PubMed Health⌕ Search

Biomedical subjects

P C Nijssen

Publications and source records attributed to P C Nijssen.

12 recordsLinked to original sources
PubMed2006

Coiling of truly incidental intracranial aneurysms.

BACKGROUND AND PURPOSE: The purpose of this study is to report the morbidity, mortality, and angiographic results of coiling of asymptomatic incidental aneurysms and compare the characteristics of these aneurysms with other asymptomatic incidental aneurysms that were not treated. PATIENTS AND METHODS: During a 10-year period, 97 patients without previous subarachnoid hemorrhage, presented with incidentally found intracranial aneurysms. In 48 patients, 58 aneurysms were coiled. The mean size of the 58 coiled incidental aneurysms was 10.9 mm (median, 9 mm; range, 3-40 mm). Twenty-six of 58 coiled aneurysms (44.8%) were > or = 10 mm. RESULTS: Permanent morbidity of coiling was 2.1% (1 of 48), mortality was 0%. Compared with untreated patients with incidental aneurysms, coiled patients were younger and more often had multiple aneurysms. Aneurysms of coiled patients more often had a small neck, were more often located on the carotid artery, and were less often located on the middle cerebral artery. Of 46 aneurysms with angiographic follow up, 45 were completely or near completely occluded. To obtain these results, 3 aneurysms were coiled more than once. Coiled incidental aneurysms did not rupture during a median follow-up period of 28.5 months. Mean hospital stay per patient was 2.5 days. CONCLUSION: Coiling of incidental intracranial aneurysms has a low complication rate in selected aneurysms and patients. Coiling should be the first treatment option in incidental aneurysms suitable for this technique.

Adult↗
PubMed2006

Procedural complications of coiling of ruptured intracranial aneurysms: incidence and risk factors in a consecutive series of 681 patients.

BACKGROUND AND PURPOSE: To report the incidence of procedural complications of coiling of ruptured intracranial aneurysms leading to permanent disability or death in a consecutive series of 681 patients and to identify risk factors for these events. PATIENTS AND METHODS: Between January 1995 and July 2005, 681 consecutive patients with ruptured intracranial aneurysms were treated with detachable coils. Procedural complications (aneurysm rupture or thromboembolic) of coiling leading to death or neurologic disability at the time of hospital discharge were recorded. For patients with procedural complications, odds ratios (OR) with corresponding 95% confidence intervals (CI) were calculated for the following patient and aneurysm characteristics: patient age and sex, use of a supporting balloon, aneurysm location, timing of treatment, clinical condition at the time of treatment, and aneurysm size. RESULTS: Procedural complications occurred in 40 of 681 patients (5.87%; 95% CI, 4.2% to 7.9%), leading to death in 18 patients (procedural mortality, 2.6%; 95% CI, 1.6% to 4.2%) and to disability in 22 patients (procedural morbidity, 3.2%; 95% CI, 2.0% to 4.9%). There were 8 procedural ruptures and 32 thromboembolic complications. The use of a temporary supporting balloon was the only significant risk factor (OR, 5.1; 95% CI, 2.3 to 15.3%) for the occurrence of procedural complications. CONCLUSION: Procedural complication rate of coiling of ruptured aneurysms leading to disability or death is 5.9%. In this series, the use of a temporary supporting balloon in the treatment of wide-necked aneurysms was the only risk factor for the occurrence of complications.

Adult↗
PubMed2001

Migraine with aura after intracranial endovascular procedures.

OBJECTIVE: To describe three cases of migraine (two with aura) after an intracranial endovascular procedure. Method.-Retrospective. RESULTS: One patient had an attack of migraine with prolonged aura after embolization of a dural arteriovenous fistula. Another patient had an attack of migraine with aura (and hemiparesis) after a diagnostic angiogram. The third patient already suffered from migraine with aura and had a migraine attack after embolization of an occipital arteriovenous malformation. A quadrantanopia persisted in this patient. Outcome of the other two patients was good. CONCLUSION: Intracranial endovascular procedures can induce migraine with aura. We could not identify the underlying pathophysiological mechanism, but mechanical, chemical, immunological, or hemodynamic factors could be involved.

