space-occupying middle cerebral artery infarct].

The aim of this paper is to review new developments in the intensive care of patients with space-occupying middle cerebral artery infarctions. Elevated blood pressure should not be treated; however, there is no scientific basis to induce arterial hypertension in these patients. It is not recommended generally to nurse the patients in a position with the head elevated. If therapy is targeted for an optimum cerebral perfusion pressure, the patients should be nursed in a flat position. Decompressive surgery is associated with a marked reduction in an otherwise high mortality. The functional outcome after surgery is similar to the outcome of the survivors after conventional treatment alone. Treatment options for an acutely raised intracranial pressure are mannitol or hypertonic saline solutions, although the long-term effects have not been ascertained yet. There is not enough evidence supporting a prophylactic standard therapy with hypertonic solutions. Patients who require artificial ventilation can be safely ventilated using PEEP or an inverse inspiration/expiration ratio, if the blood pressure is monitored and a possible drop of the arterial blood pressure is treated. Corticoids and hemodilution are obsolete therapies in these patients.

Blood Pressure↗
PubMed2002

Cruciate paralysis or man-in-the-barrel syndrome? Report of a case of brachial diplegia.

A patient who developed isolated brachial diplegia following cardiac surgery is described. The underlying cerebral lesion could not be localized using magnetic resonance imaging (MRI). Evoked potentials disclosed normal findings, while pathological latencies were seen on cortical magnetic stimulation. Their marked improvement over the following year was accompanied by almost complete clinical recovery. The preserved arm reflexes, together with the observed slow firing motor units in electromyography argued against bilateral lesions of the brachial plexus. We attribute the observed diplegia to a medullary lesion at the level of the pyramidal decussation, presumably caused by an intraoperative embolic occlusion of the anterior spinal artery. Cruciate paralysis and man-in-barrel-syndrome (MIBS) both are terms used to describe brachial diplegia; cruciate paralysis when caused by medullary lesions, MIBS when caused either by supratentorial or by medullary lesions. Exclusive use of the term MIBS for bilateral frontal lobe lesions, as in the original description, would provide more clarity in terminology.

Anterior Spinal Artery Syndrome↗
PubMed2002

Noninvasive monitoring of hypertensive breakthrough of cerebral autoregulation in a patient with acute ischemic stroke.

BACKGROUND AND PURPOSE: We describe the first documentation of hypertensive breakthrough of cerebral autoregulation in a patient with acute stroke with transcranial Doppler sonography. CASE DESCRIPTION: A 55-year-old patient with acute left hemispheric stroke was treated with moderate hypothermia. He died of transtentorial herniation 4 days after admission. Static cerebral autoregulation (sCA) of the unaffected hemisphere was evaluated 6 times during this period and always found to be intact. A bolus application of epinephrine resulted in a hypertensive episode (mean arterial pressure (MAP) 135 mm Hg); hypertensive breakthrough of cerebral autoregulation was evident when MAP exceeded approximately 110 mm Hg. Interestingly, no such breakthrough was evident during testing of sCA, even when MAP reached 120 mm Hg. CONCLUSIONS: Our observation suggests that (1) the pace of the MAP increase is crucial for the occurrence of a hypertensive breakthrough of the cerebral autoregulation and (2) the disturbance of cerebral autoregulation is potentially longer as previously assumed.

Blood Pressure Monitoring, Ambulatory↗
PubMed2002

Hemicraniectomy and moderate hypothermia in patients with severe ischemic stroke.

