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EPPP shorter > Physio and Psychopharm > Flashcards

Physio and Psychopharm Flashcards

1
Q

Neuron (Nerve Cell)

A

Neuron (Nerve Cell) is a specalized cell that conducts info. in the nervous system & neurons can vary in size & shape.

Neurons consist of 3 parts:

  1. Dendrites (Branch Like): Recieve info from other cells & conduct it toward the cell body.
  2. Cell Body (SOMA): Contains several structures including:
    • Nucleus
    • Mitochondria: Site where the cell perf. metabolic acitivites.
    • Ribosomes: Site where cell synthesizes new protien molecules.
    • Golgi Complex: System of membrane that prep neurotransmitters & other sub for secretion.
  3. Axon: Then transmit info. from the cell body to other cells by releasing neurotransmitters
  4. Synaptic Cleft: Goes into this area which is the gap btwn the axon terminal of the presynaptic cell & receptors on the dendrite of the post-synaptic cell.

Most neurons have a single axon that divides into numerous branches & many axons are connected by a Myelin Sheath: A fatty substance that acts as an insulator & speeds up the conduction of nerve impulses.

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2
Q

Neuron (Action Potential)

A

The neuron (nerve cell) is a specialized cell that is directly involved in mental processes & behavior. Messages w/in a neuron are transmitted from a neuron’s dendrites to the end of its axon through an electrical process called conduction.

With sufficient stimulation from other cells, a cell becomes:

  • Depolarized (the interior of the cell becomes less negative), which triggers an action potential- i.e. an electrical impulse that travels quickly through the cell.
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3
Q

Neuron (All-or-None Principle)

A

Predicts that an action potential will always be of the same magnitude regardless of the amount of stimulation received by a neuron as long as the minimal level of stimulation (the threshold) has been reached.

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4
Q

Neurotransmitters

A

Chemical substances that are released from axon terminals, diffuse across synapses, & excite or inhibits receptor sites on postsynaptic nerve cells.

Neurotransmitters Include:

  • Acetylcholine (ACh)
  • Dopamine (Catecholamine)
  • Norepinepherine (Catecholamine)
  • Epinepherine (Catecholamine)
  • Serotonin (5-HT)
  • Gamma-Amino Butyric Acid (GABA)
  • Glutamate
  • Endorphins
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5
Q

Acetylcholine

A

Neurotransmitter found in the somatic nervous system.

Released into neuromuscular junction that mediates neuromuscular transmission, & controls the acions of the skeletal muscles & in automatic nervous system, it controls the internal organs & glands. contract

Involved in voluntary motor movement, parasympathetic arousal, sleep, important role in learning & memory

  • Too much assoc. w/Depression
  • Too little (in Hippocampus) assoc w/Dementia (e.g. memory loss in Alzheimers disease)
    • Declines in memory assoc. w/normal aging & Alzheimer’s disease are related to deterioration of neurons that secrete ACh, especially in the hippocampus & areas of the drain that communicate directly w/the hippocampus.
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6
Q

Dopamine

A

Neurotransmitter classified as a catecholamine (Norepinepherine, epinepherine) Fx’s include:

  • Involved in mood, motivation/emotional Fx’s & voluntary movement
  • Personality, mood, memory, sleep, attention & learning
  • Too little:
    • Parkinson’s Disease: A degeneration of dopamine producing cells in the substantia nigra & basal ganglia (Muscle rigidity & tremors) &
    • Forms of Depression
  • Too Much linked to:
    • Schizophrenia: According to Dopamine Hypothesis - Is due to oversensitivity to or higher-than-normal levels of dopamine in certain regions of the brain. (Rx reduces dopamine, decrease + Sx’s; Antipsychotics)
    • Tourtte’s Disorder

​Cocaine, Amphetamines & other stimulant drugs elevate mood my increasing levels of dopamine in areas of the midbrain & limbic system that have been ID as part of the brains reward system.

Alcohol increases dopamine levels & causes the pleasurable feelings related to alcohol use leading to reinforcing effects of alcohol additction.

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7
Q

Norepinepherine

A

Neurotransmitter assoc. with:

  • Mood, attention/alertness, dreams, learning, autonimic Fx, & eating
  • Too little assoc. w/Depression (Catecholamine Hypothesis)
  • Low levels also asoc. w/Bulimia & Eating D/O’s
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8
Q

Epinephrine

A

Neurotransmitter involved in energy & glucose metabolism.

  • Too little assoc. w/Depression
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9
Q

Serotonin (5-HT)

A

Neurotransmitter that ordinarily inhibits behavior & is involved in:

  • Meditates arousal/mood regulation, appetite/hunger, thirst, sexual behavior, impulsive & aggressive behaviors, sleep, memory, body temperature, & pain
  • Too little assoc. with:
    • Affective Disorders (Dep.),
    • Mania
    • Anxiety D/O’s (OCD)
    • Bulimia (Antidepressant Rx that increases serotonin levels have been found useful to control binge & purge behaviors)
  • Too much assoc. with:
    • Schizophrenia
    • Anorexia: Assoc. w/an excess of serotonin which causes nervousness & anxiety. Food restriction helps lower serotonin levels which reduce thses unplesant feelings.
      • Rx that increases serotonin are not useful for these indiv. but once they have reached normal weight Rx may help prevent weight loss.

Evidence that low levels of serotonin are involved in cravings for alcohol in abusers.

