Abstract. Two Japanese quail which were incapable of wing movement and three normal quail were examined by histological and ultrastructural methods. The diseased birds had glycogen deposits in their skeletal muscle, cardiac muscle, smooth muscle, and nerve cells of the brain and spinal cord. According to the distribution of the lesions and the characteristics of the deposited glycogen, the diseased birds had glycogenosis which was analogous to type I1 found in man. The usefulness of this disease as a model for glycogenosis in man is discussed.
The autopsy findings in a patient with late-onset acid maltase deficiency who died following rupture of a basilar artery aneurysm are reported. The patient developed muscular weakness and wasting at the age of 20 years and died 9 years later after suddenly falling into a coma. At autopsy a giant fusiform aneurysm was found in the basilar artery which had ruptured at the base of the pons, leading to a large haematoma in the pons. The cerebral arteries and arterioles showed extensive vacuolar degeneration of smooth muscle cells in the media. It is suggested that the aneurysm was induced by fragility of the arterial wall due to this smooth muscle change.
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