Bio Bases Flashcards
what are glial cells for
Provide support for information processing neurons
what are the glial cells in the CNS/PNS
Astrocytes, oligodendrocytes, microglial (CNS);
Schwann, satellite, and enteric glia (PNS)
describe glial cells in the CNS
Astro- prun of neurons, form new neurons; Regulate blood flow, but also transfer mitochondria to neurons, and supply the building blocks of neurotransmitters, which fuel neuronal metabolism - synchronize activity of the axon by taking up chemicals released by the axon
oligo- form myelin sheath in brain and spinal cord;
micro- remove debris from injured cells (pain perception)
differences in motor, sensory, and interneurons
Motor: stimulate muscles or glands
sensory: responds to environmental stimul (light, odor, touch)
interneurons: receive input from and send input to other neurons
why is the axon hillock important
Plays important role in neural communication; cone shaped area that gives rise to the axon (site of integration); determines if signals warrant propagation of action potential and transmission of signal
why is myelination important
Helps insulate and speed conduction; it forms around the nerves; the sheath allows electrical impulses to transmit quickly and efficiently along the nerve cells
what are the nodes of ranvier
Gaps between sections of myelin where the axon is exposed
what are the two parts of the autonomic nervous system
Parasympathetic nervous system- controls body’s rest and digest functions; keep body relaxed and maintain daily functions
Sympathetic nervous system- controls the body’s fight or flight response; prepares the body for physical activity
role of the frontal, parietal, occipital, and temporal lobe
Frontal- movement and high level cognition
Parietal- spatial cognition (attention), sensory
Occipital- visual processing
Temporal- auditory processing, aspects of learning, recognition of objects
sagittal, horizontal, coronal planes
saggital: cut down the middle, left and right
horizontal (axial, transverse): cut in half, top and bottom
coronal (frontal): cut in half, front and back
grey matter vs white matter
Grey matter: consists of cell bodies that form the outer layers of the cortex and nuclei within the brain. Unmyelinated neuron cell bodies and short, unmyelinated axons
White matter: light colored interior; packed with fatty myelin that surrounds axons sending information in and out of the cortex
Glutamate is an excitatory neurotransmitter. What does that mean?
It stimulates nerve cells to take action; This action makes it more likely that chemical messages will continue to pass between nerve cells, rather than being stopped.
What are agonists and antagonists?
Agonists: An agonist is a drug that binds to the receptor, producing a similar response to the intended chemical and receptor.
Antagonist: is a drug that binds to the receptor either on the primary site, or on another site, which all together stops the receptor from producing a response.
What are the monoamine?
neurotransmitters that contain an aromatic ring connected to an amino group by a two-carbon chain.
How are the monoamines different from the catecholamines?
Monoamines are a class of neurotransmitters and neuromodulators that are derived from aromatic amino acids and are characterized by their chemical structure. Monoamines are divided into two major classes based on their chemical structure: catecholamines and indolamines:
Catecholamines
Contain a nucleus catechol group, which is a benzene group with two adjacent hydroxyl groups, and an ethylamine side chain with a single amine group. Catecholamines include dopamine, norepinephrine, and epinephrine, and are synthesized from the amino acid L-tyrosine. Catecholamines are associated with both proinflammatory and antiinflammatory effects, and can also have immunosuppressive, vasoconstrictive, and coagulative effect
Indolamines
Contain 5-hydroxytryptophan (5-HT), also known as serotonin, and melatonin, and are synthesized from the amino acid L-tryptophan
What could a monoamine oxidase inhibitor be?
Class of antidepressants that treat depression and other psychiatric illnesses by preventing the breakdown of certain brain chemicals
If a drug blocks the autoreceptors which has an effect of stimulating the release of a neurotransmitter into the synapse, is it an agonist or antagonist?
Agonist
What area of the brain do most addictive drugs have their effect?
Nucleus accumbs (basal ganglia)
What are the models of drug abuse?
Moral Model: abuse is due to failure of moral character or lack of self control.
Disease Model: addiction is considered to be a disease that requires medical treatment.
Physical Dependence Model: abusers continue to use drugs to avoid withdrawal symptoms.
Positive Reward Model: drug abuse and addiction are due to powerful reinforcement.
Which models of drug abuse work or not and why?
Moral- Little evidence that morality-based programs affect abuse rates.
Disease- no evidence of physical or biochemical abnormalities.
Physical dependence- But some people become addicted before physical dependence develops, and some addictive drugs such as cocaine don’t produce withdrawal symptoms.
Positive reward- Self-administration experiments using animals shows that addiction can occur in the absence of physical dependence or withdrawal symptoms.
What are the two original main theories of emotion?
James-Lange theory: the emotions we feel are caused by bodily changes; emotions differ due to different physiological responses.
Cannon-Bard theory: emotions precede physiological responses and help deal with a changing environment.
What are some suggestions for getting off antidepressants?
Take your time
Make a plan
Consider psychotherapy
Stay active
Seek support
Complete the taper
How can antidepressant withdraw look like depression?
Discontinuation symptoms include anxiety and depression; Anxiety and depression symptoms reason on medication in first place
What is the difference between withdrawal and depression?
Emerge within days to weeks of stopping the medication or lowering the dose, whereas relapse symptoms develop later and more gradually. Include physical complaints that aren’t commonly found in depression, such as dizziness, flulike symptoms, and abnormal sensations.
-Discontinuation symptoms disappear quickly if you take a dose of the antidepressant, while drug treatment of depression itself takes weeks to work.
-Discontinuation symptoms resolve as the body readjusts, while recurrent depression continues and may get worse.
Is having discontinuation symptoms the same as being addicted?
No it is not;
A person who is addicted craves the drug and often needs increasingly higher doses. Few people who take antidepressants develop a craving or feel a need to increase the dose
What is the difference between ED50 and LD50?
Why do we want the ED50 and LD50 to be far apart?
LD50, or lethal dose 50 is the lethal dose for 50% of individuals tested. ED50 stands for the effective dose 50, and in this case efficacy is seen as the maximum effect a drug can cause at any given dose. The smaller the ED50, the more potent the drug.
This should make sense to you because a wide or large TI can only occur if the LD50 is very high and the ED50 is much lower. In other words, this means the dose at which a drug is effective is far smaller than the dose at which the drug is lethal, giving us a wide margin of safety between the two doses.
What does the ED50 and LD50 have to do with the therapeutic index?
Both ED50 and LD50 are used to calculate the TI, or therapeutic index: the margin of safety of a drug. It is equal to LD50 divided by ED50. The higher the TI the better, as that means the margin of safety of a drug is wider.
What is the third model of emotion, how does it differ or add to James/Cannon, what research to support it?
Schachter’s cognitive attribution model: emotional labels (e.g., anger, fear, joy) are attributed to relatively nonspecific feelings of physiological arousal.
Which emotion we experience depends on cognitive systems that assess the context.
But there is evidence that patterns of autonomic activity differ between some emotions
Are there universal emotions? What are they? Do researchers agree on core emotions across all cultures?
anger, sadness, happiness, fear, disgust, surprise, contempt, and embarrassment.
But researchers do not yet agree about the number of basic emotions. One clue may come from the number of facial expressions we have.
Facial expressions are not completely universal; researchers have found isolated groups whose identifications of emotions from facial expressions did not fully agree with those of Westerners.
What areas of the brain involved in smiling and does this suggest that smiling makes you feel better?
Cingulate cortex
Facial feedback hypothesis: sensory feedback from our facial expressions can affect our mood, e.g., forcing a smile can make you feel happier.
What role does the amygdala seem to play in fear conditioning? What is the research evidence that supports this?
