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Biomedical subjects

F Graus

Publications and source records attributed to F Graus.

At least 217 records · Page 12Linked to original sources
PubMed1985

Cerebrovascular complications in patients with cancer.

In an autopsy study of patients with cancer, 14.6% had pathologic evidence of cerebrovascular disease (CVD), and in 7.4% clinical symptoms of CVD had been present in life. The usual risk factors for CVD were overshadowed by pathophysiologic abnormalities related to the neoplasm, including direct effects of the tumor, coagulation disorders, infections and diagnostic or therapeutic procedures. In patients with leukemia, hemorrhages (72.4%) were much more common than ischemic infarcts. In lymphoma patients, the incidence of cerebral bleeding was lower (36.3%). In both groups, the leading causes of ischemic infarction were septic thrombi and intravascular coagulation. In patients with carcinoma, cerebral infarctions (54.1%) were more frequent than hemorrhages. NBTE (18.5%) and intravascular coagulation (9.6%) were the most common etiologies. Hemorrhages other than intratumoral bleeding in patients with melanoma or germ cell tumors were unusual. The clinical presentation of CVD in patients with cancer is more often a diffuse encephalopathy, with or without localizing signs, than the typical acute onset of a focal deficit. This was particularly true with intravascular coagulation, septic infarction and subdural hematoma. Our study suggests that by knowing the clinical setting, neurologic features and laboratory findings, one can, in many instances, make an accurate clinical diagnosis that, in some cases, leads to effective treatment.

Arteriosclerosis↗
PubMed1985

Neuronal antinuclear antibody in sensory neuronopathy from lung cancer.

We found an antinuclear antibody highly restricted to nuclei of neurons in two patients with subacute sensory neuronopathy complicating oat cell carcinoma of the lung. Serum was tested by indirect immunofluorescence and immunoperoxidase staining. At low concentrations of antibody, only the nuclei of the neurons were stained. At high concentrations, there was also staining of the nuclei of glial cells and fetal nonneural tissues. The cytoplasm of most neurons was stained with the immunoperoxidase method.

Antibodies, Antinuclear↗
PubMed1984

Distribution of the ganglioside GD3 in the human nervous system detected by R24 mouse monoclonal antibody.

Immunohistochemical staining with mouse monoclonal antibody R24 recognizing the ganglioside GD3 was used to study the distribution of GD3 in the human brain. Positive staining was primarily found in the surrounding neuropil of many neuronal groups in the brainstem and spinal cord, cerebellum, retina and dentate gyrus of hippocampus. In addition, staining was found in ependymal cells and glial processes around blood vessels and in the subependymal region.

Animals↗
PubMed1984

The palmomental reflex. Clinical study of 300 cases.

In 300 subjects divided into three equal series of healthy adults, healthy newborn children and adults with neurological diseases, a clinical study of the palmomental reflex (PMR) is carried out, showing its methodology for the examination and appraisal of the reflex response. The PMR appears in 11% of the healthy adults, in 25% of the healthy newborn children and in 72% of the adults with neurological diseases. Habituation to the reflex response is significantly different in the three series, and this is the most important data to consider whether the PMR is physiological or pathological. No significant difference was objectified on evoking the reflex response by stimulation of the thenar region or the thumb.

Adult↗
PubMed1983

Papilledema in the metastatic jugular foramen syndrome.

In a patient with Ewing's tumor, bilateral papilledema developed along with a left jugular foramen syndrome. Plain tomograms demonstrated a metastasis at the base of the skull. A digital intravenous angiogram showed an occlusion of the left transverse sinus at the level of the jugular foramen. The papilledema was explained by an increase in the intracranial pressure due to the rapid obstruction of venous drainage by the metastasis.

Adult↗
PubMed1983

Brain metastases in children.

We reviewed the records of 31 children under the age of 21 years with parenchymal brain metastases diagnosed by CT scan (13 patients) or necropsy (18). Brain metastases were found in 18 of 139 (13%) children with solid tumors in whom complete postmortem examinations were done. Osteogenic sarcoma and rhabdomyosarcoma were the most frequent primary tumors causing brain metastases in patients younger than 15 years, and testicular germ cell tumor, from age 15 to 21 years. Evidence of intratumoral hemorrhage was found in 50% of autopsy cases. Pulmonary metastases were present in 28 of 31 (90%). The median interval from recognition of pulmonary metastases to the development of brain metastases was 10 months. No patient had evidence of brain metastases at diagnosis of the systemic cancer. In only one patient was the brain the only site of relapse. Following detection of brain metastases, the median survival was seven months in six patients who underwent surgery and whole-brain radiation therapy and four months in 15 given radiotherapy (3000 rads) alone. Patients with relatively radioresistant brain metastases may benefit from surgical excision or higher doses of radiation, or both.

