2-Minute Neuroscience: Caffeine Neuroscientifically Challenged 2026-09-21 | 2-Minute Neuroscience: Caffeine
Cotards syndrome Neuroscientifically Challenged 2024-06-18 | Soundtrack: Classic Horror 1 - Dark World by Kevin MacLeod is licensed under a Creative Commons Attribution 4.0 license. creativecommons.org/licenses/by/4.0
Akinetopsia Neuroscientifically Challenged 2024-06-03 | The music March of the Mind by Kevin MacLeod is licensed under a Creative Commons Attribution 4.0 license. creativecommons.org/licenses/by/4.0
2-Minute Neuroscience: Seasonal Affective Disorder Neuroscientifically Challenged 2024-05-30 | Seasonal affective disorder is a subtype of depression or bipolar disorder in which symptoms appear at specific times of the year and go into full remission at other times. In this video, I discuss some of the hypothesized neurobiological mechanisms underlying seasonal affective disorder.TRANSCRIPT:Seasonal affective disorder is a subtype of depression or bipolar disorder in which symptoms appear at specific times of the year and go into full remission at other times. The condition most commonly develops during fall or winter, but spring or summer cases do also occur. In order to be diagnosed with seasonal affective disorder, someone must meet the criteria for major depressive disorder or bipolar disorder, but also display seasonal patterns with their symptoms for at least two years. The mechanisms underlying seasonal affective disorder are not fully understood, and are likely not the same in every case. One hypothesis is that seasonal affective disorder is linked to a disruption in circadian rhythms, the 24-hour cycles that regulate the function of our bodies. According to this hypothesis, in some individuals circadian rhythms may not adjust appropriately when the length of the day changes with the seasons. This could lead to a misalignment of circadian rhythms and environmental light, as well as a misalignment of biological processes like melatonin release and sleep. While this does not seem to explain all cases of seasonal affective disorder, it does provide an explanation for why exposure to very bright light, as is done in bright light therapy, has been found to be effective in treating some cases of the disorder.Several other hypotheses have been proposed to explain seasonal affective disorder, some of which might be also linked to circadian rhythm disruption. For example, studies have found that some individuals with seasonal affective disorder might have deficiencies in retinal sensitivity to light. Other studies suggest low levels of vitamin D could play a role in some cases, and abnormalities in levels of neurotransmitters like serotonin and norepinephrine have also been implicated.REFERENCES: Galima SV, Vogel SR, Kowalski AW. Seasonal Affective Disorder: Common Questions and Answers. Am Fam Physician. 2020 Dec 1;102(11):668-672. PMID: 33252911.Rohan KJ, Roecklein KA, Haaga DAF. Biological and Psychological Mechanisms of Seasonal Affective Disorder: A Review and Integration. Current Psychiatry Reviews. 2009;5:37-47.Sohn CH, Lam RW. Update on the biology of seasonal affective disorder. CNS Spectr. 2005 Aug;10(8):635-46; quiz 1-14. doi: 10.1017/s109285290001960x. PMID: 16041295.Image of trees appearing at the 10-second mark is the work of J. Hageluken, available at: commons.wikimedia.org/wiki/File:B%C3%A4ume_Jahreszeit_2013.jpg
2-Minute Neuroscience: Zolpidem (Ambien) Neuroscientifically Challenged 2024-05-10 | Zolpidem, better known by the brand name Ambien, is a medication primarily used to treat insomnia and other sleep-related problems. In this video, I discuss the safety and effectiveness of zolpidem as well as how it works in the brain to promote sleep. TRANSCRIPT:Zolpidem, better known by the brand name Ambien, is a medication primarily used to treat insomnia and other sleep-related problems. Studies have found zolpidem to be effective in reducing sleep latency, or the amount of time it takes someone to fall asleep, as well as in increasing total sleep time. Zolpidem belongs to a class of medications known as non-benzodiazepine hypnotics, sometimes called Z-drugs because many of the first of these drugs to be sold had names that started with the letter Z.Similar to the benzodiazepines, zolpidem exerts its effects by increasing activity at receptors for the neurotransmitter GABA. GABA is primarily an inhibitory neurotransmitter, and increasing GABA activity can promote sleep as GABA can decrease activity in parts of the brain that promote wakefulness. Unlike benzodiazepines, however, zolpidem is thought to selectively bind to specific GABA receptor subtypes that are especially involved in sleep-inducing effects.While zolpidem has been found to be effective and safe in the short-term management of sleep problems, the drug can also cause tolerance, dependence, and withdrawal symptoms when someone stops taking it, even when taken as prescribed at typical doses. Additionally, while most of the side effects of zolpidem, such as next day drowsiness, are common side effects of sleep medications, some zolpidem users have reported sleepwalking, sleep eating (which involves getting up and eating without waking), and even more dangerous activities like sleep driving, while under the influence of the drug. And due to various concerns, such as potentially impaired metabolism of the drug, an increased risk of falls, and an increased risk of cognitive impairment, zolpidem may pose more problems for older populations. Thus, despite its effectiveness, zolpidem should be prescribed cautiously and used only for as long as is absolutely necessary.REFERENCES:Edinoff AN, Wu N, Ghaffar YT, Prejean R, Gremillion R, Cogburn M, Chami AA, Kaye AM, Kaye AD. Zolpidem: Efficacy and Side Effects for Insomnia. Health Psychol Res. 2021 Jun 18;9(1):24927. doi: 10.52965/001c.24927. PMID: 34746488; PMCID: PMC8567759.Fitzgerald AC, Wright BT, Heldt SA. The behavioral pharmacology of zolpidem: evidence for the functional significance of α1-containing GABA(A) receptors. Psychopharmacology (Berl). 2014 May;231(9):1865-96. doi: 10.1007/s00213-014-3457-x. Epub 2014 Feb 22. PMID: 24563183.Gunja N. In the Zzz zone: the effects of Z-drugs on human performance and driving. J Med Toxicol. 2013 Jun;9(2):163-71. doi: 10.1007/s13181-013-0294-y. PMID: 23456542; PMCID: PMC3657033.Huedo-Medina TB, Kirsch I, Middlemass J, Klonizakis M, Siriwardena AN. Effectiveness of non-benzodiazepine hypnotics in treatment of adult insomnia: meta-analysis of data submitted to the Food and Drug Administration. BMJ. 2012 Dec 17;345:e8343. doi: 10.1136/bmj.e8343. PMID: 23248080; PMCID: PMC3544552.Matheson E, Hainer BL. Insomnia: Pharmacologic Therapy. Am Fam Physician. 2017 Jul 1;96(1):29-35. PMID: 28671376.Salvà P, Costa J. Clinical pharmacokinetics and pharmacodynamics of zolpidem. Therapeutic implications. Clin Pharmacokinet. 1995 Sep;29(3):142-53. doi: 10.2165/00003088-199529030-00002. PMID: 8521677.Wong E, Nguyen TV. Zolpidem Use in the Elderly and Recent Safety Data. Prescription Pad. 2014 Feb;10(2):140-141.Xiang T, Cai Y, Hong Z, Pan J. Efficacy and safety of Zolpidem in the treatment of insomnia disorder for one month: a meta-analysis of a randomized controlled trial. Sleep Med. 2021 Nov;87:250-256. doi: 10.1016/j.sleep.2021.09.005. Epub 2021 Sep 20. PMID: 34688027.
10-Minute Neuroscience: Depression Neuroscientifically Challenged 2023-12-16 | In this video, I discuss the neuroscience of depression. First, I cover the serotonin hypothesis, which suggests depression is caused by low levels of serotonin in the brain, and I explain why this hypothesis does not fully explain what’s happening in the brain to cause depression. Then, I cover several other hypotheses, including those that focus on dysregulation in the HPA axis, immune system dysfunction, and impaired neuroplasticity and neurogenesis (linked to low levels of BDNF). Along the way, I also explain the mechanisms behind some common antidepressants, such as SSRIs.Key points:00:00 Introduction1:01 Serotonin hypothesis3:48 Flaws with serotonin hypothesis4:57 HPA axis dysregulation6:19 Immune system dysfunction7:30 Neuroplasticity, neurogenesis, and BDNFREFERENCES: Dean J, Keshavan M. The neurobiology of depression: An integrated view. Asian J Psychiatr. 2017 Jun;27:101-111. doi: 10.1016/j.ajp.2017.01.025. Epub 2017 Jan 29. PMID: 28558878.Krishnan V, Nestler EJ. The molecular neurobiology of depression. Nature. 2008 Oct 16;455(7215):894-902. doi: 10.1038/nature07455. PMID: 18923511; PMCID: PMC2721780.López-Muñoz F, Alamo C. Monoaminergic neurotransmission: the history of the discovery of antidepressants from 1950s until today. Curr Pharm Des. 2009;15(14):1563-86. doi: 10.2174/138161209788168001. PMID: 19442174.López-Muñoz F, Alamo C, Juckel G, Assion HJ. Half a century of antidepressant drugs: on the clinical introduction of monoamine oxidase inhibitors, tricyclics, and tetracyclics. Part I: monoamine oxidase inhibitors. J Clin Psychopharmacol. 2007 Dec;27(6):555-9. doi: 10.1097/jcp.0b013e3181bb617. PMID: 18004120.Moncrieff J, Cooper RE, Stockmann T, Amendola S, Hengartner MP, Horowitz MA. The serotonin theory of depression: a systematic umbrella review of the evidence. Mol Psychiatry. 2023 Aug;28(8):3243-3256. doi: 10.1038/s41380-022-01661-0. Epub 2022 Jul 20. PMID: 35854107; PMCID: PMC10618090.Otte C, Gold SM, Penninx BW, Pariante CM, Etkin A, Fava M, Mohr DC, Schatzberg AF. Major depressive disorder. Nat Rev Dis Primers. 2016 Sep 15;2:16065. doi: 10.1038/nrdp.2016.65. PMID: 27629598.
2-Minute Neuroscience: Sleepwalking Neuroscientifically Challenged 2023-11-04 | Sleepwalking, or somnambulism, involves walking and other behaviors that are performed during incomplete arousal from sleep. In this video, I discuss some hypotheses about what happens in the brain to cause sleepwalking. TRANSCRIPT:Sleepwalking, or somnambulism, involves walking and other behaviors that are performed during incomplete arousal from sleep. Sleepwalking episodes can last for anywhere from a few seconds to longer than 30 minutes, and sleepwalking behaviors can vary in their complexity from basic behaviors such as pointing or walking around a room, to complicated procedures like getting dressed, cooking, or driving a car. Sleepwalkers may be difficult to arouse during a sleepwalking episode and confused when they awake from one, and they may have complete or partial amnesia for the episode. Sleepwalking occurs more frequently in children than in adults, but childhood sleepwalking is typically benign, while adult sleepwalking is more likely to result in injury to the sleepwalker or others.During sleep, the brain transitions through several stages characterized by unique patterns of brain activity. Sleepwalking typically occurs during stage 3 non-rem sleep, also known as slow-wave sleep. The neuroscience underlying sleepwalking is not completely understood, but current evidence suggests that it may emerge from a coexistence of wake and sleep-like activity occurring in different parts of the brain at the same time. For example, some studies of sleepwalkers during sleepwalking episodes have found brain activity suggestive of wakefulness in areas like the motor cortex, which is involved with movement, but activity suggestive of slow wave sleep in areas involved in complex cognition and conscious awareness, such as the prefrontal cortex. This type of incongruity might explain why sleepwalkers move around with limited awareness of their actions. Wake-like activity during sleep in other areas of the brain—such as those involved in emotional reactions—could explain other aspects of sleepwalking, such as the fact that many sleepwalkers report experiencing strong emotions associated with their episodes. On the other hand, persistence of sleep states in areas like the hippocampus, which is involved in memory consolidation, could explain why sleepwalkers sometimes do not remember the sleepwalking incident or certain aspects of it. REFERENCES:Arnulf I. Sleepwalking. Curr Biol. 2018 Nov 19;28(22):R1288-R1289. doi: 10.1016/j.cub.2018.09.062. Epub 2018 Nov 19. PMID: 30458142.Zadra A, Desautels A, Petit D, Montplaisir J. Somnambulism: clinical aspects and pathophysiological hypotheses. Lancet Neurol. 2013 Mar;12(3):285-94. doi: 10.1016/S1474-4422(12)70322-8. PMID: 23415568.Credit to cottonbro studios for photo of sleepwalker.
2-Minute Neuroscience: Vertigo Neuroscientifically Challenged 2023-10-21 | Vertigo involves the illusion of movement, where someone either feels like they or the environment around them is moving—usually in a spinning manner. In this video I discuss the role of the vestibular system and related structures in producing vertigo.TRANSCRIPT:Vertigo involves the illusion of movement, where someone either feels like they, or the environment around them, is moving—usually in a spinning manner. Vertigo may range in severity from mild to so severe that it’s difficult to maintain one’s balance, and it frequently involves other symptoms as well, including sweating, nausea, and vomiting. While vertigo is often described as dizziness, dizziness is a more general term, and vertigo is considered a subtype of dizziness. There are many potential causes of vertigo, including conditions such as benign paroxysmal positional vertigo, migraine, or Meniere’s disease, as well as a number of other causes such as infections, head injuries, and tumors, among others.Our sense of stability is maintained primarily by the activity of the vestibular system, which includes the semicircular canals and otolith organs of the inner ear as well as the vestibular nuclei in the brainstem. The inner ear structures receive information about head movement and communicate this information to other brain regions, including the brainstem, cerebellum, and cerebral cortex. Vertigo is typically associated with a disruption in function of either the vestibular system or one of the regions it communicates with to maintain our sense of balance and stability.Vertigo can be classified as peripheral or central, with peripheral vertigo referring to vertigo typically caused by dysfunction in the vestibular structures of the inner ear or of the vestibular nerve, which carries information from those structures to the brain. Central vertigo involves disruption to regions of the central nervous system that handle vestibular information. The symptoms a patient is experiencing can help to determine if vertigo has a peripheral or central origin; for example, peripheral vertigo is more likely to result in short-lived episodes with more severe nausea and vomiting, while central vertigo may cause longer episodes that involve other neurological symptoms–but of course these commonalities may not hold true in every case. REFERENCES:Baloh RW. Vertigo. Lancet. 1998 Dec 5;352(9143):1841-6. doi: 10.1016/S0140-6736(98)05430-0. PMID: 9851400.Labuguen RH. Initial evaluation of vertigo. Am Fam Physician. 2006 Jan 15;73(2):244-51. Erratum in: Am Fam Physician. 2006 May 15;73(10):1704. PMID: 16445269.Noij KS, Shapiro SB, Samy RN, Naples JG. Vertigo: Streamlining the Evaluation through Symptom Localization. Med Clin North Am. 2021 Sep;105(5):901-916. doi: 10.1016/j.mcna.2021.05.011. Epub 2021 Jul 12. PMID: 34391542.Stanton M, Freeman AM. Vertigo. 2023 Mar 13. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan–. PMID: 29493978.
