Parkinson's disease is a severe neurodegenerative disorder. Currently, deep brain electrical stimulation (DBS) is the first line of surgical treatment. However, serious neurological impairments such as speech disorders, disturbances of consciousness, and depression after surgery limit the efficacy of treatment. In this review, we summarize the recent experimental and clinical studies that have explored the possible causes of neurological deficits after DBS. Furthermore, we tried to identify clues from oxidative stress and pathological changes in patients that could lead to the activation of microglia and astrocytes in DBS surgical injury. Notably, reliable evidence supports the idea that neuroinflammation is caused by microglia and astrocytes, which may contribute to caspase-1 pathway-mediated neuronal pyroptosis. Finally, existing drugs and treatments may partially ameliorate the loss of neurological function in patients following DBS surgery by exerting neuroprotective effects.
Keyphrases
- deep brain stimulation
- oxidative stress
- end stage renal disease
- cerebral ischemia
- newly diagnosed
- ejection fraction
- minimally invasive
- traumatic brain injury
- chronic kidney disease
- spinal cord injury
- multiple sclerosis
- cell death
- patient reported outcomes
- inflammatory response
- depressive symptoms
- prognostic factors
- coronary artery bypass
- dna damage
- cognitive impairment
- white matter
- neuropathic pain
- induced apoptosis
- lipopolysaccharide induced
- brain injury
- subarachnoid hemorrhage
- atrial fibrillation
- blood brain barrier
- nlrp inflammasome
- coronary artery disease
- endoplasmic reticulum stress