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Biomedical subjects

F Graus

Publications and source records attributed to F Graus.

At least 37 records · Page 2Linked to original sources
PubMed1991

Effect of intraventricular injection of an anti-Purkinje cell antibody (anti-Yo) in a guinea pig model.

Female guinea pigs had intraventricular injections of either IgG from a patient with paraneoplastic cerebellar degeneration (PCD) and anti-Purkinje cell antibodies (anti-Yo IgG) or control IgG. In animals that received a single injection of control or anti-Yo IgG and were killed at different time intervals, IgG immunoreactivity was present in the cytoplasm of Purkinje cells at 2 h and persisted at 24 h. In guinea pigs injected for 15 days with control or anti-Yo IgG and sacrificed 24 h after the last injection, IgG was detected into the Purkinje cells in both groups, whereas animals killed 7 and 30 days after the last injection had no staining for IgG in the Purkinje cells. Clinical or pathologic evidence of cerebellar involvement was not seen in any of the animals. This study suggests that anti-Yo antibody alone may not be the cause of the Purkinje cell loss in PCD.

Animals↗
PubMed1991

Trends and survival for AIDS patients presenting with indicative neurologic diseases.

Nervous system involvement in patients with AIDS is frequent either due to direct infection by the HIV-1 or to opportunistic infections or neoplasms. In the present study we evaluate the epidemiologic characteristics of patients in whom the first AIDS manifestation was an indicative neurologic disease (IND) and the influence of such a presenting form in the patients' survival. Out of 1250 reported cases, 252 (20.2%) presented with one of the INDs, according with the CDC AIDS definition criteria. Neither sex nor age differences were found between patients presenting with and without an IND. IVDUs were more likely to present with an IND than homosexual/bisexual men (p = 0.024). Cerebral toxoplasmosis (CT) was the only IND with a significant proportional increase over time. Although some of the IND have a specific treatment, as a whole patients presenting with an IND lived shorter than those presenting with any of the other indicative disorders (p less than 0.0001). The incidence of IND is greater than elsewhere, mainly because of CT. The increment of CT may be in part due to the introduction of the new AIDS definition criteria.

AIDS Dementia Complex↗
PubMed1991

Detection of the anti-Hu antibody in specific regions of the nervous system and tumor from patients with paraneoplastic encephalomyelitis/sensory neuronopathy.

We studied the nervous systems and tumors of five patients with anti-Hu-positive paraneoplastic encephalomyelitis/sensory neuronopathy (PEM/PSN) to determine if the autoantibody found in the serum and CSF was also present in those tissues. Immunohistochemical studies of the nervous system revealed the presence of IgG bound predominantly to the nuclei of most of the neurons and the cytoplasm of some glial cells. IgG was also present to a lesser degree in the neuropil. In brains of patients who died of cancer without the paraneoplastic syndrome, IgG was present in the immediate perivascular areas and to a very limited degree in the neuropil. There was no IgG in neurons, and in only some of the controls a few glial cells showed IgG immunoreactivity in the cytoplasm. The amount of anti-Hu IgG relative to total IgG in various brain regions and tumor was determined by quantitative Western blot analysis. The proportion of anti-Hu IgG was greater in some areas of the brain and tumor than in serum and CSF. Control brains did not contain anti-Hu IgG. There was a limited correlation among (1) the principal clinical symptoms, (2) regions of major tissue injury, and (3) the quantitative anti-Hu IgG distribution. We conclude that although the role of the antibody in the pathogenesis of the disease is still uncertain, its specific localization in the nervous system and tumor suggests an immunologic etiology of this paraneoplastic syndrome.

Aged↗
PubMed1990

[Postherpetic vasculopathy. A study of 3 cases in immunosuppressed patients].

We report three cases of postherpetic vasculopathy in immunologically compromised patients. Two had ophthalmic herpes zoster, contralateral to the physical signs, and the third case developed after disseminated herpes zoster. The initial CT images consisted of small ischemic infarcts in capsular regions and basal ganglia. The arteriography showed images consistent with vasculitis or thrombosis of great vessels of the Willis' polygon, which were ipsilateral to the herpetic lesion in two cases. In one patient the neurological defect remained stable, while the other two developed new ischemic episodes, all in the same cerebral hemisphere. It can be assumed from the delayed development of neurologic disease after cutaneous lesions that some cases go unnoticed if the zoster infection is not specifically looked for in retrospect.

Adult↗
PubMed1990

[Encephalic toxoplasmosis in patients with the acquired immunodeficiency syndrome. A clinico-radiological study and the therapeutic results in 78 cases].