Adolescent↗
PubMed1983

Mixed carcinomatous neuropathy in patients with lung cancer and lymphoma.

A clinical, electrophysiological and histological study of the peripheral nerve was performed on 62 patients with lung cancer and 30 patients with lymphoma. There was a mild peripheral neuropathy (MPN) in 17.7% of patients with lung cancer and in 10% of those with lymphoma. MPN was related to the degree of weight loss. Histological studies of 5 patients with MPN demonstrated a loss of large myelinated fibers in all patients, axonal degeneration in 2 and remyelination in 3 patients. Electromyographic and histological findings indicate a primary axonal neuropathy with remyelination, probably secondary to axonal damage. 2 patients with lymphoma developed a severe neuropathy that remitted in 1 patient. The main pathological abnormality was segmental demyelination in both cases. Immunofluorescence studies were negative in all cases with mild or severe neuropathy.

Adolescent↗
PubMed1981

[Peripheral neuropathy and insulinoma (author's transl)].

A case of insulinoma is reported with disease of the peripheral nervous system and pathological demonstration of a primary nerve lesion. On admission the female patient gave a history of hypoglycemic episodes and paresthesias and loss of strength in both hands. Physical examination disclosed loss of strength and atrophy of the distal musculature of the extremities, predominating in the upper ones and without fasciculations. Muscle biopsy demonstrated changes suggestive of neurogenous atrophy, and biopsy of the sural nerve showed reduction of the myelin fibers with axonal degeneration, important signs of demyelinization, and remyelinization figures. The neuropathy was unchanged two months after removal of the insulinoma. The exact location of the nerve lesion in insulinoma is controversial, some authors placing it in the peripheral nerve while others believe the motor neurons of the anterior horns to be diseased. The pathological findings in the present case suggest primary nerve disease, but an associated lesion of the anterior horns could also be present.

Adenoma, Islet Cell↗
PubMedDate not supplied

Cerebral infarction of the basal ganglia due to embolism from the heart.

We studied 8 patients with cerebral infarction in the deep territory of the middle cerebral artery (MCA). All patients had a definite cardiac source of emboli and no known factors for thrombosis. Mixed sensory and motor deficit was found in all but one patient and CT scan showed larger lesions than usually reported in lacunar infarcts. Contrast enhancement was seen in all cases in which CT scan was performed in the second or third week. It is concluded that embolic infarcts in deep cerebral territory of MCA from a cardiac source are more frequent than previously reported. This diagnosis has to be considered when CT scan demonstrates a deep cerebral infarct.

Adult↗
PubMedDate not supplied

[Paraneoplastic syndromes in otoneuro-ophthalmology].

INTRODUCTION AND OBJECTIVE: The so-called neurological paraneoplastic syndromes (NPNS) are a group of diseases of the central nervous system of unknown etiology which are seen almost exclusively in patients with cancer. We review the main NPNS paying particular attention to those with ophthalmological and otological features. DEVELOPMENT: Certain neuro-ophthalmological findings may constitute, at least partly, some paraneoplastic syndromes. There are alterations of vision in paraneoplastic retinopathy and in optic neuritis of paraneoplastic origin. The latter, unlike the retinopathy, usually coexists with involvement of other structures of the nervous system. Oculomotor function is affected in the opsoclonus-myoclonus syndrome. Diplopia and/or ophthalmoplegia may be a predominant or initial symptom, in patients with paraneoplastic neurological degeneration or brainstem encephalitis. In the Lambert-Eaton syndrome and in paraneoplastic encephalomyelitis, may have blurred vision and alterations of the pupil. Cases of paraneoplastic uveitis have also been described. Paraneoplastic otological involvement is less frequent. Patients with sensorineural deafness in the context of a paraneoplastic encephalomyelitis have been reported. In the NPNS vertigo is caused by cerebellar or brainstem lesions and not by lesions of peripheral organs. When nystagmus occurs in a NPNS it may be of various types and is due to involvement of structures in the brain stem or cerebellum. CONCLUSIONS: The diagnosis of NPNS in patients with no known cancer is important because it may lead to the detection of an occult cancer which is localized or scarcely extended, and therefore is still potentially treatable. Oto-neuro-ophthalmological manifestations may be the first or only symptom of presentation of a paraneoplastic neurological clinical picture.

