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Chapter 4

PSYC32 Chapter 4.docx

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University of Toronto St. George
Michael Inzlicht

Chapter 4: Neuropathology: Acquired Disorders Case: • Cathy lived in an old building • Found that her concentration and memory were poorer + severe headaches + nosebleeds • Her family found the same • Bc high lvls of heavy metals in bloodstream bc toxin exposure (pesticides, fertilizers, herbicides used by lcal farmers + the basement of the house had a lot of cleaning sol’ns, chemicals to strip wood, remove paint, etc. ever since they began living in the country) • Also abstract reasoning deficits • They moved to the city and the symptoms subsided and never returned • Doctor first assumed emotional factors before thinking of enviro toxins though TBI/Head Injury: • hard to say exactly how many have had TBIs bc mild ones not always treated • 1.25 mill Americans/yr treated for it, 250K hospitalized, 50K died • 150/100K die per year • Very similar rates to UK + France. But, China only has a quarter of that number • TBI Act of 1996: provides various services to victim (while they get to track the number of cases) • Peak age = 15-24 (males espec) • But also >64 (females espec) and <5 (females espec) are at high risk, after the peak age group • Open vs closed depends on more than just nature of injury (also the psychopathological processes) • James Brady, former press secretary to Reagan, was shot, in a foiled Reagan assassination attempt, in right frontal lobe ( paralyzed on left side) o Brady Handgun Violence Prevention Act of 1993 = requires a criminal background check before firearms can be purchase • Severity of ~’s are determined by combo of the following factors: o Length of PTA (Posttraumatic Amnesia) = period between receiving injury till regaining continuous day to day memory o Depth of Unconsciousness (usually measured immediately after resuscitation w/ GCS (Glasgow Coma Scale = measures depth of coma through determining individual’s responsiveness on criteria like opening eyes, motor movement, verbal comm. Scores range from 3-15, with higher scores indicating more intact fxns. 3-8 = severe TBI, 9-12 = moderate TBI. Also, 6-8 = severe, 3-5 = very severe. 13-15 = mild.) o Length of Unconsciousness and Presence of Neurological Signs Δ1: Open Head Injury • Skull is penetrated and cortex is exposed • Most common = gunshot wound. Ex. JFK • Most often people don’t survive • Clean wounds (= damage is mainly along the path of invading object, i.e. no fragments or ricochet) cause less damage • Secondary effects of ~ = hypotension, hypovolemia = low blood volume, contusions (= bruising), intracranial hematomas • Neuro deficits will depend on site of lesion but there will also be general, diffuse brain imp such as difficulties w/ concn, attn, mem + overall mental slowing • ~ is highly related to epilepsy (80% of patients experience seizures within the first 24 hrs) • Rapid recovery can happen in first 1-2 yrs, with smaller gains afterwards (which is the standard TBI pattern) Δ2: Closed Head Injury • Brain is never exposed to the elements • Still considered a form of severe injury • 2 stages = coup and contrecoup • Primary difficulties include diffuse axonal (=white matter) damage (caused by acceleration + deceleration of brain impacting against the skull), contusion (often occurs under the frontal and temporal poles where shearing forces of the brain are impacting on the sharpest and most confined parts of the skulls. They can also occur under point of impact or at contrecoup), hemorrhage (blood vessels supplying O2 to brain are ruptured) • Secondary damage: injuries resulting from hematomas, hemorrhage, infection, hydrocephalus, anoxic damage, low b.p. • Also, there may be neurochem difficulties like excitotoxicity, cell membrane degradation, cellular edema, or changes in neuropeptides, electrolytes, excitatory amino acids • 15-24 most likely to suffer ~, especially MVCs (including ATVs, boats, etc.) • Though another major cause is athletic injury (especially boxing and soccer, bc no protective headwear. But also other sports, i.e. football has a helmet but it does not cover base of brain or upper spinal column) • Npsych difficulties of closed and open are similar, but closed is less severe • Typically: lower speed of info processing and problems with concn, attn, mem, rxn time • Also often behv + personality changes afterwards (those around them acknowledge it before actual person does) • Very likely to experience depression or other emotional difficulty bc changes to life circumstances • PTSD is likely if caused by trauma • Also, inability to deal with strong emotions, especially anger o Poor anger management  their relationships suffer o TBI victims do not actually have a higher rate of divorce than avg pop’n though • Also, they tend to “look normal” even though they experience lots of problems that are not so apparent to others (like fatigue, cog problems) • TBI pt’s also often have a lack of awareness of their behv, cog, phys deficits • Many try to return to their life as if nothing happened but they cannot fxn as they once did and so they feel like they’re failures and thus angry and frustrated • Treatment for open + closed are very similar • Main thing is to prevent brain swelling • Atypical antipsychotics and anticonvulsants can help with anger management and to lesson behv outbursts Δ3: Postconcussion Sydrome • Milder form of