Psych 280 Final Exam

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where drugs exert their effects

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Because transmission between neurons is a CHEMICAL PROCESS, it is primarily at SYNAPSES that DRUGS exert their effects.

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*** AGONISTS ***

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Drugs that ENHANCE or INCREASE the activity of the neurotransmitter for which they are agonistic.

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AGNOSTIC EFFECTS can be accomplished by way of the drug BINDING to the receptor sites of the NT for which it is an agonist and MIMICKING the effects of the NT that should bind there.

EXAMPLE :

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NICOTINE is an example of such an ACh agonist. It binds to the NICOTINIC RECEPTOR SITES for ACh and mimics the action of ACh there, having a STIMULANT EFFECT (in low doses) on the subject.

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COCAINE

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another example of an agonist.

It affects the activity of both DA and NE (it is a catecholamine agonist) by BLOCKING their RE-UPTAKE by the pre-synaptic neuron

causing EUPHORIA, INSOMNIA, LOSS OF APPETITE.

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*** ANTAGONISTS ***

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Drugs that DIMINISH or DECREASE the activity of the neurotransmitter for which they are antagonistic.

ANTAGONISTIC EFFECTS can be accomplished by way of the drug BINDING to the receptor sites of the NT for which it is an antagonist and BLOCKING the NT that should bind there but having NO EFFECT.

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CURARE

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an example of an ACh antagonist.

It blocks the NICOTINIC RECEPTOR sites for ACh preventing muscles from being able to move and PARALYZING the subject.

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Botox

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Antagonist

affects the activity of ACh by BLOCKING the release of ACh at neuromuscular junctions and thereby effectively PARALYZING the muscle controlled by this junction.

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Events of Chemical Transmission:

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1. SYNTHESIS OF THE NT

2. STORAGE OF THE NT IN THE TERMINAL BUTTON VESICLES

3. BREAKDOWN IN THE CYTOPLASM OF NT THAT LEAKS FROM THE VESICLES

4. EXOCYTOSIS (THE PROCESS OF FUSION BETWEEN THE MEMBRANE OF THE SYNAPTIC VESICLE AND THE MEMBRANE OF THE TERMINAL BUTTON & THE CONSEQUENT RELEASE OF THE NT INTO THE SYNAPTIC CLEFT)

5. AUTORECEPTOR FEEDBACK ON THE PRE-SYNAPTIC MEMBRANE INHIBITING THE CONTINUED RELEASE OF NT

6. ACTIVATION OF POST-SYNAPTIC RECEPTORS BY NT

7. DEACTIVATION OF THE NT (REUPTAKE OR ENZYMATIC DEGRADATION)

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AGONISTIC (enhancing) EFFECTS:

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1. Drug serves as a precursor for NT

e.g.: L-DOPA for dopamine (treatment for Parkinson’s disease)



2. Drug stimulates the release of NT

e.g.: black widow venom for acetylcholine



3. Drug stimulates post-synaptic receptors for NT

e.g.: nicotine for acetylcholine



4. Drug blocks pre-synaptic autoreceptors for NT

e.g.: clonidine for norepinephrine



5. Drug blocks reuptake of NT

e.g.: cocaine for dopamine



6. Drug inactivates breakdown enzyme for NT

e.g.: physostigmine for acetylcholine (treatment for myasthenia gravis)

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ANTAGONISTIC (inhibiting) EFFECTS:

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1. Drug prevents storage of NT in synaptic vesicles

e.g.: reserpine for dopamine (treatment for schizophrenia)



2. Drug inhibits release of NT

e.g.: botulinum toxin for acetylcholine



3. Drug blocks post-synaptic receptors for NT

e.g.: curare for acetylcholine



4. Drug inactivates synthetic enzyme for NT

e.g.: PCPA for serotonin



5. Drug stimulates autoreceptors for NT

e.g.: apomorphine for dopamine

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The Blood Brain Barrier is not well developed in human infants, only reaching complete development after one or two years of age. This explains ....

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the heightened effect of many drugs on the fetus (leading in some cases, to such disorders as fetal alcohol syndrome) and on young children (which is it is prudent to avoid taking psychoactive drugs during pregnancy and while breast-feeding).

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The EASE with which drugs cross the BBB predicts the EXTENT to which these drugs influence psychological processes.

example:

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Heroine for example, is a semi-synthetic opiate that crosses the BBB much faster than its relative morphine, and produces a 'rush' of euphoria in the user almost immediately upon entering the bloodstream. For this (and other) reasons, it is a more highly sought-after drug than some of the opiate alternatives.

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Blood Brain Barrier can be compromised by:

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trauma such as concussions and tumors and by invasion by foreign substances such as drugs and organisms such as viruses and bacteria. Any of these can cause enough trauma to impair the effectiveness of the BBB.

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PSYCHOTROPIC DRUGS

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Drugs that have an effect on our mental, emotional, or behavioural functioning

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PHARMACOKINETICS

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movement of psychotropic drugs through our bodies once we have been exposed to them

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Most common routes of drug administration

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Injection

NOT BY INJECTION:

1. ORAL (in mouth)
2. INTRARECTAL (in rectum)
3. INHALATION (breath in)
4. TOPICAL (cutaneous, sublingual or intranasal)

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types of injection (common)

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1.SUBCUTANEOUS (sc): needle is inserted just under the skin (in humans often under the skin of the arm or thigh). E.g.: Insulin (diabetes treatment)

2. INTRAMUSCULAR (im): needle is inserted into a muscle (in humans often in the upper arm muscles or the buttock muscles). E.g.: Demerol (pain killer) A DEPOT INJECTION is a special type of im injection in which the vehicle is oil, slowing the diffusion of the drug in the body fluids over a longer period of time. E.g.: Depot Vera (birth control)

3. INTRAPERITONEAL (ip): needle is inserted through the abdominal wall into the peritoneal cavity which is the area surrounding the intestines, liver, stomach and other abdominal organs. E.g.: Heparin (blood thinner)

4. INTRAVENOUS (iv): needle is inserted into a vein so that the drug moves directly into the bloodstream. E.g.: Morphine (pain killer)

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less common types of injection

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These methods of administration by-pass the BBB.

1. INTRACEREBRAL: injection of the drug directly into brain tissue at the desired site

2. INTRACEREBROVENTRICULAR: injection of the drug into the cerebral ventricles

3. INTRATHECAL: injection of the drug into the nervous system between the base of the skull and the first vertebra

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***DOSE-RESPONSE CURVE***

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"A graph of the magnitude of effect of a drug as a function of the amount of drug administered."


The EFFECT of a drug is assessed by PLOTTING the DOSE OF DRUG administered against the STRENGTH of the EFFECT the drug has on the subject(s) to whom it has been administered.

The RANGE of such a CURVE should cover a dose so low that there is no detectable effect to a dose so high that further increases in dose have no further effect.

Such a PLOT is called a DOSE RESPONSE CURVE.

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A common way to use the dose response curve to compare the effectiveness of different drugs

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compare the dose at which 50% of subjects who receive each drug experience the effect under investigation. This dose is referred to as the ED50.

(ED50 = EFFECTIVE DOSE).

Similarly, the LD50 represents the dose at which 50% of the subjects who receive each drug die.

(LD50 = LETHAL DOSE).

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**THERAPEUTIC INDEX**

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"The ratio between the dose that produces lethal effects in 50% of the subjects to whom it is given and the dose that produces the desired effects in 50% of the subjects to whom it is given = (LD50 / ED50)."

The RATIO between the LD50 and the ED50 (LD50/ED50) is referred to as the THERAPEUTIC INDEX (TI). The HIGHER the therapeutic index, the LESS LIKELY an accidental OVERDOSE of the drug is to take place, because the ED50 is much smaller than the LD50. So, the higher the TI, the SAFER the drug is to take.

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Tolerance

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When a drug loses its EFFECTIVENESS, the user is said to have built up a “TOLERANCE” to it and requires HIGHER & HIGHER DOSES of the drug to produce the desired effect.

a GREATER DOSE of the drug is required to produce the SAME MAGNITUDE of effect in subjects.

Tolerance can develop to SOME of the effects of a drug BUT NOT TO OTHER EFFECTS. For example, it is possible for tolerance to develop to the pain-killing effects of a drug but NOT to the LETHAL effects of the same drug, making the drug increasingly DANGEROUS if the user continues to increase the does in order to counter tolerance to the effect of the drug he/she is using for.

E.g.: among the effects of morphine is NAUSEA & VOMITING. These effects show RAPID TOLERANCE, but the ability of morphine to CONSTRICT PUPILS of the eyes shows NO TOLERANCE at all, no matter how long the drug is taken.

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Why tolerance to some drug effects and not others?

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tolerance is not caused by one mechanism in the nervous system. Many different kinds of changes in the nervous system are responsible for the many difference effects of each drug (think back to the 7 steps that are involved in chemical neural transmission).

Consequently, it is more appropriate to think of tolerance developing to the particular effect of a drug than to the drug itself (refer to my previous comments about dose response curves being specific to a particular effect of the drug and not to the drug itself).

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Reverse tolerance / sensitivity

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Tolerance can develop to some of the effects of a drug while SENSITIVITY (sometimes called “REVERSE TOLERANCE”) develops to some of the other effects.

Sensitivity represents a SHIFT in the DOSE-RESPONSE CURVE to the LEFT. That is, a SMALLER DOSE of the drug produces the same MAGNITUDE OF EFFECT in the subject as a larger dose did originally.

E.G.: someone may become tolerant to the nausea effects of ALCOHOL but become more sensitive to the cognitive impairment effects.

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cross tolerance

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Exposure to one drug can result in tolerance to other drugs (= CROSS TOLERANCE). Cross tolerance typically occurs between members of the same class of drugs (e.g., heroine and morphine), presumably because they have similar mechanisms of action.

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WITHDRAWAL SYMPTOMS

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Withdrawal symptoms are typically the OPPOSITE of the effects of taking the drug itself. Heroine for example, causes euphoria, relaxation and constipation. Withdrawal from heroine is associated with dysphoria, nausea/diarrhea, and agitation.

Withdrawal symptoms can be STOPPED virtually INSTANTLY by simply re-administering the drug that has been stopped.

Often another drug of the SAME FAMILY can be given instead of the drug of addiction to stop withdrawal symptoms such as is the intent behind METHADONE CLINICS for heroine addictions.

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Methadone as a Treatment for Heroine Addiction:

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METHADONE is a HEROINE ANTAGONIST. It exerts its effect by BLOCKING the receptor sites for heroine causing the heroine receptor sites to be occupied despite the fact that the addict is not taking heroine.