During a 40-month period 78 episodes of encephalic toxoplasmosis (ET) were diagnosed in 57 patients among 394 with acquired immunodeficiency syndrome (AIDS) (based on CDC criteria) in the Hospital Clinic from Barcelona. 38 patients were parenteral drug abusers (66.7%), 17 were homosexual males (29.8%) and 2 were heterosexual females (3.5%). ET was the first opportunistic infection in 28 patients (49.1%). The most common symptoms at the time of diagnosis were focal neurological signs (62.8%) and fever (52.6%). Usually, computed tomography showed single or multiple hypodense lesions (70.3%) with ring-like (46.1%) or nodular (28.3%) uptake. Serology (indirect immunofluorescence) was diagnostic in only 24 cases (42.1%). The acute episodes were treated with the combination pyrimethamine/sulfadiazine (P/S) during 3-6 weeks, and folinic acid was associated. If the patient had previous allergy to sulfonamides or allergy developed during the acute phase, clindamycin (C) was given instead of S. The patients surviving the acute episode (49, 86, 0%) underwent, if they consented, maintenance therapy with P/S two days per week (15 patients) or with C if sulfonamide allergy was present (10 patients). No relapse was observed in those receiving P/S, but 40% of those treated with P/C relapsed. It was concluded that ET is a common opportunistic infection in the AIDS patients, that the treatment of the acute phase with P/S or with P/C is satisfactory, and that maintenance therapy with P/S two days per week may be effective to prevent relapses.

Acquired Immunodeficiency Syndrome↗
PubMed1990

Selective expression of Purkinje-cell antigens in tumor tissue from patients with paraneoplastic cerebellar degeneration.

Paraneoplastic cerebellar degeneration is a rare syndrome that occurs in patients with gynecologic cancer and is characterized by widespread loss of Purkinje cells. To determine whether Purkinje-cell antigens are selectively expressed in the tumors of patients with the syndrome, we examined tumor tissue from 10 patients whose serum contained anti-Purkinje-cell (anti-Yo) antibodies. The origins of the cancers were the breast (five patients), ovary (three), endometrium (one), and fallopian tube (one). We used as controls tumor tissue from 11 patients with ovarian cancer and 10 patients with breast cancer who were neurologically normal. Using immunohistochemical and Western blot analysis, we found that Purkinje-cell antigens were expressed in all the tumors from the 10 patients with paraneoplastic cerebellar degeneration but in none of the tumors from the 21 neurologically normal patients. When IgG from patients with paraneoplastic cerebellar degeneration was affinity-purified to cerebellar Purkinje-cell antigen, immunohistochemical analysis showed that it reacted specifically with the tumor tissue from those patients. We conclude that in patients with paraneoplastic cerebellar degeneration, the anti-Yo antibody results from an immune response to neural antigens expressed by the gynecologic tumors in the patients.

Antigens, Neoplasm↗
PubMed1990

Analysis of a neuronal antigen (Hu) expression in the developing rat brain detected by autoantibodies from patients with paraneoplastic encephalomyelitis.

Anti-Hu is an autoantibody that recognizes an antigen (Hu) highly restricted to neuronal nuclei. In the developing rat brain all neurons and the germinal cell layer were anti-Hu positive. Ependyma and choroid plexus were positive only in the early stages of development. The strongest expression of Hu was seen in the most mature neurons. The transitory nature of Cajal-Retzius and subplate neurons was confirmed with the anti-Hu staining. Although the Hu is also expressed by neural cells other than neurons, the strongest staining of mature neurons could indicate that Hu plays a role in the process of neuronal differentiation.

Aging↗
PubMed1990

Normal proprioceptive trigeminal afferents in patients with Sjögren's syndrome and sensory neuronopathy.

A pure sensory neuropathy due to neuronal damage in the gasserian and spinal ganglia has been described in patients with Sjögren's syndrome. Conventional electromyographic (EMG) studies can demonstrate the selective involvement of the sensory pathways but they do not provide definite evidence for the site of the lesion. Noting that the trigeminal sensory neurons carrying cutaneous and muscular afferents are differentially located in the gasserian and mesencephalic nuclei, respectively, we carried out an electrophysiological study of the trigeminofacial and trigeminotrigeminal reflexes in 5 patients with Sjögren's syndrome and pure sensory neuropathy, in 10 patients with sensory-motor neuropathies of other causes, and in 10 healthy subjects. Our results show that patients with Sjögren's syndrome and pure sensory neuropathy who exhibited abnormal blink reflexes and an abnormal, cutaneous-induced masseter silent period had normal jaw jerks, whereas patients with sensory-motor neuropathies who exhibited abnormal cutaneous responses had abnormal jaw jerks. These findings suggest that the lesion in pure sensory neuropathy involves damage to the neurons of the gasserian ganglia and not to the trigeminal axons, since an axonal lesion would be expected to involve the large axons from muscle spindle receptors.

Adult↗
PubMed1990

Expression of lymphocyte, macrophage and class I and II major histocompatibility complex antigens in normal human dorsal root ganglia.