Adult↗
PubMed2001

Rupture of intracranial aneurysms during treatment with Guglielmi detachable coils: incidence, outcome, and risk factors.

OBJECT: The aim of this study was to assess the incidence and outcome of procedure-related rupture of intracranial aneurysms in patients treated with Guglielmi detachable coils (GDCs) and to identify risk factors for this complication. METHODS: Procedure-related rupture occurred in seven of 264 treated aneurysms in 239 consecutive patients. Aneurysm size, history of previous subarachnoid hemorrhage (SAH) caused by the treated aneurysm, timing of treatment after SAH, and the use of a temporary occlusion balloon in the seven procedures in which rupture occurred were compared with the remaining 257 procedures, and these findings were correlated with data from 13 studies in the literature, in which results of 2030 aneurysm treatments were reported. CONCLUSIONS: Procedure-related rupture of intracranial aneurysms during GDC treatment occurs in 2.5% of cases and is responsible for 1% of treatment-related deaths. Risk factors are as follows: small aneurysm size, previous SAH, and probably the use of a temporary occlusion balloon.

Adult↗
PubMed2000

[Neuroradiologic intervention in two patients with cerebral sinus thrombosis].

Two patients with cerebral sinus thrombosis were successfully treated with neuroradiological intervention procedures, one with local thrombolysis and the other with mechanical thrombosuction using a hydrolyser catheter. The first patient, a 20-year-old woman, was treated with asparaginase for acute lymphatic leukaemia. She lapsed into coma with extensor posturing due to superior sagittal and right transverse sinus thrombosis. She recovered completely after local thrombolysis with 2,940,000 units urokinase, administered over a period of 40 hours. The second patient was a 29-year-old man who presented with clinical deterioration after seizures due to superior sagittal, left transverse and straight sinus thrombosis. A CT-scan demonstrated bilateral haemorrhagic cerebral infarctions. Since the risk of haemorrhage during thrombolysis with urokinase was considered to be high, mechanical thrombosuction with a hydrolyser catheter was performed. This procedure took only 4 hours. The patient recovered completely in two weeks. These cases add further evidence to the effectiveness of thrombolysis and thrombosuction in selected patients with severe cerebral sinus thrombosis.

Adult↗
PubMed2000

Carotid balloon occlusion for large and giant aneurysms: evaluation of a new test occlusion protocol.

OBJECTIVE: Validation of a new angiographic test occlusion protocol before carotid balloon occlusion in patients with carotid aneurysms. METHODS: Carotid occlusion was considered for 29 consecutive patients. From 1993 to 1995, test occlusion in four patients consisted of clinical observation for 30 minutes and during electroencephalographic registration. From 1996 onward, test occlusion in 25 patients consisted of clinical observation and angiography of collateral vessels. Permanent balloon occlusion was performed only when the cortical veins in both the occluded and the collateral vascular territories filled synchronously. RESULTS: Two of the four patients with normal clinical and electroencephalographic findings during test occlusion developed delayed hypoperfusion infarction after permanent carotid occlusion. Seventeen of 25 patients (68%) demonstrated both clinical and angiographic tolerance, and no ischemic events occurred after permanent carotid occlusion. In one patient with clinical tolerance but angiographic nontolerance, permanent carotid occlusion had to be performed, which resulted in delayed hypoperfusion infarction. In two patients with angiographic nontolerance, venous filling became synchronous after bypass surgery. Long-term clinical follow-up showed an alleviation of the symptoms of mass effect in 14 of 21 patients (67%). Magnetic resonance imaging follow-up (range, 3-70 mo) revealed a reduction in the size of the aneurysm in 19 of 21 patients (90%). CONCLUSION: Test occlusion with clinical and angiographic control is reliable, safe, and simple to perform.