Because METHADONE occupies the receptor sites for heroine, it PREVENTS some of the WITHDRAWAL SYMPTOMS that would normally accompany the cessation of heroine use and makes it easier for the addict to carry on without heroine.

But because METHADONE is an ANTAGONIST for heroine, it does NOT cause the EUPHORIC RUSH typically associated with heroine use and furthermore, while it occupies the receptor site, if the addict RELAPSES and uses heroine while on methadone, he/she will not experience the RUSH typically associated with heroine. This has the added BENEFIT of decreasing the tendency to return to using heroine while on methadone.

Other ADVANTAGES of methadone are that it can be taken ORALLY thereby ELIMINATING the risk of needles and since the effects of methadone last about 24 hours, it can be given 1x/day. Consequently there is no need to take it home and addicts can be monitored daily on an OUT-PATIENT basis.

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The DISADVANTAGES of methadone

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include that it produces some of the same SIDE EFFECTS as those produced with heroine use: sweating, constipation, sexual dysfunction. Furthermore, ultimately, the user must be WEANED OFF the METHADONE just as he/she would have been weaned off the HEROINE and RELAPSE RATES of methadone use are approximately the SAME as those of heroine use: 80-90%.

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CONDITIONED DRUG TOLERANCE

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This refers to the fact that the fact that both CLASSICAL & OPERANT conditioning can alter the effects of drugs and can be used to explain TOLERANCE & WITHDRAWAL.

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how conditioned withdrawal effects play an important role in the RELAPSE of to drug use in abstaining addicts.

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If the user later returns to the environment in which the drug is normally administered, but does not take the drug, the compensatory changes are still produced. In this way, withdrawal effects can be conditioned and may be evoked by specific stimuli previously associated with the administration of the drug (such as the environment in which the drug was typically used).


Conditioned compensatory responses also explain accidental overdoses that often occur when an addict administers the drug in a novel environment. The compensatory response is much reduced in the novel environment and if the addict administers the usual dose, his/her body is not as ‘prepared’ for the drug effects and he/she overdoses.

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Psychoactive drugs can be DIVIDED into 6 major categories:

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1. NARCOTICS
2. SEDATIVE-HYPNOTICS
3. ALCOHOL
4. STIMULANTS (I will include NICOTINE here although your textbook discusses it in a category of its own)
5. HALLUCINOGENS
I will consider ECSTASY separately as it doesn’t fit well into any one of these drug classifications.
6. CANNABIS

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Narcotics

Names, effects, side effects
natural & semisynthetic

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Are called OPIATES (because natural sources are derived from OPIUM which comes from the POPPY PLANT)

· Are called ANALGESICS (because they used primarily to RELIEVE PAIN)

· NATURAL opiates = MORPHINE & CODEINE

· SEMISYNTHETIC opiates = HEROINE (is made by chemically ALTERING the MORPHINE MOLECULE resulting in a compound that travels to the BRAIN much FASTER than morphine)

· Exert their effects at naturally-occurring (endogenous) receptors in the brain (ENDORPHINS & ENKEPHALINS---endogenous opiate-like neurotransmitters bind here)

· EFFECTS = EUPHORIA--- an extreme well-being which is typically what they are used to achieve recreationally

· SIDE EFFECTS = NAUSEA & VOMITING (these typically DISAPPEAR after the FIRST ADMINISTRATION and then the drug acts to INHIBIT nausea & vomiting---these symptoms return during withdrawal), CONSTIPATION, LETHARGY, IMPAIRED MENTAL and MOTOR functioning

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Sedative-Hypnotics

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· Contains 2 FAMILIES of drugs: BARBITURATES (anti-convulsant drugs) & BENZODIAZEPINES (anti-anxiety drugs)

· Exert their effects on the neurotransmitter GABA (increasing its inhibitory activity)

· EFFECTS = SIMILAR to taking ALCOHOL and include feelings of RELAXATION and INACTIVITY (CNS depressant)

· SIDE EFFECTS = SLEEPINESS, severe MOTOR & MENTAL impairment.

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Alcohol

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· Has many sites of action including at the GLUTAMATE (decreases activity), GABA (increases activity) and SEROTONIN (increases activity) receptors.

· Also changes the properties of the cell membrane perhaps by dissolving in the lipid layer and thereby interfering with the ability of the ion channels to operate properly. This is not well understood

· EFFECTS = Low doses can stimulate neural firing (responsible for social disinhibition), moderate to high doses can depress neural firing (responsible for relaxation, sleepiness & slow cognitive & motor responses) and at very high doses, it can lead to UNCONSCIOUSNESS, and risk of DEATH from RESPIRATORY FAILURE (blood alcohol levels of > .5%).

· MILD WITHDRAWAL (such as in a “hangover”) leads to HEADACHE, NAUSEA, VOMITING and TREMULOUSNESS.

· SERIOUS WITHDRAWAL is LIFE-THREATENING and includes the DT’s (delirium tremens) and convulsions.

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Stimulants

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· = several SUB-CLASSES of drug: COCAINE (naturally-occurring), AMPHETAMINES (synthetic stimulants), CAFFEINE and NICOTINE (tobacco)

·Exert their main effects on the MONOAMINE neurotransmitters (DA, NE & SE) and ACh, increasing activity

· EFFECTS = energized, awake and stimulated feeling.

· SIDE EFFECTS = restlessness, anxiety, insomnia and paranoia. The side effect syndrome of cocaine use looks much like an ACUTE ONSET of PARANOIA as seen in patients with schizophrenia.

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Hallucinogens

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- Heterogeneous group of drugs that includes LSD, PSILOCYBIN (found in “MAGIC” MUSHROOMS), MESCALINE (found in Mexican CACTUS known as the PEYOTE), PCP (synthetic drug called phencyclidine)

- Exert their main effect on SE & NE receptors (increasing activity) but mechanism of action is poorly understood.

· EFFECTS = sensory and perceptual DISTORTION effects. Users report KEENER & MORE ACUTE sensory & perceptual experiences (“good trips” refer to the pleasurable euphoria and visions experienced and “bad trips” refer to the nightmarish hallucinations that can be experienced)

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Cannabis

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· = MARIJUANA & HASHISH. Both of these come from the CANNABIS PLANT. Marijuana comes from the LEAVES & FLOWERS and hashish comes from the RESIN at the top of the female cannabis plant.

· Exerts its effect on naturally-occurring THC receptors in the brain

· EFFECTS = RELAXATION and ENHANCED SENSORY awareness.

· SIDE EFFECTS = ANXIETY, SLOW MENTAL functioning and IMPAIRED MEMORY.

· used EXPERIMENTALLY to treat NAUSEA in CANCER PATIENTS being treated with chemotherapy.

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Ecstacy

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ECSTASY was originally classed as an HALUCINOGEN because it is a synthetic MESCALINE-LIKE drug (it has since been re-classified as a STIMULANT because it is an amphetamine derivative).

It is otherwise known as MDMA and was originally synthesized by a drug company and patented in 1914 (i.e., not a “new” drug). It first appeared on the drug scene in the late 1960’s and achieved considerable popularity in the mid-1980’s.

Lower to moderate doses of Ecstasy produces a state similar to that caused by MARIJUANA or low doses of PCP with no hallucinations or enhanced sensory or emotional awareness.

Before 1985, it was administered by some psychiatrists to their patients because it seemed to enhance intimacy and communication between the patient and the therapist.

NEUROTOXIC SIDE EFFECTS include depletion of SE in the brain at very high doses.

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1.EEG (electroencephalography)
2.EOG (electrooculography)
3.EMG (electromyography)

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1.EEG (electroencephalography): electrical activity of the brain

Sleep can be broken down into stages and each stage is defined by the EEG, EOG and EMG activity that characterizes it.

2.EOG (electrooculography): electrical activity of the eyes

3.EMG (electromyography): electrical activity of the muscles

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Note that EEG recordings DO NOT represent the ACTIVITY OF ONE NEURON or even a CLEARLY LOCALIZED GROUP of neurons.

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Rather, EEG recordings represent the activity of MANY NEURONS with some RATHER MINIMAL degree of LOCALIZATION such as in which CEREBRAL LOBE or HEMISPHERE the activity is located.

For this reason, using EEG recordings to study human brain activity has been likened to standing outside of a FACTORY without windows and attempting to GUESS at what is being manufactured inside on the basis of the NOISES that can be heard coming from inside the factory (author unknown)

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As you lie in bed with your eyes closed, your EEG pattern changes from ...

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As you lie in bed with your eyes closed, your EEG pattern changes from

beta waves (13-24 Hz, characteristic of being awake and alert)

to alpha waves (8-12 Hz, characteristic of being drowsy & relaxed but still awake).

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As you DRIFT off to sleep, your EOG shows ...

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SLOW, ROLLING EYE MOVEMENTS

and your EEG shows less and less BETA wave activity

and more and more THETA wave activity (4-7 Hz).

You also exhibit a DECREASE in other signs of physiological arousal, including HEART RATE, BREATHING RATE, BODY TEMPERATURE & MUSCLE TONE (as measured by EMG). These indicators continue to decline through the stages of sleep. REM sleep is an exception to this as we will see later.

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The CESSATION of the rolling eye movements signifies :

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the onset of stage one sleep. This is a LIGHT SLEEP and typically lasts only a FEW MINUTES. THETA waves predominate during this stage of sleep.

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Stage one sleep

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This is a LIGHT SLEEP and typically lasts only a FEW MINUTES. THETA waves predominate during this stage of sleep.

It is common during this phase to experience fleeting images and sensations not as complex as a dream (called HYPNAGOGIC IMAGERY) such as falling or tripping and you may experience TWITCHING & JERKING of your leg or arm muscles and thereby wake yourself (or someone else!) up. These twitches and jerks are referred to as HYPNOTIC JERKS.

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Stage two sleep

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After a few minutes in stage one sleep, you enter the slightly DEEPER stage two sleep. This stage is characterized by a pattern of periodic BURSTS of higher-frequency brain waves known as SLEEP SPINDLES

and by a pattern of single large negative waves

followed by single large positive waves known as K-complexes.

Sleep spindles are thought by some research to signal the absence of ENVIRONMENTAL AWARENESS of the sleeper. This stage of sleep lasts about 20-25 minutes.

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Stage three sleep

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The defining characteristic of stage three sleep is the presence of DELTA wave activity (1-2 Hz) in the EEG.

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Stage four sleep

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The stage at which 50 % of your brain wave activity is DELTA is called stage four sleep.