2-Minute Neuroscience: Migraine Neuroscientifically Challenged 2023-10-01 | Migraine is a chronic neurological condition involving repeated headaches as well as a variety of other symptoms. In this video, I discuss the neurological mechanisms thought to underlie migraine.TRANSCRIPT: Migraine is a chronic neurological condition involving repeated headaches that are frequently severe and are accompanied by other symptoms, such as nausea, vomiting, and an increased sensitivity to light or sound. Migraine headaches are often throbbing, experienced on one side of the head, and worsened by movement or physical activity. About ⅓ of migraine sufferers experience a migraine aura, which consists of neurological symptoms such as visual disturbances that occur before or during the onset of pain.The headache phase of a migraine is thought to be attributable to activation of the trigeminal nerve, a cranial nerve that acts as the main sensory nerve for the head. The trigeminal nerve supplies a variety of pain-sensitive structures, including the eye, dura mater, and various blood vessels. Activation of the trigeminal nerve can elicit pain in these structures, which might explain the characteristic head and eye pain of migraine. Activation of the trigeminal nerve also prompts the release of neurotransmitters that can dilate cranial blood vessels and further stimulate and sensitize pain receptors. Additionally, trigeminal nerve fibers synapse on neurons that project to various brain regions, and these connections might be responsible for eliciting other common symptoms, such as auditory, visual, emotional, and cognitive effects. People who experience migraines may undergo neurological changes that increase sensitivity to migraine triggers, but it’s still not completely clear what causes a migraine attack to begin. Migraine aura has been linked to a spreading abnormality in the electrical activity in the brain known as cortical spreading depression, which prompts other alterations in brain activity and is linked to the activation of the trigeminal system. This spreading depression has been suggested as a mechanism for the initiation of migraine without aura as well, although there is no consensus on this point, and other mechanisms that lead to trigeminal nerve stimulation may be involved.REFERENCES:Dodick DW. Migraine. Lancet. 2018 Mar 31;391(10127):1315-1330. doi: 10.1016/S0140-6736(18)30478-1. Epub 2018 Mar 6. PMID: 29523342.Ferrari MD, Goadsby PJ, Burstein R, Kurth T, Ayata C, Charles A, Ashina M, van den Maagdenberg AMJM, Dodick DW. Migraine. Nat Rev Dis Primers. 2022 Jan 13;8(1):2. doi: 10.1038/s41572-021-00328-4. PMID: 35027572.Image credit: Photo by Andrea Piacquadio from Pexels: pexels.com/photo/female-student-suffering-from-headache-at-home-3808016
2-Minute Neuroscience: Methylphenidate Neuroscientifically Challenged 2023-09-15 | Methylphenidate, better known as Ritalin or Concerta, is a stimulant medication primarily used to treat ADHD. In this video, I discuss how methylphenidate affects the brain and how this is thought to lead to therapeutic effects in ADHD. TRANSCRIPT:Methylphenidate is a stimulant medication primarily used to treat ADHD, although it is sometimes also used to treat daytime sleepiness associated with narcolepsy and has several other off-label uses. Methylphenidate is better known as Ritalin or Concerta, which are two of the numerous brand names the drug is sold under.Methylphenidate is a stimulant drug. Its primary mechanism of action is thought to be the inhibition of reuptake of the neurotransmitters dopamine and norepinephrine. Reuptake is a process used by neurons to remove excess neurotransmitters from the synaptic cleft. In reuptake, proteins called transport proteins move neurotransmitters out of the synaptic cleft and typically back into the neuron that released them. Thus, by inhibiting reuptake, methylphenidate increases levels of dopamine and norepinephrine in the synaptic cleft. These elevated levels of dopamine and norepinephrine lead to increased activity at the receptors for these neurotransmitters, and cause various alterations in brain activity. For example, methylphenidate has been shown to increase activity in the prefrontal cortex, an area of the brain that’s considered important to attention and other executive functions. The exact way the pharmacological actions of methylphenidate help improve the symptoms of ADHD is not fully understood, but in general it’s thought that dopamine and norepinephrine signaling are important to attention and other executive functions, and thus increasing levels of these neurotransmitters leads to therapeutic effects in ADHD. Although inhibiting dopamine and norepinephrine reuptake appears to be the primary mechanism of action for methylphenidate, the drug does have a number of other actions in the nervous system. For example, it also stimulates serotonergic and adrenergic receptors. It’s unclear exactly what contribution these other actions may make to methylphenidate’s therapeutic effects, but studies have found that the effect on adrenergic receptors specifically may be important to the drug’s ability to enhance cognitive function.REFERENCES:Faraone SV. The pharmacology of amphetamine and methylphenidate: Relevance to the neurobiology of attention-deficit/hyperactivity disorder and other psychiatric comorbidities. Neurosci Biobehav Rev. 2018 Apr;87:255-270. doi: 10.1016/j.neubiorev.2018.02.001. Epub 2018 Feb 8. PMID: 29428394; PMCID: PMC8063758.Shellenberg TP, Stoops WW, Lile JA, Rush CR. An update on the clinical pharmacology of methylphenidate: therapeutic efficacy, abuse potential and future considerations. Expert Rev Clin Pharmacol. 2020 Aug;13(8):825-833. doi: 10.1080/17512433.2020.1796636. Epub 2020 Jul 25. PMID: 32715789.
10-Minute Neuroscience: Visual Pathways Neuroscientifically Challenged 2023-08-26 | In this video, I cover the pathway visual information travels moving from the eye to the visual cortex and surrounding areas. First, I discuss the components of the eye that focus light on the retina. Then, I describe the anatomy of the retina along with the functions of the different cell types found there. Next, I cover the pathways that carry visual information from the retina to the primary visual cortex. Finally, I describe how the primary visual cortex recruits surrounding visual areas to further process visual information.Key points:00:00 Introduction00:22 Anatomy of the eye1:35 The retina2:48 Rods and cones4:44 Other retinal cells6:25 Pathway from the retina to visual cortex8:04 Primary visual cortex and surrounding areasREFERENCES:Albright TD, Freiwald WA. 2021. High-Level Visual Processing: From Vision to Cognition. In: Kandel ER, Koester JD, Mack SH, Siegelbaum SA, eds. Principles of Neural Science, 6th ed. New York: McGraw-Hill.Breedlove SM, Watson NV. 2018. Behavioral Neuroscience. 8th ed. Sunderland, MA: Sinauer Associates, Inc. Meister M, Tessier-Lavigne M. 2021. Low-Level Visual Processing: The Retina. In: Kandel ER, Koester JD, Mack SH, Siegelbaum SA, eds. Principles of Neural Science, 6th ed. New York: McGraw-Hill.Purves D, Augustine GJ, Fitzpatrick D, Hall WC, Lamantia AS, Mooney RD, Platt ML, White LE. 2018. Neuroscience. 6th ed. New York: Sinauer Associates.Vanderah TW, Gould DJ. 2021. Nolte's The Human Brain: An Introduction to its Functional Anatomy. 8th ed. Philadelphia, PA: Elsevier.
2-Minute Neuroscience: DMT Neuroscientifically Challenged 2023-08-07 | DMT is naturally produced in a variety of plants and animals (including humans) and is also a potent psychoactive drug known for its ability to cause intense hallucinations and psychedelic experiences. In this video, I discuss how DMT might act in the brain to produce its unique effects. TRANSCRIPT: DMT is a substance that’s produced naturally in a variety of plants and animals, including humans. The functions of naturally-produced DMT are unclear, but DMT is also a potent psychoactive drug known for its ability to produce intense but relatively short-lived hallucinations and psychedelic experiences. When used recreationally, DMT is typically smoked, but it’s also the main psychoactive ingredient in ayahuasca, a brewed drink that produces longer-lasting psychedelic effects. Although orally administered DMT is rapidly degraded by an enzyme called monoamine oxidase, ayahuasca is brewed with plants that contain inhibitors of this enzyme, enabling the DMT in ayahuasca to remain active even though it’s administered orally. The pharmacology of DMT is not well understood. The drug has actions at a variety of receptors in the nervous system, but its best characterized effects are its ability to stimulate a wide range of serotonin receptor subtypes. Studies suggest that DMT’s action at the 5-HT2A serotonin receptor is especially important for producing its characteristically intense visual hallucinations. At the same time, stimulation of the 5-HT2A receptor alone does not seem to be sufficient to cause the hallucinations experienced by DMT users. Thus, it’s thought that other serotonin receptor subtypes might be involved in these effects, and some evidence suggests that receptors for the neurotransmitter glutamate may play a role as well. It’s also possible that DMT’s actions at other receptors, such as sigma-1 receptors and trace amine-associated receptors, may contribute to the drug’s effects, but more research is needed to elucidate DMT’s full mechanism of action. DMT, like many other psychedelic drugs, is now gaining attention for its therapeutic potential. Studies with ayahuasca have found the drink to have beneficial effects in the treatment of depression, anxiety, and addiction, and studies are currently underway to investigate the possibility of DMT alone offering some of the same benefits. REFERENCES: Cameron LP, Olson DE. Dark Classics in Chemical Neuroscience: N, N-Dimethyltryptamine (DMT). ACS Chem Neurosci. 2018 Oct 17;9(10):2344-2357. doi: 10.1021/acschemneuro.8b00101. Epub 2018 Jul 23. PMID: 30036036. Carbonaro TM, Gatch MB. Neuropharmacology of N,N-dimethyltryptamine. Brain Res Bull. 2016 Sep;126(Pt 1):74-88. doi: 10.1016/j.brainresbull.2016.04.016. Epub 2016 Apr 25. PMID: 27126737; PMCID: PMC5048497. CREDITS:The image of ayahuasca is a CC image courtesy of Terpsichore. The work can be seen here: commons.wikimedia.org/wiki/File:Ayahuasca_prep.JPG The background kaleidoscope image is courtesy of Merlin Lightpainting. The work can be seen here: pexels.com/@merlin/gallery
2-Minute Neuroscience: Cochlear Implants Neuroscientifically Challenged 2023-07-15 | A cochlear implant is an electronic device that can restore sound perception in people with certain types of severe hearing loss by picking up sound from the environment, converting that sound into electrical impulses, and transmitting those impulses directly to the auditory nerve. In this video, I discuss the components of a cochlear implant and how they work together to create sound perception.TRANSCRIPT:A cochlear implant is an electronic device that can restore sound perception in people with certain types of severe hearing loss by picking up sound from the environment, converting that sound into electrical impulses, and transmitting those impulses directly to the auditory nerve. Cochlear implants provide an option for hearing restoration in patients who have more extensive hearing loss, and for whom a device that simply amplifies sound (such as a hearing aid) may not be as effective. A cochlear implant is an example of a neural prosthesis, as it replaces the disrupted functionality of the cochlea with an electronic device to restore functional hearing.Cochlear implants consist of both external and internal components. The external component typically sits behind the ear and picks up sound through a microphone; when sound is detected, a sound processor converts the auditory information into a radio frequency signal. The signal is transmitted to a receiver implanted under the skin behind the ear. The receiver decodes the signal, then converts it into electrical currents, which are sent along wires that have been surgically inserted into the cochlea. The wires stimulate the auditory nerve (a job typically reserved for the damaged cochlear cells), and stimulation of the nerve causes auditory information to be sent to the brain to create sound perception. A cochlear implant does require surgery, but major complications are uncommon. Studies have generally found cochlear implants to be beneficial, but the extent of the benefit does vary depending on the patient, with children who get cochlear implants earlier and adults who get them soon after hearing loss typically experiencing the greatest benefits.REFERENCES:Naples JG, Ruckenstein MJ. Cochlear Implant. Otolaryngol Clin North Am. 2020 Feb;53(1):87-102. doi: 10.1016/j.otc.2019.09.004. Epub 2019 Oct 31. PMID: 31677740.Zeng FG, Rebscher S, Harrison W, Sun X, Feng H. Cochlear implants: system design, integration, and evaluation. IEEE Rev Biomed Eng. 2008;1:115-42. doi: 10.1109/RBME.2008.2008250. Epub 2008 Nov 5. PMID: 19946565; PMCID: PMC2782849.Image of cochlear implant on head at :05 drawn by Michelle Dingman.
10-Minute Neuroscience: Action Potentials Neuroscientifically Challenged 2023-07-06 | In this video, I cover the basics of the action potential beginning with an explanation of membrane potential and how it sets the stage for the action potential. Then, I describe how an action potential is generated and how it ends. I cover the propagation of an action potential down the axon and the role myelin plays in this process. Finally, I discuss the absolute and relative refractory periods and what they mean for repeated action potential firing. Key points: 00:00 Introduction 0:17 Membrane potential 4:18 Action potential 7:20 Propagation down the axon and role of myelin 8:51 Absolute and relative refractory periods REFERENCES: Bean BP, Koester JD. 2021. Propagated Signaling: The Action Potential. In: Kandel ER, Koester JD, Mack SH, Siegelbaum SA, eds. Principles of Neural Science, 6th ed. New York: McGraw-Hill. Koester JD, Siegelbaum SA. 2021. Membrane Potential and the Passive Electrical Properties of the Neuron. In: Kandel ER, Koester JD, Mack SH, Siegelbaum SA, eds. Principles of Neural Science, 6th ed. New York: McGraw-Hill. Pinel JPJ. 2014. Biopsychology. 9th ed. New York: Pearson.
10-Minute Neuroscience: Synapses Neuroscientifically Challenged 2023-05-26 | In this video, I cover the different components of a synapse, including the presynaptic neuron, postsynaptic neuron, synaptic cleft, and synaptic vesicles. I discuss how signals are propagated at chemical synapses through the use of neurotransmitters, as well as how neurotransmitters are removed from the synaptic cleft by enzymes and/or reuptake. I also cover the components and function of electrical synapses.Key points:00:00 General introduction to synapses1:23 Different components of a chemical synapse4:28 Termination of synaptic transmission (e.g., enzymes, reuptake)6:55 Electrical synapsesREFERENCES:Purves D, Augustine GJ, Fitzpatrick D, Hall WC, Lamantia AS, Mooney RD, Platt ML, White LE, eds. 2018. Neuroscience. 6th ed. New York. Sinauer Associates.Siegelbaum ST, Fischbach GD. 2021. Overview of Synaptic Transmission. In: Kandel ER, Koester JD, Mack SH, Siegelbaum SA, eds. Principles of Neural Science, 6th ed. New York: McGraw-Hill.
