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Biomedical subjects

M Gille

Publications and source records attributed to M Gille.

At least 19 recordsLinked to original sources
PubMed2006

[Acute pain management in proximal femoral fractures: femoral nerve block (catheter technique) vs. systemic pain therapy using a clinic internal organisation model].

BACKGROUND: The aim of this study was to compare safety and efficacy of catheter-mediated femoral nerve block analgesia with systemic pain therapy in patients with proximal femoral fractures in the pre-operative and post-operative setting using a protocol for coordinating pain management. METHODS: In a prospective randomised trial of patients attending the emergency department, 100 individuals were selected with a clinically diagnosed proximal femoral fracture. Patients were divided into two equal groups A and B. Group A (n=50) received a catheter-mediated femoral nerve block with 1% prilocaine (40 ml) and post-operatively 0.2% ropivacaine (30 ml) 6 hourly. Group B (n=50) initially received intravenous metamizol (1 g) and a fixed combination of oral tilidine (100 mg) + naloxone (8 mg). Patients aged 90 years or more received a reduced dose (tilidine 75 mg + naloxone 6 mg). In the post-operative period regular oral ibuprofen (400 mg, 8 hourly) in addition to oral tilidine (50 mg) + naloxone (4 mg) was given as required for break through pain. Pain intensity was measured using a verbal rating scale (VRS) from 1 to 5: pain free (=1), mild pain (=2), moderate pain (=3), severe pain (=4), excruciating pain (=5). Pain scores were recorded at rest (R), during passive anteflection (30 degrees) of the hip (PA) on arrival and at 15 and 30 min after initial administration of analgesia. Thereafter, recordings were made 4 times a day up to the third post-operative day. RESULTS: Pain scores were comparable for both groups on admission (VRS in R 2.50 vs. 2.46; VRS during PA 4.30 vs. 4.34). Significant pain relief was achieved in both groups following initial administration of analgesia, but the total pain scores in group A were significantly lower than in group B (VRS in R 1.22 vs. 1.58, p<0.01 and VRS during PA 2.66 vs. 3.26; p<0.001). No difference was noted between the two groups during the first 3 post-operative days. No severe complications occurred as a result of analgesia, however, the catheter was dislodged in 20% of patients in group A resulting in the need for systemically administered analgesia. CONCLUSION: All patients presenting with proximal femoral fractures should receive adequate analgesia within the emergency department even prior to radiographic imaging. Femoral nerve block should be considered as the method of choice. The insertion of a femoral nerve block catheter has the dual advantage of early analgesia permitting repeated clinical examination in addition to continued post-operative pain management. The cumbersome logistics inherent in this technique within the clinical setting limits its practical application. An initial single-shot regional nerve block followed by a systemic post-operative analgesia protocol was considered an appropriate alternative. The execution of safe, consistent and appropriate regional nerve block anaesthesia is reliant on formal guidelines and protocols as agreed by the multidisciplinary teams involved with patient-directed pain management and good clinical practice.

Acute Disease↗
PubMed2006

[Wernicke's encephalopathy associated with chronic disulfiram intoxication].

INTRODUCTION: We report the case of a patient with an unusual association of Wernicke encephalopathy and chronic disulfiram intoxication. CASE REPORT: A 41-year-old man presented with progressive frontal decline and akineto-rigid parkinsonism under chronic disulfiram therapy. He also developed acute confusion with ataxia, blepharospasm, and supranuclear ophthalmoplegia following a severe malnutrition due to refusal of food intake. Brain MRI revealed symmetrical and reversible hyperintense lesions on T2 and FLAIR in the posterior putaminal regions, dorso-medial thalamic and subthalamic nuclei, the periaqueducal gray matter, the cerebellar peduncles, and the pontine tegmentum. A slow partial clinical recovery with persistent frontal syndrome was observed after discontinuation of disulfiram and parenteral administration of thiamine. DISCUSSION: The symmetry and reversibility of the MRI lesions in the basal ganglia and brain stem were suggestive of a deficiency, a toxic or a metabolic neurological disease. The dorso-medial thalamo-subthalamic and brainstem localizations, as well as their occurrence in a state of malnutrition, were consistent with Wernicke encephalopathy. Moreover, chronic disulfiram intoxication might explain the frontal syndrome and the akineto-rigid parkinsonism, associated with MRI putaminal lesions. Similar MRI lesions have been described in the so-called "energy deprivation syndromes", which are toxic, genetic or nutritional disorders that disrupt enzymes involved in energy generating metabolic pathways such as glycolysis and pyruvate oxidation.

Adult↗
PubMed2005

The scoliosis (sco) mouse: a new allele of Pax1.

