Acute striatal necrosis can be divided into three stages [70].The first stage is cytotoxic edema in the basal ganglia, cerebral ischemia, and increased blood volume in the gray matter, which occurs within 24 h after motor deficits, and cranial MRI shows increased signal intensity on T2-weighted imaging of the shell nucleus and caudate nucleus [71], along with diffusion limitation [72]
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We also implanted DBS electrodes into the centrolateral nucleus of the thalamus, a region implicated in mediating the communication between the cerebellum and basal ganglia in dystonia [29]
As fasting continues, autophagy remains elevated while the body continues to target damaged cells, pathogens, liver fat, and visceral fat
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