10-Minute Neuroscience: Neurons Neuroscientifically Challenged 2023-05-14 | In this video, I cover all of the main parts of a neuron including the dendrites, cell body (soma), axon hillock, axon, and axon terminals (synaptic boutons). I describe how a signal travels from the dendrites of a neuron, down the axon, and to the axon terminals to communicate with another neuron through the release of neurotransmitters. I also describe ways of categorizing neurons based on structure (i.e., multipolar, bipolar, unipolar, and pseudo-unipolar) and function (i.e., motor, sensory, and interneurons).Key points:00:00 General introduction to neurons1:17 How neurons communicate2:12 Parts of a neuron7:00 Classifying neurons based on structure8:17 Classifying neurons based on functionREFERENCES:Breedlove SM, Watson NV. Behavioral Neuroscience. 8th ed. Sunderland, MA: Sinauer Associates, Inc.; 2018. Kandel ER, Barres BA, Hudspeth AJ. 2013. Nerve Cells, Neural Circuitry, and Behavior. In: Kandel ER, Schwartz JH, Jessell TM, eds. Principles of Neural Science, 5th ed. New York: McGraw-Hill.
2-Minute Neuroscience: Frontotemporal Dementia (FTD) Neuroscientifically Challenged 2023-03-06 | Frontotemporal dementia, or FTD, is a term used to describe a collection of related brain disorders that involve the neurodegeneration of the frontal and temporal lobes. In this video, I discuss the symptoms and subtypes of FTD as well as the pathological brain mechanisms underlying FTD.TRANSCRIPT:Frontotemporal dementia, or FTD, is a term used to describe a collection of related brain disorders that involve the neurodegeneration of the frontal and temporal lobes. The neurodegeneration in FTD is associated with a variety of symptoms, and different presentations of symptoms have been used to establish multiple subtypes of FTD. The three main subtypes are: behavioral variant FTD, semantic variant primary progressive aphasia, and nonfluent variant primary progressive aphasia. In behavioral variant FTD, patients display a variety of changes in behavior, emotions, personality, and executive control. For example, they may exhibit compulsive behavior, apathy, and/or socially inappropriate behavior. In primary progressive aphasias, the main impairment is with language. Patients who have the semantic variant of primary progressive aphasia display deficits in word comprehension as well as trouble recalling certain words, along with other language difficulties. Patients who have the non-fluent variant primary progressive aphasia have difficulty producing fluent speech, which might involve trouble speaking at all or problems with the use of grammar to produce understandable speech.FTD is associated with a pathological process called frontotemporal lobar degeneration, which involves the death of neurons and other pathological changes in the frontal and temporal lobes, as well as other areas of the brain such as the anterior cingulate cortex and insular cortex. In FTD, the degeneration of neurons is associated with the accumulation of structurally abnormal proteins, which might contribute to cell death through multiple mechanisms. The protein accumulation and associated damage spreads, causing the symptoms of FTD to get progressively worse over time. While initially a patient may display symptoms linked to just one of the FTD subtypes, the spreading neurodegeneration may eventually lead to the manifestation of symptoms from multiple subtypes. Unfortunately at this point there are no drugs approved to treat FTD, so treatment primarily involves managing symptoms.REFERENCES:Bang J, Spina S, Miller BL. Frontotemporal dementia. Lancet. 2015 Oct 24;386(10004):1672-82. doi: 10.1016/S0140-6736(15)00461-4. PMID: 26595641; PMCID: PMC5970949.Olney NT, Spina S, Miller BL. Frontotemporal Dementia. Neurol Clin. 2017 May;35(2):339-374. doi: 10.1016/j.ncl.2017.01.008. PMID: 28410663; PMCID: PMC5472209.Young JJ, Lavakumar M, Tampi D, Balachandran S, Tampi RR. Frontotemporal dementia: latest evidence and clinical implications. Ther Adv Psychopharmacol. 2018
2-Minute Neuroscience: Spina Bifida Neuroscientifically Challenged 2023-02-23 | Spina bifida is a birth defect that involves disrupted formation of a structure called the neural tube. In this video, I discuss spina bifida, focusing primarily on the most common form of spina bifida: myelomeningocele.TRANSCRIPT:Spina bifida is a birth defect that involves disrupted formation of a structure called the neural tube. The neural tube forms in early neural development, and eventually will become the brain and spinal cord. In spina bifida, the neural tube either does not form or close properly. This can result in three types of spina bifida: myelomeningocele, meningocele, and spina bifida occulta. The latter two forms are less common and do not typically cause any symptoms. Myelomeningocele, which is the most common form of spina bifida, is more likely to result in complications and disability.In myelomeningocele, the failed closure of the neural tube leads to the disrupted formation of the spinal column and causes the spinal cord to be exposed. The spinal cord below the level of the defect does not develop properly, potentially resulting in a variety of neurological problems and associated symptoms, such as incontinence and weakness or paralysis in the legs. Additionally, the open lesion in the spinal column can cause cerebrospinal fluid leakage, which is thought to be connected to abnormalities in the size and shape of the ventricles as well as related brain conditions, such as Chiari II malformation and hydrocephalus.Spina bifida is thought to be caused due to an interaction between genetic and non-genetic factors. There are a number of non-genetic risk factors for spina bifida, but the best established one is inadequate intake of folate or folic acid before and during early pregnancy. Although it’s not completely clear why low folate levels are linked to spina bifida, folate plays important roles in neural development and thus a deficiency is thought to have the potential to interfere with healthy development. Treatment for spina bifida typically involves closing the spinal lesion after birth (although prenatal surgery is also sometimes an option) and treating any associated problems, such as hydrocephalus.REFERENCES:Copp AJ, Adzick NS, Chitty LS, Fletcher JM, Holmbeck GN, Shaw GM. Spina bifida. Nat Rev Dis Primers. 2015 Apr 30;1:15007. doi: 10.1038/nrdp.2015.7. PMID: 27189655; PMCID: PMC4898641.Iskandar BJ, Finnell RH. Spina Bifida. N Engl J Med. 2022 Aug 4;387(5):444-450. doi: 10.1056/NEJMra2116032. PMID: 35921452.Mitchell LE, Adzick NS, Melchionne J, Pasquariello PS, Sutton LN, Whitehead AS. Spina bifida. Lancet. 2004 Nov 20-26;364(9448):1885-95. doi: 10.1016/S0140-6736(04)17445-X. PMID: 15555669.
2-Minute Neuroscience: Sleep Paralysis Neuroscientifically Challenged 2023-01-06 | Sleep paralysis is a relatively common phenomenon in which someone experiences a state of immobility just before falling asleep or upon awakening. In this video, I discuss what might be happening in the brain to cause sleep paralysis.TRANSCRIPT:Sleep paralysis is a relatively common phenomenon in which someone experiences a state of immobility just before falling asleep or upon awakening. People who experience sleep paralysis are awake and generally aware of their surroundings during the episode; they typically can open their eyes but are otherwise unable to move. On average, an episode only lasts several minutes. During an episode of sleep paralysis a person may also experience hallucinations and abnormal sensations, including perceptions that there is someone else in the room, out-of-body experiences, and feelings of suffocation or choking. Some have hypothesized that these types of experiences may be the basis for various accounts of supernatural and other unusual encounters, such as contact with ghosts, demons, and aliens.Although sleep paralysis is not fully understood, it is generally believed to occur due to an overlap between REM sleep and wakefulness. During REM sleep, neurons in the pons act to inhibit motor neurons in the spinal cord, causing a pervasive loss of muscle movement. And yet, there is a great deal of brain activity occurring in REM sleep, and it is the stage of sleep when we typically experience our most vivid dreams. Sleep paralysis is thought to either involve a failure to activate neurons that inhibit REM sleep or a hyperactivation of neurons that promote REM sleep during a time when a person is either waking or falling asleep. Thus, they experience aspects of REM sleep that spill over into wakeful consciousness. Despite being awake they experience the paralysis that occurs during REM sleep and sometimes hallucinations that resemble experiences more likely to occur in dreams. The feelings of suffocation or choking that some report might be due to difficulty breathing deeply caused by interference with normal respiratory muscle function that occurs in REM sleep.REFERENCES:Cheyne JA, Rueffer SD, Newby-Clark IR. Hypnagogic and hypnopompic hallucinations during sleep paralysis: neurological and cultural construction of the night-mare. Conscious Cogn. 1999 Sep;8(3):319-37. doi: 10.1006/ccog.1999.0404. PMID: 10487786.Hishikawa Y, Shimizu T. Physiology of REM sleep, cataplexy, and sleep paralysis. Adv Neurol. 1995;67:245-71. PMID: 8848973.Sharpless BA. A clinician's guide to recurrent isolated sleep paralysis. Neuropsychiatr Dis Treat. 2016 Jul 19;12:1761-7. doi: 10.2147/NDT.S100307. PMID: 27486325; PMCID: PMC4958367.
Book announcement #2! Neuroscientifically Challenged 2022-12-28 | Bizarre: The Most Peculiar Cases of Human Behavior and What They Tell Us about How the Brain Works is available for pre-order now (links below)! The official release is February 7, 2023. Here is a link you can use to read the Intro & Ch. 1: drive.google.com/file/d/1yg7tjVcPqV35XR6DWNn_wvrmJ5S3L31A/viewOrdering links:Amazon: amazon.com/Bizarre-Peculiar-Cases-Human-Behavior/dp/1399801201Barnes & Noble: barnesandnoble.com/w/bizarre-marc-dingman/1142645916Indiebound: indiebound.org/book/9781399801201
2-Minute Neuroscience: Fatal Insomnia Neuroscientifically Challenged 2022-11-22 | Fatal insomnia is a very rare neurodegenerative disease characterized by progressively worsening insomnia and eventual death. In this video, I explain the symptoms of fatal insomnia as well as what happens in the brain during the disease.TRANSCRIPT:Fatal insomnia is a very rare terminal condition characterized by difficulty sleeping that becomes progressively worse over time. Although the disease is typically genetic in origin, some sporadic cases without a clear genetic basis have also been documented. The condition usually begins in middle age or later, and early symptoms include trouble sleeping as well as autonomic nervous system disturbances, such as increased body temperature and increased heart rate. The disease gets worse over time as the amount of sleep patients get continues to decline. Patients will sometimes lapse into a state of unresponsiveness during which they make involuntary movements that seem to be related to acting out dreams, and they can develop a variety of additional symptoms including difficulties with balance and coordination, trouble speaking and swallowing, hallucinations, and personality changes. Eventually, most patients lose the ability to enter deep sleep at all, and fall into a stupor that it is difficult to rouse them from. This stupor sometimes leads to coma, and the disease is always fatal, with death occurring in just over 18 months on average.Fatal insomnia is a prion disease, meaning it is associated with the conversion of a protein called prion protein into a form that cannot be broken down. The new pathological form of prion protein accumulates in the brain, and its accumulation is associated with the death of neurons and other pathological changes such as the brain taking on a spongy texture. The neuronal death eventually becomes insurmountable and is linked to the death of the patient. In fatal insomnia, the most severe neuronal loss often occurs in the thalamus and inferior olivary nuclei, but pathological changes are sometimes seen through other areas of the brain such as the cerebral cortex. Damage to the sleep-promoting regions of the thalamus is thought to be especially important to causing the insomnia that occurs in the disease.REFERENCES:Cracco L, Appleby BS, Gambetti P. Fatal familial insomnia and sporadic fatal insomnia. Handb Clin Neurol. 2018;153:271-299. doi: 10.1016/B978-0-444-63945-5.00015-5. PMID: 29887141. Montagna P. Fatal familial insomnia and the role of the thalamus in sleep regulation. Handb Clin Neurol. 2011;99:981-96. doi: 10.1016/B978-0-444-52007-4.00018-7. PMID: 21056239. Montagna P, Gambetti P, Cortelli P, Lugaresi E. Familial and sporadic fatal insomnia. Lancet Neurol. 2003 Mar;2(3):167-76. doi: 10.1016/s1474-4422(03)00323-5. PMID: 12849238.
2-Minute Neuroscience: PTSD Neuroscientifically Challenged 2022-08-16 | Post-traumatic stress disorder, or PTSD, is a disorder that develops after someone experiences a traumatic event; it involves a variety of intrusive symptoms related to the trauma. In this video, I discuss hypotheses about what might be going on in the brain to cause PTSD.TRANSCRIPT:Post-traumatic stress disorder, or PTSD, is a condition that develops after someone experiences a traumatic event. It involves the occurrence of intrusive symptoms like nightmares or distressing memories that are linked to the trauma and may cause the person to feel like they are reliving aspects of the traumatic event. These symptoms also lead to the avoidance of things that remind a person of the trauma. PTSD may cause various other issues such as difficulty sleeping, negative emotions like fear, guilt, or sadness, trouble concentrating, and irritability. Although the neurocircuitry underlying PTSD is still not completely clear, one supported hypothesis suggests that PTSD involves decreased activity in the medial prefrontal cortex and increased activity in subnuclei of the amygdala that are involved in the identification of threats. According to this hypothesis, the medial prefrontal cortex normally acts to regulate amygdala function, inhibiting it when there is not an immediate threat to devote attention to. In an individual with PTSD, however, the amygdala might be hyperactive and provoke a fearful reaction in response to trauma-related stimuli. The medial prefrontal cortex fails to inhibit this unnecessary amygdala activation, causing patients to experience responses that are disproportionate to the threat that trauma-related stimuli currently pose.Some patients with PTSD, however, also experience the suppression of emotions, which causes symptoms like social detachment and emotional numbness. This might be caused by an opposing mechanism where increased activity in the medial prefrontal cortex dampens activity in regions such as the amygdala and other areas involved in emotional expression. Thus, the neuroscience of the disorder is complex and the neurocircuitry involved likely depends on the symptoms a particular patient displays. Additionally, more recent research has suggested a role for other networks that span larger areas of the brain in bringing about the symptoms of PTSD.REFERENCES:Etkin A, Wager TD. Functional neuroimaging of anxiety: a meta-analysis of emotional processing in PTSD, social anxiety disorder, and specific phobia. Am J Psychiatry. 2007 Oct;164(10):1476-88. doi: 10.1176/appi.ajp.2007.07030504. PMID: 17898336; PMCID: PMC3318959.Rauch SL, Shin LM, Whalen PJ, Pitman RK. Neuroimaging and the Neuroanatomy of Posttraumatic Stress Disorder. CNS Spectrums. 1998 July/August;3(7):31-41.Yehuda R, Hoge CW, McFarlane AC, Vermetten E, Lanius RA, Nievergelt CM, Hobfoll SE, Koenen KC, Neylan TC, Hyman SE. Post-traumatic stress disorder. Nat Rev Dis Primers. 2015 Oct 8;1:15057. doi: 10.1038/nrdp.2015.57. PMID: 27189040.
