Journal of Clinical and Experimental Ophthalmology considers articles on clinical ophthalmology related issues such as ophthalmia neonatorum, pterygium histology, aphakic glaucoma, acute zonal occult outer retinopathy (AZOOR), hypertrophic pachymeningitis, phacomorphic glaucoma, pseudoexfoliation syndrome, binasal hemianopsia, bitemporal heteronymous hemianopsia, cycloplegic refraction, cycloplegic drugs, macular edema optical coherence tomography (OCT), juxta fovea retinal telangiectasis, central serous retinopathy treatment, involutional ectropion, impaired depth perception, lacrimal fistula, sagging eye syndrome, spontaneous periorbital ecchymosis, neonatal conjunctivitis, ocular pemphigoid, Non-Arteritic Anterior Ischemic Optic Neuropathy (NAION) and Arteritic Anterior Ischemic Optic Neuropathy (AAION) eye, macular pseudohole, scleromalacia perforans, and subperiosteal haemorrhage. Quality articles are welcome for submission which will aid in attaining high impact factor.

Emerging practices and the experiences in this field needs a critical and thorough discussion to spread the knowledge so that the researchers, ophthalmologists and pharmacist adopt them to pass on the benefits to the needy. The Journal of Clinical & Experimental Ophthalmology accepts articles in the form of research articles, review articles, short communications, letter to editors, commentaries, case reports, etc. This ophthalmology journal is a peer reviewed open access scholarly journal dedicated towards distribution of valuable information for the societal benefit. Ophthalmology journal impact factor is 1.42* for last 5 Years.

Eyeblink classical conditioning (EBCC) is a model paradigm for associative learning, one of the most basic forms of learning and memory. Two major EBCC paradigms are utilized with human subjects. In delay EBCC, a conditioned stimulus (CS; e.g., an auditory tone) co-terminates with the unconditioned stimulus (US; e.g., a corneal airpuff). In trace EBCC, CS presentation is followed by a silent interstimulus interval (which Pavlov termed the “trace” interval), with the US non-overlapping with the CS in time. Because EBCC paradigms are readily adapted across species, the neural substrates of EBCC are well studied, and include the cerebellum and anterior interpositus nucleus, hippocampus, and prefrontal cortex. Functional impairments of the latter regions predominantly impair trace EBCC, while cerebellar circuits are active in both delay and trace EBCC. Age-associated EBCC impairments are well documented, with both delay and trace EBCC declining with age. Although additional factors such as sensory alterations or varying stimulus parameters may also impact EBCC performance, performance in EBCC has been strongly linked to changes in the underlying neural structures involved. Exciting cross-fertilization of ideas have emerged from studies assessing both animal and human subjects acquiring, discriminating, or extinguishing classically conditioned eyeblink responses.

EBCC paradigms have been employed to assess individuals with a range of neurological deficits. For example, amnestic Korsakoff’s patients with specific cerebellar damage exhibit impaired delay EBCC. Abstinent alcoholics with or without amnesia show consistent performance profiles across both EBCC paradigms, i.e. if impaired on delay EBCC, individuals are also impaired on trace EBCC. While the amnestic H.M., with severe hippocampal damage, showed enhanced trace EBCC that transferred across sessions, Alzheimer patients are typically impaired on trace EBBC. Trace EBCC is also impaired in dyslexics, while delay EBCC is impaired in patients with inflammatory tremor, dystonia, or multiple sclerosis. Both acquisition and extinction of delay EBCC is altered in autism. In many conditions, complex interactions have been observed between comorbid states, with effects on both production and magnitude of conditioned responses.

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