BACKGROUND AND PURPOSE: We compared the clinical course of 36 consecutive patients with severe acute ischemic stroke (more than two thirds of the middle cerebral artery territory) treated with hemicraniectomy (CE; n=17) or moderate hypothermia (MH; n=19) in terms of intracranial pressure control, mortality, and specific treatment parameters. METHODS: Over a period of 18 months, patients with severe ischemic stroke were treated with CE when the nondominant hemisphere was affected and with MH when the dominant hemisphere was affected. MH (33 degrees C) was induced with either cold blankets and fans (n=11) or endovascular cooling (n=8). Intracranial pressure was monitored invasively in all cases. RESULTS: Age, sex, cranial CT findings, level of consciousness, and time to treatment were similar between the 2 groups; significant differences were noted in National Institute of Health Stroke Scale (NIHSS) score (20 [range, 18 to 22] and 17 [range, 16 to 18] for MH and CE, respectively) but were not present when NIHSS score was corrected for aphasia (17 [range, 15 to 19] and 17 [range, 16 to 18] for MH and CE, respectively). Mortality was 12% for CE and 47% for MH; 1 patient treated with MH died as a result of treatment complications (sepsis) and 3 of intracranial pressure crises that occurred during rewarming. Duration of mechanical ventilation and of neurological intensive care unit stay did not significantly differ, but duration of catecholamine application and maximal catecholamine dosage were significantly higher in the MH group. CONCLUSIONS: In patients with severe ischemic stroke, CE results in lower mortality and lower complication rates compared with MH. Both treatment modalities, however, are associated with intensive medical treatment and a prolonged stay in the neurological intensive care unit.

Adult↗
PubMed2002

Neuroprotective effect of delayed moderate hypothermia after focal cerebral ischemia: an MRI study.

BACKGROUND AND PURPOSE: In contrast to early hypothermia, the effects of delayed hypothermia in focal cerebral ischemia have not been widely addressed. We examined the influence of delayed hypothermia on secondary ischemic injury, MRI lesion size, and neurological outcome after transient focal cerebral ischemia in a rat model. METHODS: Rats (n=30) were subjected to transient middle cerebral artery occlusion (MCAO, 120 minutes) by use of the intraluminal filament model. Animals of the treatment group (n=12) were exposed to whole-body hypothermia of 33 degrees C for 5 hours starting 3 hours after MCAO, whereas the control group (n=18) was kept at 37 degrees C throughout the whole experiment. The normothermia- and hypothermia-treated animals were investigated daily by using the Menzies neurological score. Serial MRI was performed 1, 3, and 6 hours after MCAO and on days 1, 2, 3, and 5. After the final MRI scan, the rats were euthanized, and brain slices were stained by 2,3,5-triphenyltetrazolium chloride. RESULTS: Delayed hypothermia resulted in a significant increase of survival rate and a significant improvement of the Menzies score. Moreover, a significant decrease in the extent of hyperintense volumes in T2-weighted scans and a reduction of cerebral edema as calculated from T2-weighted scans throughout the examination period were obvious. The extent of cerebral infarct volume and cerebral brain edema examined by MRI was consistent with 2,3,5-triphenyltetrazolium chloride staining. CONCLUSIONS: Our results suggest that even delayed postischemic hypothermia can reduce the extent of infarct volume and brain edema after transient focal cerebral ischemia.

Animals↗
PubMed2002

Cerebral autoregulation under moderate hypothermia in patients with acute stroke.

BACKGROUND AND PURPOSE: We undertook this study to examine the integrity of cerebral autoregulation in patients with acute ischemic stroke treated with moderate hypothermia (33 degrees C). METHODS: Fourteen patients, aged 58+/-11 years, with an acute anterior circulation infarction and National Institutes of Health Stroke Scale score >15 were evaluated. Patients received catecholamines (norepinephrine) via continuous intravenous infusion and were mechanically ventilated. Alpha-stat was used for pH maintenance. Arterial pressure (AP) and intracranial pressure (ICP) were invasively monitored. Flow velocity in the middle cerebral artery (MCA) supplying the unaffected hemisphere was continuously monitored. Instantaneous maximum flow velocity (V(max) MCA), ICP, and AP were simultaneously recorded in real time. Mean values of V(max) MCA (V(mean) MCA) and AP (MAP) were calculated over 1 minute. Static cerebral autoregulation (sCA) was calculated as sCA=(%DeltaCVR/%DeltaMAP)x100% (where %DeltaCVR is an estimate of percent change in cerebrovascular resistance). An sCA value of 0% indicates absent autoregulation, and a value of 100% indicates perfect autoregulation. Autoregulation is considered impaired when sCA values are <40%. MAP changes were produced by increasing the rate of the norepinephrine infusion. Six patients were examined under both normothermic and hypothermic conditions, while 8 were examined only under hypothermia. RESULTS: The induced MAP increase was 22+/-7 mm Hg (minimum 13, maximum 40 mm Hg). Mean sCA was 64+/-16% (minimum 40%, maximum 100%). No effect of moderate hypothermia on sCA or V(mean) MCA was evident in any of the 6 serially examined patients. Normocapnia was observed in all cases. CONCLUSIONS: sCA appears intact under moderate hypothermia with the use of alpha-stat for pH maintenance.