2-Minute Neuroscience: Schizophrenia Neuroscientifically Challenged 2022-06-03 | Schizophrenia is a potentially severe psychiatric condition that involves a variety of symptoms. In this video, I discuss the neuroscience of schizophrenia.TRANSCRIPT:Schizophrenia is a potentially severe psychiatric condition that involves a variety of symptoms. The symptoms of schizophrenia are often categorized as positive, negative, or cognitive. Positive symptoms involve the development of a behavior or thought pattern that isn’t normally present, such as hallucinations and/or delusions. Negative symptoms involve the loss of a normal function, and include lack of motivation, blunted emotion, or difficulty experiencing pleasure. Cognitive symptoms are those that affect someone’s ability to think clearly, and include deficits in attention, memory, and/or concentration.The neuroscience of schizophrenia has been difficult to sort out, but a great deal of research has focused on neurotransmitter abnormalities at the root of the disorder. Dopamine has received much of this attention, with the general hypothesis being that dopamine activity is too high in certain parts of the brain in schizophrenia. This hypothesis was originally formulated based on the findings that drugs used to treat schizophrenia act to reduce dopamine activity, and drugs that increase dopamine levels (such as amphetamine) can induce behavior that in some ways resembles the psychotic states schizophrenic patients experience. The idea that increased dopamine activity plays a role in schizophrenic symptoms is now supported by a large body of evidence.However, dopamine irregularities alone do not seem to explain all the symptoms of schizophrenia. Glutamate abnormalities, such as dysfunctional glutamate receptors, also occur in schizophrenia, and these may be capable of accounting for some negative and cognitive symptoms—something that dopamine levels have been less successful in explaining. Additionally, it has been proposed that dysfunction in glutamate systems may precede and lead to the dopamine hyperactivity observed in schizophrenia. While it’s uncertain what causes these neurotransmitter abnormalities to emerge in the first place, it’s generally believed that schizophrenia can be traced back to disruptions in early neural development that occur due to the influence of both genetic and environmental factors.REFERENCES:Howes O, McCutcheon R, Stone J. Glutamate and dopamine in schizophrenia: an update for the 21st century. J Psychopharmacol. 2015 Feb;29(2):97-115. doi: 10.1177/0269881114563634. Epub 2015 Jan 13. PMID: 25586400; PMCID: PMC4902122.Howes OD, Murray RM. Schizophrenia: an integrated sociodevelopmental-cognitive model. Lancet. 2014 May 10;383(9929):1677-1687. doi: 10.1016/S0140-6736(13)62036-X. Epub 2013 Dec 6. PMID: 24315522; PMCID: PMC4127444.Kahn RS, Sommer IE, Murray RM, Meyer-Lindenberg A, Weinberger DR, Cannon TD, O'Donovan M, Correll CU, Kane JM, van Os J, Insel TR. Schizophrenia. Nat Rev Dis Primers. 2015 Nov 12;1:15067. doi: 10.1038/nrdp.2015.67. PMID: 27189524.Owen MJ, Sawa A, Mortensen PB. Schizophrenia. Lancet. 2016 Jul 2;388(10039):86-97. doi: 10.1016/S0140-6736(15)01121-6. Epub 2016 Jan 15. PMID: 26777917; PMCID: PMC4940219.
2-Minute Neuroscience: COVID-19 & the Brain Neuroscientifically Challenged 2022-04-16 | COVID-19 is associated with a wide range of neurological symptoms. In this video, I discuss current hypotheses that attempt to explain how SARS-CoV-2 (the virus that causes COVID-19) affects the brain.TRANSCRIPT:Although COVID-19 is generally considered a respiratory illness, it is associated with a wide range of symptoms, a number of which involve the nervous system. These neurological symptoms range from very common symptoms such as disturbances in smell and taste, to complications such as confusion, impaired consciousness, and stroke. Additionally, some patients develop long-term symptoms that involve the nervous system, such as headaches, depression, and impaired concentration. These symptoms can last well after a COVID infection, and are part of a condition sometimes referred to as long COVID. At this point there is still uncertainty about how SARS-CoV-2, the virus that causes COVID-19, leads to neurological symptoms. Initially, it was suspected that the virus might enter the nervous system through one of several potential routes such as through the olfactory nerve or across the blood-brain barrier. Studies so far, however, have found very low levels of virus in the brain and cerebrospinal fluid, suggesting that the virus migrating to the brain and infecting brain cells may not play the primary role in causing the neurological effects of COVID-19. There is, however, evidence of a robust immune response to SARS-CoV-2 in the brain. Thus, one hypothesis is that this immune reaction and the associated inflammation that occurs may interfere with brain function and potentially damage neurons, resulting in neurological symptoms. SARS-CoV-2 is also known to damage blood vessels and impair vascular function, and thus issues such as microscopic blood clots and disruptions of blood supply may be responsible for neurological symptoms as well. Additionally, studies have found changes in brain structure after COVID-19 infection and altered metabolic activity in the brains of people with Long COVID. These neurological changes might contribute to long COVID symptoms, although the underlying mechanisms are still unclear.REFERENCES:Al-Sarraj S, Troakes C, Hanley B, Osborn M, Richardson MP, Hotopf M, Bullmore E, Everall IP. Invited Review: The spectrum of neuropathology in COVID-19. Neuropathol Appl Neurobiol. 2021 Feb;47(1):3-16. doi: 10.1111/nan.12667. Epub 2020 Oct 20. PMID: 32935873. Boldrini M, Canoll PD, Klein RS. How COVID-19 Affects the Brain. JAMA Psychiatry. 2021 Jun 1;78(6):682-683. doi: 10.1001/jamapsychiatry.2021.0500. PMID: 33769431.Spudich S, Nath A. Nervous system consequences of COVID-19. Science. 2022 Jan 21;375(6578):267-269. doi: 10.1126/science.abm2052. Epub 2022 Jan 20. PMID: 35050660.
2-Minute Neuroscience: Obsessive-Compulsive Disorder (OCD) Neuroscientifically Challenged 2022-03-18 | Obsessive-compulsive disorder, or OCD, is a condition characterized by obsessions and/or compulsions. Although the neuroscience of OCD is not completely understood, in this video I discuss one supported perspective on what happens in the brain to cause the obsessions and compulsions that occur in OCD.For a more in-depth discussion of the neuroscience of OCD (on my website), click this link: neuroscientificallychallenged.com/posts/know-your-brain-obsessive-compulsive-disorder-ocdTRANSCRIPT:Obsessive-compulsive disorder, or OCD, is a condition characterized by obsessions and/or compulsions. Obsessions are recurrent unwanted thoughts, while compulsions are repetitive behaviors or mental acts often performed in response to obsessions, typically with the goal of reducing anxiety and discomfort. It’s important to note that OCD is often very distressing, and is not just a preference for orderliness, as the term is sometimes used to imply.The neuroscience of OCD is not completely understood, and it’s likely that different neural circuits may be involved based on a person’s age and symptom profile, among other factors. One supported perspective on the neuroscience of OCD, however, points to a prominent role for circuits that connect the orbitofrontal cortex with a group of structures called the basal ganglia. According to this perspective, increased activity in the orbitofrontal cortex is associated with a heightened focus on concerns that spawn obsessive thoughts. When the orbitofrontal cortex is activated in response to something the brain perceives as a danger or concern, it communicates with the basal ganglia. A simplified version of basal ganglia circuitry suggests it consists of two opposing pathways: an excitatory pathway called the direct pathway, and an inhibitory pathway called the indirect pathway. When the orbitofrontal cortex sends a signal to the basal ganglia, it often leads to an action designed to alleviate the discomfort caused by the perceived danger; that action is mediated by the direct pathway. In a healthy person, the indirect pathway then inhibits further action. In someone with OCD, however, the direct pathway is over-excitable, drowning out the activity of the indirect pathway and causing a difficult time switching to a different behavior or turning focus away from the concern causing the discomfort. Thus, according to this model, overactivity in the orbitofrontal cortex and the direct pathway of the basal ganglia increases the occurrence of both obsessions and compulsions.REFERENCES:Lanciego JL, Luquin N, Obeso JA. Functional neuroanatomy of the basal ganglia. Cold Spring Harb Perspect Med. 2012 Dec 1;2(12):a009621. doi: 10.1101/cshperspect.a009621. PMID: 23071379; PMCID: PMC3543080.Pauls DL, Abramovitch A, Rauch SL, Geller DA. Obsessive-compulsive disorder: an integrative genetic and neurobiological perspective. Nat Rev Neurosci. 2014 Jun;15(6):410-24. doi: 10.1038/nrn3746. PMID: 24840803. Saxena S, Rauch SL. Functional neuroimaging and the neuroanatomy of obsessive-compulsive disorder. Psychiatr Clin North Am. 2000 Sep;23(3):563-86. doi: 10.1016/s0193-953x(05)70181-7. PMID: 10986728. Stein DJ, Costa DLC, Lochner C, Miguel EC, Reddy YCJ, Shavitt RG, van den Heuvel OA, Simpson HB. Obsessive-compulsive disorder. Nat Rev Dis Primers. 2019 Aug 1;5(1):52. doi: 10.1038/s41572-019-0102-3. PMID: 31371720; PMCID: PMC7370844.
2-Minute Neuroscience: ADHD Neuroscientifically Challenged 2022-02-12 | Attention-deficit/hyperactivity disorder, or ADHD, is a condition characterized by difficulties with attention and/or hyperactivity and impulsivity. In this video, I discuss perspectives on the neuroscience of ADHD.TRANSCRIPT:Attention-deficit/hyperactivity disorder, or ADHD, is a condition characterized by difficulties with attention and/or hyperactivity and impulsivity. ADHD involves strong genetic influences, but environmental factors, and interactions between genetics and the environment, are thought to play an important role in ADHD as well.Much of the recent research into the neuroscience of ADHD has focused on understanding the brain networks that might underlie different aspects of cognitive function in ADHD. One example is the default mode network, which is a collection of brain regions that is more active during mind-wandering and introspection, and less active when a person is attempting to complete a specific task. Studies have found that people with ADHD have atypical connectivity in the default mode network, which might be associated with distractibility.Individuals with ADHD also display lower activity in brain networks that are involved in attention and cognitive control. Typically, activity in these networks increases when activity in the default mode network decreases, and vice versa. Thus, one hypothesis is that in ADHD activity in the default mode network is dysregulated and interferes with the function of networks involved in attention and cognitive control. Studies have also found that people with ADHD tend to display atypical activity in the reward system, a group of structures that are involved in motivated behavior, anticipation, and reinforced learning. This atypical reward system activity might be associated with a tendency to overestimate the value of short-term rewards in comparison to long-term rewards, which could also affect planning and decision-making. The reward system includes some of the major dopamine pathways in the brain, and dopamine is often implicated in ADHD because medications that are commonly used to treat the condition, such as amphetamine and methylphenidate, cause increased transmission of dopamine and norepinephrine.REFERENCES:Faraone SV, Asherson P, Banaschewski T, Biederman J, Buitelaar JK, Ramos-Quiroga JA, Rohde LA, Sonuga-Barke EJ, Tannock R, Franke B. Attention-deficit/hyperactivity disorder. Nat Rev Dis Primers. 2015 Aug 6;1:15020. doi: 10.1038/nrdp.2015.20. PMID: 27189265. Gallo EF, Posner J. Moving towards causality in attention-deficit hyperactivity disorder: overview of neural and genetic mechanisms. Lancet Psychiatry. 2016 Jun;3(6):555-67. doi: 10.1016/S2215-0366(16)00096-1. Epub 2016 May 13. PMID: 27183902; PMCID: PMC4893880.Posner J, Polanczyk GV, Sonuga-Barke E. Attention-deficit hyperactivity disorder. Lancet. 2020 Feb 8;395(10222):450-462. doi: 10.1016/S0140-6736(19)33004-1. Epub 2020 Jan 23. PMID: 31982036; PMCID: PMC7880081.
2-Minute Neuroscience: Restless Legs Syndrome Neuroscientifically Challenged 2022-01-21 | Restless legs syndrome (RLS) is a condition that causes an urge to move the legs that often occurs along with uncomfortable sensations in the legs. In this video, I discuss RLS and the neurological mechanisms that might underlie it.TRANSCRIPT:Restless legs syndrome or RLS is a condition that causes an urge to move the legs that often occurs along with uncomfortable sensations in the legs or sometimes in other body parts. The unpleasant sensations and urges to move the legs typically begin or become worse when someone is at rest, and they often only occur in the evening or at night. Movement tends to relieve the unpleasant sensations and urges to move, at least for as long as the movement lasts. Patients with RLS also often have insomnia and experience involuntary periodic leg movements during sleep or resting wakefulness. The mechanisms underlying RLS are not well understood. Genetic factors play a large role in susceptibility, but it’s thought that in most patients environmental factors must interact with genetics to bring about the condition. The most commonly-identified environmental factor in RLS is iron deficiency, and iron deficiency in the brain is the best-known neurological feature of RLS. It’s thought that this brain iron deficiency might be the result of an impaired ability of the brain to take iron up out of the blood and import it into neurons, and it may have multiple effects on brain function. For example, brain iron deficiency may disrupt oxygen transport and impair myelination, and it might be related to abnormal signaling in multiple neurotransmitter systems. Abnormalities in dopamine signaling are thought to play an important role in RLS, and drugs that increase dopamine activity can offer therapeutic benefits to RLS patients. Research, however, suggests RLS patients do not have low dopamine levels, and thus the reason for the benefit offered by dopamine-increasing drugs is not completely understood. Despite the short-term benefits, long-term use of dopamine-increasing drugs tends to cause what is known as augmentation, where RLS symptoms worsen with continued use of medication. Thus, alternative drugs are often used when possible.REFERENCES:Allen RP. Restless Leg Syndrome/Willis-Ekbom Disease Pathophysiology. Sleep Med Clin. 2015 Sep;10(3):207-14, xi. doi: 10.1016/j.jsmc.2015.05.022. Epub 2015 Jul 15. PMID: 26329430; PMCID: PMC4559751. Allen RP, Earley CJ. The role of iron in restless legs syndrome. Mov Disord. 2007;22 Suppl 18:S440-8. doi: 10.1002/mds.21607. Erratum in: Mov Disord. 2008 Jun;23(8):1200-2. PMID: 17566122.Manconi M, Garcia-Borreguero D, Schormair B, Videnovic A, Berger K, Ferri R, Dauvilliers Y. Restless legs syndrome. Nat Rev Dis Primers. 2021 Nov 3;7(1):80. doi: 10.1038/s41572-021-00311-z. PMID: 34732752.Trenkwalder C, Allen R, Högl B, Clemens S, Patton S, Schormair B, Winkelmann J. Comorbidities, treatment, and pathophysiology in restless legs syndrome. Lancet Neurol. 2018 Nov;17(11):994-1005. doi: 10.1016/S1474-4422(18)30311-9. Epub 2018 Sep 21. PMID: 30244828.
