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Biomedical subjects

F Bolgert

Publications and source records attributed to F Bolgert.

At least 19 recordsLinked to original sources
PubMed1995

[Hiccups in adults].

Hiccoughs are an involuntary spasmodic and coordinated contractions of the inspiratory muscles associated with a delayed and sudden closure of the glottis which is responsible for the characteristic noise. The pathophysiology of hiccoughs have not been elucidated. There have only been a few observations describing the sequence of inspiratory muscle activation and these suggest that the control of hiccoughs is within the central nervous system. The clinical circumstances associated with acute benign hiccoughs are both numerous and disparate. In these cases, when they stop spontaneously or as a result of simple physical manoeuvres hiccoughs do not require any particular medical attention. Chronic hiccoughs, defined as hiccoughs persisting for more than 24 hours or recurring as repetitive attacks are a rare phenomenon. The causes cover the whole of organic pathology. Systematic protocols of complementary examinations most often enable an underlying organic cause to be found. Amongst these, particular attention should be paid to oesophageal causes by the reason of their being the most frequent. An important place should be reserved for the aetiological treatment as is frequently enables a remission of chronic hiccough.

Acute Disease↗
PubMed1995

[An oneiroid experience during severe acute polyradiculoneuritis].

This study is to present a psychopathological analysis of complex hallucinatory symptoms--without consciousness breaking up in confusional state--occurring in patients with acute Guillain-Barré's syndrome diagnosis requiring neurological intensive care. Finally the patients experience an unitary and closed situation "close to dream without being dream". This experience is corresponding to the semeiology of the "oneiroid experience" (Mayer-Gross, 1924). The "oneiroid experience" appears to be of syndromic nature independent of any etiological and/or nosological classification. But its conceptualization does probably need widening: the oneiroid world appears to be a creation of a primitive function which inserts us in the world before any science or verification.

Acute Disease↗
PubMed1994

[Endocrine diseases in POEMS syndrome. Apropos of 4 cases].

POEMS syndrome is a rare systemic multi-organ disease usually reported in Japanese patients. The clinical course is slow with a 5-year survival of 60%. Death is caused by polyneuropathy and or anasarka. We observed four cases in our ward (all males, aged 39, 57, 54 and 54 years) who all presented at least four characteristic clinical signs. Gynecomasty together with impotency was seen in all patients. All had hypogonadism and borderline hyperprolactinaemia. Hyperoestrogenism was seen in two. In three patients, rare endocrinopathies were part of the POEMS syndrome. One patient had diabetes mellitus. The clinical course was variable and a function of the effectiveness of plasmocyte dyscrasia therapy. Little work has been done on endocrinopathies in POEMS syndrome. In most cases, gonadotrope function is impaired with gynecomasty and impotency in men, amenorrhoea in women. Generally the hypogonadism is hypogonadotropic. Hyperoestrogenism is frequent and prolactin levels are normal or high with an exaggerated response to thyroid releasing hormone stimulation. The aetiology of POEMS syndrome is unknown. Current research is based on an immunologic theory based on the discovery of high levels of interleukin 6 in POEMS patients with or without Castleman's disease. The cytokine would affect the different organs and lead to clinical expression. Corticosteroids are usually effective in most patients, particularly in reducing the oedema and controlling the polyneuropathy.

Adult↗
PubMed1993

Diffuse noxious inhibitory controls in humans: a neurophysiological investigation of a patient with a form of Brown-Séquard syndrome.