We describe the spontaneous mutant mouse scoliosis (sco) that carries a new allele of Pax1 (un-i, undulated intermediate). The Pax1(un-i) allele is lacking the 5'-flanking region and exon 1 to 4 which is mapped to nt -2636 to -640 and -272 to 4271 of the Pax1 gene. Homozygous mice show a mild form of the known phenotypes of other Pax1 mutants. Adult mice have a lumbar scoliosis and kinky tails. In homozygous embryos the skeleton ossifies early, ossification centers of the vertebral bodies are fused with the ossification centers of the pedicles. Neural arches and spinous processes are underdeveloped but the pedicles and transverse processes are overdeveloped which is in contrast to other Pax1 mutants. In the scapula, the acromion is missing and the deltoid tuberosity of the proximal humerus is shortened and thickened. Among the inner organs the thymus development is affected. In late embryos, the thymus is small and thymocyte numbers are reduced. T-cell development from CD4- and CD8- double negative (DN) to CD4+ and CD8+ double positive (DP) is decelerated. The percentage of CD90+ cells is also reduced but in contrast to other Pax1 mutants no alteration of the expression level of the CD90 (Thy-1) could be found.

Animals↗
PubMed2004

[Chorea-athetosis in the anti-Hu syndrome].

INTRODUCTION: Paraneoplastic choreo-athetoses are rare. We report a case of anti-Hu syndrome with choreo-athetosis. CASE REPORT: A 48-year-old woman developed a small-cell lung carcinoma revealed by an anti-Hu syndrome. The neurological features included choreo-athetosis predominating in the upper limbs, chronic sensorimotor axonal polyneuropathy, and opsoclonus. The cerebrospinal fluid was acellular and contained several oligoclonal IgG bands, not found in the corresponding serum. Magnetic resonance imaging revealed bilateral high-intensity lesions on T2/FLAIR sequence in the corona radiata. Moderate transitory improvement of the paraneoplastic neurological syndrome was observed after several carboplatin-etoposid cycles. CONCLUSION: A paraneoplastic origin must be considered in all cases of unexplained choreo-athetosis. Paraneoplastic choreo-athetosis is most often associated with other neurological symptoms. The most frequent associated tumor is a small-cell lung carcinoma with anti-CRMP5 and/or anti-Hu antibodies. Our patient developed paraneoplastic choreo-athetosis related to an anti-Hu syndrome in the absence of anti-CRMP5/CV2 antibodies. Paraneoplastic choreo-athetosis might result from a central lesion, and/or from proprioceptive deafferentation subsequent to peripheral neuropathy.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed2002

[Fulminant thrombotic thrombocytopenic purpura in the course of ciprofloxacin therapy].

We report on a 43-year-old woman who developed a fulminant thrombotic thrombocytopenic purpura (TTP) in the early course of an oral ciprofloxacin therapy. An acute bacterial meningo-encephalitis with disseminated intravascular coagulation was first suspected. She also presented with haemolytic anaemia and a severe thrombocytopenia. The lumbar puncture was delayed and only performed after platelets transfusions. CSF examination ruled out meningo-encephalitis. A diagnosis of TTP was made and she was given plasma exchanges. However, her neurological status worsened and the cranial CT revealed a subarachnoidal hemorrhage in left sylvian valley with diffuse oedema predominating in the left cerebral hemisphere and multiple ischemic lacunes. She died four days after admission.

Adult↗
PubMed2000

[Thoracic myelopathy revealing a chronic ossificans arachnoiditis of the thoraco-lumbar spinal cord].

We report a case of chronic spinal, ossificans, thoraco-lumbar arachnoiditis, associated with an arachnoidal cyst at the level of TH7, and revealed by a rapidly progressive thoracic myelopathy. Two years ago, he had presented with a spinal intrathecal haemorrhage of unknown etiology. There was no evidence of spinal traumatism, arterial hypertension or coagulation disorder. The finding of several small cysts and angiomas in the liver of this patient lead us to suspect an associated spinal vascular malformation, not detected on the spinal magnetic resonance imaging. A partial neurologic improvement was observed after laminectomy and cysto-peritoneal derivation.

Aged↗
PubMed1998

Neurological complications of intravenous immunoglobulin (IVIg) therapy: an illustrative case of acute encephalopathy following IVIg therapy and a review of the literature.

