Endothelial cell function is essential to maintain corneal transparency, but unfortunately the regenerative capacity of the endothelium is limited. There are only a few reports describing the effect of age on morphologic appearance of corneal endothelial cells of dogs. Studies of normal corneal endothelial cells in humans and dogs have shown a decrease in endothelial cell density (ECD) and an increase in pleomorphism and polymegethism with advancing age. The purpose of this study was to investigate the effect of age on ECD and endothelial cell morphology in dogs. A total of 30 dogs were divided into three groups (10 dogs/group) based on age: group 1 (2-12 months old), group 2 (24-72 months old), and group 3 (84 months or older). Corneas were processed for light and scanning electron microscopy. Results showed only difference in cell density between group 1 and groups 2 and 3, showing an initial decrease in cell density as the animal matured. Whereas there was significantly greater variation in cell size within the dogs in group 3 than there was within the other two groups, suggesting that there was increased polymegethism and pleomorphism with advancing age.

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-We report a case of a 26-year-old man who presented a lower motor neuron syndrome due to hyperparathyroidism. Electromyography showed neurogenic features with normal nerve conduction studies. Hypercalcemia led to the discovery of a primary hyperparathyroidism with gland hyperplasia. Following parathyroid surgery there was recovery of the neurological symptoms.KEY WORDS: parathyroid gland, hyperparathyroidism, spinal muscular atrophy, gland hyperplasia.Hiperparatiroidismo primário simulando doença do neurônio motor: relato de caso RESUMO -Descrevemos o caso de homem de 26 anos que apresentou síndrome do neurônio motor inferior devido a hiperparatiroidismo. A eletromiografia mostrou aspecto neurogênico com estudos da condução normal. Hipercalcemia levou à descoberta de hiperparatiroidismo primário com hiperplasia da glândula. A p ó s a cirurgia de ressecção da paratiróide, houve regressão dos sintomas neurológicos.PA L AV R A S -C H AVE: glândula paratiróidea, hiperparatiroidismo, atrofia muscular espinal, hiperplasia glandular.The neurological clinical syndrome of hyperparathyroidism includes easy fatigability, weakness and especially amyotrophy, of proximal muscles with preserved reflexes in most cases. Neuromuscular symptoms resemble lower motor neuron disord e r s with or without upper motor neuron signs. Neurological complications are common but are minor i n most cases; in some instances, however, they are s o severe as to suggest a primary and even untreatable neurological disorder. Treatable neurological d i sorders mimicking motor neuron disease must be e xcluded and the calcium and phosphorus levels h a v e to be measured since hyperparathyroidism can be cured as in the case we report. CASEA 26-year-old caucasian man presented with a oneyear history of symmetric proximal weakness and leg p a i n s , resulting in frequent falls and walking difficulties. He reported difficulty in swallowing, chewing, breathing and speaking. In addition and noted a chest deformity.Examination revealed a short man with slight proximal muscle atrophy in the upper limbs and proximal e d i stal atrophy in the lower limbs (Fig 1). There were no fasciculations and both mental status and speech were normal, whilst cranial nerves were intact. Muscle power (according to MRC) was grade 4 in all proximal limbs. The sensory examination was normal. Muscle stretch reflexes were grade 2 in the upper and lower limbs with flexor plantar responses bilaterally. Laboratory studies including routine chemistries, c r eatinephosfokinase and thyroid function were normal. T h e first electrophysiological study (April 2002) showed a neurogenic pattern characterized by polyphasic motor unit potentials with decreased recruitment in several musc l e s of the upper and lower limbs. No fasciculations and fibrillations were seen. Nerve conduction studies were unremarkable. The molecular diagnosis for spinal muscular atrophy (SMA) -(SMN gene) was negative. Five m o n t h s l a t e r, the patient was hospitalized with spontaneous femur fracture. ...

To our knowledge, autoimmune keratolysis secondary to cutaneous LCCV (EED) has not been described previously, and there has been no description of granulomatous reaction (in the conjunctiva) in EED.