closed head injury • Involves the traits and behvs that exist after an individual has received a TBI caused by a concussion. • Not currently listed in DSM-IV, but should be included in -V, along with mild neurocog disorder • Concussion is primarily caused by diffuse axonal injury o Symptoms include loss of consciousness, PTA, sometimes seizures • Npsych deficits of ~ = poor attention, verbal retrieval, and forgetfulness. Also could exp headaches, dizziness, irritability, sleep disturbance, fatigue • A premorbid personality, and psychiatric disorders make ppl more susceptible to the stress they exp’d when TBI happened, thus making them more likely to exp ~ o In fact, the reduced info processing is linked to a stress-producing factor • Also, the E4 allele of the ApoE gene (which is related to AD) is a contributor to the severity of TBI damage outcome • Treatment = pain relievers (such as nonsteroidal analgesics for headaches) + meds for depression, nausea, or dizziness. Rest is recommended. • Deficits are supposed to rectify themselves over time. o Education is also very effective in preventing re-emergence of symptoms • Athletes are at greater risk for subsequent concussions after the first one • But, the syndrome is also common in malingerers Toxic Conditions: • Usually an infrequent occurrence for an individual to see a clin npsy’ist for a toxic condition, except in the case of alcohol • ~ often complicate differential diagnosis bc the symptom presentation is more varied Δ1: Alcohol-Related Disorders • Only one of the toxins that has both positive protective effects and negative physio effects • Protective = not like medicinal use of marijuana = protective effects from cardio - and cerebro- vascular disease. If in moderation (social drinking lvls) = 1-2 drinks/day, depending on gender) • Social drinking leads to little to no npsy impairment o Alcohol abstinence by social drinkers does not tend to improve cog fxn or memory • Alcohol abuse = excess use of alcohol for 1 yr o Shown to negatively impact social/occu fxn • Alcohol dependence = abuse + tolerance and/or withdrawal o Tolerance = needing more of a substance over time to attain same lvl of intoxication o Withdrawl = pattern of symptoms after cessation of use • Binge drinking (the npsy implications are underresearched) • Alcohol is a CNS depressant • But also has a paradoxical effect whereby it produces euphoric feelings before depressive ones • Alcohol is a neurotoxin (therefore could be considered a poison) • Is metabolized differently than other drugs in a process called zero-order kinetics (= metabolized at a steady rate of approx 1 drink/hour, regardless of the amount consumed. • Metabolized through several different routes which explain it effects on CNS + organs • Females metabolize alcohol more slowly bc body comp + fat distrib • Asians lack the form of aldehdye hydrogenase that eliminates low lvls of the first breakdown product of alcohol (acetaldehyde) • Whites and Blacks have similar rates of alcohol abuse and dependence. But Latino males have somewhat higher rates and Latino females lower. Natives have higher rates. • Chronic alcohol use  complex visuospatial deficits, decreased psychomotor speed. o Well-learned tasks like arithmetic, lang, attn are not as greatly affected o Memory deficit often exist and are severe. But, not actually a hallmark of chronic alcohol use (some don’t have mem imp)  But, as the mem task increases in complexity, there is a higher chance of impairment being apparent • Alcohol dementia = widespread cog deterioration, similar to other dementias. Progressive. Involves cog + mem + abstract reasoning deficits. o Sometimes difficult to differentiate from other dementias o There should be some recovery of cog fxns if they become abstinent from alcohol • Korsakoff’s Syndrome = short-term mem + other mem deficits. Manic confusion, unable to clearly state thoughts. Disoriented eye + limb movements. o Cause is significant alcohol intake over a period with subsequent vitamin deficiency (alcohol interferes with GI absorption of the vitamin thiamine)  Thiamine deficiency  cog + emotional changes o Is treatable if caught early and given thiamine and no more alcohol • During the intital detox period of alcohol abstinence, 1-2 weeks of cog + memdeficits o After this, the greatest amount of return of fxn occurs o But, for the next 3-6 weeks, rate of return of fxn slows down. o After that, rates of return of fxn are inconsistent in the research lit Marijuana • ~/cannabis = herbal form • Hashish = resinous form of the plant Cannabis sativa • The bio active compound is THC = tetrahydrocannabinol • ~ is native to Central Asia th • Only became illegal in most parts of the world in 20 century • Became very popular in U.S. during the counterculture movement of the 60s • Can induce good/bad hallucinations + emotional states • Also, time distortion, memory loss • Similar to alcohol in terms of how it feels + the link of how it feels to a person’s expectations + mental state prior to using • Intensity of the effects is dose-dependent (i.e. high dose  psychotic-like symptoms) o Even lesser doses would be enough in those predisposed/vulnerable to schizophrenia • Use before age of 17  more likely to dev npsych deficits than those who start using at a later date • Some studies show poorer performance on cog activities, especially memory, but others show no effects • ~ is known to act on hippo and impact short-term mem + attn • Some studies show personality