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SLOW WAVE SLEEP (SWS)

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Stage three and four

It is very DIFFICULT to wake people from SWS.

SLEEP ENURESIS (bed-wetting) in young children for example, is most often associated with this stage of sleep presumably due to the fact that children are much less aware of and therefore relatively unresponsive to autonomic cues regarding the fullness of their bladder in these stages of deep sleep.

SOMNAMBULISM (sleepwalking) typically occurs in SWS. Can you guess why this would be so as opposed to for example, in REM sleep?

NIGHT TERRORS (panic-inducing experiences not typically associated with dreaming, in which the individual wakes up suddenly in the throws of extreme autonomic arousal) are also associated with SWS.

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How long is SWS?

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We typically reach SWS within about 1/2 to 1 HOUR of falling asleep

and remain there for about 1/2 hour before the sleep cycle REVERSES itself and we MOVE BACK through the cycles of sleep from stage 4, through stage 3, to stage 2.

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Stage five (REM) sleep

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When we reach what would be stage one sleep again, we do NOT enter this stage of sleep. Instead of cycling through stage one sleep again, we enter REM sleep. The EEG pattern characteristic of REM sleep consists of a combination of BETA & THETA activity.

REM stands for RAPID EYE MOVEMENTS and describes the fact that during this stage of sleep, our eyes move back and forth rapidly under our eyelids.

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How long is REM sleep?

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The first time we experience REM sleep a night, it only lasts a few minutes. However, we cycle through the 5 stages of sleep several times a night and subsequent cycles of REM sleep last longer. An ENTIRE SLEEP CYCLE, consisting of the 4 stages of non-REM sleep plus REM sleep typically lasts about 90 MINUTES.

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Physiological arousal in REM sleep

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despite the fact that REM sleep is a RELATIVELY DEEP SLEEP in the sense that it is quite difficult to wake someone in REM sleep, it is marked by INCREASED PHYSIOLOGICAL AROUSAL

unlike the other four stages of sleep during which the physiological indicators discussed earlier continue to decrease.

Despite the increase in physiological arousal during REM, muscle tone during REM sleep is extremely RELAXED---so much so, that the body is virtually PARALYZED and therefore INCAPABLE of coordinated movement.

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REM sleep and dreaming

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Although DREAMING is thought to occur in other stages of sleep, REM sleep is the stage of sleep most highly associated with dreaming. It has therefore been suggested that the purpose of the MUSCLE PARALYSIS experienced during REM may be to PREVENT us from ACTING OUT our dreams in real time while we sleep.

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REM BEHAVIOUR DISORDER (RBD)

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Some people do appear to act out their dreams.

behave in ways similar to cats who have undergone lesions of the LOCUS COERULEUS, a nucleus of the PONS that seems to be involved in the regulation of REM paralysis.

Lesioned cats also appear to be acting out their dreams, pawing and meowing during REM sleep.

RBD has an onset of post-50 years of age and is sometimes associated with the early stages of PARKINSON'S disease.

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Restorative or Recuperation Theories

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Sleep is necessary to maintain the physiological processes that are required for the brain and body to function normally and is therefore necessary for survival.

Sleep is triggered by a departure from physiological homeostasis and not by a biorhythm.

Sleep provides a period of RELATIVE INACTIVITY and therefore allows the body and brain to RECOVER from the day’s wear and tear of waking activities.

Proponents of these theories of sleep argue that the CORTICAL ACTIVITY that occurs while we are AWAKE, such as that involved in PROCESSING SENSORY INFORMATION, MEMORY & THINKING, requires energy and results in CELLULAR CHANGES.

Since these cortical functions are DIMINISHED during SLEEP, proponents have concluded that CELLULAR REST & REPAIRS are made during sleep.

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Circadian or Evolutionary Theories

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Sleep provides relative safety from nocturnal predators and conserves energy and therefore has survival value.

Sleep is triggered by a biological mechanism and is based on a (circadian) biorhythm and not a biological need.

Proponents of these theories argue that sleep has SURVIVAL VALUE in that it CONSERVES ENERGY and keeps animals safer than they would be running around in the open and exposing themselves to predators.

This is especially important during times when FOOD supplies are LOW (increased likelihood for predation and increased need to conserve energy from limited food supplies).

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Three theories of dreaming

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The PSYCHODYNAMIC THEORY

the COGNITIVE THEORY

the ACTIVATION-SYNTHESIS THEORY.

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ACTIVATION-SYNTHESIS THEORY

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dreams are the SIDE-EFFECTS of SPONTANEOUS NEURAL FIRING at the sub-cortical levels which are then INTERPRETED by higher cortical centers.

Remember, our brains do not ‘shut off’ while we sleep consequently, the cortex continues with its day job of making sense out of neural signals, whatever they may be.

This may account for the disjointed, random and sometimes bizarre content and nature of dreams.

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Four main brain systems have been implicated in the regulation of sleep.

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1) the FOREBRAIN
2) the RETICULAR FORMATION
3) the PONS
4) the HYPOTHALAMUS.

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The forebrain seems to promote SLOW WAVE SLEEP by ...

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releasing GABA (recall that GABA is an inhibitory neurotransmitter) and would apparently, continue to do so indefinitely if it weren’t for the reticular formation.

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The role of the reticular formation in sleep seems to be ...

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to ‘wake up’ the forebrain bringing an end to SWS and thereby earning its alternate name of ‘reticular activating system.’

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role of pons in REM sleep

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It seems to control the muscle paralysis that generally accompanies REM sleep.

Not surprisingly, injury to the brainstem, including the pons, is often accompanied by COMA and damage to a nucleus of the pons called the LOCUS COERULEUS in cats, leads to the loss of muscle paralysis during REM sleep as already mentioned.

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Role of hypothalamus in sleep

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neurons in the hypothalamus that produce a neuropeptide called HYPOCRETIN, send out axons to the pons, reticular formation and forebrain

The destruction of hypocretin-producing neurons seems to cause the sleep disorder NARCOLEPSY in which patients lapse directly and uncontrollably into REM sleep.

On the basis of these and related findings, it has been proposed that the hypothalamus may have a role in preventing the transition from wakefulness directly into REM sleep.

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VISUAL AGNOSIA

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unable to RECOGNIZE or IDENTIFY common visual objects despite being fully able to SEE THEM.

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PROSOPAGNOSIA

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inability to recognize FACES. This disorder is thought to arise from damage to the VISUAL ASSOCIATION AREAS of the TEMPORAL CORTEX which we will discuss later.

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Sensation

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the process of DETECTING the PRESENCE of a STIMULUS

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Perception

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the process of INTERPRETATION of that STIMULUS.

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Our ability to experience the visual world in three dimensions is the result of

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DEPTH/DISTANCE CUES such as RETINAL DISPARITY among others.DEPTH/DISTANCE CUES such as RETINAL DISPARITY among others.

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he RETINAL IMAGE of the visual stimulus is 2-DIMENSIONAL but our perception of that visual stimulus is

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3 dimensional

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The RETINAL IMAGE of the visual stimulus is an UPSIDE-DOWN and REVERSED image of the actual stimulus. This is the result of ...

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the fact that the light reflected from the visual stimulus and arriving at our eyes, travels in straight lines.

yet our perception of the visual stimulus is RIGHT SIDE UP and UN-REVERSED.

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Our ability to experience the visual world without a hole in the center of it is a result of the fact that ...

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our sensory apparatus fills in the missing information by extrapolating from the information surrounding the blindspot.

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The RETINAL IMAGE of a moving visual stimulus CHANGES SHAPE, SIZE and COLOUR under various MOVEMENT and LIGHTING conditions, yet we perceive the visual stimulus ...

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as CONSTANT with respect to all three of these characteristics.

These are referred to as PERCEPTUAL CONSTANCIES.

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Light waves are reflected by the visual stimulus and travel to the eye, where they are projected onto the...

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retina

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sclera

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the elastic membrane that serves as the outer cover of the eye.

This is what we see as the white of the eye.

The sclera maintains the shape of the eye from the pressure of the liquid in the eye (the aqueous and vitreous humours) ---like the skin of a grape.

Front 75

cornea

Back 75

the transparent bulge at the front of the eye that acts as a fixed lens, letting light in and focusing it a little.

Front 76

iris

Back 76

the colored ring within the cornea which gives us our eye color.

The iris is home to the muscles that control the amount of light entering the eye by constricting and dilating the pupils, like a camera aperture.

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pupil

Back 77

the whole in the centre of the iris.

The pupil gets larger (dilates) or gets smaller (constricts) to control the amount of light entering the eye.

Our pupils adjust according to the amount of light available to the eye---constricting in bright sunlight to keep out harmful rays and dilating in dim light to gather more light.

They also dilate when we are INTERESTED in something, functioning to gather as much light (i.e., information) from the subject of our interest as possible.

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lens

Back 78

located behind the pupil and changes shape to focus the light on the back of the eyeball where the retina is located.

A set of muscles called the ciliary muscles change the shape of the lens to accommodate to the distance of the observed subject.

The lens is normally round for viewing close objects, and flattened out for viewing distant objects.

Front 79

retina

Back 79

The “screen of neural elements” at the back of the eye. This is about as thick as a piece of paper, on which the light reflected form the visual stimulus is focused.

Front 80

Olfaction receptors

Back 80

the receptor organ is the NOSE and in it are the OLFACTORY CILIA, which are the receptor cells for olfaction.

Front 81

Gustation receptors

Back 81

receptor organ is the TONGUE and on it are the TASTE BUDS, which are the receptor cells for gustation.

Front 82

Audition receptors

Back 82

the receptor organ is the EAR and in it are the AUDITORY CILIA, which are the receptor cells for audition.

Front 83

Somatosensation receptors

Back 83

the receptor organ is the SKIN and on it are a number of different receptor cells such as FREE NERVE ENDINGS which are receptive to PAIN and TEMPERATURE.

Front 84

Vision receptors

Back 84

receptor organ is the EYE and in it are the RODS AND CONES which are the receptor cells for vision.

Front 85

The type of energy used by the nervous system is ...

Back 85

ELECTRICAL, taking the form of an ACTION POTENTIAL, and CHEMICAL, taking the form of NEUROTRANSMITTERS.

Front 86

***TRANSDUCTION***

Back 86

The conversion of environmental energy into biochemical energy that can be used by the nervous system.

takes place in the receptor cell.

Front 87

Type of energy for Gustation and Olfaction in transduction (environmental energy into biochemical)

Back 87

various CHEMICALS carried by the AIR or contained in FOOD fit themselves into receptors of various shapes to activate the neural response, resulting in the perception of TASTE and SMELL.