In normal subjects, the application of heterotopic painful stimuli induces simultaneous and parallel decrease in the sensation of pain and of the spinal nociceptive flexion (RIII) reflex evoked by electrical stimulation of the sural nerve. This inhibition of the RIII reflex is absent in tetraplegic patient with clinically complete spinal cord transections and can be triggered only from the analgesic hand in patients with Wallenberg's syndrome. These findings suggest that the inhibitory phenomena observed in normal subjects are likely to be examples of diffuse noxious inhibitory controls (DNICs), being sustained by a loop involving supraspinal structures, the ascending part of which is localized in the spinoreticular tract. We now report an exceptional case of a patient with Brown-Séquard syndrome due to a 4-year-old spinal cord lesion (left side, T-6 level) produced by a knife-wound in the back. Nociceptive flexion (RIII) reflexes elicited by stimulation of cutaneous afferents in the ulnar and sural nerves were studied in the upper and lower limbs by recording from the biceps brachialis and biceps femoris muscles, respectively. For each limb, the RIII reflex threshold was determined. The reflex was then elicited regularly by stimuli of 1.2 times threshold before, during, and after periods of nociceptive electrical conditioning stimulation (15 mA; 4 Hz; 1 min) applied successively to the other three limbs.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Virological markers in the cerebrospinal fluid from HIV-1-infected individuals.

We analysed 127 specimens of cerebrospinal fluid (CSF) from 118 HIV-1-infected individuals at different stages of infection. Intrathecal antibody synthesis was evident in 23 samples tested and was more frequently directed against HIV than against rubella virus, herpes simplex virus, varicella zoster virus or cytomegalovirus. HIV was isolated from only 14% of the 127 CSF specimens, but from 82% of CSF-paired blood samples. HIV antigen was detected in 12% of CSF specimens and 44% of paired plasma samples. Twenty specimens analysed using the polymerase chain reaction (PCR) detected proviral DNA in 75% of CSF specimens. The low rate of virus recovery from CSF was caused by neither the freezing of specimens prior to culture nor therapy. In contrast, virus isolation from CSF was significantly associated with CSF cell count. Virus isolation and antigen detection in CSF were not correlated with either the Centers for Disease Control disease stage or the peripheral CD4+ lymphocyte count, whereas viraemia was significantly associated with a low CD4+ lymphocyte count. Moreover, virus isolation and antigen detection in CSF were not associated with symptoms of subacute HIV encephalitis, suggesting that these markers are not of potential value in the diagnosis of HIV-specific neurologic complications. The value of PCR in this field merits further investigation.

AIDS Dementia Complex↗
PubMed1991

[Slowly progressive apraxia: a MRI and positron tomography in 4 cases].

Four right-handed patients (69, 58 and 68 year-old men; 85 year-old woman) complained of motor difficulties with their left hand (3 cases), or both hands predominant on the left side (1 case). Continuous (1 case) or intermittent (2 cases) myoclonus was noted in the left arm. These disorders gradually progressed for 3 to 10 years. Clinical examination disclosed absence of motor, sensory (except in 1 case), or visual deficit. There were no cerebellar signs, no parkinsonian features (except for mild rigidity in 1 case), and no oculomotor abnormality. On the other hand, neuropsychological examination showed evidence of visuo-constructive apraxia in all cases, dressing apraxia in 3/4 cases and writing impairment in 3/4 cases. There was no amnesia, no aphasia and no intellectual impairment. MRI showed atrophy of the parietal areas, predominant on the right side. A positron emission tomography study was performed in all cases, and twice in 1 case. Cortical energy metabolism was measured using either 18 F-fluorodeoxyglucose or 15 O-Oxygen, to calculate the cerebral metabolic rate of glucose (CMRglu) or oxygen (CMRO2) respectively. Cortical metabolism was significantly decreased in the whole cortex of the right hemisphere in 3 cases, and was also reduced in the cortex of the left hemisphere, significantly in 1/3 studied planes. Moreover, regional metabolic indices (CMRO2 or CMRglu/cortex) showed a significant decrease in both the right and left posterior associative areas (temporo-parieto-occipital cortex), predominantly marked on the right side in 3 cases, indicating bilateral cortical dysfunction. At follow-up, one patient became progressively demented, another had visuo-spatial disorders indicating a lesion of both parietal areas. The relationships of our cases with the slowly progressive apraxia syndrome and with corticobasal degeneration are discussed.

Aged↗
PubMed1990

Human immunodeficiency virus (HIV) leukoencephalopathy and the microcirculation.