Adult↗
PubMed1999

Unilateral pallidotomy in Parkinson's disease: a randomised, single-blind, multicentre trial.

BACKGROUND: The results of several cohort studies suggest that patients with advanced Parkinson's disease would benefit from unilateral pallidotomy. We have assessed the efficacy of unilateral pallidotomy in a randomised, single-blind, multicentre trial. METHODS: We enrolled 37 patients with advanced Parkinson's disease who had, despite optimum pharmacological treatment, at least one of the following symptoms: severe response fluctuations, dyskinesias, painful dystonias, or bradykinesia. Patients were randomly assigned to unilateral pallidotomy within 1 month or to pallidotomy after the primary outcome assessment (6 months later). The primary outcome was the difference between the groups in median changes on the motor examination section of the unified Parkinson's disease rating scale (UPDRS 3) score done in the off phase. Secondary outcome measures included levodopa-induced dyskinesias (dyskinesia rating scale [DRS]) and extent of disability (UPDRS 2). FINDINGS: The median UPDRS 3 off score of the pallidotomy patients improved from 47 to 32.5, whereas that of control patients slightly worsened from 52.5 to 56.5 (p<0.001). In the on phase the median DRS score improved 50% in pallidotomy patients compared with no change in controls. The UPDRS 2 off score improved with a median of 7 in the pallidotomy group. Two treated patients had major adverse effects. INTERPRETATION: Unilateral pallidotomy is an effective treatment in patients with advanced Parkinson's disease, who have an unsatisfactory response to pharmacological treatment.

Aged↗
PubMed1997

Alpha rhythms: noise, dynamics and models.

Alpha rhythms appear as sinusoidal-like oscillations in the electroencephalogram (EEG) within the frequency range 8-12 Hz that waxe and wane in a more or less irregular way. The irregularity may have various origins. It may be due to noise or the oscillations may have an intrinsic irregular character, e.g. they may be generated by chaotic processes [Jansen (1991) Quantitative analysis of electroencephalograms: is there chaos in the future? Int. J. Biomed. Comput., 27: 95-123; Pradham, N. and Dutt, D.N. (1993) A nonlinear perspective in understanding the neurodynamics of EEG. Comput. Biol. Med., 23: 425-442; Pritchard et al. (1995) Dimensional analysis of resting human EEG II: Surrogate-data testing indicates nonlinearily but not low-dimensional chaos. Psychophysiology. 32: 486]. The term noise is often used in neurophysiology with different connotations as pointed out by Bullock (1990), either meaning an unwanted signal from the point of view of the receiver of a message, or a signal with intrinsic random fluctuations, i.e. with a stochastic character. Here we consider noise in this sense, as random or quasi-random neural activity. In this overview, we concentrate on the question of whether alpha rhythms should be considered generated in neuronal networks (1) as forms of filtered noise, (2) as deterministic oscillations influenced by noise or (3) as the result of chaotic dynamics. A clear answer to this question can have theoretical value because it may lead to a general model of the generation of this important EEG signal. Such a model, of course, would be a macroscopic one, since it would primarily account for the properties of the alpha rhythms at the neuronal network level. A translation of these properties to the microscopic, i.e. neuronal, level will not be easy to achieve without more direct knowledge of the membrane and synaptic basic properties of the neurons involved. Here we consider the question formulated above by presenting some relevant experimental evidence and theoretical arguments. The consideration whether alpha rhythms may have noise or chaotic sources implies examining how and where such sources can occur in the neuronal networks of the brain. Therefore we present, first, some basic data regarding the possible origin of noise and of chaos in neuronal networks. Second, the signal analysis methods that have to be applied in order to discriminate between filtered noise activities and chaotic oscillations are introduced. Third, the implications of these signal analyses regarding the possible answer to the initial question are discussed.