2-Minute Neuroscience: Autism Neuroscientifically Challenged 2021-12-20 | Autism is characterized by impairments in social communication and interaction and restricted and repetitive behaviors. In this video, I discuss the neuroscience of autism along with potential factors and mechanisms involved in the development of autism.TRANSCRIPT:Autism, also known as autism spectrum disorder, is characterized by symptoms that include impairments in social communication and interaction and restricted and repetitive behaviors. Although the neuroscience of autism is still poorly understood, autism is considered to be a complex developmental disorder that involves atypical brain organization starting early in development. Individuals with autism often experience a period of unusually rapid brain growth in infancy and early childhood. This accelerated brain growth is linked to an atypical pattern of connectivity between brain regions. A number of studies report that alterations in brain circuitry involved with social interaction and attention can be detected well before the symptoms of autism begin to appear. At this point, however, it’s unclear how brain overgrowth and atypical connectivity might be linked to the occurrence of autism symptoms. Research suggests that the risk of autism is strongly influenced by genetics, yet studies consistently report that environmental factors also play a large role. Although a number of potential environmental factors have been identified, the risk factors for autism are far from definitive, and it remains unclear which factors are responsible for causing an increase in autism risk, and which are associated in a non-causal way. The risk factors that are most strongly linked to autism are associated with the prenatal or perinatal period. Thus, it’s possible they might be responsible for disruptions to typical neural development, leading to symptoms of autism months or years later. How these risk factors might interfere with neural development is still uncertain, but hypotheses have suggested potential mechanisms such as epigenetic effects, inflammation, oxidative stress, or damage caused by oxygen deficiency. More work needs to be done, however, to fully elucidate the genetic and environmental risk factors for autism, as well as the mechanisms for the development of autism symptoms. REFERENCES:Lord C, Brugha TS, Charman T, Cusack J, Dumas G, Frazier T, Jones EJH, Jones RM, Pickles A, State MW, Taylor JL, Veenstra-VanderWeele J. Autism spectrum disorder. Nat Rev Dis Primers. 2020 Jan 16;6(1):5. doi: 10.1038/s41572-019-0138-4. PMID: 31949163.Lord C, Elsabbagh M, Baird G, Veenstra-Vanderweele J. Autism spectrum disorder. Lancet. 2018 Aug 11;392(10146):508-520. doi: 10.1016/S0140-6736(18)31129-2. Epub 2018 Aug 2. PMID: 30078460; PMCID: PMC7398158.Modabbernia A, Velthorst E, Reichenberg A. Environmental risk factors for autism: an evidence-based review of systematic reviews and meta-analyses. Mol Autism. 2017 Mar 17;8:13. doi: 10.1186/s13229-017-0121-4. PMID: 28331572; PMCID: PMC5356236.Muhle RA, Reed HE, Stratigos KA, Veenstra-VanderWeele J. The Emerging Clinical Neuroscience of Autism Spectrum Disorder: A Review. JAMA Psychiatry. 2018 May 1;75(5):514-523. doi: 10.1001/jamapsychiatry.2017.4685. PMID: 29590280.
2-Minute Neuroscience: Narcolepsy Neuroscientifically Challenged 2021-11-15 | Narcolepsy is a chronic condition that causes excessive daytime sleepiness and leads to an increased tendency to fall asleep during daytime activities. In this video, I discuss the symptoms of narcolepsy and explain what may happen in the brain to cause those symptoms to occur.TRANSCRIPT:Narcolepsy is a chronic condition that causes excessive daytime sleepiness and leads to an increased tendency to fall asleep during daytime activities. The majority of people who suffer from narcolepsy also experience cataplexy, which involves brief, sudden episodes of muscle weakness or paralysis---often brought on by strong positive emotions. The muscle weakness in cataplexy may be severe enough to cause someone to fall to the ground and be unable to speak or move for a short period of time despite remaining conscious. Patients with narcolepsy also often experience other sleep-related problems, such as disrupted sleep, sleep paralysis, and hallucinations when falling asleep or waking up. Today, narcolepsy is often classified as narcolepsy type 1 or narcolepsy type 2. Type 1 typically involves narcolepsy with cataplexy, and low levels of a neuropeptide called orexin, also known as hypocretin. Type 2 does not involve cataplexy, and levels of orexin are normal. Narcolepsy type 2 generally has less severe symptoms, but little is known about its cause. Narcolepsy type 1 is linked to a loss of orexin-producing neurons in the hypothalamus, leading to low orexin levels. Orexin neurons have an excitatory effect on several regions of the brain that are involved in promoting wakefulness and suppressing REM sleep. Thus, the loss of these neurons leads to deficiencies in maintaining wakefulness and is linked to the dysregulation of REM sleep. This REM sleep dysregulation is thought to cause episodes of muscle paralysis and other aspects of REM sleep to occur during wakefulness, which is the basis for cataplexy.The cause of the loss of orexin neurons in narcolepsy is not completely understood, but several lines of evidence implicate an autoimmune mechanism. According to this view, a combination of genetic and environmental factors leads to an inflammatory process in the brain that causes the immune-mediated destruction of orexin neurons, bringing about the symptoms of narcolepsy.REFERENCES:Bassetti CLA, Adamantidis A, Burdakov D, Han F, Gay S, Kallweit U, Khatami R, Koning F, Kornum BR, Lammers GJ, Liblau RS, Luppi PH, Mayer G, Pollmächer T, Sakurai T, Sallusto F, Scammell TE, Tafti M, Dauvilliers Y. Narcolepsy - clinical spectrum, aetiopathophysiology, diagnosis and treatment. Nat Rev Neurol. 2019 Sep;15(9):519-539. doi: 10.1038/s41582-019-0226-9. Epub 2019 Jul 19. PMID: 31324898. Kornum BR, Knudsen S, Ollila HM, Pizza F, Jennum PJ, Dauvilliers Y, Overeem S. Narcolepsy. Nat Rev Dis Primers. 2017 Feb 9;3:16100. doi: 10.1038/nrdp.2016.100. PMID: 28179647.Mahoney CE, Cogswell A, Koralnik IJ, Scammell TE. The neurobiological basis of narcolepsy. Nat Rev Neurosci. 2019 Feb;20(2):83-93. doi: 10.1038/s41583-018-0097-x. PMID: 30546103; PMCID: PMC6492289.Sateia MJ. International classification of sleep disorders-third edition: highlights and modifications. Chest. 2014 Nov;146(5):1387-1394. doi: 10.1378/chest.14-0970. PMID: 25367475.
2-Minute Neuroscience: MDMA Neuroscientifically Challenged 2021-09-28 | MDMA, better known as ecstasy, molly, or one of a number of other street names, is a stimulant drug with unique prosocial effects. In this video, I discuss the current understanding of how MDMA acts on the brain to produce its effects.TRANSCRIPT:MDMA, better known as ecstasy, molly, or one of a number of other street names, is a stimulant drug that is chemically related to amphetamine. Like other stimulants, MDMA causes increased alertness and a positive mood. But MDMA’s effects are also distinct from the effects of other stimulants, as the drug causes unique prosocial effects such as strong feelings of trust, openness, and closeness with others.Although we don’t have a full understanding of the effects of MDMA on the brain, MDMA’s mechanism is similar in many ways to the mechanism of other amphetamines. MDMA inhibits the function of proteins called transporter proteins, which typically remove neurotransmitters like serotonin, dopamine, and norepinephrine from the space between neurons known as the synaptic cleft. By inhibiting transporter proteins, MDMA causes serotonin, dopamine, and norepinephrine to accumulate in the synaptic cleft, increasing neurotransmitter activity there. In contrast to other amphetamines, MDMA inhibits the serotonin transporter more potently than the dopamine or norepinephrine transporter. MDMA also uses transporter proteins to enter neurons; once inside, MDMA disrupts the storage of neurotransmitters in synaptic vesicles, causing the buildup of serotonin, dopamine, and norepinephrine inside neurons; then, MDMA facilitates the release of these neurotransmitters into the synaptic cleft, leading to increased neurotransmitter levels and activity. In addition to these mechanisms, MDMA also binds to a number of receptors directly, including specific subtypes of the serotonin receptor; these interactions may contribute to the effects of MDMA.It’s not clear what mechanism accounts for the unique prosocial effects of MDMA. A number of studies have found that MDMA promotes the release of the hormone oxytocin, which itself has been linked to prosocial effects. At the same time, most studies have failed to find a link between increasing oxytocin levels and the prosocial effects of MDMA, leaving these effects still unexplained.REFERENCES:Dunlap LE, Andrews AM, Olson DE. Dark Classics in Chemical Neuroscience: 3,4-Methylenedioxymethamphetamine. ACS Chem Neurosci. 2018 Oct 17;9(10):2408-2427. doi: 10.1021/acschemneuro.8b00155. Epub 2018 Jul 12. PMID: 30001118; PMCID: PMC6197894. Oeri HE. Beyond ecstasy: Alternative entactogens to 3,4-methylenedioxymethamphetamine with potential applications in psychotherapy. J Psychopharmacol. 2021 May;35(5):512-536. doi: 10.1177/0269881120920420. Epub 2020 Sep 10. PMID: 32909493; PMCID: PMC8155739. Schenk S, Highgate Q. Methylenedioxymethamphetamine (MDMA): Serotonergic and dopaminergic mechanisms related to its use and misuse. J Neurochem. 2021 Jun;157(5):1714-1724. doi: 10.1111/jnc.15348. Epub 2021 Mar 25. PMID: 33711169.
2-Minute Neuroscience: Brain Aneurysms Neuroscientifically Challenged 2021-08-27 | A brain aneurysm is a weakened area in the lining of a blood vessel in the brain where blood accumulates, causing a bulging of the blood vessel wall. Most brain aneurysms do not cause any symptoms, but a ruptured aneurysm can lead to bleeding into the area surrounding the brain—a dangerous condition known as subarachnoid hemorrhage. In this video, I discuss the characteristics, formation, rupture, and treatment of brain aneurysms.TRANSCRIPT:A brain aneurysm is a weakened area in the lining of a blood vessel in the brain where blood accumulates, causing a bulging of the blood vessel wall. While estimates vary, it is thought that brain aneurysms may occur in somewhere between 2 and 5% of the population. Most brain aneurysms, however, do not cause any symptoms, but larger aneurysms may cause symptoms by putting pressure on brain tissue and in a small percentage of cases, an aneurysm may rupture. The rupture of a brain aneurysm can cause bleeding into the area surrounding the brain---a condition known as subarachnoid hemorrhage. Subarachnoid hemorrhage is an extremely dangerous situation with high rates of fatality. The mechanisms underlying the formation and rupture of brain aneurysms are still not completely understood. It is thought, however, that an aneurysm may typically originate with damage to the wall of a blood vessel, followed by an inflammatory response that ends up further weakening the blood vessel wall. The weakened vessel wall allows blood to accumulate in that section of the blood vessel and increases the risk of the vessel rupturing. There are a number of factors that may influence the likelihood of aneurysm rupture, such as the size, location, and rate of growth of the aneurysm, as well as patient factors such as smoking, alcohol consumption, hypertension, and a family or personal history of aneurysm rupture. A ruptured aneurysm requires emergency treatment, which typically involves one of two approaches: surgical clipping or endovascular coiling. Clipping involves surgery to open the skull and place a metal clip at the base of the aneurysm to prevent blood flow into the aneurysm. Coiling is a less invasive procedure that involves passing a catheter into an artery and threading it through the body to reach the aneurysm. Tiny platinum coils are then released into the aneurysm to block blood flow into the aneurysm. REFERENCES:Brisman JL, Song JK, Newell DW. Cerebral aneurysms. N Engl J Med. 2006 Aug 31;355(9):928-39. doi: 10.1056/NEJMra052760. PMID: 16943405."Cerebral Aneurysms Fact Sheet", NINDS, Publication date May 2018.NIH Publication No. 18-NS-5506 Chalouhi N, Hoh BL, Hasan D. Review of cerebral aneurysm formation, growth, and rupture. Stroke. 2013 Dec;44(12):3613-22. doi: 10.1161/STROKEAHA.113.002390. Epub 2013 Oct 15. PMID: 24130141. Jung KH. New Pathophysiological Considerations on Cerebral Aneurysms. Neurointervention. 2018 Sep;13(2):73-83. doi: 10.5469/neuroint.2018.01011. Epub 2018 Aug 31. PMID: 30196677; PMCID: PMC6132027.Thompson BG, Brown RD Jr, Amin-Hanjani S, Broderick JP, Cockroft KM, Connolly ES Jr, Duckwiler GR, Harris CC, Howard VJ, Johnston SC, Meyers PM, Molyneux A, Ogilvy CS, Ringer AJ, Torner J; American Heart Association Stroke Council, Council on Cardiovascular and Stroke Nursing, and Council on Epidemiology and Prevention; American Heart Association; American Stroke Association. Guidelines for the Management of Patients With Unruptured Intracranial Aneurysms: A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association. Stroke. 2015 Aug;46(8):2368-400. doi: 10.1161/STR.0000000000000070. Epub 2015 Jun 18. PMID: 26089327.Vlak MH, Algra A, Brandenburg R, Rinkel GJ. Prevalence of unruptured intracranial aneurysms, with emphasis on sex, age, comorbidity, country, and time period: a systematic review and meta-analysis. Lancet Neurol. 2011 Jul;10(7):626-36. doi: 10.1016/S1474-4422(11)70109-0. PMID: 21641282.