The environmental energy involved here = CHEMICAL ENERGY

Front 88

Type of energy for Audition in transduction (environmental energy into biochemical)

Back 88

AIR PRESSURE WAVES displace the AUDITORY CILIA, activating the neural response and resulting in the perception of SOUND.

The environmental energy involved here = MECHANICAL ENERGY.

Front 89

Type of energy for Somatosensation in transduction (environmental energy into biochemical)

Back 89

tissue damage releases a CHEMICAL that functions as a NEUROTRANSMITTER activating the nerve endings directly and resulting in the perception of PAIN.

The environmental energy involved here = CHEMICAL & MECHANICAL ENERGY.

Front 90

Type of energy for Vision in transduction (environmental energy into biochemical)

Back 90

LIGHT WAVES are converted into chemical energy in the RODS and CONES which are located in the RETINA of the eye, resulting in the perception of SIGHT.

The environmental energy involved here = ELECTROMAGNETIC ENERGY.

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SENSORY ADAPTATION OR HABITUATION

Back 91

This ability to “TUNE OUT” constant stimuli

Front 92

WHY doesn’t your vision DISSAPEAR after you have been staring at the same stimulus for a few minutes the way a CONSTANT SMELL or SOMATOSENSATION does after you have been smelling or feeling the same stimulus for a few minutes?

Back 92

The ANSWER lies in the fact that you DO NOT actually FIXATE upon the visual scene you THINK you are fixating upon. The visual system has ADAPTED TO COMPENSATE for this tendency to filter out the visual scene if we stare at it for too long by having the EYE continually SCAN the visual field with a SERIES of VERY SMALL MOVEMENTS.

These movements are called SACCADES. They result in about 3 BRIEF FIXATIONS of the eyes every second or so. In this way, new visual receptors are being stimulated with each new fixation as opposed to the same receptors being continually stimulated which would result in the disappearance of the visual scene (ANALOGY: computer screen savers). The visual system then INTEGRATES (called TEMPORAL INTEGRATION because it is happening over time) these FIXATIONS to create a stable perception of the visual scene you are looking at.

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3 layers of retina

Back 93

·photoreceptors (rods and cones) = first layer
·horizontal, bipolar, and amacrine cells = second layer
·ganglion cells = third layer

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Why are the RODS and CONES are located at the BACK of the eye?

the LIGHT must PASS THROUGH all the cells (ganglion, amacrine, bipolar and horizontal cells) before reaching them.

Back 94

the rods and cones REQUIRE A LOT OF OXYGEN in order to TRANSDUCE the incoming electromagnetic energy into a neural signal that can be used by the nervous system, so they must be in CLOSE PHYSICAL PROXIMITY to the BLOOD VESSELS of the eye which are carrying this oxygen.

Since the blood vessels are LOCATED in the EPITHELIUM at the BACK of the eye, the rods and cones must also locate themselves at the back of the eye

Front 95

cells that begin the process of ORGANIZATION & AMALGAMATION of all of the signals generated by the RODS and CONES.

Back 95

The BIPOLAR, HORIZONTAL & AMACRINE CELLS

Front 96

why the RETINA is considered to be part of the CNS

Back 96

the processing of the visual signal has already begun at the level of the retina by The BIPOLAR, HORIZONTAL & AMACRINE CELLS

Front 97

The GANGLION CELLS TRANSMIT the visual signal to the brain via the:

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optic nerve

Front 98

blind spot

Back 98

The point at which the axons of the ganglion cells come together to form the OPTIC NERVE and EXIT EACH EYE is of course, devoid of any rods and cones and is the location of the BLIND SPOT (since without any rods or cones, no light energy following on this area of the retina can be transduced)

Front 99

The TOP-DOWN THEORY of visual perception

Back 99

states that we perceive form by FIRST developing a PERCEPTUAL HYPOTHESIS about what the visual stimulus is (based upon previous experience, memory, expectations, etc) and THEN sort of ‘FIT IN’ the individual FEATURES of the stimulus to MATCH this hypothesis.

Front 100

The PERCEPTUAL HYPOTHESIS

Back 100

is formed by applying the GESTALT principles (e.g., proximity, closure, simplicity, etc) to the individual features of the visual stimulus, resulting in a complete, continuous perception of the WHOLE VISUAL STIMULUS.

Front 101

how many rods in each eye?

Back 101

between 115 - 120 MILLION RODS and 5 - 7 MILLION CONES in each eye

Front 102

Where are rods spread?

Back 102

spread over the whole retina, except for the fovea (center of retina), where there are essentially no rods at all and are consequently primarily responsible for PERIPHERAL VISION

Front 103

Where are cones spread?

Back 103

concentrated in the fovea of the eye and are consequently primarily responsible for CENTER VISION ---i.e., vision in which the “eye is squarely centered on the subject of interest.”

Front 104

The axons of only about 800,000 GANGLION CELLS (NOT rods and cones) actually leave the eye in the optic nerve. This means that ...

Back 104

there are approximately 15 photoreceptors to 1 ganglion cell conveying the visual information to the brain.

The signals from the RODS and CONES are COMBINED in various ways by the MIDDLE LAYER of cells in the retina (this is the processing I referred to earlier taking place by the bipolar, horizontal, and amacrine cells and the reason for the inclusion of the retina in CNS) and the resulting amalgamated signals are sent to the brain via the ganglion cells.

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***RECEPTIVE FIELD***

Back 105

The area of the visual field within which it is possible for a visual stimulus to influence the responses of one particular cell.


Since each ganglion cell carries a signal that is an AMALGAMATION of the signals of about 15 or so photoreceptors, each ganglion cell “DESCRIBES” a spot on the retina where those 15 or so photoreceptors “live.” That “SPOT” on the retina to which the ganglion cell responds is referred to as the RECEPTIVE FIELD of that ganglion cell.

Front 106

Consequently, a typical ganglion cell can respond to a change in the intensity of a stimulation in its RECEPTIVE FIELD by either ...

Back 106

INCREASING its rate of firing ABOVE that of its BASELINE ACTIVITY or by DECREASING its rate of firing BELOW that of its BASELINE ACTIVITY.

Front 107

The typical RECEPTIVE FIELD of the ganglion cell is approximately CIRCULAR in shape and falls into one of 2 RESPONSE CATEGORIES. This means that...

Back 107

the ganglion cell corresponds to a small circular area on the retina and its firing activity takes the form of one of 2 possible PATTERNS.

1. ON-CENTER CELLS
2. OFF-CENTER CELLS

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ON-CENTER CELLS

Back 108

respond to light in the CENTRAL REGION of their receptive fields with an ON-RESPONSE (the firing rate of these cells INCREASES when light falls anywhere in the CENTER of their receptive fields and DECREASES when that light is turned off) AND...

They respond to light in the PERIPHERY of their receptive fields with an OFF-RESPONSE (the firing rate of these cells DECREASES when light falls anywhere in the PERIPHERY of their receptive fields and INCREASES when that light is turned off).

Front 109

OFF-CENTER CELLS

Back 109

demonstrate the opposite pattern to on-center cells. They respond to light anywhere in the CENTRAL REGION of their receptive fields with an OFF-RESPONSE AND...

to light anywhere in the PERIPHERY of their receptive fields with an ON-RESPONSE.


As a result of this RESPONSE PATTERN, GANGLION CELLS respond best to CONTRAST between the center and periphery of their receptive fields. Therefore, the most effective way to influence the firing rate of an ON- or OFF-CENTER CELL is to illuminate either the entire center or the entire surround while leaving the other region entirely dark.

Front 110

***HIERARCHICAL ORGANIZATION***

Back 110

The organization of the cortex such that each subsequent projection area performs progressively more complex analyses of the stimulus.


The receptive fields of the majority of cells in the PRIMARY VISUAL CORTEX (cells here are called SIMPLE and COMPLEX cells) are MORE COMPLEX than those of ganglion cells, processing increasingly more specific information about the visual stimulus in keeping with one of several principles of organization of the sensory system: The principle of HIERARCHICAL ORGANIZATION.

Front 111

***PARALLEL PROCESSING***

Back 111

The organization of the cortex such that unique information about the same sensory stimulus is simultaneously passed from one hierarchical level to the next through independent pathways.

Front 112

PRIMARY VISUAL PATHWAY

Back 112

From the Retina to the Brain:

Approximately 80% of the visual signals take the PRIMARY VISUAL PATHWAY, following the GENICULOSTRIATE system.

After leaving the eye, this pathway goes to the lateral geniculate nucleus (LGN) in the THALAMUS.

From the thalamus, it proceeds to the PRIMARY VISUAL CORTEX in the OCCIPITAL LOBES (called the striate cortex).

Front 113

SECONDARY VISUAL PATHWAY

Back 113

From the Retina to the Brain:

The remaining 20% of the visual signals take a SECONDARY VISUAL PATHWAY, following the TECTOPULVINAR system.

After leaving the eye, this pathway goes to an area in the BRAINSTEM called the TECTUM (specifically to the SUPERIOR COLLICULI there) and then on to a part of the THALAMUS called the PULVINAR NUCLEUS.

From the thalamus, the SECONDARY PATHWAY ALSO goes to the VISUAL CORTEX in the OCCIPITAL LOBES, but NOT to the primary visual cortex, rather it goes to DIRECTLY to the SECONDARY VISUAL AREAS.

Front 114

the PARVO and MAGNO CHANNELS

Back 114

Visual signals FOLLOWING THE PRIMARY VISUAL PATHWAY via the GENICULATESTRIATE system further SEPARATE into 2 pathways: the PARVO and MAGNO CHANNELS.

Front 115

The PARVO channel

Back 115

flows through the TOP 4 LAYERS of the thalamus, called the PARVOCELLULAR or P-LAYERS (hence the name 'PARVO') because the cell bodies of the cells comprising these layers are relatively SMALL (parvo = small).

carries information about the COLOUR, FORM and PATTERN DETAIL of STATIONARY or SLOW-MOVING objects and

ORIGINATES primarily in the CONES of the RETINA, FEEDING the VENTRAL STREAM or WHAT? PATHWAY we discussed earlier, and ultimately terminating in TEMPORAL tertiary or association cortex.

Front 116

The MAGNO channel

Back 116

flows through the BOTTOM 2 LAYERS of the thalamus, called the MAGNOCELLULAR or M- LAYERS (hence the name 'MAGNO') because the cell bodies of the cells comprising these layers are relatively LARGE (magno = large).

carries information about the MOVEMENT of objects and

ORIGINATES primarily in the RODS of the RETINA, FEEDING the DORSAL STREAM or WHERE? PATHWAY we discussed earlier, and ultimately terminating in PARIETAL tertiary or association cortex.

