400 Years after Thomas Willis: beyond the Polygon / 400 Anos depois de Thomas Willis: além do Polígono

Thomas Willis is famous for the cerebral arterial polygon that bears his name, but his contribution to neuroanatomy goes beyond that. Probably the first anatomist physician to attempt the study of the basal nuclei was Galenus. However, it was only in the 17th century that there was a leap in neuroanatomical knowledge of the region based on the studies by Willis, using a dissection technique with a caudal to cranial perspective.

Cortex: Gross Anatomy

The cerebral cortex consists of 2 hemispheres, the left and the right. These are divided by the falx cerebri, a dural-derived structure. The cerebral cortex receives input from various subcortical structures, often connecting through the thalamus and from other areas of the cortex by association fibers. The cortex then projects back to wide regions of the central nervous system, including the cortex, thalamus, basal nuclei, cerebellum, brainstem, and spinal cord. The types of fibers connecting areas of the central nervous system are designated according to the regions they connect. For instance, the fibers connecting the cortex to subcortical structures are called projection fibers. The fibers connecting 1 hemisphere to the opposite hemisphere are called callosal fibers, and the fibers connecting areas within the same hemisphere are called association fibers. Fibers connecting the cortex to the thalamus are designated corticothalamic fibers.

Experience of joint management of patient with Huntington's chorea by neurological and dental specialists with use of tetrabenazine

Huntington's chorea is a hereditary disease causing progressive degeneration of the central nervous system with the damage to extrapyramidal structures: basal nuclei, striatum, subthalamic nucleus with increased activity of the central dopaminergic pathways, with the development of neurological, psychiatric, and emotional/personality disorders [1, 17]. The inheritance pattern of the disorder is autosomal dominance. The prevalence of Huntington's disease ranges from 3 to 17 cases per 100,000 population, averaging 5–7 cases per 100,000 population in Russia [2]. The development of the disease is associated with the expansion of CAG (cytosine-adenine-guanine) trinucleotide repeats in the frst exon of the HTT gene encoding the huntingtin protein. This expansion of trinucleotides (long sections of glutamine residues) leads to the selective loss of neurons that connect the striatum and the globus pallidus. This leads to a loss of inhibitory activity and an increase in the excitation impulse, which leads to uncontrolled movements.Unfortunately, medical treatment does not slow down the progression of this disease (a lethal outcome occurs within 15–20 years). Improvement of the quality of life of people with Huntington's chorea, with the provision of medical services at an appropriate level, remains an urgent issue. This direction is especially relevant in providing dental care to patients with Huntington's chorea. Due to the pronounced hyperkinetic syndrome and compulsive movements in the muscles of the arms, trunk, neck and face, it is almost impossible to provide dental care for these patients. Currently, general anesthesia is used to enable dental intervention, but patients note that with frequent use of anesthesia, the patient's condition deteriorates, with an increase in hyperkinetic symptoms. Tetrabenazine is known to reduce the severity of hyperkinetic symptoms and is used in many countries [5].However, in our country many specialists are not familiar with it. During the follow-up of a patient with Huntington's chorea, with the selection of a therapeutic dose of tetrabenazine, it was possible to provide three stages of dental care for the patient without the use of general anesthesia. The material presented in the article can provide useful information on the use of tetrabenazine in patients with Huntington's chorea.

Moon Triggers “Menstrual Clock”

The study presents that Human Basal Ganglia situated underneath the Human Brain is a plausible reflection of the Solar System wherein the nine celestial bodies are the cosmic counterparts of the nine Basal Nuclei Orders in many aspects such as their orbital location and their significations in astrology of their organization and functions. Moon, the cosmic counterpart of Hypothalamus, together with the other messengers, namely the pituitary gland and the ovary, plausibly regulate human female menstrual cycle. The releasing of hormones by Hypothalamus and its messengers in a rhythmic fashion appear to be the result of variation in the intensity of lunar magnetism. Human females plausibly have an internal ‘menstrual clock’ that helps them anticipate and adapt to the regular rhythm so that it is synchronized with the Moon’s revolutions.

P14.23 Relation between neurological deficits and location of postsurgical ischemia in glioma resection

BACKGROUND Postoperative ischemia is a known complications of glioma resection and can lead to neurological deficits. New or worsened postoperative deficits are often transient, but some patients experience persisting effects after surgery. Neuroanatomical location of ischemia is suspected to play an important role in the development as well as persistence of neurological deficits. Therefore, the aim of this study was to investigate the spatial relation between postoperative ischemia and short-term and long-term neurological deficits. MATERIAL AND METHODS Postoperative ischemia was defined as new confluent areas of diffusion restriction on DWI in a retrospective database of 144 adult WHO grade II-IV supratentorial glioma patients, who received MRI within 3 days after resection in 2012–2014. New or worsened neurological deficits of any grade at discharge and after 3 months was assessed in relation to postoperative ischemia by an experienced neuro-oncologist. We manually delineated ischemic lesions and spatially normalized these to stereotaxic MNI space. Next, we performed voxel-based analysis (VBA) to identify locations of ischemia associated with new or worsened neurological deficits and corrected for multiple comparisons using family-wise error correction to eliminate false positive results. Delineations were labeled using the Harvard-Oxford cortical and subcortical atlases and a white matter atlas (XTRACT). RESULTS Any new or worsened neurological deficits were present in 44 (30.5%) cases at discharge and in 27 (20.9%) cases after 3 months, of which respectively 26 (18%) and 21 (16.3%) were related to ischemia. Volume of ischemia was significantly associated with deficits at discharge (P = 0.003) and after 3 months (P = 0.039). No areas of ischemia were associated with a lack of new or worsened deficits. A statistically significant cluster of 42.96cc was associated with deficits at discharge and encompassed the right frontal, insular and tempo-occipital regions. Voxels associated only with deficits at discharge included lateral occipital cortices and supramarginal gyri. A cluster of 17.68cc in the right frontal and insular lobes was significantly associated with deficits after 3 months. Overlapping areas included the right thalamus, caudate nucleus, putamen, globus pallidum, insular cortex, middle and inferior temporal gyri, corticospinal tract and superior thalamic radiation. CONCLUSION Transient and persisting new or worsened deficits after glioma resection were significantly associated with volume of postoperative ischemia. Ischemic lesions in right frontal and insular regions, including the basal nuclei, corticospinal tract and superior thalamic radiation were significantly associated with persisting neurological deficits after 3 months, while temporo-occipital lesions were associated with transient deficits only found at discharge.