2-Minute Neuroscience: Bells Palsy Neuroscientifically Challenged 2021-07-14 | Bell’s palsy is a disorder characterized by facial weakness or paralysis, typically on one side of the face. It results from the dysfunction of cranial nerve VII, the facial nerve, but the cause of the facial nerve dysfunction is unknown. In this video, I discuss the symptoms, possible causes, and prognosis for Bell’s palsy.TRANSCRIPT: Bell’s palsy is a disorder that results from the dysfunction of cranial nerve VII, the facial nerve. It involves weakness or paralysis, typically on one side of the face. The onset of the condition is rapid, usually progressing to maximum severity within 72 hours. While there can be a number of causes of facial weakness or paralysis, the cause of Bell’s palsy is unknown, and diagnosis is made by ruling out other potential causes like Lyme disease, trauma, tumors, etc. In other words, Bell’s palsy is only diagnosed when there is not another identifiable cause of the facial paralysis.The symptoms of Bell’s palsy can vary from case to case in both form and severity, but the most common symptom is rapidly developing weakness on one side of the face. There can be a number of other symptoms that emerge from facial nerve dysfunction, including drooping of the eyelid, drooping of one side of the mouth, drooling, an inability to completely close the eye, excessive tearing and pain in the eye, facial pain, loss of taste, hypersensitivity to sound on the affected side, and other symptoms depending on the case.Although the cause of Bell’s palsy is unclear, there is evidence that many cases may have a viral origin. Reactivation of latent viruses such as the herpes simplex virus has been hypothesized to be an important factor in many cases of Bell’s palsy, but how exactly viruses might damage the facial nerve is still uncertain. Other factors potentially involved in the development of Bell’s palsy include reduced blood supply to the facial nerve and damage to the facial nerve caused by inflammation. Most cases of Bell’s palsy start to improve without any medical intervention within a few weeks, and recover completely within 3 to 4 months. Less commonly, symptoms may last longer, never completely disappear, or fade away and then reoccur.REFERENCES:Baugh RF, Basura GJ, Ishii LE, Schwartz SR, Drumheller CM, Burkholder R, Deckard NA, Dawson C, Driscoll C, Gillespie MB, Gurgel RK, Halperin J, Khalid AN, Kumar KA, Micco A, Munsell D, Rosenbaum S, Vaughan W. Clinical practice guideline: Bell's palsy. Otolaryngol Head Neck Surg. 2013 Nov;149(3 Suppl):S1-27. doi: 10.1177/0194599813505967. PMID: 24189771. The National Institute of Mental Health. Bell’s Palsy Fact Sheet. NIH Publication No. 18-NS-5114. 2018. Retrieved from: ninds.nih.gov/Disorders/Patient-Caregiver-Education/Fact-Sheets/Bells-Palsy-Fact-SheetReich SG. Bell's Palsy. Continuum (Minneap Minn). 2017 Apr;23(2, Selected Topics in Outpatient Neurology):447-466. doi: 10.1212/CON.0000000000000447. PMID: 28375913.Zhang W, Xu L, Luo T, Wu F, Zhao B, Li X. The etiology of Bell's palsy: a review. J Neurol. 2020 Jul;267(7):1896-1905. doi: 10.1007/s00415-019-09282-4. Epub 2019 Mar 28. PMID: 30923934; PMCID: PMC7320932.
2-Minute Neuroscience: Tinnitus Neuroscientifically Challenged 2021-06-12 | Tinnitus, sometimes called “ringing in the ears,” involves hearing a sound that cannot be linked to an external stimulus. In this video, I discuss nervous system mechanisms that might underlie tinnitus.TRANSCRIPT:Tinnitus, sometimes called “ringing in the ears,” involves hearing a sound that cannot be linked to an external stimulus. The nature of the perceived sound can vary in complexity, but common manifestations include ringing, hissing, or sizzling. Prevalence estimates vary, but most studies suggest tinnitus occurs in somewhere between 10 and 15% of the population. Although most cases are manageable, severe cases of tinnitus can significantly impact quality of life. Tinnitus can occur as a symptom linked to a number of different conditions, and thus there is not a single mechanism that can explain all cases. The most common predisposing condition, however, is hearing loss, which is found in up to 90% of patients with tinnitus. The mechanisms underlying tinnitus are not well understood, but it’s thought that hearing loss might be linked to tinnitus in a number of ways. Damage to the cochlea, for example, may lead to increased signaling in other auditory structures to compensate for the reduction in auditory input from the cochlea, and the resultant amplification of neural noise may lead to tinnitus. Additionally, there may be a reorganization in the auditory cortex where neurons that normally respond to frequencies that are missing due to cochlea damage now respond to other frequencies and display abnormal levels of activity. Neuroimaging studies have revealed other potential abnormalities in tinnitus, such as increased activity in the auditory cortex and decreased activity in areas like the prefrontal cortex. The latter may be linked to a failure to inhibit increased auditory signaling. Other studies have found increased activity in regions involved with memory like the hippocampus and surrounding areas. These might be involved with retrieving a sound from memory that becomes the perceived sound in tinnitus. Activation of areas like the anterior cingulate cortex and insula, which are involved in identifying important stimuli, may prevent habituation to the perceived sound in tinnitus.REFERENCES:Baguley D, McFerran D, Hall D. Tinnitus. Lancet. 2013 Nov 9;382(9904):1600-7. doi: 10.1016/S0140-6736(13)60142-7. Epub 2013 Jul 2. PMID: 23827090.Elgoyhen AB, Langguth B, De Ridder D, Vanneste S. Tinnitus: perspectives from human neuroimaging. Nat Rev Neurosci. 2015 Oct;16(10):632-42. doi: 10.1038/nrn4003. Epub 2015 Sep 16. Erratum in: Nat Rev Neurosci. 2015 Nov;16(11):700. PMID: 26373470.Shore SE, Roberts LE, Langguth B. Maladaptive plasticity in tinnitus--triggers, mechanisms and treatment. Nat Rev Neurol. 2016 Mar;12(3):150-60. doi: 10.1038/nrneurol.2016.12. Epub 2016 Feb 12. PMID: 26868680; PMCID: PMC4895692.
2-Minute Neuroscience: Ketamine Neuroscientifically Challenged 2021-05-15 | Ketamine is an anesthetic, analgesic, antidepressant, and recreationally used drug. In this video, I discuss hypotheses about how ketamine produces its effects.TRANSCRIPT: Ketamine was initially developed as an anesthetic, but today it is also used as an analgesic and an antidepressant. It has been used as a recreational drug since the 1970s.After administration, ketamine is rapidly and extensively metabolized into an active metabolite called norketamine, which is thought to play an important role in ketamine’s anesthetic and analgesic effects. Ketamine and norketamine both act at a receptor for the neurotransmitter glutamate called the NMDA receptor. Glutamate is the primary excitatory neurotransmitter in the brain, and ketamine and norketamine act as antagonists at the NMDA receptor, which means that they block the receptor and inhibit activity there. Inhibition of NMDA receptors can substantially affect neurotransmission, and is thought to be critical to the anesthetic and analgesic effects of ketamine.While most other antidepressants take several weeks to achieve a therapeutic effect, ketamine can begin to improve depressive symptoms within hours and last for up to 2 weeks after a single administration. The mechanisms underlying ketamine’s antidepressant action are not fully understood, but it’s thought that it cannot be explained by NMDA antagonism alone. One hypothesis is that another glutamate receptor known as an AMPA receptor may play a key role. AMPA receptors may be stimulated indirectly by ketamine or directly by other ketamine metabolites such as hydroxynorketamine. Stimulation of AMPA receptors may lead to the activation of multiple signaling pathways. and downstream effects such as new synapse formation in areas of the brain like the prefrontal cortex and hippocampus. These synaptic connections may bolster neural circuits involved with regulating stress and mood. Ketamine also acts on a number of other receptors, however, and there is still much more to learn about ketamine’s antidepressant mechanism of action. Additionally, more evidence about the safety and effectiveness of ketamine needs to be collected for more physicians to support the use of ketamine as an antidepressant.REFERENCES:Nowacka A, Borczyk M. Ketamine applications beyond anesthesia - A literature review. Eur J Pharmacol. 2019 Oct 5;860:172547. doi: 10.1016/j.ejphar.2019.172547. Epub 2019 Jul 23. PMID: 31348905. Tyler MW, Yourish HB, Ionescu DF, Haggarty SJ. Classics in Chemical Neuroscience: Ketamine. ACS Chem Neurosci. 2017 Jun 21;8(6):1122-1134. doi: 10.1021/acschemneuro.7b00074. Epub 2017 Apr 21. PMID: 28418641. Zanos P, Gould TD. Mechanisms of ketamine action as an antidepressant. Mol Psychiatry. 2018 Apr;23(4):801-811. doi: 10.1038/mp.2017.255. Epub 2018 Mar 13. PMID: 29532791; PMCID: PMC5999402.
2-Minute Neuroscience: Chronic Traumatic Encephalopathy (CTE) Neuroscientifically Challenged 2021-04-18 | Chronic traumatic encephalopathy, or CTE, is a neurological condition linked primarily to repetitive head trauma. In this video, I discuss what happens in the brain during CTE.For an article (on my website) that discusses CTE more in-depth, click this link: neuroscientificallychallenged.com/posts/know-your-brain-chronic-traumatic-encephalopathy-cteTRANSCRIPT:Chronic traumatic encephalopathy, or CTE, is a neurological condition linked primarily to repetitive head trauma. Most cases of CTE occur in those who play sports where head injuries are common, but anyone who has experienced repeated head trauma is at risk. CTE symptoms generally begin to appear years after head trauma and may include: memory deficits and other cognitive impairment, abnormal behavior such as paranoia, aggression and impulsivity, mood disturbances such as depression, and movement problems such as tremor and other symptoms similar to those seen in Parkinson’s disease. In most cases, CTE is a progressive condition that gets worse over time.Although the pathology of CTE in the brain is not fully understood, a common feature of CTE involves a protein called tau that’s normally involved in maintaining the structure of the cell. In CTE, tau proteins accumulate in neurons and other cells like astrocytes to form abnormal clusters or aggregates. The tau aggregates are called neurofibrillary tangles when they form in neurons and astrocytic or glial tangles when they form in astrocytes. The role of tau aggregates in disease progression is still not fully understood, but it’s thought they can disrupt cellular communication, and their presence is associated with the degeneration and death of neurons. They also seem to be able to spread throughout the brain, so a neuron that develops neurofibrillary tangles may cause surrounding neurons to develop them as well.Initially, tau aggregates primarily form close to the surface of the cerebral cortex, but as the disease progresses they spread throughout the cortex and to other areas of the brain like the hippocampus, amygdala, and various other regions. The spread of the tau pathology is correlated with other degenerative signs, such as general atrophy of the brain, severe neuronal loss in areas such as the hippocampus and amygdala, and less substantial neuronal loss in a number of other brain regions. REFERENCES:Asken BM, Sullan MJ, DeKosky ST, Jaffee MS, Bauer RM. Research Gaps and Controversies in Chronic Traumatic Encephalopathy: A Review. JAMA Neurol. 2017 Oct 1;74(10):1255-1262. doi: 10.1001/jamaneurol.2017.2396. PMID: 28975240.Baugh CM, Stamm JM, Riley DO, Gavett BE, Shenton ME, Lin A, Nowinski CJ, Cantu RC, McKee AC, Stern RA. Chronic traumatic encephalopathy: neurodegeneration following repetitive concussive and subconcussive brain trauma. Brain Imaging Behav. 2012 Jun;6(2):244-54. doi: 10.1007/s11682-012-9164-5. PMID: 22552850. McKee AC, Stern RA, Nowinski CJ, Stein TD, Alvarez VE, Daneshvar DH, Lee HS, Wojtowicz SM, Hall G, Baugh CM, Riley DO, Kubilus CA, Cormier KA, Jacobs MA, Martin BR, Abraham CR, Ikezu T, Reichard RR, Wolozin BL, Budson AE, Goldstein LE, Kowall NW, Cantu RC. The spectrum of disease in chronic traumatic encephalopathy. Brain. 2013 Jan;136(Pt 1):43-64. doi: 10.1093/brain/aws307. Epub 2012 Dec 2. Erratum in: Brain. 2013 Oct;136(Pt 10):e255. PMID: 23208308; PMCID: PMC3624697. Montenigro PH, Corp DT, Stein TD, Cantu RC, Stern RA. Chronic traumatic encephalopathy: historical origins and current perspective. Annu Rev Clin Psychol. 2015;11:309-30. doi: 10.1146/annurev-clinpsy-032814-112814. Epub 2015 Jan 12. PMID: 25581233.
2-Minute Neuroscience: Motor Neurons Neuroscientifically Challenged 2021-03-23 | In this video, I discuss upper and lower motor neurons as well as the syndromes (i.e., upper and lower motor neuron syndrome) that occur when a motor neuron is damaged.TRANSCRIPT: A motor neuron is a type of neuron that carries information from the brain or spinal cord and is involved in regulating activity in muscles or glands. There are two types of motor neurons: upper motor neurons and lower motor neurons, which interact with one another to cause movement and other responses. Upper motor neurons originate in multiple areas of the brain and brainstem and carry information about desired movements or other responses in descending tracts like the corticobulbar and corticospinal tracts. Upper motor neurons descend to various levels of the brainstem and spinal cord and form connections with lower motor neurons. Lower motor neurons then influence the activity of muscles or glands. There are three broad categories of lower motor neurons: somatic motor neurons, which extend to skeletal muscle to control movement and muscle tone; special visceral or branchial motor neurons, which supply muscles in the head and neck; and general visceral motor neurons, which are involved in the autonomic nervous system. Somatic motor neurons can be further subdivided into alpha, beta, and gamma motor neurons depending on the type of muscle fiber they supply.The consequences of upper and lower motor neuron damage are distinct. Symptoms of upper motor neuron damage, which are collectively called upper motor neuron syndrome, can include weakness or paralysis, spasticity, increased muscle tone, over-responsive reflexes, and a positive Babinski sign, which occurs when the bottom of the foot is stroked and---instead of the toes curling down---the big toe extends up and the other toes fan out. Lower motor neuron damage leads to a collection of symptoms known as lower motor neuron syndrome, which may involve weakness or paralysis, decreased or absent muscle tone, decreased or absent reflexes, involuntary muscle twitches, and muscle atrophy.REFERENCES:Purves D, Augustine GJ, Fitzpatrick D, Hall WC, Lamantia AS, Mooney RD, Platt ML, White LE, eds. Neuroscience. 6th ed. New York. Sinauer Associates; 2018.Zayia LC, Tadi P. Neuroanatomy, Motor Neuron. [Updated 2020 Jul 31]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan-. Available from: ncbi.nlm.nih.gov/books/NBK554616
2-Minute Neuroscience: Phantom Limb Neuroscientifically Challenged 2021-02-12 | Phantom limb is a condition in which someone who has lost a part of their body (e.g., due to amputation) continues to experience phantom sensations coming from the missing body part. In this video, I discuss some of the hypotheses that have been proposed to explain this strange phenomenon.For an article (on my website) that discusses phantom limb more in-depth, click this link: neuroscientificallychallenged.com/posts/know-your-brain-phantom-limbTRANSCRIPT:Phantom limb is a condition in which someone who has lost a part of their body continues to experience phantom sensations coming from that body part. Despite the name, phantom limb doesn’t only occur in limbs, and has also been recorded after the loss of other body parts like breasts, genitals, and even teeth. Phantom sensations are thought to be experienced by almost all amputees, and most suffer from some degree of phantom pain.Scientists have proposed a number of hypotheses to explain phantom limb, but the phenomenon is still poorly understood. The prevailing explanation is an idea known as cortical reorganization. According to this hypothesis, when a limb is lost, the neurons in the somatosensory cortex that used to respond to signals from that limb begin to respond to signals from other nearby neurons. This can cause sensations felt in other parts of the body to lead to the stimulation of neurons in the somatosensory cortex devoted to the now missing limb, which causes the brain to perceive sensations in the missing limb.Another hypothesis suggests that your brain maintains an internal representation of your body, which aids in body positioning and movement among other things. But when a limb is lost the body representation can remain intact. This persistent neural representation might lead to the sense that the limb is still there, and could even generate pain when the intention to move the limb is discordant with the lack of sensory feedback from the missing body part.The peripheral nervous system might also be involved. When a limb is lost, damaged neurons often attempt to repair themselves by growing new extensions. But without a limb to grow into, the new extensions have nowhere to go, and they form a mass of neural tissue called a neuroma. The neuroma can generate erratic signals, which may underlie the sensations and pain associated with phantom limb.REFERENCES:Collins KL, Russell HG, Schumacher PJ, Robinson-Freeman KE, O'Conor EC, Gibney KD, Yambem O, Dykes RW, Waters RS, Tsao JW. A review of current theories and treatments for phantom limb pain. J Clin Invest. 2018 Jun 1;128(6):2168-2176. doi: 10.1172/JCI94003. Epub 2018 Jun 1. PMID: 29856366; PMCID: PMC5983333.Flor H, Nikolajsen L, Staehelin Jensen T. Phantom limb pain: a case of maladaptive CNS plasticity? Nat Rev Neurosci. 2006 Nov;7(11):873-81. doi: 10.1038/nrn1991. PMID: 17053811.Ramachandran VS, Hirstein W. The perception of phantom limbs. The D. O. Hebb lecture. Brain. 1998 Sep;121 ( Pt 9):1603-30. doi: 10.1093/brain/121.9.1603. PMID: 9762952.Weeks SR, Anderson-Barnes VC, Tsao JW. Phantom limb pain: theories and therapies. Neurologist. 2010 Sep;16(5):277-86. doi: 10.1097/NRL.0b013e3181edf128. PMID: 20827116.
