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.

[Mentalization or theory of mind as an aspect of our social cognition, is our ability to infer mental states of others (intentions, desires, thoughts, emotions) and to predict their behavior accordingly. This function significantly affects our participation and orientation in the social world and plays an important role in conversational situations, social interactions, social integ­ration and adaptation. The brain regions that serve as the basis for mind-reading function can be damaged as a consequence of traumatic brain injury, which frequently occurs among the younger population. Traumatic brain injury can cause focal or diffuse cerebral injuries, often leading to theory of mind deficit. In this topic such publications were researched that compared theory of mind ability between traumatic brain injury patients and control subjects (comparative case-control studies). We searched for the studies in the following internet based/online databases: PubMed, Web of Science, ScienceDirect, Google Scholar, APA PsycNET (PsycARTICLES) and EBSCO Host. The search was performed using the following key word combinations: theory of mind or mentalizing or social cognition AND traumatic brain injury or head/brain injury or diffuse axonal injury. Based on the results of the included and processed studies (21 pc), traumatic brain injury often leads to mentalization deficit with different severity. With this present review we aim to draw attention to the fact that the appearance and severity of mind reading dysfunction can considerably affect the outcome of the disease, the length of rehabilitation time and the prognosis of traumatic brain injury patients. Besides this, with this review, we aim to take sides in whether theory of mind ability is domain-specific or domian-general based on studies including traumatic brain injury patients.]

[Dizziness is one of the most common causes of medical visits. Management of the dizzy patient may be challenging both for the general practitioner, in emergency departments, and special clinics, as behind a seemingly homogeneous clinical presentation several very different etiologies may occur. Research of the last two century enriched our knowledge about physiology and pathophysiology of the vestibular system. Much knowledge is now available about the labyrinth being able to sense head motions and gravity, processing of afferent vestibular stimuli, reflectory oculomotor and postural control, or recovery of the vestibular system. Based on scientific results new beside tests have been introduced including provocation maneuvers for detecting ectopic otoliths in different semicircular canals, head impulse test to examine function of the vestibulo-ocular reflex, and the HINTS+ battery for differentiation of peripheral or central origin of an acute vestibular syndrome. Technical innovations like videooculography and vestibular evoked myogenic potentials enable us to selectively and side-specifically examine the function of all six semicircular canals and two otolith organs. Pathomechanism of disorders with vertigo and dizziness became more clear resulting in the development or amendment of diagnostic criteria of several vestibular disorders including vestibular migraine, Menière’s disease, benign paroxysmal positional vertigo, persistent postural-perceptual dizziness, bilateral vestibulopathy. Broader knowledge about the pathomechanism promoted the development of new therapeutic methods like different repositioning maneuvers in benign paroxysmal positional vertigo, pharmaceutical therapies, vestibular rehabilitation, and psychotherapy. We aimed to summarize the novelties in the field of oto-neurology.]

[Necrotizing fasciitis is a rare and high mortality condition. Most commonly it is spreading in the extremi­ties, abdominal wall soft tissues and perineal region, but occurs rarely in the retroperitoneal space too. Primary treatment is debridement with administered antibiotics, supported by negative pressure wound care. The present case report concerns a successful treatment of an extensive necrotizing fasciitis spreading from the hip region and ending up in a retroperitoneal abscess. A gradually increasing, painful, ulcerated swelling developed in the patient’s right hip region. On the first examination, elevated laboratory markers of inflammation were identified while the necrotizing lesion raised concerns of sarcomatic background. Initially, we started antibiotics and took tissue samples. The prompt CT scan confirmed a large abscess complex involving also the retroperitoneal space. The surgical exploration verified a typical necrotizing fasciitis and after removing debridement negative pressure wound care was started. After 14 days of this treatment the patient recovered successfully. Negative pressure wound therapy is pivotal in the treatment of necrotizing fasciitis. The number of wound dressings and of medical staff – patient contacts can be significantly reduced by this me­thod. It has a major advantage in the COVID-19 pandemic, since minimalizing close contacts is of vital importance in controlling the spread of the virus.]

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.