It is a key structure in the mediation of fear; lesions abolish fear
Forms associations between emotional responses and specific memories of stimuli stored elsewhere in the brain
Research- circuitry of fear (rat), tone with shock
Are cannabinoids involved in fear extinction? How do we know?
Yes; mice missing one type of cannabinoid receptors have a harder time extinguishing fear responses, suggesting cannabinoid signaling is important for fear extinction
Do different emotions activate different areas of the brain?
Yes; brain imaging shows unique network of brain areas is responsible for the emotion of love
Emotions are associated with bilateral changes in insula, amygdala, caudate, putamen, cingulate cortex, and prefrontal cortex activity
What factors affect the stress response in early development for rat pups?
Separated for long periods and received little maternal attention
Is fight or flight the only stress response?
No, there is also freeze
How does generational stress lead to epigenetic changes?
Epigenetic regulation- maternal deprivation exerts negative effect on adult stress responses by causing long-lasting changes in the expression of genes for adrenal steroid receptors in the brain
Define stress and outline the neuroendocrine changes that acute and chronic stress may produce in humans and other animals.
Stress is any circumstance that upsets homeostatic balance
Stimulates adrenal medulla to release epinephrine and noreprinephirne (increase heart rate and breathing)
Discuss possible explanations for what appears to be a marked sex difference in the prevalence of depression.
Women more susceptible to depression than men
May involve reproductive hormones; clinical depression often related to events in female reproductive cycle
Postpartum depression suggests some combo of hormones can precipitate depression
Outline the three stages of memory formation; include the regions of the brain believed to be involved and refer to evidence as appropriate.
Encoding- sensory info passed to short term memory (medial temporal lobe)
Consolidation – short term memory passed to long term memory (hippocampus and other medial temporal structures)
Retrieval- stored information is used (medial temporal)
Describe the symptoms of Broca’s and Wernicke’s aphasias; discuss organization of language in the brain based on studies of patients with neurological damage.
Broca- interfere with speech production
Werncke- interfere with language comprehension
Fluent aphasia- not understand read/hear
Global aphasia- total loss of ability to understand language, speak, read, write
What is selective attention and explain the difference between top-down and bottom-up processes.
Selective attention- select/process information while surpressing irrelevant distractors
Bottom-up processing involves taking in sensory information and processing it to form a coherent understanding of the task at hand. Top-down processing, on the other hand, involves using pre-existing knowledge and context to guide the understanding and execution of the task
What is the importance of studying monozygotic and dizygotic twins in epidemiological studies of disease models? What do they tell us about the genetic influence on disease heritability? What do the monozygotic and dizogotic twin studies tell us about the heritability of schizophrenia?
Mono- share identical genes; dizy- share 50% genes
Identical concordance rate is 50% pointing to genetic factor
More closely related a person is, greater that person’s chances are of also developing it
What are some of the brain differences that have been found in those with and without schizophrenia?
Cerebral ventricals enlarged (lateral ventricals)
Hippocampus and amygdala smaller
Abnormalities in activity of limbic networks
Corpus callosum has altered structure/function
Loss of gray matter
Reduced metabolic activity in frontal lobes
Is excess dopamine the main cause of schizophrenia? What is the evidence for or against this hypothesis?
It is one hypothesis of many
Says excess synaptic dopamine or dopamine receptors
Support came from amphetamine users who develop symptoms similar. Amphetamine promotes release of dopamine and blocks its reuptake
What role might stress play in the development of schizophrenia?
Stressful events increase risk of dev.; appears in adolescents (puberty, college)
Prenatal stress- influenza, low birth weight, lack of oxygen
Caused by interaction of genetic factors and stress
What are the three different generations of antipsychotics? How do they generally work?
1st gen: D2 receptor antagonists (block D2)
2nd gen: affinity for other receptors (block serotonin receptors and D2 receptors); increase dopamine release
3rd: blocking dopamine D2 receptors in areas with high dopamine levels and promoting dopamine in areas with low dopamine levels. They also balance serotonin activity, which affects mood and sleep.
What areas of the brain show increased and decreased activation among individuals with depression? What are the implications of this/ in other words what do these brain areas do?
Increased activity in prefrontal cortex (thinking, problem solving) and amygdala (fear/stress)
Decreased blood flow in parietal (social beh, self consciousness) and posterior temporal cortex (managing emotions) and anterior cingulate (motivation, emotion regulation, pain perception)
What is the McGill Pain Scale?
Describes three aspects of pain:
Sensory-discriminative quality (e.g. throbbing, gnawing, shooting)
Motivational-affective (emotional) quality (e.g. tiring, sickening, fearful)
Cognitive eval. Quality (e.g. no pain, mild, excruc)
What is Gate Control Theory?
Gate control theory of pain is a theory that explains how non-painful sensations can reduce or override painful sensations
Stimuli that compete with nociceptive stimuli and reach the brain faster will reduce the perception of the painful stimulus
What is the difference between pain and nociception?
Nociception is the sensation of pain
Pain is the perception
What is synesthesia? What are some examples of synesthesia that you have either heard of or looked up that are unique?
Condition in which stimuli in one modality evoke the involuntary experience of an additional sensation in another modality
What causes pain?
Sensory nerve endings nociceptors (pain receptors) come into contact with a painful or noxious stimulus
How is social rejection related to pain?
SJ activates the anterior cingulate cortex, upset level corelates with activation of region (pos. correlation)
Ppl who took Tylenol reported fewer hurt feelings than those taking placebo; less activation of the anterior cingulate
What is an analgesic? What are other medicines to treat pain?
A drug that reduces pain
Acupuncture- only some ppl achieve continued relief from chronic pain
—-acts by releasing endogenous opiates (Nal. Blocks or reduces its analgesic effects)
What is the main brain area associated with the pain pathway?
The anterolateral (spinothalamic) system transmits sensations of pain and temperature
Sensation of pain travels from its origin to the brain via spin crossing midline in spinal cord before ascending to the thalamus
What are ways that we or other animals can thermoregulate?
Responses to cold: shivering of muscles, constriction of blood vessels, metabolism of brown fat, increased thyroid activity
Responses to heat: accelerated respiration, perspiration, dilation of vessels
What does redundancy mean in reference to thermoregulation?
The body has multiple systems for regulating the internal environment; allows for compensation if one monitoring system fails
Neurons of the preoptic area integrate sensory inputs and drive physiological thermoregulatory responses
How does the size and myelination of an axon influence sensation transmission?
Large axons conduct action potentials faster than small axons do; myelination speeds conduction even more
Light tough receptors use moderately large, myelinated fibers and send information to the CNS rapidly
What is the purpose of fevers?
Helps fight infections
What are the two different kinds of thirst and how are they triggered?
Osmotic thirst- stimulated by high extracellular solute concentration. Water is pulled out of the cells when extracellular salt concentration is too high.
Hypovolemic thirst- stimulated by low extracellular fluid volume
What is the relationship between glucose and glucogen?
Glucose is a form of glucogen that can be stored
Glucose- principal sugar used for energy, especially in the brain
Glucogen- complex cab made of glucose molecules; stored for short term in the liver and muscles
Can a person or animal simply cut significant calories to reduce weight? What happens to their metabolism?
Ppl and animals adjust their metabolism in response to under or overnutrition, thus tend to resist losing or gaining weight
Start of diet, the basal metabolic rate will fall to prevent losing weight
What are the roles of the ventral medial and lateral hypothalamus in hunger signals?
VMH lesions cause animals to eat to excess and become obese; suggests that VMH is a satiety center
LH lesions cause cessation of eating; suggests LH is a hunger center
Is there a brain region for attention? What is it?
Yes
Posterior parietal lobe
Cingulate cortex
What is the role of the thalamus in processing most sensory information?