We studied the brains of three patients with acquired immune deficiency syndrome (AIDS), all of whom developed subacutely progressive dementia unassociated with opportunistic infection or neoplasm in the central nervous system. Computed tomographic (CT) scans of the head revealed cortical atrophy, ventricular dilation, and diffuse hypodensity of the centrum semiovale. On microscopic examination, the cerebral and cerebellar white matter in all cases showed diffuse and focal, angiocentric regions of myelin pallor, focal vacuolization, and extensive gliosis. Variable axonal loss and axonal spheroids were evident. The microvasculature showed striking changes, including mural thickening, increased cellularity, and enlargement and pleomorphism of endothelial cells with variable numbers of macrophages and multinucleated giant cells (MNGC), which often contained hemosiderin pigment. Human immunodeficiency virus type 1 (HIV-1) antigens were identified immunocytochemically within perivascular macrophages and MNGC and in some microglial cells. We suggest that the morphologic abnormalities of the microcirculation may be associated with an alteration of the blood-brain barrier. The increased vascular permeability could contribute to damage and loss of the white matter including both myelin and axons, and result in subcortical cerebral atrophy. The HIV-1 infected cells present in relation to the microvasculature may play a role in mediating the vascular injury.

Acquired Immunodeficiency Syndrome↗
PubMed1989

Chronic myelopathies associated with human T-lymphotropic virus type I. A clinical, serologic, and immunovirologic study of ten patients in France.

Chronic myelopathy associated with human T-lymphotropic virus type I (HTLV-I) has been described in HTLV-I endemic areas. In Paris, 167 neurologic patients were screened for HTLV-I by enzyme-linked immunosorbent, indirect immunofluorescent, and Western blot assays. Ten of the 11 patients with positive results had a chronic spastic paraparesis with IgG oligoclonal bands and elevated HTLV-I antibody index. Two of them had been born and were living in France, without HTLV-I risk factors. Evoked potentials were abnormal in the nine tested patients and brain magnetic resonance images in three of seven patients. No improvement was observed with steroid treatment. A retrovirus similar to HTLV-I was isolated in five cases at different periods of the disease. Hypotheses of limited endemic areas in western countries are discussed. Early presence and persistence of HTLV-I suggest that it is the etiologic agent.

Adult↗
PubMed1989

Brain potentials reveal covert facial recognition in prosopagnosia.

Brain potentials were recorded in a prosopagnosic patient, in response to familiar and unfamiliar faces he was asked to recognize. The amplitude of the P300 component was found to be an inverse function of probability for each category of faces despite the patient's inability to consciously recognize the familiarity of these faces. In addition, P300 latency varied from 700 to 800 msec according to the familiarity of the faces, and P300 scalp location was different as a function of faces probability and overt recognition. The results imply that covert facial recognition may be evidenced in using event-related potentials of the brain. They also demonstrate that automatic and covert processing of face familiarity are preserved, but prolonged in this patient.

Agnosia↗
PubMed1989

The spectrum of polyneuropathies in patients infected with HIV.

Twenty five patients with peripheral neuropathy at different stages of human immunodeficiency virus (HIV) infection are reported. Cerebrospinal fluid (CSF) findings were available in 17 cases, electrophysiology in all and a neuromuscular biopsy in 11. Of six otherwise asymptomatic HIV+ patients, five had chronic inflammatory demyelinating polyneuropathy (CIDP) and one acute inflammatory demyelinating polyneuropathy (AIDP). CSF showed pleocytosis in all cases. Infiltration of the endoneurium and/or the epineurium by mononuclear cells was seen in biopsies from three cases. These six patients recovered either spontaneously, or with corticosteroids or plasmaphereses. Of five patients with AIDS related complex (ARC), three had distal predominantly sensory peripheral neuropathy (DSPN), one CIDP and one mixed neuropathy. Of 14 patients with AIDS, one had mononeuropathy multiplex and 13 painful DSPN. Electrophysiological studies were consistent with an axonopathy. Nerve biopsies in six cases showed axonal changes but surprisingly associated with marked segmental demyelination in two cases. Cell infiltration was present in nerve samples in two cases. Five patients died within six months after the onset of the neuropathy.