Acute Disease↗
PubMed2001

Cerebral vasoconstriction in vasovagal syncope: any link with symptoms? A transcranial Doppler study.

BACKGROUND: Cerebral vasoconstriction has been described previously in vasovagal syncope (VVS). This phenomenon appears paradoxical in view of the well-known decrease of systemic vascular resistances taking places during VVS. We aimed to assess (1) whether cerebral vasoconstriction in VVS is an independent paradoxical phenomenon and (2) whether cerebral vasoconstriction has any link with symptoms and/or VVS onsets. METHODS AND RESULTS: Seven young patients with recurrent VVS participated in the study. Each patient underwent monitoring of heart rate, blood pressure, cerebral blood flow velocity (by means of transcranial Doppler), end-tidal PCO(2), peripheral oximetry, respiratory rate, and tidal volumes both at rest and during head-up tilt. All the subjects experienced tilt-induced VVS. A significant increase of respiratory tidal volumes was observed in each subject >/=160 seconds before VVS. This deep breathing induced a PCO(2) decrease and, consequently, also a decrease in cerebral blood flow velocity and increase in cerebrovascular resistance (expressed by the increase of the pulsatility index). Within 40 seconds, 5 subjects started complaining of discomfort, in the absence of any significant blood pressure drop. CONCLUSIONS: Cerebral vasoconstriction is not a paradoxical phenomenon when it occurs before tilt-induced VVS but rather is only the physiological consequence of the hyperventilation-induced hypocapnia that occurs in habitual fainters. The large lag between the onset of syncope and cerebral vasoconstriction excludes the hypothesis that VVS is dependent on abnormal behavior of cerebral hemodynamics.

Adolescent↗
PubMed2001

Synthesis and comparative study on the reactivity of peptidyl-type phosphinic esters: intramolecular effects in the alkaline and acidic cleavage of methyl beta-carboxyphosphinates.

Using the phosphinic analogue of Cbz-Phe-Gly-OEt 1a as a template for this study, several phosphinic esters (2a-g) were prepared, employing an efficient method for each case. The reactivity of these derivatives under conventional deprotection conditions was studied, and the results are listed comparatively. The effect of steric hindrance as well as the contribution of neighboring groups in the rate of hydrolysis of suitably selected beta-carboxyphosphinates under acidic and alkaline deprotection conditions was examined. The results clearly demonstrate that a significant acceleration of phosphinate cleavage occurs due to the intermediacy of a five-membered, mixed anhydride-type species. This was supported by the observation that similar interactions were not observed in the case of hindered alpha-carboxyphosphinate homologous derivatives.

Carboxylic Acids↗
PubMed2001

Convenient synthesis and diversification of dehydroalaninyl phosphinic peptide analogues.

[structure: see text]. Dehydroalaninyl phosphinic dipeptide analogues were synthesized, via an efficient tandem Arbuzov addition/allylic rearrangement, in high yields. The susceptibility of the conjugate system to 1,4 nucleophilic additions was investigated. C-Elongation of the dipeptides was performed, and the efficiency of 1,4 addition to the resulting acrylamidic moiety was evaluated. Derivatization of such phosphinic templates is a powerful approach for rapid access to large number of phosphinic pseudopeptides bearing various side chains in the P1' position.

Alanine↗
PubMed2001

Discharge patterns of spontaneous activity and motor units on concentric needle electromyography.

