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Biomedical subjects

J Roquer

Publications and source records attributed to J Roquer.

At least 19 recordsLinked to original sources

[Neurologic syndromes associated with anti-Hu antibody. Study of 24 patients].

BACKGROUND: Twenty-four patients with neurologic involvement and anti-Hu antibodies were studied with the aim of defining the type of tumor associated, evaluating whether the clinico-pathologic picture agreed with the concept of paraneoplastic encephalomyelitis (PEM) and evaluating the treatments used. METHODS: The study was retrospective with the clinical histories being reviewed to define the neurologic syndromes, their evolution and response to the different treatments, time of appearance and type of tumor as well as the neuropathologic changes in the patients undergoing autopsy. RESULTS: In 18 patients a neoplasm was diagnosed as small cell pulmonary carcinoma (SCPC) in 89% of the cases. The neurologic picture preceded the tumor by an average of five months. The clinical pictures included: sensitive neuropathy (20 patients), cerebellous and truncus encephalicus involvement (8 patients), motor neuropathy (6 patients), cortical involvement (5 patients) and neurovegetative dysfunction (4 patients). In 55% of the patients more than one area was altered. Post mortem studies carried out on 5 patients demonstrated inflammatory infiltrates and neuronal loss in multiple areas of the nervous system. None of the patients improved with treatment. The 9 patients who only received immunodepressants evolved in a way similar to those who were not treated. In 7 of the 11 patients who received antitumoral therapy, the neurologic syndrome stabilized for at least 6 months. CONCLUSIONS: The clinicopathological picture and the associated tumor seen in patients with anti-Hu antibodies are identical to those seen in PEM. Antitumoral treatment seems to be more effective than immunodepressant treatment.

Adult

Lipoprotein and apolipoprotein profile in men with ischemic stroke. Role of lipoprotein(a), triglyceride-rich lipoproteins, and apolipoprotein E polymorphism.

BACKGROUND AND PURPOSE: The role of lipoprotein abnormalities in the development of ischemic cerebrovascular disease has not been sufficiently clarified. The aim of this study was to identify the lipoprotein profile in ischemic cerebrovascular disease and the possible role of apolipoprotein E polymorphism. METHODS: The relation between the concentrations of lipoprotein(a), intermediate density lipoproteins, apolipoprotein A-I, apolipoprotein B, apolipoprotein E, and other lipoproteins was studied in 100 men with ischemic cerebrovascular disease (48 atherothrombotic, 28 lacunar, and 24 of unknown type) and in 100 healthy age-matched men as a control group. RESULTS: Patients with ischemic cerebrovascular disease had significantly higher levels of lipoprotein(a), lipids carried by intermediate density lipoproteins, and low density lipoprotein cholesterol and lower levels of high density lipoproteins than control subjects. Patients with atherothrombotic infarction had higher total serum cholesterol and low density lipoprotein cholesterol concentrations than patients with lacunar infarction. To assess lipoprotein abnormalities in normolipidemic subjects, a subgroup of 38 patients with ischemic cerebrovascular disease and 53 control subjects, both with serum cholesterol levels < 5.2 mmol/l (200 mg/dl) and triglycerides < 2.3 mmol/l (200 mg/dl), was analyzed. Serum lipoprotein(a), lipids carried by very low density lipoproteins and intermediate density lipoproteins, and low density lipoprotein triglycerides were significantly higher in normolipidemic patients compared with normolipidemic control subjects, whereas high density lipoprotein cholesterol levels were lower. Apolipoprotein E polymorphism in our ischemic cerebrovascular patients differed from that of the control group, with the epsilon 4 allele being more prevalent. CONCLUSIONS: Increased serum lipoprotein(a) levels and intermediate density lipoprotein abnormalities together with decreased high density lipoprotein levels are major risk factors for ischemic cerebrovascular disease, even in normocholesterolemic and normotriglyceridemic subjects. Finally, the epsilon 4 allele could probably be a predisposing genetic marker for ischemic cerebrovascular disease.

Adult

Primary cerebral abscess due to nocardia presenting as 'ghost tumor'. Clinical and pathological study.

We report a case of a primary cerebral abscess due to Nocardia asteroides in a nonimmunocompromised patient with a particular clinical course. The first symptom (right subacute brachial palsy) and the lesion in a computed tomographic (CT) scan (left parietofrontal edema suggestive of brain tumor) disappeared after corticosteroid treatment and the patient was discharged with total recovery. After 2 months she complained of headache and visual disturbance. A new CT scan showed an annular lesion in the left occipital lobe. A cerebral biopsy was diagnosed of nocardia infection. The patient died 2 weeks after this biopsy. A postmortem study showed an occipital brain abscess but not structural abnormalities were seen in the left parietofrontal area. We believe that the first episode could be a local inflammatory response to cerebral implantation of nocardia which disappeared clinically in the CT scan and in the postmortem study after corticosteroid treatment. Then the nocardia could have displaced by the hematological route to the second and definitive cerebral lesion.

Aged

[Moyamoya syndrome. Diagnosis with angio-MRI].

We present a case of Moya-Moya syndrome in a 28-year-old female patient with an unusual debut in the form of mirror-image writing. The patient was studied by CAT, conventional cerebral angiography, MRI and angio-MRI. The results obtained show a very good correlation between the images of conventional angiography and those obtained by angio-MRI. Angio-MRI requires no contrast, is noninvasive and rapid, promising to be a first class alternative in the diagnosis and follow-up of Moya-Moya syndrome.

Adult

[Hemangioblastoma associated with syringomyelia and syringobulbia in a patient with rheumatoid arthritis].

A 80-year-old woman with a 25-year history of seropositive, erosive rheumatoid arthritis (RA) presented with a neurological clinical picture consistent with cervical cord compression, secondary to a hemangioblastoma with medulla, cerebellum and spinal cord involvement, with associated syringomyelia and syringobulbia. We present a review of the literature remarking the low frequency of this tumor (1%-2% of all intracranial tumors) and its exceptional presentation over the age of 70. We have not been able to find no cases of hemangioblastoma associated with rheumatoid arthritis, thus, we think, this association may be casual. Nevertheless, it emphasizes the need for careful evaluation of patients with rheumatoid arthritis and neurological symptoms before ascribing them to complications due to the rheumatoid disease itself.

Aged