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Biomedical subjects

J Hildebrand

Publications and source records attributed to J Hildebrand.

At least 19 recordsLinked to original sources
PubMed2007

Acute confusion in patients with systemic cancer.

OBJECTIVE: To determine the incidence, the causes and the prognostic value for survival of acute confusion (delirium) in patients admitted to a general cancer hospital. PATIENTS: Hundred consecutive patients with confusion were examined; 78 had a metastatic disease, 11 had local tumor and 11 had no sign of tumor recurrence at admission. Patients with confusion represented 11.8% (95%CI: 9.7-14.2%) of admissions. Follow-up period lasted 18 months from the inclusion of the last patient. RESULTS: Structural brain lesions (SBL) were mostly metastatic and caused confusion in 36 patients. 57 patients had a toxic or metabolic encephalopathy (TME). The cause remained unexplained in 6 cases, and in one patient the final diagnosis was psychotic state. Most patients with TME had more than one abnormality which could cause confusion. Confusion was reversible in 34 patients, and the odds for its regression was 3-fold higher in patients with TME (P = 0.02). Survival was significantly shorter (P = 0.02) in patients with SBL (median: 3 weeks) than in patients with TME (median: 8 weeks). However, the survival was significantly longer (P = 0.007) in patients with only one toxic or metabolic disorder (median: 20.5 weeks) than in patients with multiple changes (median: 5 weeks). CONCLUSION: Confusion is common in general cancer population. TME is the leading etiology and it is due to multiple causes in most patients. SBL causes confusion in one third of the patients. Patients with TME have a greater chance to recover, and survive longer especially if they have only one toxic or metabolic change.

Adult↗
PubMed2006

Clinical and molecular cytogenetic characterisation of a newly recognised microdeletion syndrome involving 2p15-16.1.

BACKGROUND: During whole genome microarray-based comparative genomic hybridisation (array CGH) screening of subjects with idiopathic intellectual disability, we identified two unrelated individuals with a similar de novo interstitial microdeletion at 2p15-2p16.1. Both individuals share a similar clinical phenotype including moderate to severe intellectual disability, autism/autistic features, microcephaly, structural brain anomalies including cortical dysplasia/pachygyria, renal anomalies (multicystic kidney, hydronephrosis), digital camptodactyly, visual impairment, strabismus, neuromotor deficits, communication and attention impairments, and a distinctive pattern of craniofacial features. Dysmorphic craniofacial features include progressive microcephaly, flat occiput, widened inner canthal distance, small palpebral fissures, ptosis, long and straight eyelashes, broad and high nasal root extending to a widened, prominent nasal tip with elongated, smooth philtrum, rounding of the upper vermillion border and everted lower lips. METHODS: Clinical assessments, and cytogenetic, array CGH and fluorescence in situ hybridisation (FISH) analyses were performed. RESULTS: The microdeletions discovered in each individual measured 4.5 Mb and 5.7 Mb, spanning the chromosome 2p region from 57.2 to 61.7 Mb and from 56 to 61.7 Mb, respectively. Each deleted clone in this range demonstrated a dosage reduction from two to one copy in each proband except for clone RP11-79K21, which was present in three copies in each proband and in four copies in their respective parents (two per each chromosome 2 homologue). DISCUSSION: The common constellation of features found in the two affected subjects indicates that they have a newly recognised microdeletion syndrome involving haploinsufficiency of one or more genes deleted within at least a 4.5-Mb segment of the 2p15-16.1 region.

Abnormalities, Multiple↗
PubMed2006

EFNS Guidelines on diagnosis and treatment of brain metastases: report of an EFNS Task Force.

The objectives have been to establish evidence-based guidelines and identify controversies regarding the management of patients with brain metastases. The collection of scientific data was obtained by consulting the Cochrane Library, bibliographic databases, overview papers and previous guidelines from scientific societies and organizations. A tissue diagnosis is necessary when the primary tumor is unknown or the aspect on computed tomography/magnetic resonance imaging is atypical. Dexamethasone is the corticosteroid of choice for cerebral edema. Anticonvulsants should not be prescribed prophylactically. Surgery should be considered in patients with up to three brain metastases, being effective in prolonging survival when the systemic disease is absent/controlled and the performance status is high. Stereotactic radiosurgery should be considered in patients with metastases of 3-3.5 cm of maximum diameter. Whole-brain radiotherapy (WBRT) after surgery or radiosurgery is debated: in case of absent/controlled systemic cancer and Karnofsky Performance score of 70 or more, one can either withhold initial WBRT or deliver early WBRT with conventional fractionation to avoid late neurotoxicity. WBRT alone is the treatment of choice for patients with single or multiple brain metastases not amenable to surgery or radiosurgery. Chemotherapy may be the initial treatment for patients with brain metastases from chemosensitive tumors.