The thalamus transmits the information to the cerebral cortex
Most sensory pathways pass through regions of the thalamus
Why is adaptation important from an evolutionary perspective?
important from an evolutionary perspective because it allows the evolutionary process to occur piecemeal. Adaptations are inheritable characteristics that increase an organism’s ability to: find food and water, protect itself, and manage in extreme environments
What are the different kinds of sensory information transmitted on the skin cells?
Vibrations
Touch (fast adapting)
Touch (slow adapting)
Stretch (slow adapting)
How does outside energy get converted to information in the nervous system for different sensory systems?
Utilize receptor organs to convert outside information (light, sound) into neural activity
All senses use same type of energy to communicate with brain- action potentials
What is the treatment for Tourette’s Syndrome? What mechanism is it working on?
Haloperidol, a dopamine antagonist, is a primary treatment
Dopamin D2 receptors are denser in caudate nucleus of person with disorder
Is there a brain based treatment for OCD? Is that the most recommended treatment?
Cingulatomy (surgical disruption of circuits in the cingulate cortex) benefits some severly disabled OCD patients
OCD responds to SSRIs in most cases; suggests serotonin dysfunction plays a major role
What are used to treat anxiety disorders and what mechanisms are they working on? In other words, what are they doing in the brain?
Benzos are an anxiolytic (anxiety reducing)
They bind to GABA receptors and enhance GABA’s inhibitory actions by increasing the flow of Cl- ions into cells
Serotonin 5-HTIA receptor agonists and SSRIs are also used
What is bipolar disorder, how is it generally treated pharmacologically and how does that work?
Periods of depression alternating with expansive mood
Lithium treats it; mechanism is unknown
Widespread actions in the brain; interacts with circadian clock, boosts BDNF activity
What are the gender differences in depression and why?
Women have greater susceptibility to depression
May involve reproductive hormones
GABA and glutamate are inhibitory neurotransmitters. What does this mean?
prevent chemical messages from being passed along, which decreases the likelihood of a neuron firing an action potential. This prevents neurons from becoming overexcited, and can also make neurons less sensitive to incoming stimuli. In some cases, inhibitory neurotransmitters can have a relaxing effect
Why would the nervous system need inhibition?
to function properly. It helps shape and organize the flow of information through neuronal networks to create a precise neural code.
stabilizing and tuning the responses of networks of excitatory neurons.
generations of anti-depressants
1st-Monoamine oxidase inhibitors (MAOIs)
1st- Tricyclic antidepressants (TCAs)
2nd- Dopamine re-uptake inhibitors
2nd- 5-HT2 receptor antagonists
2nd- Selective Norephinephrine Re-uptake inhibitors
2nd- Selective Serotonin Re-uptake inhibitors(SSRIs)
how MAOIs and TCAs work
by blocking the monoamine oxidase (MAO) enzyme, which breaks down neurotransmitters in the brain.
blocking the reabsorption of serotonin and norepinephrine, neurotransmitters that regulate mood and behavior, in the brain.
How Dopamine re-uptake inhibitors
and
5-HT2 receptor antagonists work
increase dopamine levels in the brain by blocking the dopamine transporter (DAT).
by binding to serotonin 5-HT2 receptors without activating them, which blocks the actions of serotonin or serotonin 5-HT2 receptor agonists
How does Selective Norephinephrine Re-uptake inhibitors
AND
Selective Serotonin Re-uptake inhibitors
increase norepinephrine levels in the brain by blocking its reabsorption into nerve cells.
by preventing nerve cells from reabsorbing serotonin, a chemical messenger that carries signals between brain cells
Is there a role for cortisol/ stress in depression?
*Suggests that dysfunction of the hypothalamic-pituitary-adrenal axis may be involved in depression.
*Dexamethasone suppression test: reveals tendency to release excess cortisol.
Cortisol and depression information continued
Circulating cortisol levels are usually higher in people with depression than in psychiatric or healthy controls. In this plot, each dot represents an individual case. (C) People with depression may display increased levels of cortisol across the circadian rhythm of release.
Evidence that cortisol and stress impact depression
Evidence shows that the hypothalamic-pituitary-adrenal system is involved in depression.
Dexamethasone suppression test: reveals tendency to release excess cortisol.
The same dose of dexamethasone is far less effective at suppressing the next day’s cortisol release in people with depression.
Why not to quit antidepressants cold turkey
What is the reason the author gives for why not to quit cold turkey?
Coming off your medication can cause antidepressant withdrawal – and could set you up for a relapse of depression.
Neurons eventually adapt to the current level of neurotransmitters, and symptoms that range from mild to distressing may arise if the level changes too much too fast-for example, because you’ve suddenly stopped taking your antidepressant.
neurons
how many are there
do they stay consistent or change
grey matter or white matter?
Neuron: responsible for the communication between neuron via electrochemical impulses (neurotransmission)
-Human brain contains 100 billion
-They are modified by experience (they learn, remember, forget)
-make up grey matter in the brain
three kinds of neurons
Can either be excitatory, inhibitory, or a combination of both
apoptosis
During early development many more neurons are created than will survive due to neuronal pruning called apoptosis (refinery process)
-Helps with growth, immune surveillance, and neuroplastic development
-Neurons can malfunction causing changes in cognition, emotions, and behavior
-If too many cells get a chance to grow cancer tumors can develop
cell body (soma)
“control center,” contains RNA and DNA
The bulbous, non-process portion of a neuron or other brain cell type, containing the cell nucleus.
axon
long projection fiber from the cell body that transmits nerve impulses away from the cell body to the terminal buttons where neurotransmitters are stored and released into the synapse
-Axons begin to sprout from neuron’s cell body as they migrate to their targets
-Begin to grow during the prenatal period with the anterior commissure visible at 3 months gestation
myelin sheath
white matter or gray matter?
what myelinates first?
