Biomedical subjects

F R Costa-Jussà

Publications and source records attributed to F R Costa-Jussà.

6 recordsLinked to original sources

PubMed2001

Long-term effects of bilateral frontal brain lesion: 60 years after injury with an iron bar.

BACKGROUND: Harlow's report of the case of Phineas P. Gage in 1848 was one of the earliest description of the personality and behavioral changes following frontal lobe damage. Since Harlow's articles, a few more case reports of frontal lobe damage have been published. As standard neuropsychological and neurologic evaluations may reveal subtle defects, case reports have been particularly useful in characterizing the behavioral changes that follow frontal lobe damage. OBJECTIVE: To describe the long-term outcome of an 81-year-old patient who sustained a severe frontal brain lesion 60 years ago caused by the passage of an iron spike through his head. RESULTS: The patient has bilateral damage affecting the orbital and dorsolateral frontal regions. He displays many of the typical frontal behavioral disturbances described in the literature. His conduct is characterized by dependence on others, cheerfulness, planning difficulties, problems establishing realistic goals, lack of drive, and difficulties in initiating, continuing, and finishing activities. Although gross cognitive functioning is intact, neuropsychological deficits are present in the executive functioning, memory, and visuoconstructive domains. CONCLUSIONS: In contrast with the antisocial conduct pattern usually associated with frontal damage in the literature, this case suggests that large frontal lesions can produce behavioral and personality changes that are compatible with stable functioning in family, professional, and social settings. In addition to the localization of the lesion, many other factors should be considered in the long-term prognosis of frontal brain injured patients.

Adult↗

PubMed1988

Changes in denervated skeletal muscle of amiodarone-fed mice.

Prolonged dosing of mice with amiodarone produced a myopathy characterized by autophagic vacuolation and phospholipid inclusions. A previous morphological study had shown that amiodarone did not affect the rate of nerve regeneration after sciatic nerve crush. In the present study, reinnervation was assessed by the reappearance of miniature endplate potentials that confirmed that axonal regeneration and motor reinnervation was not affected by amiodarone. However, there was a marked delay in the recovery of motor function in the amiodarone-treated mice. Denervation was found to induce an extensive necrosis of muscle fibers in the deeper parts of fast-twitch muscles. Histochemical studies showed that type 1 fibers were spared, necrosis affecting mainly type 2 fibers with relatively high oxidative enzyme activity (fast-twitch oxidative fibers). Biochemical studies showed a significant increase in the amount of amiodarone and its metabolite in denervated muscle of amiodarone-treated mice when compared with contralateral, normally innervated muscles.

Amiodarone↗

PubMed1985

The pathology of amiodarone neurotoxicity. I. Experimental studies with reference to changes in other tissues.

Rats and mice were given amiodarone by mouth at doses of 50 mg/kg/day. The drug induced accumulations of lipids within lysosomes, leading to the formation of cytoplasmic bodies. These were found in many tissues, both nervous and nonnervous, but were excluded from regions with blood-brain or blood-nerve barriers. Of nervous system regions lying outside a vascular barrier, autonomic ganglia were the most affected, with large accumulations of lysosomal bodies in nerve cells and processes, and evidence of degenerative changes. the myenteric plexus was also involved. No significant changes were seen in peripheral nerves. A limited period of increased permeability caused by nerve crush, or due to immaturity of the blood-nerve barrier resulted in the short-lived appearance of drug-induced inclusions. The rate of regeneration of axons following nerve crush was not affected, although there were small defects in myelination.

Amiodarone↗

PubMed1985

The pathology of amiodarone neurotoxicity. II. Peripheral neuropathy in man.

Sural nerve changes are described in 2 cases of amiodarone neuropathy. Clinically, 1 patient developed a sensorimotor neuropathy, whereas in the other it was predominantly motor. Examination of sural nerves showed demyelination with only mild axonal loss. Cytoplasmic changes developed in Schwann cells of myelinated and unmyelinated axons, and involved loss of most recognizable organelles. These changes were associated with, and possibly preceded, myelin sheath breakdown. Inclusions, mainly of a lamellated type, were found in all cell types in the nerves. These inclusions, known to be lysosomal in origin, are a characteristic finding in amiodarone-induced neuropathy. The pathogenesis of the neuropathy is discussed, with particular reference to the findings in a parallel experimental study.

Adult↗

PubMed1985

The induction of pulmonary phospholipidosis and the inhibition of lysosomal phospholipases by amiodarone.

Administration of high doses of amiodarone to young adult rats leads to phospholipidosis of the lung, with extensive phospholipid storage by type II pneumonocytes and alveolar macrophages. Biochemical analysis reveals an increase in the total phospholipid content of the lung and in the proportion of phosphatidylcholine. The cause of the phospholipidosis is suggested to be the inhibition of lysosomal phospholipases, responsible for catabolizing phospholipids. It is shown that amiodarone is a potent inhibitor of phospholipases prepared from the soluble fraction of adult rabbit lung lysosomes.

Amiodarone↗

PubMed1984

Amiodarone lung toxicity: a human and experimental study.

This paper describes the pathology of pulmonary histiocytosis developing in a patient treated with amiodarone, and reports comparable changes in the lungs of rats and mice to which this drug had been administered. Ultrastructural studies indicate that the experimental lung changes are similar to those produced by iprindole and chlorphentermine. The patient also displayed focal necroses and an eosinophilic bronchiolitis; these may represent further effects of amiodarone on the lung.

Adult↗