AIDS-Related Complex↗
PubMed1989

[Visual object agnosia: current conceptions].

Visual agnosia for objects is a difficulty in recognizing objects presented visually. This difficulty can not be explained by a mental deterioration, a disorder of attention or a lack of familiarity with the object. Two criteria are essential but disputed: the absence of visual sensory difficulty necessary for adequate perception; possible recognition of the object by another sensory modality. An object is characterized by a triple representation: formal, semantic, lexical. The clinical, cognitive, pathophysiological analysis lead to distinguish 3 types of visual agnosia. 1) Aperceptive visual agnosia: patients see badly with morphological errors; the disorder concerns visual informations processing that is a necessary condition for identifying the formal representation of the object; the lesions are bilateral and involve the occipito-temporal cortex. 2) Associative visual agnosia: patients can copy, are not aphasic, but give erroneous verbal responses; the disorder concerns the links between formal representations and semantic, lexical representations; the lesions are unilateral and involve the left gyrus angularis connections. 3) Asemantic visual agnosia: patients have lost the meanings of objects and words; the disorder concerns semantic representations; the lesions are bilateral and involve the temporo-limbic cortex.

Agnosia↗
PubMed1988

[The peripheral nervous system and HIV infection. 13 cases].

Disorders of the peripheral nervous system occur at all stages of HIV infection. From 13 patients referred for a peripheral neuropathy, 9 were known to be HIV seropositive and 4 were found to be seropositive. All were Caucasian males aged 27 to 58. Ten were homosexual, 2 were drug-addicts. Patients fell into several groups: the first group was made of 5 patients, 4 asymptomatic and 1 AIDS-related-complex (ARC), with an inflammatory demyelinating polyneuropathy, acute in 1 case and subacute in 4; the CSF showed pleiocytosis in all cases. Motor conduction nerve velocities were markedly reduced and motor distal latencies prolonged. Three patients recovered spontaneously, 1 responded to corticosteroids, 1 to plasmapheresis. In the second group, 4 patients, 1 asymptomatic and 3 ARC, had a distal symmetrical polyneuropathy; CSF was normal in 2 cases. Electrophysiological studies and nerve biopsies indicated a mixed axonal-demyelinating polyneuropathy. Three patients recovered spontaneously, 1 is unchanged. Among both groups, an infiltration of mononuclear cells was found on nerve biopsies in 4 cases. The third group was made of 3 patients with AIDS who presented with a painful sensory polyneuropathy involving the distal lower limbs. Electrophysiological and pathological study of the nerve indicated axonal degeneration. No cell infiltration was found. The last patient with AIDS had a progressive meningoradiculopathy. These 4 patients died within 6 months after the onset of the neuropathy. These findings are close to those previously reported, and confirm the wide spectrum of disorders of the peripheral nervous system associated to HIV infection.

Acquired Immunodeficiency Syndrome↗
PubMed1988

[Human acquired immunodeficiency virus infection of the nervous system].

Neurological manifestations of HIV infection are recognised at different phases of the evolution of the disease. During the late stages opportunistic neuro-meningeal infections and tumors develop as a result of the immuno-suppression. There exist, however, various manifestations which evolve independently of the immune state, and seem to be directly related to the virus itself. One can distinguish central neuro-meningeal syndromes and peripheral syndromes at the onset, or at later stages. Their prognostic implications are uncertain, but often severe, for example in the case of the subacute dementias which, in this setting, may lead to death in several months. There are also other manifestations which may be self limited or slowly evolving in the central and peripheral nervous systems. The neuropathological changes are known for the dementias as mentioned above, though the characteristics lesions due to HIV infection per se remain controversial. The presence of the virus in the nervous system has been established by in situ hybridization techniques, immunohistochemistry and culture. Studies on CSF have also allowed virological (cultures) and immunological studies to be carried out. The physiopathological mechanisms for the apparent neurological effects of this virus remain hypothetical. A better understanding of these mechanisms should lead to a rationalisation of therapeutic strategies, in a disorder which would seem to be an early and persisting viral infection of the nervous system.

Acquired Immunodeficiency Syndrome↗