cover the axons and insulates it to facilitate neurotransmission (white in appearance)
-Make up most of the brain’s white matter
-White matter can be destroyed or damaged as a result of traumatic brain injury and neurologic disease such as Multiple Sclerosis (a disease in which the immune system eats away at the myelin sheaths of nerve cells)
-Spinal cord and sensory-motor tracts are first to myelinate
-Prefrontal cortex probably not fully myelinated until young adulthood🡪 this is why teenagers make stupid/risky decisions
-Appears to be correlated with acquisition and development of visual, motor, cognitive, and social skills
corpus callosum
connections between cortical and subcortical structures
myelination
process by which axons are “sheathed” in a protective layer of lipids and proteins
-Similar to function to the rubber coating of an electrical cord
-Myelin facilitates efficient neurotransmission (i.e., sending and receiving of impulses from the presynaptic neuron to the postsynaptic neuron)
-Increases brain weight from 400 grams at birth to 1410 grams at age 15
dendrite
(tree) structure that radiates out from the cell body and receives impulses from other neurons
-Growth visible at about 7 months gestation
-Growth and formation of synapses is heavily dependent on environmental stimulation following birth
node of ranvier
part of axon that has no sheath so that potassium and sodium can enter into the axon
dopamine neurotransmission
For example, Dopamine🡪 produces two types of behavior, please and motor functions
-Dopamine antagonist (blockers) decrease psychotic symptoms such as hallucinations
explain the process of neurotransmission
Neuron is just sitting there with a negative charge, -.70 millivolt
Ratio of ions inside favor the negative (chloride)
Outside the neuron is more positive ions (potassium and sodium)
Creates electrical gradient attraction
Concentration gradient: too much crowing of similar ions, so they want to get inside where there is more room
Dendrites pick up stimulation, opens nodes, positive ions go rushing in
The charge changes to about +.40 millivolt and pops open all the nodes down to the terminal buttons which then open as well
Channels close and become more negative than originally started
Slowly creeps back to original resting state
seizure and neurotransmission
Too many neurons firing at once can cause a seizure
action potential
the change in electrical potential associated with the passage of an impulse along the membrane of a muscle or nerve cell
absolute refractory period
when an action potential will not occur no matter how much stimulation is received by the neuron
Need this period so that the neuron doesn’t burn out, it is a measure of control
relative refractory period
when stronger than normal stimulation is needed to cause an action potential
propogation
The spread of the action potential down an axon, caused by successive changes in electrical charge along the length of the axon’s membrane
when nodes open to allow chemicals in to charge the neuron
nuclei
aggregated community of neurons that are related in function
are neurons directly connected
Neurons are not directly connected, rather they send chemicals (neurotransmitters) across a microscopic gap called the synaptic gap
-Each neuron may have thousands of synapses
aggregation
process by which neurons mass to form major nuclei including the corpus callosum and basal ganglia
neuroplasticity
learning, stronger connections, making room for what is important (adaptation)
-Plasticity after a brain injury neurons will borrow from each other or assume new positions
-Adults recover better than children because they already learned skills
-Brain damage occurring prior to 1 year of age tends to result in disproportionality greater impairments than those occurring later
-The brain may benefit considerably from plasticity is damage occurs between 1 and 5 years
-Benefits of plasticity are likely to dimmish substantially for injured brain following 5 years of age, although functions may recover by another process
crowding and neuroplasticity
▪ Crowding happens when too much borrowing is taking place🡪 verbal functioning may go from 50% to 85% but visual functioning may drop from 100% to 85%
neuroglia or glial cells (Nerve glue)
-Makes up 50% of the total volume of the Central Nervous System
-Is the structural support for neurons
-Will fill cavities with scar tissues caused by brain damage/lesions
-Insulates synapses
-Produces Cerebral Spinal fluid
-Repairs damaged neurons
-Facilitates transmission of signals across neurons
astrocytes
are a type of glial cell that helps synchronize activity of the axon by wrapping around the presynaptic terminal and taking up chemicals release by the axon
astrocytoma
giant tumor of astrocytes that overproduced because of a lack of apoptosis
microglia
removes waste material and other microorganisms that could prove harmful to the neuron
oligodendrocytes (brain) and schwann cells (spinal)
build the myelin sheath, in the brain and spinal cord respectively, that surrounds the axon of some neurons
radial glia
guides the migration of neurons and the growth of their axons and dendrites during embryonic development
-If the radical glia do not work🡪 abnormality in neural migration (ex. Dyslexia)
brain development from 25 days to 33 years
25 days gestation: neural tube forms
-When it does not close, spina bifida occurs
40 weeks gestation: the spinal cord, brain stem, and a substantial amount of forebrain (cerebral cortex and some subcortical structures like the thalamus) develop
Birth-First Year: cerebellum’s maximum growth rate
3-33 years old: everything is the same except myelination, which finishes at 23-24 years of age
proliferation and cell migration
-Nerve cells form via mitosis in the ventricular lining of the brain
-form axons and dendrites
-Fastest rate of brain growth occurs prenatally when 250,000 brain cells are formed each minute of mitosis
neuronal migration
consists of neurons being guided by the radial fibers of glial cells to the proper neuroanatomical destination, likely to be governed by a number of variables including genetic, physiological, chemical, and environmental factors
5th month of fetal development and migration
migration process is rapid as several layers of the cerebral cortex are visible
nerve growth factor and most severe abnormality in neural migration
chemical that helps neurons figure out where to go
-Abnormalities in neural migration
▪ Most severe: Lissencephaly- “smooth brain” when brain fails to form sulci and gyri, the brain is equivalent to a 12-week embryo
heterotopia
a neurodevelopmental disorder that is characterized by displaced pocket of grey matter (neurons) that appear in the ventricular walls or white matter due to aborted neural migration (seizures may result)
brain derived neurotrophic factor (BDNF)
proteins that guide axon and promotes survival, growth, and the formation of new synapses
-Needs environmental stimulation
-One area that an infant forms (myelinates) very early is lips🡪 to nurse
-Stimulation may increase BDNF
-Plasticity also dependent on environmental stimulation
If there is an alteration in neuronal migration due to neurotoxins or disease, neurons may migrate short of or beyond their proper destination, ending up at the wrong neuroanatomical region
Luria’s Model of Brain development (5 stages)
Stage 1: Pre-post-birth: basic arousal systems and attention
Stage 2: Pre-post-birth: basic sensory and motor areas (ex. Sucking)
Stage 3: Birht-4years: refinement of stages 1 and 2, including smoothing out motor movements and developing secondary auditory and visual skills
Stage 4: 5-8years: development of posterior areas of the brain (linking perception with academic skills)
Stage 5: 9year-on: development of anterior (frontal) areas of the brain (ex. Planning a response to sensory input processed by the posterior regions of the brain)
Maureen Dennis model of brain damage
Damage during infancy: will affect emerging skills by delaying their onset or disrupting the sequential order of the arrival of a given skill
Damage during childhood: will affect the rate of skill development, the strategy to employ the skill, or the competent use of the skill
Damage after skill has been established: affects the control and long-term maintenance of the skill
top of brain
superior, dorsal
bottom of brain
inferior, ventral
front of brain
anterior, rostral, coronal
rear of brain
posterior, caudal
middle of brain
medial, mesial
side of brain
lateral, sagittal
sylvian fissure / lateral sulcus
gap that separates frontal from temporal
contralateral
Brain is contralateral: right hemisphere controls left side of body and left hemisphere controls right side of body
skull
temporal bone over the temporal lobe, inside surface is rough, jagged, and relatively close to the temporal lobes (TMI usually causes memory impairment and impairment of executive functioning)
meninges and three kinds of matter
protect coverings of the brain
Dura mater: right under the skull, fatty (like turkey skin, ew)
Arachnoid mater: webbing
Pia mater: thin layer
All can be pieced by a skull fracture
All three are important when understanding brain bleeds
meningitis
inflammation of the meninges
-Viral: can use antibiotics
-Bacterial: can be treated at first, but if not cognitive/sensory impairment or death
parts of the forebrain
top is the cerebral cortex, gyri, sulci, fissure
gyri
convolutions (hills) of the cerebral cortex
sulci
relatively shallow valleys or grooves that separate gyri from each other
global atrophy
gyri shrink
widening of sulci
gaps get bigger
fissure
deep sulci