We report the case of a 73-year-old man who developed an acute encephalopathy during IVIg therapy for AIDP. The signs and symptoms of the encephalopathy completely resolved after discontinuation of the treatment. We also reviewed the literature over the major neurological complications of IVIg therapy, including aseptic meningitis, cerebral infarction, and acute encephalopathy. About 30 cases of aseptic meningitis are reported. They are probably related to an immunoallergic reaction, caused by the entry of the exogenous IgG into the CSF compartment. CSF examinations usually show a neutrophilic or a mixed pleocytosis. Three cases of cerebral infarction and 2 patients with acute encephalopathy, following IVIg therapy, were also reported in the literature. Cerebral vasospasm, cerebral vasculitis, and/or serum hyperviscosity may be implicated in the pathogenesis of these neurological complications. There is a clinical similarity between these IVIg-related encephalopathy and the "reversible posterior leukoencephalopathy syndrome", described by Hinchey et al., 1996.

Acute Disease↗
PubMed1997

[Acute encephalomyopathy and persistent cerebellar syndrome after lithium salt and haloperidol poisoning].

A 44-year-old maniacodepressive woman developed acute encephalopathy due to the association of lithium carbonate and haloperidol. She was treated with lithium salts for many years and the serum level of lithium was within the therapeutic range. The encephalopathy was worsened by hyperthermia, dehydration, and reintroduction of haloperidol, 5 days after the first discontinuation of the neuroleptic. The clinical features were characterized by a persistent cerebellar syndrome, more than one year after the interruption of these medications.

Acute Disease↗
PubMed1997

[Folic acid deficiency with leukoencephalopathy and chronic axonal neuropathy of sensory predominance].

A 44-year-old, alcoholic, woman developed a prolonged folate deficiency with a chronic predominantly axonal sensory polyneuropathy. The cerebral CT and MRI revealed a diffuse, clinically asymptomatic, leukoencephalopathy. A partial improvement of the neurological symptoms was observed after two months of oral administration of folate. Neurological complications of folate deficiency are rare and similar to those observed in cobalamin deficiency. Both cobalamin and folate deficiencies may interfere with the synthesis of the central myelin. This case report illustrates the possibility to observe a leukoencephalopathy due to folate deficiency, in association with the classical polyneuropathies and/or subacute combined degenerations of the spinal cord.

Adult↗
PubMed1996

Delayed-onset hemidystonia and chorea following contralateral infarction of the posterolateral thalamus. A case report.

A 68 year-old man developed progressive hemidystonia and chorea 8 months after a contralateral thalamic stroke. The neurological examination also showed a right pyramidal syndrome without hemiparesis, a right horizontal sectoranopia, and a right hemihypesthesia for all sensory modalities. The MRI revealed infarctions in the left medial temporo-occipital lobes and left posterolateral thalamus, corresponding to the vascular territories of both the thalamo-geniculate and posterolateral choroidal arterial pedicles. The thalamic lesion involved the pulvinar, the lateral geniculate body, and the ventro-postero-lateral, dorso-lateral, posterolateral, and dorso-medial nuclei, but apparently did not extent to the ventrolateral thalamic nucleus, and the subthalamic and midbrain regions. Thalamic and striatopallidal dystonia have not a common pathophysiological mechanism. The involvement of the pulvinar nucleus and of the strategic crossing of proprioceptive, cerebellar, pyramidal, and subthalamic pathways may play a role in the genesis of the posterolateral thalamic dystonia.

Aged↗
PubMed1994

[Cerebral cysticercosis treated by albendazole: development of cerebral magnetic resonance imaging].

A 36-year-old Indian man presented with a generalized tonic-clonic seizure. The diagnosis of neurocysticercosis was suspected by the presence of multiple cystic and nodular cerebral lesions on MRI, and was confirmed by serological studies (ELISA). He was treated with albendazole during one week at the daily dose of 15 mg/kg. This case illustrates the advantage of MRI over CT for the detection and the therapeutical follow-up of neurocysticercosis. Moreover, the MRI findings can be correlated to the anatomical stage of neurocysticercosis, proposed by Escobar (1983); four stages are described: I = vesicular stage (living larvae), II = vesicular colloidal stage (degenerating larvae), III and IV, granular nodular and nodular calcified inactive stages respectively.

Adult↗
PubMed1994

[Agenesis of the corpus callosum, heterotopia of the gray cortex and interhemispheric cyst. Late radiologic diagnosis in an asymptomatic adult].

Agenesis of the corpus callosum may occur as an isolated finding; most often, it is present in association with other cerebral malformations such as cortical heterotopias. Computerized tomography and magnetic resonance imaging are methods of choice to detect these cerebral prenatal abnormalities, especially asymptomatic forms. We report the case of an asymptomatic young adult with complete callosal agenesis, cortical heterotopia and interhemispheric cyst, on CT and MR imaging.

Adult↗