Interest in the hippocampal formation and its role in navigation and memory arose in the second part of the 20th century, at least in part due to the curious case of Henry G. Molaison, who underwent brain surgery for intractable epilepsy. The temporal association observed between the removal of his entorhinal cortex along with a significant part of hippocampus and the developing severe memory deficit inspired scientists to focus on these regions. The subsequent discovery of the so-called place cells in the hippocampus launched the description of many other functional cell types and neuronal networks throughout the Papez-circuit that has a key role in memory processes and spatial information coding (speed, head direction, border, grid, object-vector etc). Each of these cell types has its own unique characteristics, and together they form the so-called “Brain GPS”. The aim of this short survey is to highlight for practicing neurologists the types of cells and neuronal networks that represent the anatomical substrates and physiological correlates of pathological entities affecting the limbic system, especially in the temporal lobe. For that purpose, we survey early discoveries along with the most relevant neuroscience observations from the recent literature. By this brief survey, we highlight main cell types in the hippocampal formation, and describe their roles in spatial navigation and memory processes. In recent decades, an array of new and functionally unique neuron types has been recognized in the hippocampal formation, but likely more remain to be discovered. For a better understanding of the heterogeneous presentations of neurological disorders affecting this anatomical region, insights into the constantly evolving neuroscience behind may be helpful. The public health consequences of diseases that affect memory and spatial navigation are high, and grow as the population ages, prompting scientist to focus on further exploring this brain region.

Drop foot is defined as difficulty of dorsiflexion of the foot and ankle due to weak anterior tibial, extensor hallucis longus and extensor digitorum longus muscles. Cauda equina syndrome, local peroneal nerve damage due to trauma, nerve entrapment, compartment syndrome and tumors are common etiologies. A 32-year-old male patient was applied with difficulty in dorsiflexion of both of his toes, feet and ankles after he had squatted in toilette for 6-7 hours (because of his haemorrhoid) after intense alcohol intake 2 weeks before. Acute, partial, demyelinating lesion in head of fibula segment of peroneal nerves was diagnosed by electromyography. This case was reported since prolonged squatting is an extremely rare cause of acute bilateral peroneal neuropathy. This type of neuropathy is mostly demyelination and has good prognosis with physical therapy and mechanical devices, but surgical intervention may be required due to axonal damage. People such as workers and farmers working in the squatting position for long hours should be advised to change their position as soon as the compression symptoms (numbness, tingling) appear.

Purpose - Methylation is a key epigenetic modification of DNA and regarding its impact on epilepsy, it is argued that “DNA methylation may play an important role in seizure susceptibility and maintenance of the disorder”. DNA methylation status of KCC2 (SCL12A5) and NKCC1 (SCL12A2) associated with refractory temporal lobe epilepsy was investigated in our study. Materials and methods - Thirty-eight patients with temporal lobe epilepsy (TLE) who were diagnosed by video EEG monitoring and 32 healthy control subjects were included in the study. Twenty-three patients in TLE group were men and the remaining 15 were women. Among them, 27 had unilateral temporal focus (9 with right; 18 with left) and 11 patients had bilateral TLE. We analyzed promoter region methylation status of the KCC2 (SCL12A5) and NKCC1 (SCL12A2) genes in the case and control groups. Gene regions of interest were amplified through PCR and sequencing was accomplished with pyro-sequencing. Results - We found a significant relationship between TLE and methylation on the NKCC1. However, there was no association between TLE and methylation on the KCC2 gene. Also, we found no association between right or left and unilateral or bilateral foci of TLE. There was no relationship between TLE and methylation on the NKCC1and KCC2 genes in terms of mesial temporal sclerosis in cranial MRI, head trauma or febrile convulsions. Conclusion - The methylation of NKCC1 can be a mecha­nism of refractory temporal lobe epilepsy. There are limited findings about DNA methylation in TLE. Therefore, further studies with large sample sizes are necessary.

[Here one case report of the posterior ischaemic optic neuropathy, a rare and underdiagnosed form of the non arteritic ischaemic optic neuropathy is presented, to underline the value of the MRI in the diagnosis. The ischaemic optic neuropathy is the infarction of the optic nerve. Depending on the affected segment of optic nerve (optic nerve head or retrobulbar segment) two subclasses exist: the anterior (AION) and the posterior (PION) ischaemic optic neuropathy. Ischaemic optic neuropathy characterized by sudden, painless, mononuclear loss of vision, and/or visual field defect, that is accompanied by a diagnostic picture of the optic disc fundus only in the case of the AION. The diagnosis of the PION is based on a diagnosis of exclusion described by Hayreh in 1981. The macular and retinal laesions, the etiological role of toxic agent, the compression and the inflammation of the optic nerve all have to be excluded. The differential diagnosis between the PION and the retrobulbar neuritis is more difficult. Nowadays, in addition to the case history and the clinical data the diagnosis of the PION could be confirmed with help of VEP (visual evoked potential) and MRI. In the case of an old woman who had a sudden, painless visual loss of left eye we confirmed the diagnosis of PION with MRI which was presumed after had excluding other etiological factors.]

[Several diseases are accompanied by hypoxic stress; elimination of it is an important physiological process. Our body provides a protective function which delays damage and destruction by hypoxia. In case of necrosis, it provides the mop up of the damaged area. This security system starts the regeneration in cells of the hypoxic zone which surrounds the necrotic area, resulting in the survival of the cells in hypoxic environment and ensuring the handling of the necrosis. The key molecules of the system are the hypoxia-induced factor molecules. The review discusses the physiological role of tissue hypoxia and normoxia and its effects on tissue regeneration. The physiological system triggered by the hypoxia-induced factor plays an important role in embryonic development, in wound healing and in numerous diseases (eg. myocardial infarction, stroke, vaculities, etc). Unfortunately, this system also plays a key role in several malignant tumors by rising the development of cells with increased aggressive fenotypes as well. The physiological process of regeneration starts in the hypoxic tumor cells aided by the hypoxia-induced factor system. The process results in neovascularization, and in the case of tissue damage, in the mop up of the necrotic tissue and in the restoration of tissue oxygenisation. However, after the formation of the new vascular network, tumor cells accustomed to hypoxia will not die but keep their original uncontrolled proliferation and anaerobic nature. Moreover the malignant nature of the cells will be increased by the genetic changes generated by the system of hypoxia- induced factors. The role of the hypoxia-induced factor system in tumor progression is discussed by the example of one of the most malignant tumors, malignant melanoma.]