longitudinal fissure
separates both hemispheres
frontal lobe and what it consists of
(output lobes) where you decide what to do with input data
primary motor cortex, premotor cortex, supplementary motor cortex, prefrontal motor cortex
primary motor cortex
(motor strip): located at the precentral gyrus; controls the muscles on the contralateral side of the body and executes individual motor movements
premotor cortex
Broca’s area (expressive language) is in the lateral premotor area of the left frontal lobe; directs more complex, coordinated movements; fluid, sequential movements; selects the movements to be executed
supplementary motor cortex
planning and organizing a rapid sequence of movements; motor inhibitionp
prefrontal cortex
executive functioning and consists of dorsolateral, medial, orbitofrontal
-Receives information via projections from multiple cortical and subcortical regions including the temporal, parietal, and occipital association zones as well as the thalamus and limbi systems. This permits complex, integrative functions
-Primary function consists of planning and executing responses to information received from other cortical and subcortical regions
central sulcus
is clear and dividing line between frontal and partial lobes
frontal lobes
most anatomically and functionally distinct
parietal lobes
separated from the frontal lobes by the central sulcus, primary somatosensory cortex (i.e. somatosensory strip) located on the postcentral gyrus
occipital lobes
primary visual cortex
temporal lobes and what it consists of
lateral or Sylvian fissure separates the temporal lobe from the frontal and parietal lobes, primary auditory cortex
wernickes area
arcuate fassiculus
hippocampus and amygdala
wernickes area
located in the posterior region of the superior temporal gyrus on the left hemisphere
arcuate fasciculus
Nerve projections that connect the temporal and frontal lobes allowing Broca’s and Wernicke’s areas to communicate
hippocampus and amygdala
buried deep within the mesial region of the temporal lobes
interhemispheric connections
large bundles of myelinated fibers (axons) that allow the two cerebral hemispheres to communicate with each other
corpus callosum
large bundle of nerve fibers (about 300 million) that allows rapid communication between the two hemispheres
anterior commissure
connects the temporal lobes of the right and left hemisphere
intrahemispheric connections
consist of association fibers that allow different cortical regions within a hemisphere to communicate with each other
Each gyrus is connected by short association fibers
Longer fibers connect lobes to each other
The arcuate fascicules connect the frontal and temporal lobes of the left hemisphere (Broca’s and Wernicke’s areas)
how anxiety looks
How anxiety (habitual) looks… singular gyri, amygdala, and hippocampus overwhelmed by amount of energy🡪 not enough energy for other areas (like executive functioning)🡪 these networks become hypertensive (take less to trigger them, more to deescalate)
Psychotherapy has more impact cortically
SSRI’s have more impact subcortically
damage to intrahemispheric connections
can cause considerable neurocognitive and/or behavioral problems
things in the forebrain (subcortical)
thalamus, hypothalamus, basal ganglia, limbic system, ventricles, cerebral aqueduct
thalamus
generally located at the superior (top) region of the brain stem
-Consists of several nuclei tracts that each relay specific sensory information to the cortex
-Most sensory input through the Thalamus and then on to the cortex it needs to be projected to
The brain’s sensory switchboard, located on top of the brainstem; it directs messages to the sensory receiving areas in the cortex and transmits replies to the cerebellum and medulla
hypothalamus
located anterior (in front of) and inferior (below) the thalamus
-Has connection (nerve fibers/axons) to the autonomic nervous system, limbic system, midbrain, and forebrain
it directs several maintenance activities (eating, drinking, body temperature), helps govern the endocrine system via the pituitary gland, and is linked to emotion and reward; maintains homeostasis
basal ganglia
masses of grey matter (caudate nucleus) that provide connections between cortical and subcortical structures
-Located lateral to the Thalamus
-Involved with the initiation and inhibition of several functions including motor functioning and the inhibition of emotional responses via connections to the prefrontal cortex
-Also crucial to procedural memory and initiating the motor movements involved in expressive language
caudate nucleus
implicated in Parkinson’s Disease and Huntington’s Disease
-Damage to the basal ganglia causes problems controlling speech, movement and posture (aka Parkinson’s); therefore, damage is subcortical
globus pallidus
involved in moto modulation
Component of the basal ganglia that connects to the thalamus which relays information to the motor areas and the prefrontal cortex - involved in motor modulation - control conscious and proprioceptive movements.
putamen
movement regulation
Large subcortical structure, a part of the basal ganglia, that is involved in movement regulation - It is involved in a very complex feedback loop that prepares and aids in movement of the limbs. It is closely intertwined with the caudate nucleus, nucleus accumbens, and globus pallidus, which are together known as the corpus striatum.
limbic system or limbic lobe and what it consists of
located within cortical and subcortical regions, has numerous connections throughout the brain regions
-Consists of hippocampus, cingulate gyrus, amygdala, and hypothalamus
-Amygdala sits right on top of hippocampus because evolutionarily we should remember what is dangerous and what we fear (Psychopathology🡪 PTSD arousal without real threat)
ventricles
naturally occurring cavities in the brain that produce, store, and circulate cerebrospinal fluid. CSF is also located in the arachnoid space and cushions the brain from sudden, forceful movements due to trauma
lateral ventricles
(important landmark for neuroimaging) located up in the forebrain
the two largest ventricles of the brain (located in the forebrain) and contain cerebrospinal fluid (CSF). Each cerebral hemisphere contains a lateral ventricle, known as the left or right ventricle, respectively
contain cerebrospinal fluid, a clear, watery fluid that provides cushioning for the brain while also helping to circulate nutrients and remove waste
third ventricle
located in the diencephalon
One of the four connected ventricles of the ventricular system within the mammalian brain. It is a slit-like cavity formed in the diencephalon between the two thalami, in the midline between the right and left lateral ventricles, and is filled with cerebrospinal fluid (CSF).
Main function is to produce, secrete, and convey cerebrospinal fluid
fourth ventricle
located in the brain stem
● Ventricles are space occupying, they will fill any void
The most inferiorly located ventricle (located in the brain stem), draining directly into the central canal of the spinal cord. Superiorly, it connects to the third ventricle through a thin canal called the cerebral aqueduct of Sylvius
The main function of this ventricle is to protect the human brain from trauma (via a cushioning effect) and to help form the central canal, which runs the length of the spinal cord.
cerebral aqueduct
Connects the 3rd and 4th ventricles; allows cerebrospinal fluid to pass between them. - if it gets blocked it can cause brain damage
if it gets blocked and does not get fixed (causes a lot of brain damage)
-Hydrocephalus: minute to hours
-Brain damage: loner
-Buildup of CSF enlarges ventricles leading to headaches, balance issues, incomitance, nausea
empathy
comes from connectivity between cortex and cingulate gyrus and from affective thinking and processing that takes place in the temporal lobe
midbrain and what it consists of
Generally, beneath the limbic system and on top of the brain stem (i.e. middle of the brain)
Superior Colliculus: visual processing
Inferior Colliculus: auditory processing
Substantia Nigra (black stuff)
-Major dopaminergic neurons/pathway
-Readiness for movement
-Involved in Parkinson’s Disease
Where bulk of force in TBI comes downward
Tectum: roof of the midbrain
Tegmentum: covering of several midbrain structures that is itself covered by the Tectum
hindbrain and what it consists of
cerebellum, pons, medulla, brain stem
cerebellum
located behind the brain stem and connects to the midbrain, pons, and medulla
-Has more neurons than the rest of the brain combined
-Receives sensory information regarding the location of limbs in space and helps determine where muscles should be positioned
-Determining timing for auditory and visual stimuli
-Shifting attention
A large structure of the hindbrain that controls fine motor skills, receives sensory information regarding the location of limbs in space and helps determine where muscles should be positioned - located behind the brain stem and connects to the midbrain, pons, and medulla
three divisions of the brain
forebrain: top of brain midbrain: middle portion of brain, hind brain: brain stem and bottom
pons(bridge)
located between the medulla and midbrain and above the cerebellum and is a bridge between the two hemispheres
-Consists of major motor and sensory pathways (nerve fiber tracts/axons)
**
-controls many unconscious processes (sleeping, breathing, relaying signals)
medulla oblongata
where major motor/sensory tracks cross over
-Continuation of the spinal cord at the base of the brain stem
-Includes groups of motor and sensory nuclei