Autoimmune Diseases of the Nervous System↗
PubMedDate not supplied

[Transplantation of haematopoietic stem cells in multiple sclerosis].

INTRODUCTION AND METHOD: The idea of treating auto immune diseases which are resistant to conventional immunodepressive treatment by autologous transplantation of haematopoietic stem cells obtained from peripheral blood (TAPH) is based on the hypothesis that immuno ablative treatment would destroy the patients anti self lymphocytes and the reinfusion of stem cells would give rise to lymphocytes which would be tolerant of the antigens responsible for the auto immune response. By July 2000 90 patients with multiple sclerosis (ES) had received a TAPH according to data of the European Group for Blood and Marrow Transplantation/European League against Rheumatism (EBMT/EULAR). In the literature there are reports of the results obtained in 43 patients in whom EM was the sole indication for treatment [30 secondary progressive (SP), 10 primary progressive (PP) and 3 progressive relapsing (PR) ES]. The transplant related mortality (death within the first 100 days) was 4.6% (2/43), in both cases caused by infection. In the study which included 24 patients, the TAPH was considered to have been effective, since 92% of the patients with SP MS had no further progression after 3 years. However, of the patients with PP EM only 40% scored the same or better on the EDSS, as compared to their basal scores, at the end of the study. In any case, this treatment cannot be considered to cure the MS since the probability of patients having no signs of active disease 3 years after transplantation is 12% in SP MS and 0% in PP MS. CONCLUSIONS: TAPH remains an experimental treatment. Only in the future will it be clear whether this treatment is really useful for patients with multiple sclerosis.

Disease Progression↗
PubMedDate not supplied

[Limbic encephalitis: a probably under-recognized syndrome].

Limbic encephalitis was identified as a clinicopathological entity in 1968. Up to a few years ago, 200 cases were described, most associated with lung cancer and more infrequently with other tumors. The recent identification of patients with this syndrome, idiopathic limbic encephalitis, who never develop cancer and have high titers of antibodies to voltage-gated potassium channels (VGKC) and an excellent response to immunosuppressive therapy, has extended the etiological spectrum and suggests that the syndrome may be under-recognized. The disorder, which develops in a few days or weeks, is characterized by the development of short-term memory loss, seizures, confusion and psychiatric features. The presence of symptoms beyond the limbic system is highly suggestive of a paraneoplastic origin. When limbic encephalitis is suspected, the following tests should be performed in order to demonstrate: a) involvement of the temporal lobes (EEG and brain MRI); b) presence of inflammatory abnormalities in the CSF, and c) the presence of onconeural antibodies or anti-VGKC. Once the diagnosis is confirmed by the clinical picture and MRI findings, treatment must be initiated without waiting for the antibody results because its negativity does not exclude the diagnosis. Detection of an onconeural antibody will confirm that the limbic syndrome is paraneoplastic and will help us to search for an underlying tumor and to predict possible response to the treatment. The recommended treatment is cycles of methylprednisolone (1 g/day for 3 to 5 days). Therapeutic response in the idiopathic limbic encephalitis is excellent and may be good in limbic encephalitis with anti-Ma2 or without onconeural antibodies. On the contrary, immunosuppressant treatment is not usually effective in limbic encephalitis associated to anti-Hu antibodies.

Humans↗
PubMedDate not supplied

[NMO-IgG antibodies in neuromyelitis optica: a report of 2 cases].

INTRODUCTION: Neuromyelitis optica is an inflammatory demyelination disease that selectively affects optic nerves and spinal cord. Recently it has been described that the NMO-IgG antibodies, are highly specific for the diagnosis, although they are also present in partial forms of the disease. The antigen responsible for this immune response seems to be aquaporin-4 water channel. CLINICAL CASE: We describe the detection in our laboratory of NMO-IgG antibodies in two patients, one of them with a neuromyelitis optica and the other one with a recurrent myelitis and subclinical involvement of the optic nerve. CONCLUSIONS: By using dual immunostaining, confocal microscopy showed that the antibodies of both patients colocalized with that of an anti-aquaporin-4.

Adult↗