Advisory Committees↗
PubMed2004

Tegaserod (HTF 919) stimulates gut motility in normal horses.

REASONS FOR PERFORMING STUDY: It has been shown that the selective 5-HT4 receptor agonist tegaserod induces an increase in frequency and amplitude of contractions in isolated muscle preparations of equine ileum and pelvic flexure. OBJECTIVES: To investigate the effects of tegaserod on gut motility and transit of spheres in normal horses. METHODS: Six mature Freiberger horses were kept under standardised conditions. Effects of tegaserod (0.02 mg/kg bwt i.v. b.i.d. for 2 days) or vehicle on intestinal transit of barium-filled spheres, defaecation and gut sounds were studied in a cross-over design. Spheres were given via stomach tube prior to the first dosing of tegaserod or vehicle. Faeces were collected every 3 h and spheres eliminated were identified radiologically in the faeces. RESULTS: Tegaserod significantly accelerated the gastrointestinal (GI) transit time of spheres and increased the frequency of defaecation and scores of gut sounds compared to vehicle. The compound was well tolerated; no effects on behaviour, body temperature, heart rate, respiratory rate and clinical laboratory data were observed. CONCLUSIONS: Tegaserod efficaciously stimulated motility and accelerate GI transit in healthy horses. POTENTIAL RELEVANCE: Tegaserod may offer therapeutic potential in horses suffering from impaction or paralytic ileus.

Animals↗
PubMed2003

Chemotherapy alone as initial treatment for primary CNS lymphoma in patients older than 60 years: a multicenter phase II study (26952) of the European Organization for Research and Treatment of Cancer Brain Tumor Group.

PURPOSE: To assess the efficacy and toxicity of chemotherapy alone in patients older than 60 years with primary CNS lymphoma. PATIENTS AND METHODS: Fifty patients with a median age of 72 years and a median Karnofsky performance score (KPS) of 50 were eligible for this multicenter phase II study. The protocol consisted of high-dose methotrexate (MTX), lomustine, procarbazine, methylprednisolone, and intrathecal chemotherapy with MTX and cytarabine. The patients received one induction cycle; if objective response was achieved, five additional maintenance cycles were administered every 6 weeks. The median follow-up of patients was 3 years. RESULTS: Twenty four patients (48%) achieved an objective response (compete response [CR], 42%; partial response, 6%), with a median duration of CR of 27 months (range, 3 to 47+ months). Overall median survival time was 14.3 months, and 1-year progression-free survival was 40% (95% confidence interval [CI], 26% to 53%). Myelosuppression was the most frequent side effect, with grade 3 to 4 neutropenia in 19% of patients. One patient died during chemotherapy, as a result of pulmonary embolism. Most patients improved or preserved their cognitive functions (47% and 45% of the patients, respectively) and KPS (36% and 52% of the patients, respectively) until relapse, whereas cognitive and KPS decline attributed to delayed treatment neurotoxicity occurred in 8% and 12% patients, respectively. CONCLUSION: In the elderly, this chemotherapy regimen compares favorably with radiotherapy (RT) alone and reduces considerably the risk of delayed neurotoxicity associated with combined chemoradiotherapy. Chemotherapy alone is an appropriate strategy in older patients to delay or avoid RT.

Age Factors↗
PubMed2003

Effects of the oral form of ondansetron on cerebellar dysfunction. A multi-center double-blind study.

The aim of this study was to assess the efficacy and the safety of ondansetron administered orally in patients with a cerebellar disorder. The study was a randomised, multi-center, double-blind trial. The patients were randomised either to oral ondansetron 8 mg or to placebo twice daily for seven days. Cerebellar dysfunction was quantified before and after treatment using the International Cooperative Ataxia Rating Scale (ICARS). We performed a global analysis (total scores), we analysed by subscores (4 subscores: oculomotor, speech, kinetic, postural) and subgroups (4 subgroups: Cerebellar Cortical Atrophy (CCA), Multiple Systemic Atrophy (MSA), Familial Cerebellar Degeneration (FCD) and miscellaneous cerebellar disorders), and we also performed an analysis by individual test items. We investigated whether ondansetron and placebo had different effects upon ICARS total scores and subscores in the 4 subgroups considered together or separately. For p values < 0.05, we subsequently applied the Mann-Whitney test to compare ondansetron and placebo effect for each individual item. We evaluated 45 of the 46 patients included. No effect was found in global analysis. We found no difference in the analysis of the ICARS subscores. Concerning the individual test items, there was a significant difference between the placebo and ondansetron for the finger-to-nose test (p = 0.049), the Heel-to-Knee test (HK); (p = 0.03), the Body Sway Eyes Closed (p = 0.017) and the Body Sway Eyes Open (BSEO); (p = 0.014). There was no significant difference for tremor in upper limbs (p = 0.32) or for gait (p = 0.49). The Mann-Whitney test showed a greater effect of ondansetron than placebo for BSEO in miscellaneous disorders (p = 0.013) and for HK in FCD (p = 0.036), but ondansetron was deleterious for HK in CCA (p = 0.019). Our study showed no effect of oral ondansetron on global cerebellar dysfunction. The analysis by subgroups showed that the oral form of ondansetron (a) is deleterious for coordination in patients with CCA, (b) has no effect upon tremor in upper limbs, and (c) has a mild effect upon posture and coordination in lower limbs in some subgroups of ataxic diseases.

