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Biomedical subjects

J A Zabala

Publications and source records attributed to J A Zabala.

11 recordsLinked to original sources
PubMed2003

[Progressive cranial neuropathy due to perineural spread of a facial squamous cell carcinoma].

The paper aims to present the case of a progressive and unilateral cranial polyneuropathy due to perineural spread of cutaneous squamous cell carcinoma. This is a case of a 73 year old man with a history of squamous cell carcinoma in the right temporal region that was removed in 1992. In May 2000 he first presented pain and numbness in the distribution of the first branch of right trigeminal nerve and weakness of the ipsilateral frontal muscle. Later on he presented right ophthalmoplegia, and damage of lower cranial nerves, leading to dysphagia and respiratory distress. He was admitted in March 2001 for a gastrostomy for feeding, when ataxia and recurrence of the right temporal lesion ensued. After three examinations with MRI, the fourth study showed meningeal carcinomatous and a metastatic lesion in the brainstem. Histopathologic examination demonstrated dermal and perineural invasion by squamous cell carcinoma. The necropsy also showed meningeal, perineural and endoneural infiltration of atypical epidermal cells and a pons mass composed of the same cells. We conclude that the perineural spread of the cutaneous carcinoma is an exceptional cause of cranial neuropathy, however it must be ruled out in patients with progressive and unilateral cranial neuropathy. In these cases, when no radiological abnormalities are noted, a biopsy may be performed on the peripheral branches of the cranial nerve to confirm the diagnosis.

Aged↗
PubMed1998

[Intracranial hemorrhage with fluid level. A case report without coagulation alterations].

The presence of intracranial hemorrhage with a fluid-blood level in patients receiving anticoagulant medication or with coagulopathy is an infrequent but well-documented complication. We reported a patient with a fluid-blood level with normal haemostasis. A 62-year-old-man was admitted with a left putaminal hemorrhage containing a fluid-blood level, but without abnormal haemostasis. Five months later the patient returned to the hospital because of a transient ischemic attack. A cranial CT demonstrated a hypodensity in the left putamen nucleus and corona radiata. Electrocardiogram revealed atrial fibrillation and a cardiac ultrasonographic examination showed mitral annulus calcification and left atrial enlargement. The finding of intracranial fluid-blood level has been seen in patients with arteriovenous malformations, primary and metastatic neoplasm, radiation-induced necroses, cerebral amyloid angiopathy, intrainfarct hematoma and without any identified aetiology. We suggest that in our patient this disorder was due to a intrainfarct hematoma.

Blood Coagulation↗
PubMed1998

[Intracerebral hemorrhage and treatment with platelet aggregation inhibitors: study of 21 cases].

INTRODUCTION: The place of platelet antiaggregants in the aetiology of intracerebral hemorrhage (IH) has not been extensively studied. OBJECTIVE: To analyze the characteristics of IH in patients treated with platelet antiaggregants and the possible clinical and prognostic differences from other primary IH. PATIENTS AND METHODS: A retrospective study of patients admitted to hospital with primary IH from 1985 to 1997. The cases were IH patients while being treated with platelet antiaggregants. For each case we selected two controls with IH and similar age and IH risk factors. The following data was analyzed: start of clinical condition; type, dose, indication and duration of treatment with antiaggregants; mortality, localization, volume and extension of IH to the ventricles. The last four variables were compared with the control group using the ji squared test (chi 2) and the t student test. RESULTS: 21one patients had a primary IH while being treated with antiaggregants: 20 with salicylates (17 aspirin and 3 riflusal) and one with ticlopidine. The dose of aspirin was 500 mg or less in 90% of the cases. In the group treated with salicylates, this was given for more than 20 months in 90% of the cases. Initially there was no clinical progression in any case. No significant differences were observed between the variable compared, although there was a tendency to greater volume, extension to the ventricles and mortality in the group treated with antiaggregants. CONCLUSIONS: More studies with larger numbers of patients are necessary to be able to confirm the tendencies observed.

Aged↗
PubMed1996

Acute painful diabetic neuropathy following severe weight loss.

A 34-year-old man, recently diagnosed as diabetic, presented an acute painful neuropathy. He reported a profound weight loss during the months preceding onset. There were no motor symptoms, and only mild neurological signs were observed on examination. Improvement was related to a good glycemic control and weight gain. Acute painful diabetic neuropathy is a condition that may affect diabetic patients shortly after development of the disease. The pathogenetic roles played by different factors are reviewed.

Acute Disease↗
PubMed1995

The gene for progressive myoclonus epilepsy of the Lafora type maps to chromosome 6q.

Progressive myoclonus epilepsy of the Lafora type (Lafora's disease) is an autosomal recessive disease characterized by epilepsy, myoclonus, dementia, and periodic acid-Schiff-positive intracellular inclusion bodies. The inclusion deposits consist of branched polysaccharides (polyglucosans) but the responsible biochemical defect has not been identified. Onset is during late childhood or adolescence and the disease leads to a fatal outcome within a decade of first symptoms. We studied nine families in which Lafora's disease had been proven by biopsy in at least one member. In order to locate the responsible gene, we screened the human genome with microsatellite markers spaced an average of 13 cM. We used linkage analysis in all nine families and homozygosity mapping in four consanguineous families to define the Lafora's disease gene region. Two point linkage analysis resulted in a total peak lod score of 10.54 for marker D6S311. Six additional chromosome 6q23-25 microsatellites yielded lod scores ranging from 5.92 to 9.60 at theta m = f = 0. An extended pedigree with five affected members independently proved linkage with peak lod scores over 3.8 at theta m = f = 0 for D6S292, D6S403, and D6S311. The multipoint one-lod-unit support interval covered a 2.5 cM region surrounding D6S403. Homozygosity mapping defined a 17 cM region in chromosome 6q23-25 flanked by D6S292 and D6S420 that contains the Lafora's disease gene.

Chromosome Mapping↗
PubMed1990

[Scrotal and perineal pain following coitus interruptus].

A case of perineal-scrotal and hypogastric pain following coitus interruptus in a young male patient is described. The physiopathological mechanisms involved in this condition in normal subjects or those with neuropathic disorders are discussed.

Adult↗
PubMedDate not supplied

[Genital brucellosis].

Since this is a systemic disease, it is not uncommon to find brucella organisms in urine during acute infection however, it frequently presents with orchi-epididymitis (2-20%) and, rarely, with granulomas in the urinary tract. We report on two cases of acute epididymitis. The pathogenesis, diagnosis and treatment of this disease entity are briefly viewed highlighting the urological problem.

Abscess↗