-Site of neural decussation
-controls many involuntary processes like sleeping and breathing, relay center
Part of the brainstem that controls vital life-sustaining functions such as heartbeat, breathing, blood pressure, and digestion - where major motor/sensory tracks cross over
reticular activating system
receives input from most sensory systems and projects to all levels of the brain
-An arousal system that assists in maintaining consciousness and attentional states. When enough stimuli reaches the RAS, it facilitates arousal wakefulness in the cortex
-Also located in the Pons & medulla
brain stem (mammalain brain)
includes structures located in the hindbrain, midbrain, and subcortical structures in the forebrain
-Located from the top of the spinal cord to the subcortical forebrain. Consists of the following structures: thalamus, midbrain, colliculi, pons, medulla oblongata
-Cerebrum gets bigger as animals get more complex
sends messages to and from spine and helps control involuntary processes
right vs left hemisphere
Language primarily in the left hemisphere
Visuospatial abilities are primarily in the right hemisphere
Both hemispheres are probably active, although one is dominant, and one is recessive
cerebral hemispheres
anatomical asymmetry
In most adults, the planum temporale is larger in the left hemisphere, this structure is associated with language
Cerebral Lateralization: functional differences
left hemisphere summary
o Language functioning
o Single modality processing
o Sequential “step by step” processing
o Temporal processing
o Analytical processing
o Distinct motoric functions
o Complex voluntary movements
o Greater ratio grey matter to white matter
right hemisphere
o Visuospatial functioning
o Multimodal processing and intraregional integration
o Holistic and simultaneous processing
o Facial recognition
o Processing of nonverbal communication including facial expression and melodies
o Judgement of emotional situations
o Perception of body in space
o Greater ratio of white matter to grey matter
frontal lobes
Executive Functions: are mediated by the prefrontal cortex
▪ Modulating and controlling emotional behaviors and impulses via connections to the limbic system
▪ Selecting appropriate behaviors based on the social context
▪ Impulse control/response inhibition
▪ Initiation (starting a behavior) and stopping behaviors
▪ Planning and prioritizing
▪ Organization
▪ Problem solving
▪ Cognitive/mental flexibility
▪ Judgment and decision making
▪ Abstract reasoning
▪ Working Memory
three cortical regions that make up the prefrontal cortex
Orbitofrontal: impulse control, social behavior, recognition of words that convey mental state
Medial: initiation (starting a response/behavior)
Dorsolateral: temporal or short-term memory, planning and response selection in goal driven behavior
temporal lobes
o Hearing via the primary auditory cortex
o Processing of auditory stimuli
o Visual object recognition
o Left Temporal Lobe: memory for verbal material (conversation, verbally presented information)
o Right Temporal Lobe: memory for nonverbal and visual information (geometric drawings, faces, tunes/melodies)
subcortical structures of temporal lobes (three)
▪ Hippocampus: memory and learning or acquisition of new information
▪ Amygdala: links emotions with sensory input and memories
▪ Wernicke’s Area: language comprehension (receptive language)
parietal lobes
o Somatosensory strip or postcentral gyrus: input area for all tactile sensation (touch/pressure); a pinch on the left leg will be processed by a portion of the somatosensory strip in the right hemisphere
o Spatial imager (judging size and distance)
o Visuospatial perception🡪 primarily right parietal-occipital
o Visuoconstruction🡪 primarily right parieto-occipital
o Facial recognition
o Left-right orientation
o Reading ability🡪 primarily parietal-occipital
o Agraphia/writing ability🡪 primarily left parieto-occipital
o Calculation/arithmetic operations🡪 primarily left parieto-occipital
occipital lobes
o Primary Visual Cortex: pure vision
o Temporo-parieto-occipital association region: complex visual perception; recognition analysis and comparison of present stimuli with past stimuli
reticular formation
group of interconnected nuclei and their projection fibers/axons that extend from the brain stem to the forebrain and interconnect with all major neural tracts in the brain (includes Reticular Activating System)
communication between sides of the brain: what is more likely communication bewteen corpus callosum or communication between cortical regions in each hemisphere?
*A cortical region is less likely to directly communicate with another cortical region in the other hemisphere via the corpus callosum. What is more likely is indirect communication between cortical regions in each hemisphere via the thalamus and possibly the basal ganglia🡪 this is why split-brain patients are generally unaffected
arousal unit (luria’s model of brain functioning)
-Primary function: to make sure CNS (central nervous system) reaches and maintains sufficient level of arousal
-Involves deep cortical structures of brain and brain stem (Reticular Activating System)
sensory input unit (Luria’s model of brain functioning)
-Primarily consist of occipital, temporal, and parietal lobes
-Processes incoming information from the environment
motor output unit (Luria’s model of brain functioning)
-Frontal lobes
-Processes and interprets information from the sensory input unit to select, organize, and plan actions/responses
three functional zones of frontal lobe
Primary zone: motor strip (basic, individual movements)
Secondary zone: premotor cortex (selects and directs more complex, coordinated movements)
Tertiary zone: prefrontal cortex (executive functions)
temporal lobe primary zone
primary auditory cortex (hearing)
parietal lobe functional zone
somatosensory cortex/strip
occipital lobe functional zone
pure vision
why are there not secondary or tertiary zones of temporal, parietal, and occipital lobes
*The secondary and tertiary zones of the temporal, parietal, and occipital lobes are not clearly defined anatomically or functionally
Instead, this large overlap of cortical region is referred to as the temporo-parieto-occipital association zone
This is where intermodal sensory integration takes place (vision, touch, body awareness, and spatial orientation)
genes
basic unites of heredity that maintain their structural identity from one generation to another
-Genes are aligned along chromosomes (strands of genes) and come in pairs
alleles
the different forms, or variants, of a gene
mutation
reserved for instances in which allele is known to have been newly formed, such as after treatment of an experimental organism with a mutagen (an agent that causes a heritable change in the DNA sequence)
genotypes
a particular set of alleles for all the genes carried by an individual
genes environment and behavior
**Both genes and environment interact to shape human behavior
**There is no single genetic variant that reliably predicts any psychiatric disorder🡪 rather, each psychiatric disorder is likely influences by hundreds or even thousands of genetic variants that are found within and often outside of the 20,000 or so human protein coding genes
-Schizophrenia, bipolar disorder, and autism is likely in excess of 70% heritability
-Depression and anxiety disorders are estimated at 30-40% heritability
research becoming increasingly collaborative
Research in human genetics is becoming increasingly collaborative. These collaborations will make large-scale genome-wide GE studies possible, and these will be increasingly common in the coming years.
gene environment reactions in research
If GE effects prove similar to genetic main effects, then we can expect to find that hundreds (and likely thousands) of gene– environment interactions, each of very small effect, contribute to individual psychiatric phenotypes.
Basically it is very hard to predict behavior on a molecular/genetic level
hope for Gene environment effects and biological pathways
● The hope is that GE effects may converge on a limited number of biological pathways, yielding an understanding of specific processes underlying psychiatric disorders that is more readily interpretable.
limbic system
includes the forebrain areas surrounding the thalamus; traditionally been regarded as critical for emotion
emotion
measurement of evoked responses indicate the brain is specialized to attend strongly to facial expressions but emotions tend not to be localized to specific brain regions (a single emotion increases activity in various parts of the brain)
behavioral activation system
activation of the frontal and temporal areas of the left hemisphere; associated with “approach”; marked by low to moderate arousal; can categorize either happiness or anger
behavioral inhibition system
associated with increased activity of the frontal and temporal lobe of the right hemisphere; increases attention and arousal; inhibits action; stimulate emotions such as fear and disgust
-Damage to right temporal cortex causes problems in the ability to identify emotions of others
attack and escape behaviors
Attack and escape behaviors are closely related; corresponding behaviors are anger and fear
-Pain, threat or other unpleasant stimuli can trigger an attack behavior.
-Attack behaviors are associated with increased activity in the corticomedial area of the amygdala.
-After experiencing a provocation, people are more likely to attack for a period of time afterwards.
-An initial attack behavior increases the probability of a second attack behavior.