changes w/ heavy usage • Most common symptoms = emotional blunting, mental sluggishness, apathy, restlessness, mental confusion, amotivational syndrome • But confounds in research are plentiful because self-report rather than lab style exp’ts bc illegal • The most consistent effect that has been found though is that there si a deleterious effect on rxn time, and it has been implicated in many traffic accidents • Whether withdrawl occurs or not is disputable • Abstinence for social users  restoration of cog/mem deficits • But for heavy users, even after 25 days, they have even worse cog performance on decision-making tasks • Marijuana Policy Project has argued the therapeutic benefits • FDA though has said high potential for abuse + no currently accepted medical use + it’s a gateway drug Cocaine • A CNS stimulant • Highly addictive due to the “rush” exp’d through inhalation o Inhalation > IV • Also, higher alertness + arousal, increased sense of well-being + confidence • Increases dopamine lvls in brain’s reward circuits which leads to craving and a higher threshold for the euphoric rxn • At first, it’ll feel like an aphrodisiac, but w/ prolonged use it lowers libido and can cause impotence • Also less pleasant effects like paranoia, delusions, hallucinations, panic attacks • Damages brain’s reward centers w/ repeated use • Long-term users will have many cog deficits w/ mem + conc’n being the most sig • Seizures can also occur w/ both habitual + new users • Hypertension + other symptoms of CNS overstim, such as stroke, may occur • Abnormal metabolism and hypoperfusion both when they are using the drug and when chronic users try to be abstinent o Consistent w/ findings of slowed mental processing, mem imp, and reduced mental flexibility • Withdrawal from ~ is neither life-threatening nor terribly painful o But, symptoms of irritability, restlessness, confusion, sleep disorder, abnormal muscle movements • Difficult to determine the complete rate of return of fxn o some suggestion that w/ chronic use, abilities may not return • ~ addicts make more errors on Erikson flanker task and were less likely to correct errors o Supposedly bc compromised dopamine sys Narcotics = Opiates • First ones were derived from opium poppy • Synthetic derivatives include heroin, morphine, codeine • Ease pain + prod euphoria • Origin = Middle East • Also mentioned in Ebers Papyrus to prevent excessive crying of children o Galen suggested caution but basically felt opiates were an overall cure-all o i.e. Paracelsus thought it was a panacea in the Renessaince o Sydenham = Father of clinical medicine = introduced laudanum (= a concoction using opium + other things dissolved in wine, as another panacea) • Many writers and other rich people in the 1800s, 1900s used opium daily. It was easy + cheap to obtain • Serturner, in 1806, discovered the synthetic version of opium = morphine o Received French Nobel Prize • Bayer Laboratories added two acetyl groups to the morphine molecule to produce heroin and this was put in the market in 1898 • After 1900s, the main addicts were: o Chinese railroad workers o Avg citizen who didn’t know of the addictive properties o Ppl in inner-city ghettos • Harrison Narcotics Tax Act was a taxation law (only intended to profit from the spread of narcotics, not meant to control the spread), passed in 1914 o Narcotics were now only available by prescription • 1973: specific opiate receptors in the brain were discovered as well as the brain’s own enkephalins and endorphins that fit into these receptor. o These substances were released during stress or pain o Opiates compete w/ naturally occurring endorphins for the receptor sites • Though it helps control pain, pt’s report they are still aware of the pain but it is just no longer aversive • Other effects of narcotics o Impacs the GI sys and can counteract diarrhea and control a disease called dysentery o Can control the medulla’s cough centre (i.e. use as cough medicine) • Tolerance develops for all forms of neurotics o Also cross-tolerance (to all other narcotics, even types you didn’t use) • There is most definitely withdrawal (described as a bad case of the flu or worse) • Psych dependence also occurs • Also, if needles or pipes or something are used, over time, just looking at these items can make one feel pleasure • Needles: risk of HIV, Hep • Excessive ~ use  decreased stress response, decreased mem storage, visuo -spatial and -motor difficulties, impulse control problems o Remaining abstinent may recover many lost abilities o Attention + mental flexibility are not affected • Death can occur because ~ depress the respiratory centre of the brain Meth • Most visible drug (= readily available, relatively cheap, target of media and law enforcement) • Causes such an extreme high (described as several simultaneous orgasms) that many other aspects of life are often neglected • When taken to excess, can give the appearance of psychosis • Not a new drug, has a long history o Medicinal use (mainly to treat ADHD) until 1940s when it was replaced by non- addictive forms (= Ritalin - methylphenidate and Dexedrine-dextroamphetamine) o Used in the 1960s as a stimulant by many musicians o Was very popular in the 90s with workers who need to stay awake for extended periods (i.e. ER doctors + nurses, truck drivers) o The internet made it possible for any individual to make their own meth  Thus, legislation to make the ingredient
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