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Neurology is the branch of medicine dealing with the diagnosis and treatment of all categories of conditions and disease involving the nervous system,which comprises the brain,the spinal cord and the peripheral nerves. Neurological practice relies heavily on the field of neuroscience,the scientific study of the nervous system.
Neurotrauma,brain damage or brain injury (BI) is the destruction or degeneration of brain cells. Brain injuries occur due to a wide range of internal and external factors. In general,brain damage refers to significant,undiscriminating trauma-induced damage.
A concussion,also known as a mild traumatic brain injury (mTBI),is a head injury that temporarily affects brain functioning. Symptoms may include loss of consciousness;memory loss;headaches;difficulty with thinking,concentration,or balance;nausea;blurred vision;dizziness;sleep disturbances,and mood changes. Any of these symptoms may begin immediately,or appear days after the injury. Concussion should be suspected if a person indirectly or directly hits their head and experiences any of the symptoms of concussion. Symptoms of a concussion may be delayed by 1–2 days after the accident. It is not unusual for symptoms to last 2 weeks in adults and 4 weeks in children. Fewer than 10% of sports-related concussions among children are associated with loss of consciousness.
A traumatic brain injury (TBI),also known as an intracranial injury,is an injury to the brain caused by an external force. TBI can be classified based on severity ranging from mild traumatic brain injury (mTBI/concussion) to severe traumatic brain injury. TBI can also be characterized based on mechanism or other features. Head injury is a broader category that may involve damage to other structures such as the scalp and skull. TBI can result in physical,cognitive,social,emotional and behavioral symptoms,and outcomes can range from complete recovery to permanent disability or death.
Cerebral atrophy is a common feature of many of the diseases that affect the brain. Atrophy of any tissue means a decrement in the size of the cell,which can be due to progressive loss of cytoplasmic proteins. In brain tissue,atrophy describes a loss of neurons and the connections between them. Brain atrophy can be classified into two main categories:generalized and focal atrophy. Generalized atrophy occurs across the entire brain whereas focal atrophy affects cells in a specific location. If the cerebral hemispheres are affected,conscious thought and voluntary processes may be impaired.
Neurofibrillary tangles (NFTs) are intracellular aggregates of hyperphosphorylated tau protein that are most commonly known as a primary biomarker of Alzheimer's disease. Their presence is also found in numerous other diseases known as tauopathies. Little is known about their exact relationship to the different pathologies.
Psychoorganic syndrome (POS),also known as organic psychosyndrome,is a progressive disease comparable to presenile dementia. It consists of psychopathological complex of symptoms that are caused by organic brain disorders that involve a reduction in memory and intellect. Psychoorganic syndrome is often accompanied by asthenia.
Memory disorders are the result of damage to neuroanatomical structures that hinders the storage,retention and recollection of memories. Memory disorders can be progressive,including Alzheimer's disease,or they can be immediate including disorders resulting from head injury.
Post-concussion syndrome (PCS),also known as persisting symptoms after concussion,is a set of symptoms that may continue for weeks,months,years after a concussion. PCS is medically classified as a mild traumatic brain injury (TBI). About 35% of people with concussion experience persistent or prolonged symptoms 3 to 6 months after injury. Prolonged concussion is defined as having concussion symptoms for over four weeks following the first accident in youth and for weeks or months in adults.
Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease linked to repeated trauma to the head. The encephalopathy symptoms can include behavioral problems,mood problems,and problems with thinking. The disease often gets worse over time and can result in dementia.
Post-traumatic epilepsy (PTE) is a form of acquired epilepsy that results from brain damage caused by physical trauma to the brain. A person with PTE experiences repeated post-traumatic seizures more than a week after the initial injury. PTE is estimated to constitute 5% of all cases of epilepsy and over 20% of cases of acquired epilepsy.
Post-traumatic seizures (PTS) are seizures that result from traumatic brain injury (TBI),brain damage caused by physical trauma. PTS may be a risk factor for post-traumatic epilepsy (PTE),but a person having a seizure or seizures due to traumatic brain injury does not necessarily have PTE,which is a form of epilepsy,a chronic condition in which seizures occur repeatedly. However,"PTS" and "PTE" may be used interchangeably in medical literature.
Steven T. DeKosky is the Aerts-Cosper Professor of Alzheimer's Research at the University of Florida (UF) College of Medicine,deputy director of UF’s Evelyn F. and William L. McKnight Brain Institute (MBI) and associate director of the 1Florida Alzheimer’s Disease Research Center.
Traumatic brain injury can cause a variety of complications,health effects that are not TBI themselves but that result from it. The risk of complications increases with the severity of the trauma;however even mild traumatic brain injury can result in disabilities that interfere with social interactions,employment,and everyday living. TBI can cause a variety of problems including physical,cognitive,emotional,and behavioral complications.
Samuel E. Gandy,is a neurologist,cell biologist,Alzheimer's disease (AD) researcher and expert in the metabolism of the sticky substance called amyloid that clogs the brain in patients with Alzheimer's. His team discovered the first drugs that could lower the formation of amyloid.
Clinical neuroscience is a branch of neuroscience that focuses on the scientific study of fundamental mechanisms that underlie diseases and disorders of the brain and central nervous system. It seeks to develop new ways of conceptualizing and diagnosing such disorders and ultimately of developing novel treatments.