Front 117

Hierarchical organization of eyes

Back 117

EYES



THALAMUS
(LGN)


1° CORTEX
(STRIATE CORTEX)


2° CORTEX 2° CORTEX
(PRE-STRIATE CORTEX) (INFERO-TEMPORAL CORTEX)


3° CORTEX 3° CORTEX
(PARIETAL LOBE) (TEMPORAL LOBE)

Front 118

PRIMARY SENSORY CORTEX

Back 118

the part of the cortex that receives information relayed from the appropriate sense FIRST through the THALAMUS and thus has the MOST DIRECT connection to the sensory organ.

Front 119

OCCIPITAL CORTEX

Back 119

In the case of vision, this area of the OCCIPITAL CORTEX has the most DIRECT CONNECTION to the EYES and receives VISUAL INFORMATION from them before any other areas of the cortex do.

Front 120

The primary visual cortex

Back 120

the most POSTERIOR ASPECT of the OCCIPITAL LOBES and much of it is TUCKED into the LONGITUDINAL FISSURE. Because of its STRIATED or BANDED APPEARANCE, the primary visual cortex is sometimes referred to as the STRIATE CORTEX.

Front 121

SECONDARY CORTEX

Back 121

The primary cortex sends its information on to the SECONDARY CORTEX, therefore the secondary cortex receives much of its information from the primary cortex but it is also highly interconnected within itself and so receives information from other areas of the secondary cortex.

There are 2 AREAS of SECONDARY VISUAL CORTEX: The first of these areas is located in the OCCIPITAL LOBE, directly ABOVE the primary visual cortex. This area is called the PRESTRIATE CORTEX (“pre” = before).

The second of these areas is located in the TEMPORAL LOBES, comprising a BAND of cortex at the BOTTOM of the temporal lobes called the INFEROTEMPORAL CORTEX (“infero” = below)

Front 122

TERTIARY CORTEX or ASSOCIATION CORTEX.

Back 122

The secondary cortex sends its information on to the TERTIARY CORTEX or ASSOCIATION CORTEX.

This THIRD area of cortex is called association cortex because it receives information from MORE THAN ONE SENSE. Hence the visual information arriving at the VISUAL ASSOCIATION CORTEX is thought to be associated/integrated here with information from other sensory modalities about that stimulus.

VISUAL ASSOCIATION CORTEX is located in SEVERAL AREAS of the cortex. One LARGE area of visual association cortex is located at back of the PARIETAL LOBES and is called the POSTERIOR PARIETAL CORTEX.

Another area is in the TEMPORAL LOBES.

Front 123

Evidence for Hierarchical Organization

Back 123

LESION STUDIES. DEFICITS that arise when the various levels are damaged are informative as to the function of each of the levels.

For example, if the EYES (which perform the basic sensory function) are removed/damaged such that the subject no longer receives visual stimulation, the subject is ENTIRELY UNABLE TO SEE. This kind of DAMAGE results in deficits that are comparatively LOW in COMPLEXITY, i.e., ALL visual function is lost.

But if the VISUAL ASSOCIATION CORTEX is damaged, the subject displays very specific and often bizarre visual deficits such as the PROSOPAGNOSIA previously discussed and others. This kind of DAMAGE results in deficits that are comparatively HIGH in COMPLEXITY, i.e., only SOME visual function is lost.

Front 124

***FUNCTIONAL SEGREGATION***

Back 124

The organization of the cortex such that different areas of the same hierarchical level process different aspects of the same sensory stimulus.


not all of the areas of each level of cortex are involved in processing the same information. There appears to be some FUNCTIONAL SPECIALIZATION within each of the levels of the cortex such that SPECIFIC areas are involved in the processing of specific aspects of the SAME SENSORY STIMULUS.

Front 125

Evidence for Functional Segregation

Back 125

STIMULATION STUDIES.

When certain cells within the PRIMARY VISUAL CORTEX are stimulated, they respond PREFERENTIALLY to COLOUR information while others respond PREFERENTIALLY to ORIENTATION information.

The DISCOVERY of this type of FUNCTIONAL SEGREGATION in the VISUAL CORTEX won DAVID HUBEL and TORSTEN WIESEL a NOBEL PRIZE in 1981.

Front 126

An example of PARALLEL PROCESSING in vision

Back 126

DORSAL and VENTRAL STREAMS of processing which are thought to carry SEPARATE INFORMATION about the characteristics of the visual stimulus.

The DORSAL STREAM carries information about MOVEMENT and LOCATION of the visual stimulus while the VENTRAL STREAM carries information about COLOUR and FORM of the same visual stimulus


These 2 streams are also sometimes called the ‘WHAT?’ and ‘WHERE?’ PATHWAYS.
Since COLOUR and FORM aid in the IDENTIFICATION of the visual stimulus, the VENTRAL STREAM has been called the ‘WHAT?’ pathway. Since MOVEMENT aids in the LOCATION of the visual stimulus in SPACE, the DORSAL STREAM has been called the ‘WHERE?’ pathway.

Front 127

***PARALLEL PROCESSING***

Back 127

The organization of the cortex such that unique information about the same sensory stimulus is simultaneously passed from one hierarchical level to the next through independent pathways.



Since DIFFERENT AREAS WITHIN EACH OF THE LEVELS of CORTEX are processing and passing on DIFFERENT INFORMATION about the SAME VISUAL STIMULUS, functional segregation implies the CO-EXISTENCE OF MORE THAN ONE PATHWAY carrying information between the various hierarchical levels of the cortex. This is referred to as PARALLEL PROCESSING. When information is processed in parallel through multiple pathways, it flows through the levels of the sensory system rapidly and decreases the reliance of the system on any one level of processing (think of a string of Christmas lights that are wired together in parallel---if one bulb goes out, the remaining bulbs are still lit---i.e., "information" from each bulb on the string travels independently but simultaneously, to/from the electric outlet). What follows is a very basic 'projection diagram' of visual information traveling along parallel pathways.

Front 128

Evidence for Parallel Processing:

Back 128

from patients with ISOLATED DAMAGE to one stream or the other.

Patients with damage to the DORSAL STREAM (this stream terminates at association cortex in the PARIETAL LOBES) have difficulty REACHING ACCURATELY for objects in space but have NO difficulty DESCRIBING those objects.

Patients with damage to the VENTRAL STREAM (this stream terminates at association cortex in the TEMPORAL LOBES) have difficulty DESCRIBING objects but have NO difficulty REACHING ACCURATELY for those objects (e.g., Dr. P. and prosopagnosia).

Front 129

***Retinotopic Representation***

Back 129

An organizational principle of the visual system in which the spatial relationships between the stimuli comprising the original retinal image are maintained at all levels of the visual system.


the RETINAL IMAGE is MAPPED onto the PRIMARY VISUAL CORTEX in a way that MAINTAINS the RELATIVE PROXIMAL RELATIONSHIPS of the individual aspects of the retinal image.

the MAP of the retinal image at the primary visual cortex is DISTORTED somewhat, designating more cortical space to the FOVEA than the fovea actually occupies on the retina.


This DISPROPORTIONATE organization of the visual cortex presumably exists for REASONS SIMILAR to those of the somatosensory and motor cortex distortions.

That is, the fovea contains the CONES which are the receptors that provide the most DETAILED information about the visual stimulus just as the HANDS and FACE of the homunculi represent the most SENSITIVE parts of the body.

Front 130

Evidence for Retinotopic Organization:

Back 130

patients who have sustained INJURIES to areas of the PRIMARY VISUAL CORTEX.

Specific lesions to the primary visual cortex are associated with specific deficits in the patient’s visual field, called SCOTOMAS.

The larger the area of the lesion in the cortex, the larger the area of vision affected thereby maintaining the PROXIMAL RELATIONSHIPS between FEATURES of the visual stimulus as REPRESENTED in the RETINAL IMAGE.

Visual deficits like these are referred to as incidents of CORTICAL BLINDNESS to distinguish them from incidents of blindness that are the result of an injury to the eye or the optic nerve.

Front 131

NEUROLOGICAL DISORDERS

Back 131

primarily defined by the PHYSICAL CONDITIONS of the BRAIN that underlie them. That is, we CLASSIFY such illnesses according BIOLOGICAL CRITERIA.

Front 132

PSYCHIATRIC DISORDERS

Back 132

primarily defined by the BEHAVIOURAL CONDITIONS that characterize them. That is, we CLASSIFY such illness according to PSYCHOLOGICAL CRITERIA.

Front 133

eight MAJOR classifications of NEUROLOGICAL DISORDERS:

Back 133

1. TUMOURS

2. SEIZURE DISORDERS (also known as epilepsy)

3. CEREBROVASCULAR DISORDERS (also known as strokes)

4. DEVELOPMENTAL DISORDERS

5. DEGENERATIVE DISORDERS

6. INFECTIOUS DISORDERS

7. CLOSED-HEAD INJURIES

8. NEUROTOXINS

Front 134

Tumours are typically named after...

Back 134

Tumours are typically NAMED after the REGION of the brain in which they are located. A MENINGIOMA, for example, is located in the cells of the MENINGES and is therefore ENCAPSULATED.

Front 135

Infiltrating tumours

Back 135

grow into and throughout the neural tissue. Infiltrating tumours can be tricky to remove as it is difficult to know when the entire tumour has been excised from healthy tissue.

Front 136

The SYMPTOMS of a brain tumour DEPEND on ...

Back 136

exactly where in the brain it is located and which surrounding structures it exerts PRESSURE on.

People with tumours in an area of the PONS for example, known as the LOCUS COERULEUS do not appear to be inhibited during REM SLEEP and VIOLENTLY act out their DREAMS at night. People with tumors in the Broca's or Wernicke's areas (recall that these are the areas of the brain that mediate language) have various difficulties producing and/or understanding language.

Front 137

Benign tumours

Back 137

Tumours that ARE NOT LIKELY TO RECUR after removal

Front 138

malignant tumours

Back 138

Tumours that ARE LIKELY TO RECUR after removal

Front 139

METASTATIC tumours

Back 139

tumours that have grown in a region of the body other than that of the originating tumour.

Metastatic tumours break off the original tumour and travel to other parts of the body via the BLOODSTREAM.

Once there, they grow to form a secondary tumour. Many METASTATIC BRAIN tumours ORIGINATE as CANCER of the LUNG.

