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Neuroimaging in Nuclear Medicine
Published in Michael Ljungberg, Handbook of Nuclear Medicine and Molecular Imaging for Physicists, 2022
Anne Larsson Strömvall, Susanna Jakobson Mo
The neurons have thin extensions, called axons, through which they interconnect via electrical impulses, causing the release of neurotransmitters. An isolating fatty covering called the myelin sheath often encases axons in order to enhance and speed up the transmission of the electrical impulses. The brain tissue beneath the cortex – that is, the subcortical white matter – is dominated by myelinated nerve fibres. Deep within the white matter of each cerebral hemisphere, there are defined areas, nuclei, of grey matter, for example, the basal ganglia. The basal ganglia include the striatum, which in turn is divided into the caudate nucleus and the putamen. A tiny, paired area of grey matter in the brainstem is called the substantia nigra, which is also considered part of the basal ganglia. The thalamus is another important subcortical nucleus lying medial to the striatum. The cerebellum also has two hemispheres and a middle part called the vermis. The cerebellum is heavily folded, and its proportion of white matter is smaller compared to the cerebrum.
Head Injury
Published in Ian Greaves, Keith Porter, Jeff Garner, Trauma Care Manual, 2021
Ian Greaves, Keith Porter, Jeff Garner
Contusions (or traumatic subpial extravasations of blood) are effectively bruises within the brain (Figure 13.7). These can coalesce to form a more distinct haematoma. Brain tissue is clearly injured in these cases. These lesions can often evolve (‘blooming’), swelling and enlarging over time in the same manner a bruise in the leg will often worsen. Classically, contusions can be under the location of direct trauma (coup injury) and/or opposite the location of impact (contrecoup) (Figure 13.8). The rough surface of the anterior and middle fossa means that the frontal inferior temporal lobes are common locations for contusions. Most contusions are managed conservatively; however, superficial haematomas are sometimes evacuated.15 If they cause a rise in intracranial pressure then a decompressive operation may be required.16
Introduction to dementia
Published in Joanne Brooke, Dementia in Prison, 2020
Diseases under the umbrella of dementia all originate in and cause damage to the brain. Alzheimer’s disease is no exception. This dementia is named after the neurologist, Dr Alois Alzheimer, who first described the disease in 1906. Dr Alzheimer reported an ‘unusual disease of the cerebral cortex’ to the 37th Meeting of South-West German Psychiatrists in Tubingen (Hippius and Neundorfer, 2003). He described the symptoms of a woman, which commenced when she turned 50. Auguste D.’s symptoms included memory loss, disorientation, hallucinations and ultimately her death at only 55 years. Dr Alzheimer performed a post-mortem, which showed various abnormalities of the brain. These included a thinner than normal cerebral cortex and senile plaques, previously only encountered in elderly people, along with neurofibrillary tangles (Hippius and Neundorfer, 2003). The impact of Alzheimer’s disease on the brain is now often referred to as plaques and tangles, which are the build-up of amyloid plaques and neurofibrillary tangles that lead to the death of brain tissue and functioning.
Altered Prostaglandin E Receptor Subtype 3 Expression in Lacrimal Glands of Patients with Chronic Stevens-Johnson Syndrome
Published in Ocular Immunology and Inflammation, 2023
Swati Singh, Boyinpally Sridhar Rao, Sayan Basu
The expression of EP3 has never been studied before in the lacrimal glands. The brain tissue (cytoplasmic expression in neurons) served as a positive control. The tissue sections of the study, control groups, and brain were stained for immunohistochemistry using antibodies against EP3 receptor (rabbit anti-human EP3 polyclonal antibody, 1:200 (101760; Cayman Chemicals Co., Ann Arbor, MI). Deparaffinized sections were rehydrated with graded alcohol of 100%, 90%, 80% dilution followed by antigen retrieval (heating the sections with EDTA buffer (pH-9.0) for 30 minutes). Then the slides were incubated with bovine serum albumin (catalog no-A7906, Sigma, USA) for 20 minutes to avoid non-specific antibody reaction. The EP3 primary antibody (1:200) was applied for one hour at room temperature. The prediluted secondary antibodies (Dako, Denmark, Europe) were incubated at room temperature for 30 minutes. Samples were analysed under an Olympus light microscope (BX51. Images were captured using Aperio image scope software (Leica biosystems, Mumbai, India). The number of mononuclear cells were counted in 10 high power fields.
Research progress of mechanisms for tight junction damage on blood–brain barrier inflammation
Published in Archives of Physiology and Biochemistry, 2022
Bo Zhao, Qiyang Yin, Yuxiang Fei, Jianping Zhu, Yanying Qiu, Weirong Fang, Yunman Li
Upon infection or injury, inflammation is a natural and necessary response. However, in some cases, immune system activation induced by inflammation has a negative impact (Straub 2017). The first step of the inflammatory response in the CNS is the activation and polarisation of microglia (Cherry et al. 2014). At the onset of some CNS diseases, microglial activation stimulates multiple inflammatory cascades in the CNS such as the TLR2/4/MyD88/NF-κB, PI3K/Akt/NF-κB, Rho/ROCK and other signalling pathways (Li et al. 2018, Zheng et al. 2018, Girolamo et al. 2019). The release of cytokines, chemokines, and growth factors resulting from pathway activation can induce the activation of TJ-degrading metalloproteinases (MMPs); increasing the permeability of the BBB. Harmful substances or immune cells entering the brain tissue will then bring about brain damage. Further, the infiltration of immune cells into the brain parenchyma will release additional cytokines which exacerbate inflammation and further break down the BBB, promoting a vicious circle of events (Patel et al. 2013, Ranieri et al. 2016, Gupta et al. 2018).
Comparison of head impact frequency and magnitude in youth tackle football and ice hockey
Published in Computer Methods in Biomechanics and Biomedical Engineering, 2022
Julia Meliambro, Clara Karton, Janie Cournoyer, Andrew Post, T. Blaine Hoshizaki, Michael D. Gilchrist
Brain trauma results when the neuronal tissues experience a magnitude of strain that causes either a pathophysiological cascade or structural deficit that affects function, which in the case of concussion presents as symptoms, but also may be asymptomatic (sub-concussive) (Meaney and Smith 2011; Prins et al. 2013; Giza and Hovda 2014; Post and Hoshizaki 2015). In a sporting environment such as tackle football or ice hockey, these impact induced strains of the brain tissue can come from multiple event types, and it is important to understand how players are being impacted so that these high risk events can be reduced. Recently there has been investigations into youth ice hockey event types and how they contribute to brain strains (Chen et al. 2020; Post et al. 2021), but no similar comparison has been made to tackle football to determine if the youths experience similar brain trauma loads during game play. There has been relatively little brain strain magnitude research in tackle football for youth populations, with the majority focused on the elite athletes (Pellman et al. 2003; Zhang et al. 2004; Karton et al. 2020).