We analyzed discharge patterns in electromyograms of 6 patients with complete nerve lesions and of 26 healthy subjects, in order to better differentiate between pathological and physiological spontaneous electromyographic (EMG) activity. Within 1639 trains of action potentials, the intervals between at least five successive discharges were measured. Discharge regularity was evaluated with three different algorithms. At 99% specificity, an abnormal discharge pattern was identified with 91 to 95% sensitivity, depending on the algorithm used. Analysis of as few as four successive interdischarge intervals allowed reliable differentiation between normal and pathological spontaneous EMG activity.

Action Potentials↗
PubMed2001

Length dependence of variables associated with temporal dispersion in human motor nerves.

Temporal dispersion in motor nerves is associated with changes of amplitude, area, duration, and Fourier spectra of compound muscle action potentials (CMAPs) when comparing responses to proximal and distal stimulation. These changes depend on the length of the nerve segment. To quantitatively assess this dependence, motor conduction studies of nerve segments of various lengths were performed in the median, ulnar, and tibial nerves of 86 test subjects, aged 4 to 73 years. Amplitude, area, duration, and spectral energy above 49 Hz of CMAPs were measured. Values after distal and proximal stimulation of each nerve segment were compared to determine amplitude decay, area decay, protraction, and high-frequency attenuation. A significant length dependence of amplitude decay was found in the tibial and ulnar nerves, of area decay in the median and ulnar nerves, and of CMAP duration in the ulnar and tibial nerves. The length dependence of the high-frequency attenuation was significant in all nerves studied. This report provides normative data for variables associated with temporal dispersion.

Action Potentials↗
PubMed2001

Activated protein C resistance and acute ischaemic stroke: relation to stroke causation and age.

OBJECTIVES: Resistance to activated protein C (APC) is the most frequent cause of thrombophilia and a well known risk factor for deep and cerebral vein thrombosis. Its causative role in ischaemic stroke is still a matter of debate. We undertook this study to determine the prevalence of APC-resistance in a cohort of consecutive patients with acute ischaemic stroke, especially with respect to patients' age and the underlying stroke causation. MATERIALS AND METHODS: 489 patients with proven ischaemic stroke were included in this study. Subtypes of stroke were classified according to the TOAST criteria, i. e. large artery artherosclerosis (LAA), small vessel occlusion (SVO), cardioembolism (CE), stroke of other etiology (SOE), and stroke of undetermined etiology (SUE). APC-resistance was determined with a functional method with high sensitivity and specificity for the factor V Leiden mutation. The results were compared with the prevalence of APC-resistance in healthy volunteers, all born in the same area. RESULTS: APC-resistance was found in 24 of 489 patients (4.9 %) and in 6 of the 112 (5.4 %) control subjects. In the stroke patients, APC-resistance was distributed as follows: LAA 6.5 % (9/138), SVO 3,9 % (4/104), CE 6.7 % (7/104), SOE 3.6 % (1/28), SUE 2.6 % (3/115). Prevalence of APC-resistance was not significantly different between young stroke patients (6-45 years) and older patients (7.7 % [5/65] versus 4.5 % [19/424]). CONCLUSIONS: Prevalence of APC-resistance is not increased in patients with ischaemic stroke. Additionally, no significant differences in the prevalence of APC-resistance are evident within the various stroke subtypes.

Acute Disease↗
PubMed2001

[Correlation of clinical and magnetic resonance imaging findings in patients with brainstem infarction].

The aim of this study was the comparison of clinical and neurological findings in 30 patients presenting with ischemic brainstem lesions. These were localized in the midbrain in 4 cases, in the medulla in 12 cases and in the pons in 11 cases, while the remaining three patients demonstrated combined lesions. Symptoms were lesions of the pyramidal tract in 77% of cases, vertigo in 57% of cases, speech disturbances in 40% of cases and gait ataxia in 37% of cases. Cranial nerve lesions were evident in 87% of patients, while 33% of patients demonstrated a Horner syndrome. Brainstem lesions were diagnosed in 22 (73%) of patients on magnetic resonance imaging, while all 30 patients had clinical signs suggestive of brainstem lesions. We conclude that neuroradiological studies can provide helpful information regarding patients with brainstem lesions, but by no means replace exact neurological examination.

Adult↗