2-Minute Neuroscience: Tourette Syndrome Neuroscientifically Challenged 2021-01-10 | In this video, I discuss what is hypothesized to occur in the brain to cause Tourette syndrome, a disorder characterized by recurrent involuntary movements or sounds called tics.For an article (on my website) that discusses Tourette syndrome more in-depth, click this link: neuroscientificallychallenged.com/posts/know-your-brain-tourette-syndromeTRANSCRIPT:Tourette syndrome is characterized by recurrent involuntary movements or sounds called tics. Tics can be classified as simple or complex. Simple tics usually involve only one group of muscles, and might consist of actions like eye blinking or throat clearing. Complex tics are more elaborate, and might involve actions like reaching out to touch something or the involuntary use of obscene language, which is known as coprolalia. It’s worth noting that coprolalia, while often associated with Tourette syndrome, is actually thought to occur in less than 20% of cases.The neuroscience of Tourette syndrome is still poorly understood, but a number of studies suggest an important role for a group of structures known as the basal ganglia, which includes the: caudate, putamen, globus pallidus, substantia nigra, and subthalamic nucleus. The basal ganglia are involved in diverse brain functions, but they are especially relevant to Tourette syndrome for their hypothesized role in suppressing unwanted actions. According to this perspective, one function of basal ganglia circuitry is to inhibit neurons in the thalamus and prevent them from sending undesired movement-related signals to the motor cortex. In Tourette syndrome, it’s thought that faulty inhibitory mechanisms in the basal ganglia may fail to stop unwanted signals from reaching the cortex. This causes the execution of an action that the patient might prefer to suppress, forming the basis for tics. The failed inhibition in the basal ganglia is thought to be coupled with increased activity in motor pathways that generate movements. Thus, patients with Tourette’s might experience a problematic combination of high motor activity that generates habitual patterns of behavior, along with abnormally low inhibitory activity that would normally keep those behaviors from being acted out. More research needs to be done, however, to fully elucidate the neural circuitry underlying the disorder.REFERENCES:Jahanshahi M, Obeso I, Rothwell JC, Obeso JA. A fronto-striato-subthalamic-pallidal network for goal-directed and habitual inhibition. Nat Rev Neurosci. 2015 Dec;16(12):719-32. doi: 10.1038/nrn4038. Epub 2015 Nov 4.McNaught KS, Mink JW. Advances in understanding and treatment of Tourette syndrome. Nat Rev Neurol. 2011 Nov 8;7(12):667-76. doi: 10.1038/nrneurol.2011.167.Robertson MM, Eapen V, Singer HS, Martino D, Scharf JM, Paschou P, Roessner V, Woods DW, Hariz M, Mathews CA, Črnčec R, Leckman JF. Gilles de la Tourette syndrome. Nat Rev Dis Primers. 2017 Feb 2;3:16097. doi: 10.1038/nrdp.2016.97.
2-Minute Neuroscience: Withdrawal Reflex Neuroscientifically Challenged 2020-12-05 | The withdrawal reflex is an automatic response that enables you to pull away from a painful stimulus (e.g., a hot stove, a tack you’ve stepped on) without having to consciously plan to do so. In this video, I explain the mechanism of the withdrawal reflex. TRANSCRIPT:The withdrawal reflex is an automatic response enacted to withdraw a limb from a painful stimulus. If, for example, you were to touch a hot stove or step on a tack, the withdrawal reflex would cause you to pull your arm or leg away from the painful stimulus without having to consciously plan to do so. The intensity of the reflex is proportional to the intensity of the painful stimulus, so a very hot stove would cause a more rapid and forceful withdrawal than a mildly hot stove.The withdrawal reflex is a polysynaptic reflex, as it uses neurons called interneurons to pass signals from sensory to motor neurons, creating multiple synaptic connections. The reflex begins when a painful stimulus is detected by receptors called nociceptors, which are specialized to detect noxious stimuli. The activation of nociceptors leads to an action potential in a sensory neuron, which carries the signal to the spinal cord, where multiple reflex pathways are activated. One of those pathways excites a motor neuron that activates the flexor muscle in the limb, causing the limb to withdraw from the painful stimulus. Another pathway inhibits the motor neuron that normally activates the opposing extensor muscle in the limb. This will keep the extensor muscle from counteracting the attempt of the flexor muscle to pull the limb away. Another pathway crosses over to the other side of the spinal cord, and causes the opposite response to occur in the opposing limb. In other words, the extensor muscle in the opposing limb will be activated and the flexor muscle will be inhibited. This is sometimes called the crossed-extension reflex, and it is enacted for postural support. If, for example, you are withdrawing your foot from a painful stimulus, then the other leg needs to be prepared to hold your weight. References:Pearson KG, Gordon JE. 2013. Spinal Reflexes. In: Kandel ER, Schwartz JH, Jessell TM, Siegelbaum SA, Hudspeth AJ, eds. Principles of Neural Science, 5th ed. New York: McGraw-Hill.
2-Minute Neuroscience: Serotonin-Norepinephrine Reuptake Inhibitors (SNRIs) Neuroscientifically Challenged 2020-11-03 | Serotonin-Norepinephrine Reuptake Inhibitors, or SNRIs, are a common treatment for depression and a variety of other ailments like anxiety disorders and chronic pain. In this video, I discuss how SNRIs work in the brain and how they are proposed to be able to treat the symptoms of depression.TRANSCRIPT:Serotonin-norepinephrine reuptake inhibitors, or SNRIs, first appeared on the market in 1993 with the introduction of venlafaxine. Several others, like duloxetine, would be introduced in the following decades. Most SNRIs were primarily developed for the treatment of depression, but some are now also used to treat a variety of other conditions like anxiety and chronic pain. The development of SNRIs was guided by research that suggests neurotransmitters like serotonin and norepinephrine play a role in depression. Specifically, this research suggests that low levels of these neurotransmitters might contribute to the symptoms of depression.SNRIs work primarily by inhibiting a mechanism called reuptake. In reuptake, a protein called a transporter transports excess neurotransmitter molecules out of the synaptic cleft, typically back into the neuron that released them. SNRIs inhibit the reuptake of serotonin and norepinephrine. When the removal of serotonin and norepinephrine from the synaptic cleft is inhibited, this causes levels of these neurotransmitters in the synaptic cleft to rise. These increases in serotonin and norepinephrine levels have been hypothesized to be the mechanism by which SNRIs can treat the symptoms of depression. It should be noted, however, that research suggests the neurobiological mechanism of depression is more complex than a simple neurotransmitter deficiency. Thus, it may be that increasing serotonin and norepinephrine levels leads to other effects that can alleviate the symptoms of depression, or that the drugs have other mechanisms that contribute to their effectiveness.Studies have found SNRIs to be comparable to other popular antidepressants, like SSRIs, in terms of effectiveness. SNRIS are also generally well-tolerated, with problems like nausea, sweating, and loss of appetite being some of the commonly reported side effects---although different snri drugs have different side effect profiles.REFERENCES:Brunello N, Mendlewicz J, Kasper S, Leonard B, Montgomery S, Nelson J, Paykel E, Versiani M, Racagni G. The role of noradrenaline and selective noradrenaline reuptake inhibition in depression. Eur Neuropsychopharmacol. 2002 Oct;12(5):461-75. doi: 10.1016/s0924-977x(02)00057-3. PMID: 12208564. Cipriani A, Furukawa TA, Salanti G, Chaimani A, Atkinson LZ, Ogawa Y, Leucht S, Ruhe HG, Turner EH, Higgins JPT, Egger M, Takeshima N, Hayasaka Y, Imai H, Shinohara K, Tajika A, Ioannidis JPA, Geddes JR. Comparative efficacy and acceptability of 21 antidepressant drugs for the acute treatment of adults with major depressive disorder: a systematic review and network meta-analysis. Lancet. 2018 Apr 7;391(10128):1357-1366. doi: 10.1016/S0140-6736(17)32802-7. Epub 2018 Feb 21. PMID: 29477251; PMCID: PMC5889788. Hillhouse TM, Porter JH. A brief history of the development of antidepressant drugs: from monoamines to glutamate. Exp Clin Psychopharmacol. 2015 Feb;23(1):1-21. doi: 10.1037/a0038550. PMID: 25643025; PMCID: PMC4428540. Lambert O, Bourin M. SNRIs: mechanism of action and clinical features. Expert Rev Neurother. 2002 Nov;2(6):849-58. doi: 10.1586/14737175.2.6.849. PMID: 19810918.Sansone RA, Sansone LA. Serotonin norepinephrine reuptake inhibitors: a pharmacological comparison. Innov Clin Neurosci. 2014 Mar;11(3-4):37-42. PMID: 24800132; PMCID: PMC4008300.
2-Minute Neuroscience: Cerebral Cortex Neuroscientifically Challenged 2020-10-15 | The cerebral cortex is the outermost layer of the brain, and is involved in a long list of brain functions---including most of the higher functions often associated with human cognition. In this video, I discuss the appearance, cellular architecture, and functional subdivisions of the cerebral cortex.For an article (on my website) that discusses the cerebral cortex, click this link: neuroscientificallychallenged.com/posts/know-your-brain-cerebral-cortexTRANSCRIPT:The cerebral cortex is the outermost layer of the brain. It is made up primarily of gray matter that is extensively folded, forming ridges called gyri and grooves called sulci. The folding substantially increases the surface area of the cerebral cortex, making room for more neural components.Most of the cerebral cortex in humans is classified as neocortex, which is so named because it is thought to have appeared relatively recently in vertebrate evolution. Neurons in the neocortex are typically arranged in six layers, which are distinguished from one another by differences in cell type and cell density. The rest of the cerebral cortex is made up of either allocortex, which has a more variable pattern of layering, or mesocortex, which is a transition area between the neocortex and allocortex. Although attempts to functionally subdivide the cerebral cortex tend to oversimplify its functions, one common approach is to divide the cortex into sensory areas, motor areas, and association areas. Sensory areas receive information related to sensation, and include regions like the primary somatosensory cortex---which processes information about sensations like touch, pain, and temperature---primary visual cortex, and primary auditory cortex, as well as other areas devoted to sensations like olfaction, taste, and the vestibular senses.The motor areas of the cerebral cortex are involved with movement, and include regions like the primary motor cortex, premotor cortex, and supplementary motor cortex. Association areas are involved in the integration of information from multiple brain regions. This integration can do things like add complexity to sensory perceptions or facilitate higher cognitive processes. For example, the association areas in the parietal cortex are thought to be involved with aspects of attention and perceptual awareness, and association areas in the frontal cortex are linked to complex processes like planning, impulse control, and self awareness.REFERENCES:Purves D, Augustine GJ, Fitzpatrick D, Hall WC, Lamantia AS, Mooney RD, Platt ML, White LE, eds. Neuroscience. 6th ed. New York. Sinauer Associates; 2018.Vanderah TW, Gould DJ. Nolte's The Human Brain. 7th ed. Philadelphia, PA. Elsevier; 2016. Zilles K, Amunts K. Architecture of the Cerebral Cortex. In: Mai JK and Paxinos G, eds. The Human Nervous System. 3rd ed. New York: Elsevier; 2012.