Svetlana Dambinova is a Russian neuroscientist,Doctor of Biological Sciences,Distinguished Professor at Laboratory of biomarkers at Medical Center "DeKalb",Atlanta,USA. Dambinova was awarded as Honored Worker of Science of the Republic of Buryatia (1996) and Russian Federation (1998). Known in the world for research of glutamate receptors. The Head of the project of the International Department of Neurology SPBGMU them. Acad. Pavlov's.
Giulio Maria Pasinetti is the Program Director of the Center on Molecular Integrative Neuroresilience and is the Saunders Family Chair in Neurology at the Icahn School of Medicine at Mount Sinai (ISMMS) in New York City. Pasinetti is a Professor of Neurology,Psychiatry,Neuroscience,and Geriatrics and Palliative Medicine at ISMMS.
Sleep disorder is a common repercussion of traumatic brain injury (TBI). It occurs in 30%-70% of patients with TBI. TBI can be distinguished into two categories,primary and secondary damage. Primary damage includes injuries of white matter,focal contusion,cerebral edema and hematomas,mostly occurring at the moment of the trauma. Secondary damage involves the damage of neurotransmitter release,inflammatory responses,mitochondrial dysfunctions and gene activation,occurring minutes to days following the trauma. Patients with sleeping disorders following TBI specifically develop insomnia,sleep apnea,narcolepsy,periodic limb movement disorder and hypersomnia. Furthermore,circadian sleep-wake disorders can occur after TBI.
Andrew E. Budson is an American neurologist,academic and researcher. He is a Professor of Neurology at Boston University School of Medicine,Lecturer in Neurology at Harvard Medical School,Chief of Cognitive and Behavioral Neurology and Associate Chief of Staff for Education at the Veterans Affairs (VA) Boston Healthcare System,where he also serves as a Director of the Center for Translational Cognitive Neuroscience. He is Associate Director and Outreach,Recruitment,and Engagement Core Leader at the Boston University Alzheimer’s Disease Research Center.
References
- 1 2 "Ramon R. Diaz-Arrastia, MD, PhD profile | PennMedicine.org". www.pennmedicine.org.
- 1 2 "Zenith Fellows | Alzheimer's Association". Zenith.
- 1 2 "Ramon Diaz-Arrastia". scholar.google.com.
- 1 2 "Ramon Diaz-arrastia | Institute for Translational Medicine and Therapeutics | Perelman School of Medicine at the University of Pennsylvania". www.med.upenn.edu.
- ↑ "Ramon Diaz-Arrastia, MD, PhD | NeuroNEXT". neuronext.org.
- ↑ "Ramon Diaz-Arrastia – Implications for the Next Generation of Clinical Trials" (PDF).
- ↑ Kenney, Kimbra; Amyot, Franck; Haber, Margalit; Pronger, Angela; Bogoslovsky, Tanya; Moore, Carol; Diaz-Arrastia, Ramon (January 27, 2016). "Cerebral Vascular Injury in Traumatic Brain Injury". Experimental Neurology. 275 Pt 3: 353–366. doi: 10.1016/j.expneurol.2015.05.019 . PMID 26048614. S2CID 5388184.
- ↑ Kenney, Kimbra; Amyot, Franck; Moore, Carol; Haber, Margalit; Turtzo, L. Christine; Shenouda, Christian; Silverman, Erika; Gong, Yunhua; Qu, Bao-Xi; Harburg, Leah; Wassermann, Eric M.; Lu, Hanzhang; Diaz-Arrastia, Ramon (April 27, 2018). "Phosphodiesterase-5 inhibition potentiates cerebrovascular reactivity in chronic traumatic brain injury". Annals of Clinical and Translational Neurology. 5 (4): 418–428. doi:10.1002/acn3.541. PMC 5899908 . PMID 29687019.
- ↑ Wang, J. Y.; Bakhadirov, K.; Abdi, H.; Devous, M. D.; Marquez de la Plata, C. D.; Moore, C.; Madden, C. J.; Diaz-Arrastia, R. (August 30, 2011). "Longitudinal changes of structural connectivity in traumatic axonal injury". Neurology. 77 (9): 818–826. doi:10.1212/WNL.0b013e31822c61d7. PMC 3162636 . PMID 21813787.
- ↑ Diaz-Arrastia, R.; Agostini, M. A.; Frol, A. B.; Mickey, B.; Fleckenstein, J.; Bigio, E.; Van Ness, P. C. (November 27, 2000). "Neurophysiologic and neuroradiologic features of intractable epilepsy after traumatic brain injury in adults". Archives of Neurology. 57 (11): 1611–1616. doi:10.1001/archneur.57.11.1611. PMID 11074793 – via PubMed.
- ↑ Gupta, Puneet K.; Sayed, Nasreen; Ding, Kan; Agostini, Mark A.; Van Ness, Paul C.; Yablon, Stuart; Madden, Christopher; Mickey, Bruce; D'Ambrosio, Raimondo; Diaz-Arrastia, Ramon (August 15, 2014). "Subtypes of post-traumatic epilepsy: clinical, electrophysiological, and imaging features". Journal of Neurotrauma. 31 (16): 1439–1443. doi:10.1089/neu.2013.3221. PMC 4132580 . PMID 24693960.
- ↑ "Extracellular vesicles as distinct biomarker reservoirs for mild traumatic brain injury diagnosis – Brain Communications".
- ↑ "Effects of age and time since injury on traumatic brain injury blood biomarkers: a TRACK-TBI study – Brain Communications".
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