Paraclinical Explorations Research Articles

Vers une nouvelle définition de la conversion hystérique

The diagnosis of conversion hysteria is difficult. On the one hand, the elimination of a somatic pathology comes up against the sensitivity limits of paraclinical explorations and on the other hand, a positive psychopathological explanation is far from being systematically found when no organicity is retained to explain the symptoms. In this work, we will progress from a Freudian conception of the conversion as a hieroglyphic inscription on the body of an unconscious decipherable conflict, to a modern vision of conversion disorders which integrates the results of recent functional cerebral neuroimaging studies. If the representation of the action at cortex level seems to be conserved in the conversion paralyses, the blocking of the gesture occurs later at an execution stage whereas hyperactivity of the medial frontal region seems to inhibit the action of the motor cortex via the influence of limbic afferents. In addition to a psychogenic origin, the conversion can also be defined as a functional paralysis of a neuronal zone which is the place of abnormal cerebral activity, potentially reversible pathological activity. All these recent data question the evolution of the definition of conversion disorders. At a time when the clinical perception was the main means of investigating illnesses, Freud had the intelligence to differentiate conversion and simulation: modern neurology has proved him right as the images confirm that conversion and simulation involve distinct cerebral mechanisms. Furthermore, the implication of similar functional neuropathological mechanisms as biological supports of dissociative and conversion disorder has restored the Freudian unity of hysteria, through a detour into neuroscience.

Rational management of intracranial hypertension

The treatment of intracranial hypertension depends on the type of intracranial hypertension and on the developmental stage of the illness. The treatment is first of all an etiologic one in order to remove the cause that has caused the intracranial pressure increase; simultaneously, there is an attempt to stop the pathogenic mechanisms that impact on the nervous structures, and a symptomatic treatment is applied in order to reduce the intensity of the clinical syndrome. The term of etiologic treatment refers to the etiology of the intracranial hypertension, that is to the immediate cause that generates the intracranial pressure increase: for instance, in the case of a cerebral metastasis leading to ICH, the name of etiologic treatment is given to the action of metastasis extirpation, and it has no connection to the etiology and the therapy of the original neoplasia (1, 2, 3, 4, 15). The intracranial hypertension treatment can be complex by combining three therapeutic methods used concomitantly or successively, or only the pathogenic therapy and the symptomatic one are used, depending on the clinical stage and the paraclinical explorations. The type of intracranial hypertension establishes the treatment that must be applied: 1. the treatment is etiologic in: expansive intracranial processes: cerebral tumors, intracranial hematomas, cerebral abscesses, hydatid cyst, etc., in the case of parenchymatous intracranial hypertension, hypertensive encephalopathy in the case of vascular intracranial hypertension, thrombosis of intracranial vessels, venous or arterial, in the case of vascular intracranial hypertension, CSF circulation disorders due to the existence of a ventricular or paraventricular tumor with the occurrence of an obstructive hydrocephalus, CSF resorption disorders in acute meningitis. 2. the pathogenic treatment is applied in: the ICH cases with known etiology, which are mentioned above, in order to stop the development of the pathogenic mechanisms that have already started, the parenchymatous intracranial hypertension due to posttraumatic brain edema, hypoxic brain edema caused by secondary posttraumatic cerebral ischemia or in the case of sub-arachnoid hemorrhage, general intoxications with neurotoxins (endogenous or exogenous), etc. the vascular intracranial hypertension due to cerebral venous thrombosis, thrombosis of superior sagittal sinus with a decrease in the venous drainage and the blockage of the CSF absorption, or in the case of the secondary ischemic brain edema

Causes of developmental delay in children of 5 to 72 months old at the child neurology unit of Yaounde Gynaeco-Obstetric and Paediatric Hospital (Cameroon)