Front 140

CHEMOTHERAPY to treat malignant brain tumours has NOT BEEN VERY SUCCESSFUL to date, largely due to ...

Back 140

the DIFFICULTY of getting the necessary drugs to PASS the BLOOD-BRAIN BARRIER and thereby get to the tumour itself.

Front 141

after the uterus, the most common site of tumours is...

Back 141

the brain

Front 142

GRAND MAL (literally “big trouble”) seizures

Back 142

seizure disorders with VIOLENT, PHYSICAL CONTORTIONS of the body

Front 143

PETITE MAL (“little trouble”).

Back 143

seizures that DO NOT actually involve violent contortions of the body

Front 144

Seizure disorders are characterized by

Back 144

excessive electrical activity of the neurons.

The activity typically begins in a particular region of the brain (the “focus”) and can spread from there to involve other areas of the brain. The further it spreads, the more PROFOUND the seizure gets.

see: generalized and partial seizures

Front 145

generalized seizures

Back 145

Seizures involving the entire brain

Front 146

partial seizures

Back 146

seizures that remain restricted in one particular hemisphere or region of the brain

Front 147

aura (before seizure)

Back 147

can alert the patient to the oncoming seizure. The aura can take a variety of forms, depending in part on the location of the electrical activity in the brain.

Front 148

Seizures that have their ORIGINS in the TEMPORAL LOBES (where many seizures begin) are often associated with

Back 148

changes in emotional states, such as feelings of foreboding, dread, or elation.

These patients also often carry out a particular simple behaviour (e.g. buttoning and unbuttoning an article of clothing), over and over again.

Front 149

COMPLEX PARTIAL SEIZURES

Back 149

often preceded by aura

often associated with changes in emotional states, such as feelings of foreboding, dread, or elation.

often carries out a particular simple behaviour (e.g. buttoning and unbuttoning an article of clothing), over and over again. Repetitive behaviours such as this as referred to as AUTOMATISMS and relatively COMPLEX seizures such as these are (not surprisingly) referred to as COMPLEX PARTIAL SEIZURES.

Front 150

SIMPLE PARTIAL SEIZURES.

Back 150

less complex seizures involving only primary motor or sensory symptoms are (equally unsurprisingly)

Front 151

CEREBROVASCULAR DISORDERS

Back 151

generally referred to as STROKES.

They involve either the BLOCKAGE or BREAKAGE of BLOOD VESSELS in the brain, or are sometimes more TRANSIENT in nature due to a TEMPORARY blockage of a blood vessel.

Front 152

OBSTRUCTIVE STROKE

Back 152

A stroke resulting from a BLOCKED blood vessel

Front 153

HEMORRHAGIC STROKE

Back 153

a stroke resulting from a BROKEN blood vessel

Front 154

ANEURYSM

Back 154

can cause stroke.

An aneurysm refers to the BURSTING of a blood vessel in the brain as a result of reduced ELASTICITY in its wall.

The area of the vessel swells in response to increases in blood pressure until the pressure becomes too great and then it BURSTS.

Front 155

THROMBOSIS

Back 155

can cause stroke.

some of the blood in a vessel has COAGULATED to form a PLUG or CLOT that has remained at the place of its formation and is now OBSTRUCTING blood flow from areas of the brain further down from the clot.

A THROMBOSIS therefore, is a STATIONARY blood clot.

Front 156

EMBOLISM
(Cerebrovascular disorder)

Back 156

a CLOT or PLUG that has traveled through the blood from a larger vessel into a smaller one downstream from its origin, where it now obstructs blood from reaching areas in the brain downstream from it.

An EMBOLISM therefore, is a MOBILE blood clot.

Front 157

TRANSIENT ISCHEMIA
(Cerebrovascular disorder)

Back 157

can occur when a blood vessel in the brain becomes temporarily blocked.

During the blockage, the patient experiences the symptoms associated with disruption of blood flow to the particular brain area affected however, the blockage resolves itself before the affected vessel bursts or the affected brain tissue dies.

Hence, the symptoms disappear once the disruption passes because the affected tissue recovers and resumes its prior function.

Front 159

FETAL ALCOHOL SYNDROME (FAS)

Back 159

an example of a developmental neurological disorder that results from exposure to alcohol during pregnancy.

The exact amount of alcohol necessary to cause fetal alcohol syndrome is still under DEBATE.

Characteristics of children with FAS include unusually wide spacing between the eyes, flat midfaces, short noses, thin upper lip, lower IQ’s, hyperactivity and related social problems.

Front 160

Phenylketonuria (PKU).

Back 160

Developmental neurological disorders can also be INHERITED. Examples include Phenylketonuria (PKU).

Patients with PKU DO NOT have the ENZYME necessary to metabolize the AMINO ACID PHENYLALANINE.

This enzyme is required for the successful myelinization process. Since much of the brain’s myelinization occurs in the months immediately following birth, the brains of children born with PKU fail to develop normally.

Unless treated, PKU results in severe mental retardation.

PKU TESTING is MANDATORY in Canada on birth.

Front 161

Still other developmental neurological disorders are CONGENITAL (i.e., present at birth) but are neither HEREDITARY nor LINKED to particular toxins. One such example is

Back 161

DOWN’S SYNDROME.

Front 162

down's syndrome

Back 162

Down’s syndrome is caused by the presence of an extra 21st chromosome. As in FSA, symptoms include both physical and intellectual manifestations.

Front 163

DEGENERATIVE NEUROLOGICAL DISORDERS:

Back 163

Degenerative neurological disorders get PROGRESSIVELY WORSE over time as neural tissue DEGENERATES (hence the name “degenerative disorders”).

Examples include ALZHEIMER’S disease, PARKINSON’S disease, MULTIPLE SCLEROSIS and HUNTINGTON’S disease.

Front 164

ENCEPHALITIS

Back 164

ENCEPHALITIS refers to an infection of the brain.

Encephalitis can be caused by a variety of AGENTS including VIRUSES, BACTERIA, FUNGI, or other PARASITES.

Front 165

NEUROTROPIC VIRUSES

Back 165

Viruses that have a special affinity for cells of the central nervous system

Front 166

PANTROPIC VIRUSES.

Back 166

Viruses that attack body tissues with no special affinity for tissue of the CNS

Front 167

MENINGITIS

Back 167

infection of the MENINGES and can be caused by VIRUSES or BACTERIA.

Front 168

POLIO & RABIES

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types of VIRAL infections that attack the brain.

The polio virus affects the MOTOR NEURONS of the brain and spinal cord, leading to PARALYSIS.

RABIES virus affects the cells of the CEREBELLUM and HIPPOCAMPUS. Rabies patients are often described as going “MAD” demonstrating a number of disturbing emotional symptoms (hippocampus---limbic system).

VACCINES for both infections are available.

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NEUROSYPHILIS

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a BACTERIAL infection of syphilis that migrates to the CNS in the later stages of the illness.

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CLOSED-HEAD INJURIES

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Closed-head injuries refers to injury to the brain that occurs when there is trauma to the head in which the brain itself is not penetrated.

This often results in a build-up of blood from underlying brain tissue that cannot escape the confines of the skull and consequently, creates pressure on the softer brain tissue, causing damage and/or death of neural tissue.

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HEMATOMA (bruise)

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localized collection of clotted blood in the brain due to injury of brain tissue and bleeding into the brain.

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CONCUSSION

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disturbance of consciousness with no hematoma thought to be due to a TEMPORARY DISRUPTION of the neural circuits of the brain.

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PUNCH-DRUNK SYNDROME

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general intellectual impairment due to additive impact of MULTIPLE CONCUSSIONS over time. This syndrome is often seen in BOXERS who have suffered many head injuries over the course of their fighting careers.

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CONTRE-COUP INJURY

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injury to the brain OPPOSITE to the site of the original impact/injury.

Contre-coup injuries result from the "sloshing" of the brain inside the skull (remember, the brain is bathed in CSF) such that when the skull suffers a blow to one side of the head, the brain sloshes forcefully into the opposite side of the skull and back again as the head moves back and forth from the force of the impact.

If the force of the "counter" impact is strong enough to damage brain tissue, the patient will demonstrate symptoms indicative of brain injury opposite to the location of the original impact.

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MERCURY

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Neurotoxin

Remember the Mad Hatter from Alice in Wonderland ?---He worked with mercury in the process of making hats.

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LEAD

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Neurotoxin

The term ‘Crackpots’ comes from lead leaking out of cracked pottery and poisoning the tea (and consequently also the tea drinker) consumed from the pottery.

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NEUROLEPTICS

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Neurotoxin

Early medications used to treat the psychotic symptoms of schizophrenia caused a MOTOR DISORDER known as TARDIVE DYSKINESIA in which patients are plagued with involuntary movements of the face such as SMACKING and SUCKING of the lips, ROLLING and THRUSTING of the tongue and PUFFING of the cheeks.

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Neurotoxic properties of ALCOHOL

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causes death of the neural tissue in the MAMMILARY BODIES secondary to THIAMINE DEPLETION and can lead to profound and irreversible memory loss (e.g., KORSAKOFF'S DISEASE resulting from prolonged, profound alcohol abuse)

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Neurotoxic properties of ECSTASY

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neurotoxic effects on the SEROTONIN-PRODUCING synapses at high doses.

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*** NEUROPLASTICITY ***

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The ability of neural tissue to undergo physical change in response to injury, the developmental process or experience.

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EXAMPLES of NEUROPLASTICITY

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1. NEURAL DEGENERATION: some aspect of a damaged neuron, DIES BACK following the damage.

2. NEURAL REGENERATION: the regrowth of damaged neurons. Much less frequent in higher vertebrates (e.g., mammals) than in lower vertebrates (e.g., starfish). Non-existent in CNS. Limited in PNS.

3. NEURAL REORGANIZATION: the process by which functions once performed by an area of the brain now damaged, are subsequently performed by another area of the brain.

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DSM-IV CRITERIA FOR SCHIZOPHRENIA

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A. CHARACTERISTIC SYMPTOMS: 2 or more of the following, each present for a significant portion of time during a 1-month period (or less if successfully treated).
1. delusions
2. hallucinations
3. disorganized speech (e.g., frequent derailment or incoherence)
4. grossly disorganized or catatonic behaviour
5. negative symptoms, i.e., affective flattening, alogia, or avolition

B. SOCIAL/OCCUPATIONAL DYSFUNCTION

C. DURATION: Continuous signs of the disturbance persisting for at least 6 months.

D. SCHIZOAFFECTIVE & MOOD DISORDER EXCLUSION

E. SUBSTANCE/GENERAL MEDICAL EXCLUSION

F. RELATIONSHIP TO A PERVASIVE DEVELOPMENTAL DISORDER: If there is a history of autistic disorder or another pervasive developmental disorder, the additional diagnosis of schizophrenia is made only if prominent delusions or hallucinations are also present for at least a month (or less if successfully treated).