-low serotonin turnover (the amount of a neurotransmitter that is released and resynthesized by neurons) has been linked to violent behavior and attempted suicide
damage to the amygdala
Damage to the amygdala interferes with:
-the learning of fear responses
-retention of fear responses previously learned
-interpreting or understanding stimuli with emotional consequences
**Excessive fear and anxiety disorders are associated with hyperactivity in the amygdala
what systems does stress activate
Activates two systems in the body:
-The sympathetic nervous system: “fight or flight” response that prepared the body for brief emergency responses
-The HPA axis- hypothalamus, pituitary gland, and adrenal cortex
prolonged stress
pituitary gland secretes adrenocorticotropic hormone (ACTH) which stimulates the adrenal cortex to secrete cortisol
-Cortisol helps to mobilize energies to fight a difficult situation but once depleted (low), it makes it more difficult to combat stress and makes one more prone to the damaging effects of stress
-PTSD victims show lower than normal cortisol after trauma-
prolonged stress and memory
Prolonged stress also harmful to hippocampus and memory: when metabolic activity is high, the neurons are more sensitive to damage by toxins or over-stimulation
-Impairs the adaptability and the production of new hippocampal neurons
-PTSD victims have a smaller than average hippocampus
stress process
hypothalamus (releasing factor)
anterior pituitary (ACTH through blood)
adrenal cortex (cortisol)
mental illness and where it comes from
*Mental illness results from the combination of biological predisposition and experiences
serotonin
neurotransmitter, sometimes considered a hormone, that the body uses to send messages between nerve cells. It appears to play a role in mood, emotions, appetite, and digestion🡪 also, helps regulate sleep-wake cycles and overall circadian rhythm
A neurotransmitter that affects hunger, sleep, arousal, and mood - it is also a hormone
It affects happiness levels and is important for regulating anxiety, appetite, pain control, and sleep cycles
It is found in the gastrointestinal tract (the gut)
It balances out excitatory neurotransmitter effects; deficit can be linked to depression, sadness, fatigue
dopamine
type of neurotransmitter and hormone that plays a role in many important body functions such as movement, memory, pleasurable reward, and motivations. High levels of dopamine or low levels of dopamine are associated with several mental health and neurological diseases
enzymes
(a catalyst) proteins that help speed up chemical reactions in our bodies. Too much or too little of a certain enzyme can cause health problems.
angiotensin converting enzyme (ACE)
inhibitors are medications that help relax the veins and arteries to lower blood pressure. ACE inhibits prevent an enzyme in the body from producing angiotensin II, a substance that narrows blood vessels
major depression at the gene / brain level
One gene identified controls the serotonin transporter protein- control the ability of the axon to reabsorb the neurotransmitter after its release
Depression is also associated with the decreased activity in the left prefrontal cortex and increased activity in the right prefrontal cortex
Benefits of antidepressant is greatest for people with severe depression
-Generally, don’t work for people who suffered abuse, neglect, or other trauma (usually they respond better to psychotherapy)
-Can increase suicidal thoughts in children and teenagers
categories of antidepressants
tricyclics
SSRIs
SNRIs
MAOIs
atypical antidepressants
electroconvulsive therapy (ECT)
tricyclics
operated by blocking transporter proteins that reabsorb serotonin, dopamine, and norepinephrine into the presynaptic neuron after release; also, block histamine receptors, acetylcholine receptors, and certain sodium channels (ex. Tofranil)
selective serotonin reputake inhibitors (SSRIs)
works by blocking the reuptake of the neurotransmitter serotonin; similar to tricyclics but are more precise by targeting serotonin specifically (Ex. Prozac, Zoloft)🡪 therefore the side effects are milder
serotonin norepinephrine reputake inhibitors (SNRIs)
block reuptake of both serotonin and norepinephrine (ex. Cymbalta, Effexor)
monoamine oxidase inhibitors (MAOIs)
blocks the enzyme monoamine oxidase that metabolizes catecholamine and serotonin into inactive forms (ex. Nardil)🡪 blockage of the enzyme results in more of the transmitters in the presynaptic terminal available for release
Must avoid cheese and other specific foods; therefore, only prescribed is SSRIs and tricycles don’t work
atypical antidperessants
a miscellaneous group of drugs with antidepressant effects that work by inhibiting the reuptake of dopamine and to some extent, norepinephrine but NOT serotonin (ex. Wellbutrin)
electroconvulsive therapy (ECT)
is an electrically induced seizure that is used for the treatment of severe depression
recommendations for mild moderate and severe depression
Mild Depression- prescribe exercise, diet sleep, psychotherapy, behavioral activation
Moderate Depression- prescribe all the above and maybe start and SSRI
Severe Depression- prescribe both psychotherapy and medication; ECT as last line to poor responders
bipolar disorder in the brain
brain use of glucose increases during periods of mania and decreases during periods of depression
lithium
a salt that stabilizes mood and prevents relapse in mania or depression
anticonvulsant drugs
such as valproate (Depakote) and carbamazepine
-These drugs work by decreasing glutamate activity and by blocking the synthesis of the brain chemical arachidonic acid, which is produced during brain inflammation
antipsychotic/neuroleptic drugs
are drugs that tend to relieve schizophrenia and similar conditions
chlorpromazine (thorazine)
is a drug used to relieve the positive symptoms of schizophrenia (works within 2-3 weeks, taken indefinitely)
two chemical families to treat schizophrenia
Two chemical families to treat schizophrenia (both block dopamine synapses)
-Phenothiazines: includes chlorpromazine
-Butyrophenones: includes haloperidol (Haldol)
dopamine hypothesis of schizophrenia
suggests that schizophrenia results from excess activity at dopamine synapses in certain areas of the brain
substance induced psychotic disorder
happens when a person uses repeated large doses of amphetamine, methamphetamines, or cocaine which qll prolong the activity of dopamine at the synapse
glutamate hypothesis of schizophrenia
suggests the problem relates partially to deficient activity at glutamate receptors (especially in the prefrontal cortex)🡪 increased dopamine thus produces the same effects as decreased glutamate (Effects of phencyclidine (PCP) support glutamate hypothesis)
tardive dyskinesia
side-effect of anti-psychotic drugs that blocks dopamine in the mesostriatal system which projects to the basal ganglia, resulting in tremors and other involuntary movements (usually in the face)
second generation antipsychotics (atypical antipsychotics)
are a class of drugs used to treat schizophrenia but seldom produce movement problems (ex. clozapine, amisulpride, risperidone, olanzapine, aripiprazole)
-More effective at treating negative symptoms of schizophrenia
-More widely used; less effect on dopamine receptors and more effect on antagonizing serotonin receptors-
acquired brain injury
caused by structural change in the brain
anoxia
brain damage due to oxygen deprivation; neuronal death, especially in cortical and hippocampal regions, may result after 5-7 minutes of oxygen deprivation
meningitis
an inflammatory disease cause by bacterium, virus, fungus, or parasite that attaches the protective tissue surrounding the brain and spinal cord
encephalitis
generalized infection of the brain cause by a virus that invades neurons (results in brain swelling)
ischemic stroke
occurs when blood vessels become obstructed, disrupting the flow of oxygen via blood to various brain regions (85% of CVA is ischemic)
thrombus
solidified blood within a vessel; usually due to plague buildup
embolus
when plague or another substance travels with the blood flow down a blood vessel to a narrower aspect of the vessel where it lodges and blocks blood flow
hemorrhagic stroke
occurs when a blood vessel bursts. Disrupting he flow of oxygen via blood to various brain regions as well as allowing blood to mix with brain tissue (more lethal, more damage than ischemic stroke)
what can both kinds of strokes cause
Both can cause: hemiparesis, language disruption, facial droop, dizziness/poor balance, and confusion
brain tumors
an abnormal new cell growth located within or adjacent to brain tissue
Directly destroy brain tissue by invading and growing within a specific region; indirectly destroys brain tissue by elevating pressure underneath the skull which may affect tissue that is distant from the tumor
hydrocephalus
caused by a blockage that interferes with the normal absorption of cerebrospinal fluid (CSF). The ventricles fill with the fluid and become enlarged causing pressure under the skull
