Experimental research on the growth of internal flaws has rarely been reported due to the fact that it is difficult to cut internal flaws in specimens and cannot capture the initiation and propagation processes of internal flaws through direct observations. This paper proposed a method for creating internal flaws in specimens by utilizing the volatilization of camphor. A series of compression tests were performed on rock-like specimens including two embedded circular flaws, and CT techniques were used to investigate the internal damage behavior of flawed specimens. Experimental results illustrate that the strength and deformation properties of flawed specimens increase nonlinearly with the confining pressure as well as flaw inclination angle. Crack coalescence patterns and failure modes of flawed specimens depend on not only the confining pressure but also the flaw inclination angle. The crack coalescence pattern varies from wing crack coalescence to mixed tension-shear crack coalescence and then to the shear crack coalescence as the crack inclination angle increases. Confining pressure contributes to shear crack growth and has an inhibiting effect on the propagation of tension cracks. For specimens with the same flaw inclination angle, the failure mode changed from tension failure to mixed shear-tension failure or from mixed shear-tension failure to pure shear failure with the increase of confining pressure.

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Spinocerebellar ataxia type 3 (SCA3) is a form of autosomal dominant cerebellar ataxia with a wide range of clinical manifestations, including ataxia and pyramidal and extrapyramidal signs. A few SCA3 patients have been noticed to be predisposed to the development of inclusion body myositis. It is still unknown whether muscle can be primarily involved in the pathogenesis of SCA3. This study reported an SCA3 family in which the index patient initially presented with parkinsonism, sensory ataxia, and distal myopathy but the absence of cerebellar and pyramidal symptoms. The clinical and electrophysiological studies implied a possible combination of distal myopathy and sensory–motor neuropathy or neuronopathy. MRI muscle showed selective fat infiltration and absence of denervated edema‐like changes, indicating the distal muscle weakness had a myopathic origin. Muscle pathology showed the myopathic involvement, besides neurogenic involvement, characterized by chronic myopathic changes with multiple autophagic vacuoles. Genetic screening revealed expanded CAG of 61 repeats in the ATXN3 gene, which showed co‐segregation in the family. Besides the neurogenic origin, the myopathic origin may be partly attributed to the limb weakness of SCA3 patients, which expands the spectrum of the clinical manifestation of SCA3.