Structural Brain Changes Associated with Overweight and Obesity

Obesity is a global health problem with a broad set of comorbidities, such as malnutrition, metabolic syndrome, diabetes, systemic hypertension, heart failure, and kidney failure. This review describes recent findings of neuroimaging and two studies of cell density regarding the roles of overnutrition-induced hypothalamic inflammation in neurodegeneration. These studies provided consistent evidence of smaller cortical thickness or reduction in the gray matter volume in people with overweight and obesity; however, the investigated brain regions varied across the studies. In general, bilateral frontal and temporal areas, basal nuclei, and cerebellum are more commonly involved. Mechanisms of volume reduction are unknown, and neuroinflammation caused by obesity is likely to induce neuronal loss. Adipocytes, macrophages of the adipose tissue, and gut dysbiosis in overweight and obese individuals result in the secretion of the cytokines and chemokines that cross the blood-brain barrier and may stimulate microglia, which in turn also release proinflammatory cytokines. This leads to chronic low-grade neuroinflammation and may be an important factor for apoptotic signaling and neuronal death. Additionally, significant microangiopathy observed in rat models may be another important mechanism of induction of apoptosis. Neuroinflammation in neurodegenerative diseases (such as Alzheimer’s and Parkinson’s diseases) may be similar to that in metabolic diseases induced by malnutrition. Poor cognitive performance, mainly in executive functions, in individuals with obesity is also discussed. This review highlights the neuroinflammatory and neurodegenerative mechanisms linked to obesity and emphasizes the importance of developing effective prevention and treatment intervention strategies for overweight and obese individuals.

Perigenual and Subgenual Anterior Cingulate Afferents Converge on Common Pyramidal Cells in Amygdala Subregions

The subgenual (sgACC) and pregenual (pgACC) anterior cingulate are important afferents of the amygdala, and have different cytoarchitecture, connectivity, and function. The sgACC is associated with arousal mechanisms linked to salient cues, while the pgACC is engaged in conflict decision-making, including in social contexts. How they influence the amygdala at the cellular level has not been explored in higher species. In monkeys, we placed same size, small volume tracer injections into sgACC and pgACC of the same hemisphere, and examined their terminal distribution to better understand how these different functional systems communicate with the amygdala. The sgACC has broad-based termination patterns in the amygdala, while the pgACC has a more restricted pattern which was always nested in sgACC terminals. Overlap of labeled fibers from each area occurred in subregions of the accessory basal and basal nuclei, termed 'hotspots'. In triple-labeling confocal studies, we found that the majority of randomly selected CAMIIα (+) cells (putative amygdala glutamatergic neurons) in 'hotspots' received dual contacts from the sgACC and pgACC. The ratio of dual contacts onto CAMIIα (+) cells occurred over a surprisingly narrow range in all 'hotspots', suggesting a consistent, tight balance of afferent contacts on postsynaptic projection neurons. We also found differences in bouton size from each afferent input. Large boutons, which are associated with greater synaptic strength, were approximately 3 times more frequent on sgACC versus pgACC axon terminals. Together, the results reveal a nested interaction in which pgACC ('conflict/social monitoring') terminals converge with the broader sgACC ('salience') terminals at both the mesoscopic and cellular level in 'hotspots', and do so in a tightly balanced manner. sgACC afferents have axonal bouton sizes consistent with a 'driver' function whereby new arousing cues (sgACC) can rapidly influence higher cognitive computations such as social/conflict monitoring.

Generalized choreoathetosis secondary to non-ketotic hyperglycemic disorder

Introduction: Type 2 diabetes mellitus is one of the diseases that is most associated with chorea, and although it is a rare complication, it is necessary tobe aware of it so that the correct diagnosis and early treatment can be made. Case report: Male patient, 78 years old, diabetic and uncontrolled hypertension. Began uncontrolled glycemic 7 days before admission. Evolves with imbalance when walking and with involuntary movements in the left upper limb. At admission, dextro 682 mg/dl and at neurological exam the presence of asymmetric choreoathetotic movements, more evident in the left dimidium. Investigation with neuroimaging, brain tomography showed the presence of hyperdensity in bilateral basal nuclei, confirmed by brain MRI. Other differential diagnoses were ruled out, such as hyperthyroidism, liver failure and rheumatic fever. The most likely diagnosis was generalized choreoathetosis secondary to a non-ketotic hyperglycemic disorder. During hospitalization, adequate glycemic control was performed and clonazepam was introduced as an aid, with significant improvement of movements and absence of the same at discharge. Conclusions: Cases of non-ketotic hyperglycemia are associated with the onset of chorea, and although it is a rare complication, it is not uncommon given the high incidence of diabetes mellitus in the Brazilian population, and clinical improvement may take weeks to months, even after adequate glycemic control.