This pressure can displace brain tissue and cause brain degeneration🡪 can be a consequence of TBI, infections, and/or brain tumors
The earlier you treat in process, the better: can be fixed by placing shunt within the brain to drain the cerebrospinal fluid
neurotoxins
mercury, lead, organic solvents (paint thinners), crack cocaine, alcohol, botulism and incest venom
external events
Traumatic Brain Injury (TBI)- is an acquired injury to the brain caused by an external force
impression injury
results when there is direct contact between a stationary head and a moving object
acceleration-deacceleration injury
occurs when there is an impact with a moving head
closed head injury
the skull remains intact, damage results from the brain compressing against the full, rupturing of blood vessels within the brain, and stretching and shearing axons (diffuse axonal injury) 🡪 accounts for 90% of TBI
Impacts several brain structures that generally reside in the midbrain🡪 hippocampus, amygdala, fornix, and corpus callosum
open head injury
results when an objects penetrated the skull and damages brain tissue. When the skull has been fractures, it may be “depressed down into brain tissue
coup injury
damage at the site where the brain initially impacts the skull
contrecoup injury
brain damage (cerebral contusion) at a site generally opposite to the initial impact site
injuries caused by external events and CT scans
Never trust date of injury CT scan as it make time for the injury to evolve (swelling, pools of blood)
Brain damage resulting from high velocity impacts always extends beyond the identifiable lesion on neuroimaging (for example, cannot see diffuse axonal injury on classical neuroimaging)
primary injuries
caused directly by the trauma-skull fracture, focal damage (with frontal and temporal lobes being the most frequently injured), and cerebral contusions (aka brain bruising)
cerebral lacerations
tearing of brain tissues, typically in the cerebral cortex
diffuse axonal injury
as the brain moves around the skull from impact, neurons are stretched or sheared beyond repair which slows or cuts off communication from that neuron to other neurons (results in slow processing)
secondary injuries
develop indirectly from the trauma
-Cerebral edema and brain swelling, increased intracranial pressure, anoxia/hypoxia/Ischemia, mass lesions
long term neuropathological effects of TBI
white matter degeneration, cerebral atrophy, posttraumatic hydrocephalus, posttraumatic seizures
82,000 individuals become permanently disabled each year because of a TBI (transportation related trauma and falls account for 75%-80% of all TBIs)
physical and motor effects of TBI
Hemiplegia (paralysis on one side of the body), Hemiparesis (weakness on one side of the body), Hypotonicity (decrease in muscle tone), Rigidity, Spasticity, Tremor, Reduced Motor Speed, Poor Motor Dexterity, Fatigue, Seizures, and Headaches
apraxia after TBI
inability to carry out a complex or skilled movement, not due to paralysis, sensory changes or impaired comprehension
ataxia after TBI
impairment in motor coordination not due to apraxia, weakness, rigidity, spasticity, or sensory loss. Typically cause by lesions in the cerebellum and/or basal ganglia
sensory effects of TBI
diminished auditory acuity or hearing loss, tactile, visual (most common)
cognitive/neurocognitive effects of TBI
orientation, cognitive processing speed, visuospatial perception and construction, executive function, language🡪 dysarthria (articulation difficulties), expressive aphasia, receptive aphasia, naming/word finding, low volume, “flat” prosody, oral apraxia
attention (TBI)
selective attention, speed of information processing, alertness, sustained attention
memory (TBI)
(most common) anterograde amnesia, retrograde amnesia, difficulty recalling previously learned information or experience, poor memory for recent events, difficulty acquiring new information and skills
Explicit memory is much more vulnerable than implicit memory after TBI
which is worse in TBI learning new info or old info
**Impairment in learning new information appears much greater than impairment in memory for previously learned information🡪 this is why it is worse to have a TBI at a younger age as children have not learned much in their earlier years
socioemotional effects of TBI
typically, a result of frontal lobe damage
Disinhibition/impulsivity, depression, apathy low self-esteem, anxiety, inappropriate social/sexual behavior, aggression
damage to right hemisphere socially
neurologically based unawareness, difficulty picking up subtle emotional cues (facial expression, humor, voice tone), difficulty recognizing limitation, indifference, emotional insensitivity, more “difficult” rehab patients
damage to left hemisphere socially
heightened awareness, “catastrophic” reactions, tearful, anxious, oversensitive, better progress in rehab
apraxia vs. ataxia
Both ataxia and apraxia may involve trouble with movement and speech, but they are different. Apraxia is a condition that affects your brain, making it hard for you to perform a familiar task or movement, even though your muscles are functioning properly. With ataxia, you lose the physical ability to control muscles.
acetylcholine
A neurotransmitter that enables learning and memory associated with motor neurons; and also triggers muscle contraction - found in the CNS and parasympathetic nervous system
Too much is linked to salvation, muscle weakening, blurred vision, and paralysis while too little is linked to learning and memory impairments - Alzheimer’s
cingulate gyrus
A component of the limbic system; it is involved in processing emotions and behavior regulation. It also helps to regulate autonomic motor function.
modulatory neurotransmitters
Can affect a number of neurons at the same time and influence the effects of other chemical messengers - do not directly activate receptors but work together with other neurotransmitters to enhance responses
hippocampus
A neural center located in the limbic system that helps process explicit memories for storage - buried deep within the medial region of the temporal lobes
cerebral cortex
The intricate fabric of interconnected neural cells covering the cerebral hemispheres; the body’s ultimate control and information-processing center.
Outer region of the cerebrum, containing sheets of nerve cells; gray matter of the brain
glutamate
A major excitatory neurotransmitter/amino acid; involved in memory and learning (cognitive functions)
Most abundant neurotransmitter found in the CNS
Excess of glutamate could cause excitotoxicity = neurons are killed due to overactivations of glutamate receptors -> Alzheimer’s diease
differences between serotonin and dopamine
serotonin: stored in gut; happiness, mood, wellbeing; regulates mood, body temperature, emotions and appetite
dopamine: released in brain, associated with feelings of reward, motivation and accomplishment; muscle movement and brains pleasure reward systems
tectum
A part of the midbrain that orients an organism in the environment - roof of the midbrain
endorphins
Inhibitory neurotransmitter which works in lowering the transmission of pain signals to the brain too promote feelings of euphoria - similar to opioids - made in hypothalamus and pituitary glands
tegmentum
A part of the midbrain that is involved in movement and arousal - covering several midbrain structures and is covered by the Tectum
cortisol
Stress hormone released by the adrenal cortex - helps mobilize energies to fight a difficult situation but once depleted, it makes it more difficult to combat stress - makes one more prone to the damaging effects of stress
epinephrine
Neurotransmitter secreted by the adrenal medulla in response to stress. Also known as adrenaline - stress hormone released into the blood via the adrenal glands
If there is too much in the blood stream = high blood pressure, anxiety, insomnia, and increase risk of stroke; but too little can lead to diminished excitement
Effects heart (norepinephrine impacts blood vessels)
norepinephrine
A neurotransmitter involved in arousal, as well as in learning and mood regulation - also produced in adrenal glands and is naturally occurring - produced in the brain stem and hypothalamus
Helps activate the body and brain to take action during times of stress or when in dangerous situations - especially prevalent during fight or flight, aiding in alertness
Effects blood vessels
GABA
gamma aminobuytric acid
Amino Acid/ Neurotransmitter that reduces activity across the synaptic cleft and thus inhibits a range of behaviors and emotions, especially generalized anxiety.
Body’s primary inhibitory messenger; located in hippocampus, thalamus, basal ganglia, hypothalamus, and brain stem
Main functions are to regulate anxiety, vision, and motor control - people who do not have enough GABA may find they have poor impulse control and could lead to seizures - lack of is seen in bipolar and mania
mutagen
An agent that causes mutation or a heritable change in the DNA sequence