Alpha Rhythm↗
PubMed1994

Familial anaplastic ependymoma: evidence of loss of chromosome 22 in tumour cells.

A family with anaplastic ependymomas, histologically verified in three cases and neuroradiologically suggested in a fourth, is presented. Two healthy brothers both had two affected sons. All four male patients were younger than 5 years at the time of diagnosis. Two boys died before the age of 3 years. Genotype analysis (with polymorphic DNA markers for chromosome 22 and interphase cytogenetic analysis) of one of the tumours showed a subpopulation of tumour cells with monosomy of (part of) chromosome 22. Non-neoplastic cells of this patient showed a normal karyotype. These findings give further evidence for the role of a tumour suppressor gene on chromosome 22 in the pathogenesis of familial ependymal tumours.

Brain Neoplasms↗
PubMed1992

Opioid-inhibited adenylyl cyclase in rat brain membranes: lack of correlation with high-affinity opioid receptor binding sites.

Opioid agonists bind to GTP-binding (G-protein)-coupled receptors to inhibit adenylyl cyclase. To explore the relationship between opioid receptor binding sites and opioid-inhibited adenylyl cyclase, membranes from rat striatum were incubated with agents that block opioid receptor binding. These agents included irreversible opioid agonists (oxymorphone-p-nitrophenylhydrazone), irreversible antagonists [naloxonazine, beta-funaltrexamine, and beta-chlornaltrexamine (beta-CNA)], and phospholipase A2. After preincubation with these agents, the same membranes were assayed for high-affinity opioid receptor binding [3H-labeled D-alanine-4-N-methylphenylalanine-5-glycine-ol-enkephalin (mu), 3H-labeled 2-D-serine-5-L-leucine-6-L-threonine enkephalin (delta), and [3H]ethylketocylazocine (EKC) sites] and opioid-inhibited adenylyl cyclase. Although most agents produced persistent blockade in binding of ligands to high-affinity mu, delta, and EKC sites, no change in opioid-inhibited adenylyl cyclase was detected. In most treated membranes, both the IC50 and the maximal inhibition of adenylyl cyclase by opioid agonists were identical to values in untreated membranes. Only beta-CNA blocked opioid-inhibited adenylyl cyclase by decreasing maximal inhibition and increasing the IC50 of opioid agonists. This effect of beta-CNA was not due to nonspecific interactions with G(i), Gs, or the catalytic unit of adenylyl cyclase, as neither guanylylimidodiphosphate-inhibited, NaF-stimulated, nor forskolin-stimulated activity was altered by beta-CNA pretreatment. Phospholipase A2 decreased opioid-inhibited adenylyl cyclase only when the enzyme was incubated with brain membranes in the presence of NaCl and GTP. These results confirm that the receptors that inhibit adenylyl cyclase in brain do not correspond to the high-affinity mu, delta, or EKC sites identified in brain by traditional binding studies.

Adenylyl Cyclase Inhibitors↗
PubMed1987

Characteristics of sodium-induced increase in opiate antagonist binding sites in rat brain membranes.

Sodium decreases agonist binding and increases antagonist binding to opiate receptor sites in brain membranes. This study characterizes in detail the 20-40% increase in [3H]naloxone binding caused by sodium. This increase in binding was specific to sodium (not mimicked by potassium or lithium) and was maximal at 10 mM NaCl. The sodium effect was reversible: washing membranes free of sodium restored binding to normal. Sodium increased Bmax, not KD, of [3H]naloxone binding. The sodium-induced increased binding was not inhibited by either N-ethylmaleimide (NEM) or phospholipase A2 at concentrations which inhibit 50-85% of normal [3H]naloxone binding. In NEM-treated membranes, the effect of sodium on increasing naloxone binding was actually increased. The regional distribution of these sodium-dependent sites were different from normal naloxone sites. These results suggest that physiological concentrations of sodium expose naloxone sites which differ in biochemical properties from naloxone sites assayed in the absence of sodium.

Animals↗