Administration, Oral↗
PubMed2003

Chronic meningitis: still a diagnostic challenge.

Chronic meningitis is characterized by a progressive, subacute onset of lepomeningeal disease and persisting cerebrospinal fluid (CSF) abnormalities such as elevated protein level and pleocytosis for at least one month. The array of aetiologies is very wide comprising non-infectious (carcinomatous, systemic disease, toxic) and infectious (classic and opportunistic pathogens). The evaluation encompasses a careful history, complete physical examination and laboratory tests. The specific diagnosis may remain a challenge in some cases. Algorithms for the differential diagnosis are provided for both immunocompetent and immunocompromised patients.

Chronic Disease↗
PubMed2002

[Drug treatment of epilepsy: update].

Medical treatment of epilepsy has evolved during the last ten years. The "Epileptic Syndrome Classification" established in 1989 and new antiepileptic drugs account for these changes. This article recalls the principal rules of medical treatment of epilepsy and reviews new antiepileptic drugs available in Belgium.

Anticonvulsants↗
PubMed1999

Cerebellar ataxia following whooping cough.

Bordetella pertussis (BP), the agent of whooping cough, has not been recognized so far as a cause of permanent cerebellar ataxia in human. We describe three patients who developed a disabling and permanent cerebellar syndrome soon after whooping cough. In two patients, diagnosis of BP infection was confirmed by culture of nasopharyngeal secretions. The infection occurred between the age of 13 and 15 years, with neurological symptoms beginning after a delay varying from 3 weeks to 3 months. In our three patients, the cerebellar syndrome was characterized by dysmetria of ocular saccades, scanning speech and ataxic gait. Brain MRI demonstrated a pancerebellar atrophy. The pathogenesis of this cerebellar degeneration is not established. Experimental studies have demonstrated that the cerebellum is particularly vulnerable to lymphocytosis-promoting factor (LPF), one of the exotoxins from BP. The mechanism of this toxicity might be a marked increase in the cellular levels of 3',5'cyclic guanosine monophosphate (cGMP). Since whooping cough is a bacterial exotoxin-mediated disease, this is the first report of a cerebellar syndrome triggered by a bacterial exotoxin.

Adult↗
PubMed1998

Different types of cerebellar hypometria associated with a distinct topography of the lesion in cerebellum.

We recorded ballistic wrist flexion movements in fifteen cerebellar patients exhibiting hypometria. The movement and the associated agonist and antagonist EMG activities were analysed. On the basis of the topography of the cerebellar lesion, our patients were divided into three groups. In the first group including five patients, lesions involved the efferent dentato-thalamo-cortical pathway and hypometria was associated with an imbalance between the rate of rise of the agonist EMG activity and the rate of rise of the antagonist EMG activity. In the three patients of group II, lesions were located at the level of the middle cerebellar peduncle, disrupting the crossed ponto-cerebellar projections. In these patients, the intensity of the agonist EMG activity was reduced and the duration of the antagonist EMG activity was increased. In the third group including seven patients presenting either a diffuse cerebellar atrophy or a stroke involving a large parenchymatous area, the agonist-antagonist EMG pattern showed a prolongation of the duration of the antagonist burst. Our results show that discrete mechanisms of cerebellar hypometria are associated with different anatomical lesions.

Adult↗
PubMed1998

Shift from hypermetria to hypometria in an aberrant recovery following cerebellar infarction.

Cerebellar hypermetria, a classical sign designating the overshoot when the patient attempts to reach rapidly an aimed target, is associated with an imbalance between timing and/or intensity of agonist and antagonist EMG activities. Recovery of hypermetria following a cerebellar ischemia or hemorrhage has been demonstrated to take place in a multistage process, but aberrant recovery following a cerebellar stroke has not been described previously. We report an 85-year-old woman presenting an abnormal recovery following a cerebellar infarction. We identified three successive stages. At stage 1, fast wrist flexion movements were severely hypermetric and associated with three EMG defects: a delayed onset latency of antagonist EMG activity, a reduction of intensity of the agonist EMG activity and a depression of intensity of antagonist EMG activity. At stage 2, movements were characterized by terminal oscillations around the target and the onset latency of the antagonist activity had returned to normal. At stage 3, movements were markedly hypometric, the intensity of the antagonist EMG activity had returned to normal, while the intensity of the agonist EMG activity remained abnormally low. This case illustrates an abnormal reprogramming of the EMG triphasic pattern, resulting in the shift from severe hypermetria to severe hypometria.