Background: According to the World Health Organization, about 5% of children world-wide of 14-year-old and under have a moderate to severe developmental disability, and up to 15% of children under 5-year-old are developmentally delayed. Purpose: To determine the prevalence, socio-demographic profile, aetiologies, and the clinical presentation of developmental delay in children less than 6-year-old at the child neurology unit in a university-affiliated hospital in Yaounde. Materials and methods: It was a crosssectional descriptive study carried out in Yaounde Gynaeco-Obstetric and Paediatric Hospital (Cameroon) from August to December 2012. Children aged between 5 - 72 months with a developmental quotient less than 70 were enrolled. Developmental delay (DD) was diagnosed and classified using the Denver developmental screening test (DDST). Data concerning the child (age, gender, severity of DD), the mother (age, age at conception, educational level, marital status), history of pregnancy and delivery, perinatal and postnatal events, results of para-clinical explorations (EEG, CT-scan, genetic tests), the severity of DD and the probable or demonstrate cause of DD were recorded on a standardized questionnaire. The chisquare test was used to compare variables. Results: During the study period, 2171 children aged 5 - 72 months consulted the paediatric department of the hospital, 296 were examined at the child neurology unit of which 153 had a developmental quotient less than 70, giving a hospital prevalence of 7.0% and a prevalence of 51.7% at the child neurology unit. The mean age was 26.6 ± 18.0 months and there were 56% males. The main reason for consulting was tonus disorder (43.8%) and the developmental area of parental concern was the motor domain (90.2%). Regarding the clinical presentation, 75.2% of our population were children with cerebral palsy. DD was severe, mild, moderate and profound respectively in 14.2%, 13.5%, 12.2%, and 11.1%. Gross DD represented 90.2% of all DD children. The causes of DD were hypoxic-ischemic encephalopathy (41.8%), epilepsy (13.7%), sequelae of meningitis (6.5%), sequelae of kernicterus (6.5%), and infectious embryofoetopathies (5.2%). Conclusion: Developmental delay is frequent in paediatric neurology, with perinatal disorders being the leading aetiologies in Cameroon. Prevention of perinatal hypoxic-ischemic encephalopathy risk factors needs to be reinforced.

Adult leptomeningeal cerebellar heterotopia in contact with the posterior inferior cerebellar artery

A leptomeningeal mass was encountered during microdissection of a 63-year-old male cadaver, located dorsal to the left side of the medulla oblongata. The structure was compressing the posterior inferior cerebellar artery (PICA) and was composed of cerebellar-like tissue. Immunohistochemistry for S100 protein, glial fibrillary acidic protein and neurofilaments (NF, the triplet proteins and the 200kD antibody) on paraffin-embedded samples confirmed the cerebellar heterotopion. Abundant Lewy-like degenerative bodies were also identified within the heterotopion; they were positive for the NF triplet and negative for the 200kD neurofilaments. Purkinje cells were rare. This is the first evidence of a leptomeningeal cerebellar heterotopia in contact with PICA in adult. Such subtentorial heterotopias, even if rare, should be searched for during clinical, paraclinical and surgical explorations of the posterior fossa.

Association hyperthyroïdie et cancer thyroïdien différencié (médullaire exclu). À propos de sept observations

The aim of this study was to draw attention to the fact that hyperthyroidism does not exclude the possibility of concurrent thyroid carcinoma. We analyzed the frequency and consequences of this association through seven cases of thyrotoxic patients with differentiated thyroid carcinoma followed by a review of literature. Patients and methodsThe nuclear medicine department of the CHU Ibn Sina has more than 3000 cases of differentiated thyroid carcinoma where 10 patients with association of hyperthyroidism could be retrieved. Our study focused on seven cases well documented and regularly followed. The main parameters collected were the following: age, sex, personal and family history of thyroid disease, clinical presentation, etiology of hyperthyroidism, preoperative paraclinical explorations, surgery performed, histopahological findings, complementary therapy and follow-up. ResultsGroup included six females and one male, average age was 41.4years. There were four cases of Graves’ disease, two cases of single toxic nodule and one case of functional multinodular goiter. All patients underwent total thyroidectomy. Final pathologic examination disclosed five papillary carcinomas and two follicular carcinomas. During 2 to 8years follow-up, there was neither local recurrence nor metastasis. ConclusionThe diagnosis of hyperthyroidism does not preclude concurrent thyroid carcinoma. Careful assessment of such patients is mandatory to exclude an associated thyroid malignancy particularly in the presence of a nodule in a hyperfunctioning thyroid.

Quel bilan complémentaire réaliser devant une épilepsie ?

Paraclinical explorations in epilepsy depend on the clinical situation of the occurrence of seizure. Epileptic seizure is first a possible symptom of a progressive cerebral disease or a systemic origin (toxic, metabolic, iatrogenic). In this situation, the aim of urgent explorations is to find the etiology of the seizure. If epileptic seizure is related to an epilepsy onset, paraclinical explorations are aimed to characterize an epileptic syndrome (idiopathic or symptomatic). Then EEG and cerebral imaging are imperative, eventually completed by specialized investigations (genetics, metabolic, functional imaging).