We analyzed the expression of lymphocyte, macrophage and class I and II (HLA-DR) major histocompatibility complex (MHC) antigens in normal dorsal root ganglia (DRG) from 19 patients without neurological disease by using an avidin-biotin immunoperoxidase technique. Satellite cells expressed class I and II MHC antigens. The intensity of HLA-DR staining varied among the DRG and was not related to age, history of cancer or infection, or number of T lymphocytes in the DRG. Monoclonal antibodies EBM11 and Leu-M3, that recognize cells of monocyte/macrophage lineage, stained a population of cells in all DRG. Positive cells had an elongated shape and were in the interstitial tissue between the satellite cells. These findings may be relevant to the understanding of the immune mechanisms involved in the neuronal damage of sensory neuropathies of presumably autoimmune origin such as those associated with small-cell lung cancer or Sjögren's syndrome.

Adolescent↗
PubMed1990

Central nervous system toxoplasmosis in AIDS patients: efficacy of an intermittent maintenance therapy.

Fifty-five episodes of central nervous system (CNS) toxoplasmosis developing in 43 of the 329 AIDS cases seen at our institution were diagnosed during a 34-month period and were prospectively studied. Acute episodes were treated with a pyrimethamine/sulfadiazine (P/S) combination for a mean of 21 days. Because of a previously known major allergy to sulfonamides, three episodes were treated with clindamycin instead of sulphadiazine. In those patients who accepted maintenance therapy, a combination of P/S or pyrimethamine and clindamycin (P/C) was administered 2 days per week. Thirty-six patients (83.7%) survived the first episode. Four of these 36 were lost to further study. Six of the 12 (50%) who decided not to undergo maintenance therapy relapsed (mean follow-up: 12 months). Fourteen patients were given P/S and none relapsed while they were on maintenance therapy (mean follow-up: 10.3 months). Six patients received an intermittent maintenance treatment with P/C and one relapsed 2 months after starting the maintenance therapy (mean follow-up: 13.7 months). We conclude that an intermittent (2 days per week) maintenance treatment for CNS toxoplasmosis with P/S was effective in preventing relapses, although prospective randomized studies remain to be done.

Acquired Immunodeficiency Syndrome↗
PubMed1990

Subacute cerebellar syndrome as the first manifestation of AIDS dementia complex.

A patient presented with a subacute cerebellar syndrome in absence of cognitive impairment or other symptoms. He became demented several months after the onset of the disease. Necropsy demonstrated the typical features of the AIDS dementia complex and severe loss of Purkinje cells of the cerebellum. Patients with subacute cerebellar dysfunction should be evaluated for the presence of human immunodeficiency virus infection.

AIDS Dementia Complex↗
PubMed1990

Pure sensory neuropathy in patients with primary Sjögren's syndrome: clinical, immunological, and electromyographic findings.

A pure sensory neuropathy caused by lymphocytic infiltration of the dorsal root ganglia has been reported in a few patients with Sjögren's syndrome. The clinical, immunological, and electromyographic findings of five patients with this type of neuropathy and primary Sjögren's syndrome were reviewed. Typical clinical indications were the presence of a chronic asymmetrical sensory deficit, initial disease in the hands with a predominant loss of the vibratory and joint position senses, and an association with Adie's pupil syndrome or trigeminal sensory neuropathy. The simultaneous impairment of the central and peripheral evoked cortical potentials suggested that there was a lesion of the neuronal cell body. The neuropathy preceded the diagnosis of Sjögren's syndrome in four patients. Four patients were positive for Ro antibodies, but systemic vasculitis or malignancy was not found after a mean follow up of six years. These findings indicate that in patients with a sensory neuropathy the diagnosis of Sjögren's syndrome has to be considered, even if the patient denies the presence of sicca symptoms, and that appropriate tests must be carried out.

Adie Syndrome↗
PubMed1990

High ethanol consumption as risk factor for intracerebral hemorrhage in young and middle-aged people.

We examined the prevalence of high ethanol intake, hypertension, and other risk factors for intracerebral hemorrhage in a case-control study of 24 young and middle-aged patients with intracerebral hemorrhage. We recorded ethanol consumption, history of hypertension, liver disease, cigarette smoking, and mild or severe coagulation disorder in each case of intracerebral hemorrhage and in 48 control patients matched by sex and age. In univariate matched analyses, the frequencies of high ethanol intake (p = 0.009), hypertension (p = 0.05), and coagulation disorder (p = 0.05) were higher in the cases than in the controls. After controlling for possible confounding factors, we found that high ethanol intake and hypertension were the only independent risk factors for intracerebral hemorrhage (p = 0.02 and p = 0.05, respectively). The hemorrhagic lesion found in cases with a high ethanol intake tended to be located in the cerebral lobes (p = 0.01), contrasting with the typical basal ganglia location of hypertensive hematomas (p = 0.009). We conclude that chronic, high ethanol intake should be considered as an important risk factor for lobar hematomas in young and middle-aged people.

Adult↗