2-Minute Neuroscience: Deep Brain Stimulation Neuroscientifically Challenged 2020-09-24 | Deep brain stimulation is a neurosurgical approach that involves the use of brain-implanted electrodes to treat a variety of neurological and psychiatric conditions. In this video, I discuss the uses, general procedure, and hypothesized mechanisms of deep brain stimulation.TRANSCRIPT:Deep brain stimulation is a neurosurgical approach that involves the use of brain-implanted electrodes to treat a variety of neurological and psychiatric conditions. It is primarily used to treat movement disorders like Parkinson’s disease, but has also been approved by the FDA for use in treating epilepsy and obsessive-compulsive disorder, and is being studied as a potential treatment for a number of other disorders like chronic pain and depression.Deep brain stimulation involves the insertion of an electrode into the brain. The electrode is connected to a wire that runs under the skin to a device called a pulse generator, which is usually implanted under the collar bone. When the pulse generator is turned on, it emits electrical impulses that alter neural functioning. In Parkinson’s disease, for example, the electrode is typically placed near structures like the subthalamic nucleus, whose overactivity in the disease is thought to contribute to movement problems like difficulty initiating movement. Modifying the activity of these overly excitable regions can alleviate the symptoms of Parkinson’s disease. It should be noted, however, that deep brain stimulation is major brain surgery, and thus there are risks associated with the procedure. Despite numerous studies that have investigated the mechanism of deep brain stimulation, there is still a lack of clarity as to how the treatment leads to beneficial effects. Several hypotheses have been proposed to explain the mechanism, and they are not necessarily mutually exclusive. For example, deep brain stimulation may inhibit action potentials by causing prolonged depolarization of neuronal membranes, reduce neuronal activity by prompting the release of inhibitory neurotransmitters like GABA, and disrupt abnormal rhythmic neuronal firing that might interfere with healthy brain function. But more research needs to be done to develop a clear understanding of the effects of this treatment on the brain.REFERENCES:Aum DJ, Tierney TS. Deep brain stimulation: foundations and future trends. Front Biosci (Landmark Ed). 2018 Jan 1;23:162-182. doi: 10.2741/4586. PMID: 28930542.Herrington TM, Cheng JJ, Eskandar EN. Mechanisms of deep brain stimulation. J Neurophysiol. 2016 Jan 1;115(1):19-38. doi: 10.1152/jn.00281.2015. Epub 2015 Oct 28. Erratum in: J Neurophysiol. 2020 Mar 1;123(3):1277. PMID: 26510756; PMCID: PMC4760496.
2-Minute Neuroscience: Meningitis Neuroscientifically Challenged 2020-09-09 | Meningitis is a potentially deadly disease characterized by an inflammation of the meninges. In this video, I discuss the meninges and the pathophysiology of meningitis.TRANSCRIPT:The term meninges refers to 3 membranes that surround the brain and spinal cord: the dura mater, the arachnoid mater, and the pia mater. The meninges protect and provide structural support for the brain as well as contain cerebrospinal fluid. Meningitis is an inflammation of the meninges. This inflammation is typically caused by an infection, although there are non-infectious causes of meningitis as well. A variety of pathogens can cause meningitis, but the most severe cases tend to involve bacterial infections.Although the central nervous system is separated from the bloodstream by barriers like the blood-brain barrier and blood-cerebrospinal fluid barrier, meningitis can occur when pathogens evade these types of barriers and enter the meninges. When a pathogen enters the cerebrospinal fluid, an immune response causes the inflammation that characterizes meningitis. As a consequence of the immune response, the blood-brain barrier is made more permeable. This causes an influx of white blood cells and constituents of blood plasma into the cerebrospinal fluid, which contributes to inflammation and increases the volume and viscosity of the cerebrospinal fluid. These changes contribute to the development of cerebral edema, or the accumulation of fluid in the brain, as well as to the build-up of the pressure inside the skull, known as intracranial pressure. The increased intracranial pressure can disrupt cerebral blood flow and result in damage to brain tissue. Common symptoms of meningitis include headache, neck stiffness, fever, and altered mental status, but the disease can cause serious long-term complications or death. A lumbar puncture, or spinal tap, is typically done to diagnose meningitis. Although treatment will vary depending on the cause of the disease, antibiotics are often started before a diagnosis is made if bacterial meningitis is suspected, as bacterial meningitis is typically fatal if left untreated.REFERENCES:Hasbun R, van de Beek D, Brouwer MC, Tunkel AR. 2010. Actue Meningitis. In: Mandell GL, Bennett JE, Dolin R, eds. Mandell, Douglas, and Bennett’s Principles and Practice of Infectious Diseases, 7th ed. Philadelphia: Elsevier.Kurrus TA, Tauber MG. 2012. Meningitis. In: Jong EC, Stevens DL, eds. Netter’s Infectious Diseases. Philadelphia: Elsevier.Sáez-Llorens X, McCracken GH Jr. Bacterial meningitis in children. Lancet. 2003;361(9375):2139-2148. doi:10.1016/S0140-6736(03)13693-8Scheld WM, Koedel U, Nathan B, Pfister HW. Pathophysiology of bacterial meningitis: mechanism(s) of neuronal injury. J Infect Dis. 2002;186 Suppl 2:S225-S233. doi:10.1086/344939
2-Minute Neuroscience: Wernicke-Korsakoff Syndrome Neuroscientifically Challenged 2020-08-05 | In this video, I discuss the symptoms, treatment, and primary cause of Wernicke-Korsakoff syndrome, as well as how the condition affects the brain.TRANSCRIPT:Wernicke-Korsakoff syndrome is a condition that involves the presence of two related disorders: Wernicke’s encephalopathy and Korsakoff syndrome. Wernicke-Korsakoff syndrome is typically linked to alcoholism, although alcohol consumption is not always a factor. Patients suffering from Wernicke’s encephalopathy commonly experience confusion and disorientation, but may also display eye movement disturbances and movement and gait abnormalities. Korsakoff’s syndrome appears in patients who do not completely recover from Wernicke’s encephalopathy. It involves extensive memory deficits as well as a number of other cognitive and behavioral changes. Korsakoff’s patients typically have a severely impaired ability to form new memories, although the recall of previously formed memories is also affected. Wernicke-Korsakoff syndrome is caused by a deficiency in the vitamin thiamine, also known as vitamin B1. Thiamine is an essential nutrient, and a thiamine deficiency can impair processes like the utilization of carbohydrates for energy, impacting all organs of the body. The brain, however, is especially affected, as thiamine deficiency can disrupt processes like the synthesis of neurotransmitters, maintenance of membrane potential, and myelination. Alcohol consumption can interfere with thiamine in a number of ways, such as by impairing its absorption from the small intestine, affecting its transport into the brain, and disrupting its utilization.Within a matter of weeks, thiamine deficiency can result in damage to the brain that is linked to the symptoms mentioned earlier. Common areas that are affected include the mammillary bodies and hypothalamus, thalamus, cerebellum, cortex, and brainstem. In order to minimize negative effects on the brain, when Wernicke’s encephalopathy is suspected, patients are treated with thiamine supplementation. When done promptly, this may lead to a full recovery, but when treatment is delayed patients may die or progress to Korsakoff’s syndrome, and Korsakoff’s syndrome is generally considered irreversible.REFERENCES:Arts NJ, Walvoort SJ, Kessels RP. Korsakoff's syndrome: a critical review. Neuropsychiatr Dis Treat. 2017;13:2875-2890. Published 2017 Nov 27. doi:10.2147/NDT.S130078Chandrakumar A, Bhardwaj A, 't Jong GW. Review of thiamine deficiency disorders: Wernicke encephalopathy and Korsakoff psychosis. J Basic Clin Physiol Pharmacol. 2018;30(2):153-162. Published 2018 Oct 2. doi:10.1515/jbcpp-2018-0075Sechi G, Serra A. Wernicke's encephalopathy: new clinical settings and recent advances in diagnosis and management. Lancet Neurol. 2007;6(5):442-455. doi:10.1016/S1474-4422(07)70104-7
2-Minute Neuroscience: Corneal Reflex Neuroscientifically Challenged 2020-07-13 | The corneal reflex is a protective reflex that causes both eyes to blink when the cornea of either eye is touched. In this video, I discuss the neural pathways underlying the corneal reflex as well as what types of damage might cause a deficit in the reflex.TRANSCRIPT: The corneal reflex is a protective reflex that occurs when the cornea of either eye is touched. When this happens, the corneal reflex causes the eye being touched to blink---but it also causes the other eye to blink at the same time. This ensures that both eyes are protected from any foreign objects or irritants in the environment.The corneal reflex involves sensory fibers in the ophthalmic division of the trigeminal nerve that are activated when the cornea is touched. These fibers synapse on neurons in the spinal trigeminal nucleus, and those spinal trigeminal neurons then project to the facial motor nuclei on both sides of the brainstem and synapse on neurons of the facial nerve. The facial nerve fibers leave the brainstem and travel to the orbicularis oculi muscle, which closes the eyelid. Thus, the reflex arc uses the sensory input being received in one eye to generate a motor signal that causes both eyes to blink simultaneously.The corneal reflex is used clinically to test the integrity of the trigeminal and facial nerves and related structures, typically by touching the cornea with a piece of cotton. The healthy response to touching one cornea would be that both eyes would blink, but damage to the trigeminal or facial nerves or other related structures may cause a deficit in the reflex. For example, damage to the right trigeminal nerve could cause a corneal touch to the right eye to elicit no response in either eye, since the sensation might not be detected. But damage to the facial nerve on the right side could cause a corneal touch on the right side to elicit a blink in only the left eye, since the touch would be detected but the right facial nerve may be incapable of carrying out the reflex response.REFERENCES:Peterson DC, Hamel RN. Corneal Reflex. [Updated 2019 Jun 22]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from: ncbi.nlm.nih.gov/books/NBK534247Vanderah TW, Gould DJ. Nolte's The Human Brain. 7th ed. Philadelphia, PA: Elsevier; 2016.Special thanks to Srikar Gade for help with fact-checking the script for this video.
2-Minute Neuroscience: CBD Neuroscientifically Challenged 2020-06-28 | CBD is one of a class of compounds known as cannabinoids, which are found in the cannabis plant. Unlike THC (the main psychoactive component of cannabis), CBD is not thought to have intoxicating effects. It is, however, believed to interact with the nervous system. In this video, I discuss what we know about CBD’s mechanism of action and its potential in treating various conditions like epilepsy and anxiety.TRANSCRIPT:CBD is one of a class of compounds known as cannabinoids, which are found in the cannabis plant. Unlike THC (the main psychoactive component of cannabis) CBD is not thought to have intoxicating effects. It is, however, believed to interact with the nervous system, which may enable it to modulate the effects of thc as well as have actions of its own.CBD is chemically similar to THC, but it does not have the same mechanism of action, and some evidence suggests it may even interfere with some of the actions of THC. One way it may do this is by binding to receptors that THC binds to known as CB1 receptors, but instead of activating them, causing a change in the receptor that reduces THC’s ability to interact with it. This type of effect is known as negative allosteric modulation, and it may enable CBD to mitigate some of the adverse effects of THC, like anxiety. Other research, however, suggests CBD can enhance certain effects of THC, and CBD is also thought to act at a number of other targets besides the CB1 receptor. For example, CBD is believed to activate serotonin receptors and may increase levels of a natural cannabinoid called anandamide by blocking anandamide reuptake and inhibiting the enzymatic breakdown of anandamide. Overall, although a number of targets for CBD have been identified, its mechanism of action is still poorly understood.CBD is generally well-tolerated, but some have raised concerns about the need for more research before we can be confident about its safety in all populations. CBD, however, is not thought to have potential for abuse, and some believe it does have potential for treating a number of conditions, like anxiety, insomnia, and pain. But most of these claims don’t yet have strong evidence to support them, and more research is needed, although CBD has been found to be a viable treatment for at least some types of epilepsy. REFERENCES:Laprairie RB, Bagher AM, Kelly ME, Denovan-Wright EM. Cannabidiol is a negative allosteric modulator of the cannabinoid CB1 receptor. Br J Pharmacol. 2015;172(20):4790-4805. doi:10.1111/bph.13250 McPartland JM, Duncan M, Di Marzo V, Pertwee RG. Are cannabidiol and Δ(9) -tetrahydrocannabivarin negative modulators of the endocannabinoid system? A systematic review. Br J Pharmacol. 2015;172(3):737-753. doi:10.1111/bph.12944 Pisanti S, Malfitano AM, Ciaglia E, et al. Cannabidiol: State of the art and new challenges for therapeutic applications. Pharmacol Ther. 2017;175:133-150. doi:10.1016/j.pharmthera.2017.02.041World Health Organization (WHO). Cannabidiol (CBD): Pre-Review Report. November 2017. Accessed June 28, 2020. https://www.who.int/medicines/access/controlled-substances/5.2_CBD.pdfSpecial thanks to Srikar Gade for help with fact-checking this video.
2-Minute Neuroscience: THC Neuroscientifically Challenged 2020-06-10 | THC is the main psychoactive component of cannabis. In this video, I discuss the effects of THC on the nervous system.TRANSCRIPT:THC is the main psychoactive component of cannabis, and one of a class of compounds known as cannabinoids. Cannabis tends to be relatively low in THC compared to its levels of a THC precursor, THCA. Heating the cannabis plant, however, causes the conversion of THCA to THC, which is part of the basis for heating or burning the plant for use. The effects of cannabis may vary depending on the variety of cannabis plant and its associated levels of THC and other cannabinoids, but common effects of THC include: euphoria, sedation, stimulation of appetite, impaired cognitive function, analgesia, and anxiety.THC is thought to exert most of its effects by binding to receptors called cannabinoid receptors. There are two known cannabinoid receptors, CB1 and CB2--both of which are g-protein coupled receptors. CB1 receptors are found throughout the nervous system, while CB2 receptors are primarily found on immune cells. THC acts as a partial agonist at cannabinoid receptors, meaning it binds to these receptors and generates a response that’s a fraction of what other substances that bind to the receptors can generate. THC interacts with a number of other targets as well, but it’s thought that its main psychoactive effects are mediated through its action at CB1 receptors.Activation of CB1 receptors is thought to lead to the modulation of the release of various neurotransmitters. It’s not fully understood how this translates into the characteristic effects of THC, but the activation of CB1 receptors in different areas of the nervous system may partially explain the effects of the drug. CB1 receptors in areas like the cortex and hippocampus, for example, may be involved in the perceptual and cognitive effects of THC, CB1 receptors in areas like the basal ganglia and cerebellum may be associated with sedation and effects on movement, and CB1 receptors in areas like the spinal cord and brainstem may be linked to analgesic effects.REFERENCES:Banister SD, Arnold JC, Connor M, Glass M, McGregor IS. Dark Classics in Chemical Neuroscience: Δ9-Tetrahydrocannabinol. ACS Chem Neurosci. 2019;10(5):2160‐2175. doi:10.1021/acschemneuro.8b00651Howlett AC, Barth F, Bonner TI, et al. International Union of Pharmacology. XXVII. Classification of cannabinoid receptors. Pharmacol Rev. 2002;54(2):161‐202. doi:10.1124/pr.54.2.161Pertwee RG. Pharmacological actions of cannabinoids. Handb Exp Pharmacol. 2005;(168):1‐51. doi:10.1007/3-540-26573-2_1Pertwee RG. The diverse CB1 and CB2 receptor pharmacology of three plant cannabinoids: delta9-tetrahydrocannabinol, cannabidiol and delta9-tetrahydrocannabivarin. Br J Pharmacol. 2008;153(2):199‐215. doi:10.1038/sj.bjp.0707442