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PARANOID SCHIZOPHRENIA

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essential feature is the presence of PROMINENT DELUSIONS OR AUDITORY HALLUCINATIONS in the context of RELATIVELY INTACT COGNITIVE FUNCTIONING AND AFFECT.

Delusions are typically PERSECUTORY or GRANDIOSE.

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DISORGANIZED SCHIZOPHRENIA

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The essential feature is the presence of DISORGANIZED SPEECH, BEHAVIOUR, and FLAT or INAPPROPRIATE AFFECT.

The disorganization often leads to CONSIDERABLE DISRUPTION in the ability of the patient to perform the tasks of DAILY LIVING.

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CATATONIC SCHIZOPHRENIA

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The essential feature is the presence of PSYCHOMOTOR DISTURBANCE that may include either RETARDATION or EXCITATION.

The patient may demonstrate CATALEPSY OR STUPOR, ECHOLALIA (parrot-like repetition of a word/phrase spoken by another), ECHOPRAXIA (repetition by imitation of the movements made by another), MUTISM, BIZARRE POSTURING.

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UNDIFFERENTIATED SCHIZOPHRENIA

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The essential feature is the ABSENCE of the symptoms of PARANOID, DISORGANIZED or CATATONIC schizophrenia, but the PRESENCE of CRITERION A symptoms for schizophrenia

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RESIDUAL SCHIZOPHRENIA

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There must have been AT LEAST one previous EPISODE of schizophrenia but the CURRENT CLINICAL PICTURE does not include PROMINENT SYMPTOMS OF DELUSIONS, HALLUCINATIONS, DISORGANIZED SPEECH OR BEHAVIOUR.

Hence, the patient is currently experiencing a sort-of ATTENUATED VERSION of schizophrenia and has had at least one full-blown episode of schizophrenia in his/her past.

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*** DOPAMINE HYPOTHESIS ***

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The suggestion that some of the symptoms of schizophrenia (primarily positive) may be caused by an excess of dopamine activity in the brains of these patients.

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The dopamine hypothesis forms the basis of ...

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neuroleptic treatment which is the primary treatment for patients with schizophrenia.

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Evidence in support of the dopamine hypothesis:

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1. Treatment with neuroleptics relieves symptoms of schizophrenia. Since these drugs are antagonistic for dopamine, it is reasonable to conclude that the symptoms are related to (if not caused by) too much dopamine activity. The extent to which neuroleptic drugs bind to the D2 receptors is strongly correlated with their antipsychotic efficacy. Atypical neuroleptic medications however, bind preferentially to D1 & D4 receptors and only weakly to D2 receptors.

2. Amphetamine (speed) produces symptoms indistinguishable from those of schizophrenia (paranoia, for example). Since neuroleptic drugs also counteract the symptoms of amphetamine overdose, it reasonable to conclude that the symptoms of amphetamine overdose and schizophrenia are caused by the same (or similar) malfunction.

3. Parkinson’s disease is caused by depletion of dopamine. Patients with Parkinson’s disease are treated with a dopamine precursor (L-Dopa) to replace the lost dopamine. Too much L-dopa produces schizophrenia-like symptoms in these patients (paranoia) and not enough neuroleptic medication causes Parkinson’s-like symptoms in patients with schizophrenia (tremors, stiffness). This suggests that Parkinson’s and schizophrenia represent two ends of some sort of neurochemical (dopamine) continuum.

4. PET scans & post-mortem studies both indicate an increased number of dopamine receptors in the brains of patients with schizophrenia, possibly accounting for the overactive dopamine activity in the brains of these patients.

5. Animal research confirms that neuroleptic medications block dopamine receptors specifically (as opposed to acting on other neurotransmitters generally).

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*** ANATOMIC DEGENERATION HYPOTHESIS***

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The suggestion that some of the symptoms of schizophrenia (primarily negative) may be caused by degeneration or pathology of brain structures in the brains of these patients.

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Evidence in support of the anatomic degeneration hypothesis:

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1. Reduced metabolic activity of the FRONTAL LOBES (associated with attention, motivation and planning/organization of behaviour). PET scans show reduced blood flow to this region. This may also be related to memory deficiency.

2. Increased ventricular volume, particularly in the left hemisphere compared to the right hemisphere. This is thought to indicate brain atrophy, consequently, patients with schizophrenia show increased overall brain atrophy when compared to normal subjects, but the left hemisphere of patients with schizophrenia seems to demonstrate more atrophy than the right hemisphere.

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MOOD DISORDERS IN DSM-IV

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Depressive Disorders
· Major depressive disorder
· Dysthymic disorder
· Depressive disorder NOS

Bipolar Disorders
· Bipolar I disorder
· Bipolar II disorder
· Cyclothymic disorder
· Bipolar disorder NOS

“Other Mood Disorders”
· Mood Disorder due to a General Medical Condition
· Substance-Induced Mood Disorder
· Mood Disorder NOS

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Depressive Disorders

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· Major depressive disorder
· Dysthymic disorder
· Depressive disorder NOS

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Bipolar Disorders

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· Bipolar I disorder
· Bipolar II disorder
· Cyclothymic disorder
· Bipolar disorder NOS

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“Other Mood Disorders”

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· Mood Disorder due to a General Medical Condition
· Substance-Induced Mood Disorder
· Mood Disorder NOS

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MAJOR DEPRESSIVE DISORDER
(mood disorder)

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requires one or more DEPRESSIVE EPISODE (that is symptoms meet those of a depressive episode and last for more than 2 weeks) without a history of mania.

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DYSTHYMIC DISORDER
(mood disorder)

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a CHRONICALLY DEPRESSED mood for “most of the day on most days” with a duration of at least 2 years, but depressive symptoms do not qualify for a major depressive episode.

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BIPOLAR I DISORDER
(mood disorder)

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requires one or more MANIC EPISODE or MIXED EPISODE (that is, criteria are met for BOTH a MANIC & DEPRESSIVE EPISODE during the SAME TIME PERIOD and lasting for greater than 1 week).

A bipolar I disorder can be thus diagnosed even if the individual has never had any previous depressive episodes.

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BIPOLAR II DISORDER
(mood disorder)

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requires one or more DEPRESSIVE EPISODE with one or more HYPOMANIC EPISODE (symptoms identical to those of a manic episode but “are not severe enough to cause marked impairment”).

Bipolar II disorder is thus characterized by a milder form of mania.

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CYCLOTHYMIC DISORDER
(mood disorder)

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is a FLUCTUATION between MANIC and DEPRESSIVE symptoms that are insufficient to meet the criteria for manic or depressive episodes and has a duration of at least 2 years.

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Depression

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thought to be caused by a DECREASE in ACTIVITY in the MONOAMINE NEUROTRANSMITTER SYSTEM. This system involves the neurotransmitters NOREPHINEPHRINE (NE) & SEROTONIN (SE) and to a lesser extent, also DOPAMINE (DA).

The three BRAIN SYSTEMS that use these MONOAMINE neurotransmitters ORIGINATE in the MIDBRAIN or UPPER BRAIN STEM areas and send PROJECTIONS to the LIMBIC SYSTEM and FOREBRAIN.

Two HYPOTHESES were originally proposed REFLECTING the involvement of NE & SE in depression. Both of these are types of MONOAMINE HYPOTHESES (remember that the catecholamines and one of the indolamines---SE---are classed as monoamines).

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***MONOAMINE HYPOTHESIS***

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The suggestion that depression is caused by a decrease in the activity of the monoamine (specifically, NE and SE) system.

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THREE MAJOR CLASSES of DRUG have been developed to treat depression.

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1. Monoamine Oxidase Inhibitors

2. Tricyclic Antidepressants

3. Selective Serotonin Re-uptake Inhibitors (SSRI’s):

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Monoamine Oxidase Inhibitors:

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act to INCREASE monoamine activity by INHIBITING the ENZYME, called monoamine oxidase, that BREAKS DOWN, and thereby, GETS RID OF, the monoamine transmitters.

With this enzyme blocked, monoamine transmitters released into the synaptic cleft will not be METABOLIZED and the LEVEL of the transmitters rise as more of them accumulate in the synaptic cleft.

Monoamine activity at the synapse will continue unless the synapse has some other means of adjusting its activity.

The FIRST MAO inhibitor (iproniazid) to be used was DISCOVERED by ACCIDENT. It was originally developed to treat TUBERCULOSIS but had significant effects on the MOOD of patients.

One of the PROBLEMS with the early MAO inhibitors was that they were NOT VERY SELECTIVE, effecting several of the MONOAMINE TRANSMITTERS simultaneously.

Newer MAO inhibitors are now available that are MORE SELECTIVE, effecting only NE or SE and having little effect on DA.

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Tricyclic Antidepressants:

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The FIRST TRICYCLIC DRUG (imipramine) was DISCOVERED by ACCIDENT during research on ANTIPSYCHOTIC DRUGS.

found to significantly ELEVATE the MOOD of patients. Unfortunately, it did nothing to relieve their PSYCHOTIC SYMPTOMS for which it was originally developed!

The TRICYCLIC drugs act in the same way as COCAINE. They INCREASE MONOAMINE transmitter activity but they accomplish this by blocking the RE-UPTAKE of the transmitters rather than blocking the enzyme that breaks them down.

Like the early MAO INHIBITORS, the TRICYCLIC drugs can also affect all of the MONOAMINE neurotransmitters (that is, NE, SE & DA) but they are generally MORE SELECTIVE than the MAO inhibitors are, with certain tricyclics affecting certain neurotransmitters and not others. This made them an appealing alternative to the MAO inhibitors.

However, the tricyclics also affect the ACETYLCHOLINE synapses, which is thought to be RESPONSIBLE for many of their SIDE EFFECTS.

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Selective Serotonin Re-uptake Inhibitors (SSRI’s):

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SO-CALLED 2nd GENERATION antidepressant drugs.

The SSRI’s DO NOT seem to be MORE EFFECTIVE or to WORK FASTER than the first generation drugs, but they do have FEWER SIDE EFFECTS than either of the first generation drugs, presumably because they affect fewer neurotransmitters.