Aged↗
PubMed1998

Asymmetry of basal ganglia glucose metabolism and dopa responsiveness in parkinsonism.

We investigated, by positron emission tomography (PET) with [18F]fluoro-2-deoxy-d-glucose (FDG) (FDG-PET), brain glucose metabolism in 19 patients with parkinsonian features. We compared local pattern of FDG uptake and asymmetry indexes in patients with therapeutic response to levodopa (L-dopa) (group 1, presumed Parkinson's disease, n = 9) and patients without L-dopa therapeutic response (group 2, presumed striatonigral degeneration, n = 10). Limb dystonia was present in 11% of patients in group 1 and in 40% of patients in group 2. Asymmetry in basal ganglia metabolism was distributed differently in the two groups (analysis of variance, p < 0.04). In superior and inferior putamen, superior and middle caudate, ventral striatum, and inferior thalamus, relative reduction in metabolism on the side contralateral to predominant parkinsonian signs was associated with L-dopa unresponsiveness. On the contrary, in middle caudate, ventral striatum, and inferior thalamus, a relative increase in metabolism on the side contralateral to the predominant side, parkinsonian signs were found in L-dopa-responsive patients. Our FDG-PET study using simple statistical procedures demonstrates inverse asymmetry of basal ganglia glucose metabolism in parkinsonian patients grouped on the sole basis of L-dopa responsiveness.

Adult↗
PubMed1998

Response of recurrent glioblastoma and anaplastic astrocytoma to dibromodulcitol, BCNU and procarbazine--a phase-II study.

Twenty six (17 males) patients with glioblastoma (GBL), median age 55 years, median Karnofsky Index (KI) 70/100, and 11 patients (9 males) with anaplastic astrocytoma (AA), median age 56 years, median KI 70/100 were treated at recurrence with dibromodulcitol (DBD) 1400 mg/m2 on day 1, BCNU 150 mg/m2 on day 2, and procarbazine (PCZ) 150 mg/day on days 1 to 15. The course was repeated every 4 weeks, but was delayed or decreased by 25% according to hematological toxicity. Response to treatment was evaluated by the criteria of MacDonald et al. (J Clin Oncol 1990; 8: 1277-1280). All GBL-patients were followed until death. One patient with complete response (CR) survived one year, and 2 patients with partial response (PR) survived 1 and 3 years. Ten patients who stabilized (SD) survived 7.5 months, and 13 patients who progressed under chemotherapy had a median survival of 3.5 months. In AA-group 3 patients were alive at the time of the analyses. Six patients: 1 CR and 5 PR survived 6 to 40+ months. Two patients with SD survived 4 and 14 months. Three patients with progressive disease had a mean survived of less than 3 months. The response rate of 55% in AA was significantly higher (p = 0.011) than the 12% response rate seen in GBL. We conclude that the regimen tested appears particularly promising in AA. The results in GBL are comparable to those obtained with a single nitrosourea, despite an increased but reversible toxicity.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1998

Effects of TRH on ballistic wrist movements in cerebellar cortical atrophy: improvement of two genuine deficiencies but not of the major one.

Thyrotropin-releasing hormone (TRH) has been claimed to improve cerebellar ataxia in patients with idiopathic sporadic cerebellar cortical atrophy (CCA). We analysed the effects of intravenous administration of TRH (1 mg) in ballistic wrist flexions movements in 10 healthy subjects and in eight patients with CCA. The associated agonist and antagonist electromyographic (EMG) activities were recorded. In healthy subjects, TRH did modify neither the movement amplitudes, nor the intensity of the agonist and antagonist EMG activities. Before TRH administration, patients with CCA exhibited a hypermetria which was associated with a delayed onset of the antagonist activity. Moreover, the intensity of EMG activity in both the agonist and the antagonist muscles were reduced. After TRH, the hypermetria and the delayed onset latencies of the antagonist EMG activities were unchanged but the intensity of both the agonist and the antagonist EMG activities increased. TRH could increase the magnitude of agonist and antagonist EMG activities in patients with CCA by exerting an excitatory effect directly on motoneurons or by modulating at the supraspinal level the central commands to agonist and antagonist motoneuron pools. Copyright Rapid Science Ltd

Journal Article↗