The pathophysiological changes underlying impairment of cognition in Parkinson's disease (PD) are complex and not fully understood till date. Hence, understanding the structural changes responsible for cognitive decline in PD is essential for early diagnosis and to offer effective treatment. In this review, we discuss the neuroanatomical changes in major brain structures responsible for cognition in PD. We have included the key findings of various studies to provide up-to-date information for better understanding of pathophysiology of PD, which will help researchers and clinicians in planning and developing new treatment methods for the benefit of PD patients.

Objective:There is a paucity of information regarding the specific anatomy and clinical significance of variations of foramen ovale (FO). The present study was undertaken to define this anatomy in more detail and to review the literature regarding these anatomic variations.Materials and Methods:A total of 124 adult human dry skulls were analyzed for the variations in appearance and number of FO being noted. The length and width of the FO of both sides were determined using digital vernier calipers and area (A) was also calculated and analyzed.Results:Of 82 adult skulls, the values for the right side was 7.64 ± 1.194 mm, 5.128 ± 0.827 mm, and 30.808 ± 7.545 mm2 and for the left side the values was 7.561 ± 1.123 mm, 5.244 ± 0.950 mm, and 31.310 ± 8.262 mm2, respectively, for the mean length, width, and area of the FO. The shape of foramen was typically ovale in most of the skulls (56.70%) with some bony variations such as spine, tubercles, bony bridge/bar, and confluence.Conclusion:Such variants in the FO could interfere with transcutaneous needle placement into the FO or distort anatomic relationships during approaches to the cranial base.

Angiotensin-converting enzymes are increasingly being tested in therapeutics of Parkinsonism. The objective of the present study was to evaluate the behavioral changes and neuroprotective role of captopril in the rotenone model of Parkinsonism in rats. Adult Wistar albino rats were divided into four groups of six each. Parkinsonism was induced with rotenone (3 mg/Kg intraperitoneal) in three groups. The experimental group was treated with captopril (20 mg/kg intraperitoneal). The effects were compared with a standard group treated with levodopa (12 mg/Kg) and Benserazide (3 mg/Kg). Behavioral effects were evaluated by the rotarod test, spontaneous locomotor activity, hole board test, forced swim test, and tail suspension test. Neuroprotection was noted with an estimation of glutathione and lipid peroxidation from rat brain homogenate. Levels of dopamine, serotonin, and GABA were also noted. Haematoxylin and eosin-stained sections of the brain evaluated for any histoarchitectural changes. Rats pre-treated with captopril have shown a significant increase in the duration of stay in the rotarod test, a significant increase in the number of head dipping in hole board test, significant lower duration of immobility in forced swim test and tail suspension test. Captopril has a significant neuroprotective role, as evidenced by a significant decrease in levels of glutathione and a significant increase in lipid peroxidase, myeloperoxidase, catalase, superoxide dismutase, and MAO-B levels. Captopril has significant effects on brain neurotransmitters, as evidenced by dopamine, serotonin, and acetylcholine. Captopril has shown significant neuronal protection by increased expression of Bcl-2 immunohistochemistry in rotenone-induced PD. Captopril has shown significant improvement in motor coordination (as evidenced through rotarod test), exploratory behavior (hole board test), depression (forced swimming test, and tail suspension test). Captopril significantly reduces oxidative stress conditions. Captopril has not shown major histoanatomical changes in the rotenone model. Angiotensin-converting enzyme inhibitors; neuroprotection; dopaminergic neurons; Parkinsonism; rotenone model

Understanding the microanatomical changes in brain structures is necessary for developing innovative therapeutic approaches to prevent/delay the cognitive impairment in epilepsy. We review here the microanatomical changes in the brain structures related to cognition in epilepsy. Here, we have presented the changes in major brain structures related to cognition, which helps the clinicians understand epilepsy more clearly and also helps researchers develop new treatment procedures.

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