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PROZAC (fluoxetine)

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The antidepressant drug PROZAC (fluoxetine) is an SSRI and was originally introduced to treat depression in the USA in 1987


It become the focus of CONTROVERSY when the MEDIA began reporting on a number of CASE STUDIES in which it appeared to have caused VIOLENT AGGRESSIVE ACTS & SUICIDE (not good news for a drug that was supposed to DECREASE depression!).

Large scale studies of prozac CONTRADICT these isolated cases, showing that it REDUCES the incidence of suicide and violence.

This is a DIFFICULT ISSUE to settle, since the drug itself is given to depressed and agitated patients who are SUICIDE RISKS before they are assigned the drug. Suicide after taking prozac may therefore reflect a LACK OF EFFECT of the drug in that patient (that is, its ineffectiveness in PREVENTING suicide) not the effect of the drug.

Curiously, PROZAC has also been successfully used in the treatment of OCD. These findings IMPLICATE SEROTONIN and MONOAMINE DRIVEN BRAIN SYSTEMS in ANXIETY DISORDERS.

Similarly, PROZAC has been used with some success to treat people with PARAPHILIAS (patients show sexual arousal in response to atypical stimuli) such as VOYEURISM & FETISHISM.

It is speculated that paraphilias may actually be a form of OCD in that people with paraphilias report having INTRUSIVE, COMPELLING thoughts or urges related to the object of their paraphilia..

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Clive Wearing

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talented musician and composer, who developed a severe case of ENCEPHALITIS (inflammation of the brain) secondary to a herpes infection.

CLIVE suffered massive destruction to his TEMPORAL LOBES, including a complete loss of both HIPPOCAMPI. His primary symptom is ANTEROGRADE AMNESIA but also had retrograde amnesia.

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*** ANTEROGRADE AMNESIA ***

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The loss of memories for events that take place after the event thought to trigger the onset of amnesia.

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*** CONSOLIDATION***

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The process of conversion of information or experience to a long-term memory.

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H.M.

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One of the BEST SCIENTIFICALLY STUDIED cases of MEMORY LOSS

H.M. underwent brain surgery to STOP the spread of severe EPILEPTIC seizures and suffered severe memory disruption as a result.

H.M. was studied for 35 years until his death by a CANADIAN RESEARCHER (among others) DR. BRENDA MILNER.

In the 11 years before his surgery, H.M. suffered at least 1 generalized GRAND MAL SEIZURE per week and several PARTIAL SEIZURES per day. EEG showed that the seizures were originating in the MEDIAL sections of both his TEMPORAL LOBES. In 1953, as a LAST RESORT, surgeons performed a complete BILATERAL MEDIAL TEMPORAL LOBECTOMY on H.M.

Along with his temporal lobes, doctors also removed his HIPPOCAMPUS, a structure in the LIMBIC SYSTEM, which is what is what was primarily thought to lead to his memory loss.

With respect to the EPILEPSY, the surgery was a SUCCESS: The frequency of his seizures dropped to 1 generalized grand mal seizure every 2-3 years, with partial seizures occurring only 1-2 per day. However, with respect to his MEMORY, the surgery was a DISASTER: Although H.M.’s memory for events that came BEFORE the surgery remained relatively INTACT, he was UNABLE to form any NEW MEMORIES after the surgery.

H.M. like CLIVE, suffered from ANTEROGRADE AMNESIA and was UNABLE to form any NEW MEMORIES from that day, in 1953, when he underwent brain surgery, until the END OF HIS LIFE.

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Cases like H.M.’s and Clive's, STRONGLY IMPLICATE

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the HIPPOCAMPUS in memory.

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Jimmie G.

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suffered from the destruction of the MAMMILARY BODIES and damage to areas of the THALAMUS as result of profound alcoholic DEPLETION of vitamin B1 (thiamin).

remained unable to form any new memories for the rest of his life, demonstrating ANTEROGRADE AMNESIA. Unlike H.M. and to a lesser extent, Clive, Jimmie G. also suffered from some RETROGRADE AMNESIA.

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*** RETROGRADE AMNESIA ***

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The loss of memories for events that take place before the event thought to trigger the onset of amnesia.

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IMPLICIT MEMORIES

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refer to memories we have for THINGS or EVENTS despite not being conscious of having such memories.

Evidence for the existence of these memories can therefore not be demonstrated directly but is inferred through improved performance on a previously experience task for example.

IMPLICIT memory seems to be UNAFFECTED by AMNESIA, AGE, DRUGS, TIME between LEARNING & RECALL, and INTERFERENCE

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EXPLICIT memories

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refer to those memories that we are conscious of having a memory for and can therefore express those memories directly verbally or in written format and can be further categorized into two types: SEMANTIC and EPISODIC memories.

affected by IMPLICIT memory seems to be UNAFFECTED by AMNESIA, AGE, DRUGS, TIME between LEARNING & RECALL, and INTERFERENCE

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INFEREOTEMPORAL CORTEX

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(visual association cortex):
Storage of visual memories.

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AMYGDALA (part of the limbic system):

role in memory

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Storage of emotional memories.

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PREFRONTAL CORTEX

role in memory

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Storage of memory for the temporal relationships between events in a sequence and WORKING (short-term) MEMORY.

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CEREBELLUM

role in memory

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Storage for sensorimotor skills.

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STRIATUM (=caudate + putamen of the basal ganglia):

role in memory

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Memory for relationships between stimuli and responses.

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According to the standard consolidation theory (see page 279 of your textbook) SUB-CORTICAL brain structures such as the HIPPOCAMPUS are NOT thought to be involved with MEMORY STORAGE per se, but rather with

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the CONSOLIDATION of memory. That is, it is here that information is thought to be CONVERTED into a MEMORY CODE or TRACE that later becomes a LONG-TERM MEMORY.

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The actual STORAGE of these MEMORY CODES or TRACES is HYPOTHESIZED to occur in the CORTEX, with those areas of the cortex associated with the MODALITY in which the memory was ORIGINALLY EXPERIENCED (e.g., if he original experience was VISUAL, then the memory of it may be “stored” in the visual cortex or OCCIPITAL LOBE). This implies that

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memories are DIFFUSELY STORED THROUGHOUT the cortex involving all of the areas of the cortex that were originally involved when the event that later became the memory was first experienced. This is still all HIGHLY SPECULATIVE.

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Donald Hebb

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famous for---among other things---his introductory use of the term ‘neuropyschology’

hypothesized that SYNAPTIC CHANGE is the FOUNDATION of memory.

He proposed that learning establishes NEURAL CONNECTIONS or CIRCUITS that “REVERBERATE” when they become activated.

Every time the learned response/behaviour is performed, the neural circuit underlying it becomes active. The more you practice something, the more you activate the neural circuit associated with the information.

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***LONG TERM POTENTIATION***

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The LONG-LASTING increase in NEURAL EXCITABILITY at synapses along a specific neural pathway thought to be ASSOCIATED with particular MEMORIES/REFLEXES/MOTOR ACTIONS.


When this occurs, the memory is said to have become consolidated, that is, transferred from SHORT-TERM to LONG-TERM MEMORY.

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Evidence to support neuroplasticity underlying learning:

Animal Research Findings

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Environmental change leading to sensory stimulation effects neural development.

For example, KITTENS that have been DEPRIVED of vision in ONE EYE have FEWER NEURONS in the VISUAL CORTEX associated with the BLOCKED EYE than kittens that have experienced vision in both eyes. RATS raised in ISOLATION and with little stimulation have been shown to have SMALLER CORTICES, LESS DENDRITIC DEVELOPMENT and FEWER SYNAPSES PER NEURON, than rats raised in complex environments and in the company of other rats.

It seems that the old adage “USE IT OR LOOSE IT” applies to the formation of the neural circuitry underlying learning and memory.

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Evidence to support neuroplasticity underlying learning:

Electroshock Therapy to Treat Depression

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The biochemical and anatomical changes in the nervous system that are thought to UNDERLIE learning and memory provide the basis for the RATIONALE in using Electroconvulsive or “Shock” Therapy (ECT) in the treatment of SEVERE CLINICAL DEPRESSION.

In ECT, an ELECTRIC CURRENT is administered to the brain of the afflicted patient. This electrical surge is thought to DISRUPT the NEURAL CIRCUITRY underlying the DEPRESSIVE THINKING, thereby freeing him/her from the experience of depression.

One of the SIDE EFFECTS of ECT is MEMORY LOSS. This should NOT BE SURPRISING since the ADMINISTRATION of the electrical current DOES NOT SELECTIVELY TARGET only the DEPRESSIVE circuitry in the patient’s brain. Instead, it disrupts ALL of the neural circuitry and consequently should also affect those circuits underlying our memories (which it does).

SHORT-TERM MEMORIES are particularly affected, presumably, reflecting the fact that these NEWLY FORMED neural circuits are the MOST VULNERABLE to disruption since they are the LEAST WELL ESTABLISHED.

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Evidence to support neuroplasticity underlying learning:

Memory Disruption as a Result of Head Trauma

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Similar memory loss is seen in situations of PHYSICAL TRAUMA to the head (e.g., patients who have been in an MVA). They typically also experience MEMORY LOSS, some of which returns later, and some of which never does.

The MOST COMMON memory losses in patients with HEAD INJURY are for the EVENTS SURROUNDING the accident and shortly before the accident (e.g., where they were driving to at the time of the accident, who was driving the vehicle, etc.). This is thought to reflect the fact that these memories did not have a chance to become firmly CONSOLIDATED into stable long-term memory traces before the TRAUMA.

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The role of neurotransmitters in memory

Acetylcholine

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Patients with Alzheimer’s disease show REDUCED LEVELS of the neurotransmitter ACETYLCHOLINE and have been experimentally treated with the drug CHOLINE which is a biochemical PRECURSOR for acetylcholine.

This kind of treatment is much like that of patients with PARKINSON’S disease who are treated with the drug L-DOPA, which is a precursor for the neurotransmitter, DOPAMINE.

In both cases, the hope is that the nervous system will USE THE PRECURSOR to make its own supplies of the missing neurotransmitter and synaptic function will return to normal or improved levels. Results have been mixed.

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The role of neurotransmitters in memory

GABA & Norepinephrine

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These neurotransmitters are thought to be effected by FLUCTUATING HORMONE LEVELS at the time of learning, or shortly thereafter.

This may help to explain why one’s EMOTIONAL STATE may affect our ability to learn. Changing HORMONE LEVELS at the time of learning and recall may affect NEUROTRANSMITTER LEVELS, disrupting established circuitry that underlies our ability to RECALL or preventing the establishment of new circuitry that underlies our ability to LEARN new things.