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10
Q

Gamma Amino Butyric Acid (GABA)

A

Neurotransmitter that is the most common inhibitory neurotransmitter & inhibits:

  • Excitation, anxiety, sleep, & seizures.
  • Abnormal levels of GABA in the motor region are associated w/Huntington’s Disease.
  • Abnormal levels have also been assoc. w/Parkinson’s Disease, Epilepsy & Sleep D/O’s
  • Too little assoc. w/Anxiety & Anxiety D/O’s. Some antianxiety Rx (Benzo’s) increase GABA at receptor sites & reduce anxiety & enhance sleep.
  • Affected by CNS Depressants
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11
Q

Glutamate

A

A major excitory neurotransmitter that helps messages pass from one neuron to the next more effectively.

Plays a role in:

  • Learning & memory
  • Long-term potentiation (LTP): Brain mechanism believed to be responsible for the formation of long-term memories.
  • Excessive levels can produce Excitotoxicity - which damages or destroys nerve cells & have been linked to stroke related brain damage, TBI, Huntington Disease & Alzhiemers Disease.
  • Alcohol alters Glutamate levels in the brain & are related to memory impairment & alcohol related black outs; responsible for the harmful effects alcohol has on memory.
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12
Q

Endorphins

A

(Endogenous Morphines) Inhibitory neuromodulator that lowers the sensitivity of postsynaptic neurons & neurotransmitters.

Have analgesic properties & involved in:

  • Pain Relief: Prevents release of substance P, involved in transmission of pain impulses.
  • Feelings of pleasure & contentedness, emotions, sexual behaviors, memory & learning.
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13
Q

Central Nervous System (CNS)

A

Consists of the:

  • Brain: Recieves & processes sensory info., initiates responses, stores memories, generates thoughts & emotions.
  • Spinal Cord: Sends signals to & from brain; controls reflex activity
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14
Q

Spinal Cord (Quadriplegia & Paraplegia)

A

The spinal cord carries info. btwn:

  • The brain & the peripheral nervous system,
  • Coordinates activities of the left & right side of the body, and
  • Controls simple reflexes that do not involve the brain.

Consists of 31 segments, which are divided into 5 groups. Each nerve consists of bundles of axons.

From the top of the spinal cord to the bottom, these are:

  1. Cervical
  2. Thoracic
  3. Lumbar
  4. Sacral
  5. Coccygeal.

Damage at different levels causes different types of paralysis:

  • Quadriplegia: Occurs at the cervical level (loss of sensory & voluntary motor Fx in the arms & legs).
  • Paraplegia: Occurs at the thoracic level (loss of functioning in the legs; below T1)
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15
Q

Brain

A
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16
Q

Cerebral Ventricles/Hydrocephalus

A

The ventricles are the 4 cavities of the brain that contain cerebrospinal fluid.

  • Hydrocephalus: Blockage of the ventricles & a resulting build-up of fluid.
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17
Q

Hydrocephalus

A

The abnormal accumulation of cerebrospinal fluid in the ventricles (aka Water head), which results in increased intracranial pressure & can lead to brain damage.

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18
Q

Peripheral Nervous System (PNS)

A

Made up of nerves (Bundles of axons) that relay messages btwn the CNS & body’s sensory organs, muscles & gland.

Peripheral Nervous System (PNS):

  1. Motor Neurons: CNS to muscles & glands
    • Somatic Nervous System (SNS): Controls Voluntary movements.
    • Automatic Nervous Systerm (ANS): Controls involuntary responses.
      • Sympathetic: “Fight or Flight”
      • Parasympathetic: Resting
  2. Sensory Neurons: Sensory organs to CNS
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19
Q

Somatic Nervous System (SNS)

A

Consists of sensory nerves that carry information from the body’s skeletal muscles & sense receptors to the CNS & motor nerves that carry information from the CNS to the skeletal muscles.

  • Governs activities that are ordinarily considered voluntary.
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20
Q

Autonomic Nervous System (ANS)

(Sympathetic & Parasympathetic Branch)

A

ANS controls the glands & muscles of the internal organs & regulates bodily processes that we ordinarily don’t consciously control such as digestion, respiration & HR.

Part of PNS & controls involuntary responses. It consists of 2 parts:

  1. Sympathetic Branch: Active during states of activity & energy output. Involved in the mediation of Flight or Fight (emergency) reactions. Activation of the sympathetic branch produces:
  • increased heart rate,
  • pupil dilation,
  • increased blood sugar, and
  • inhibition of the digestive processes
  1. Parasympathetic Branch: Active during states of relaxation & energy conservation. Involved in the conservation of energy & relaxation (Para = Parachute come down/relax). Activation is associated with:
    • slowing of heart rate,
    • lowered blood pressure,
    • contraction of pupils,
    • reduction of sweat gland output, and
    • increased activity of the digestive system.
    • Hypnosis & meditation
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21
Q

The 5 Stages of Brain Development (CNS)

A

Developmemnt of the Brain involves 5 Stage:

  1. *Proliferation:* Production of cells inside neural tube when embryo is 2.5 weeks.
  2. *Migration:* Each cell moves (migrates) to it’s ultimate destination in the nervous system.
  3. *Differentiation:* (Grow axons & dendrites) Cells devel. the unique charachteristics of nerve cells.
  4. *Myelination:* The axons of some cells become surrounded (insulated) by glial cells.
  5. *Synaptogenesis:* Formation of synapses & depends on certain areas of brain, but most occur post natally. Appears to be influenced by both endogenous (genetic) & Exogenous (exp.) factors.
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22
Q

Neuroimaging Techniques

A

Make it possible to study both the structure & function of the living brain.

Structural Techniques:

  • Computed tomography (CT):
  • Magnetic resonance imaging (MRI): uses magnetic fields & radio waves to produce high quality 2/3D images of brain structures.

Functional Techniques: Provide info. on the functional activities of the brain.

  • Positron-emission tomography (PET),
  • Single proton emission computed tomography (SPECT)
  • Functional magnetic resonance imaging (fMRI): Measure brain activity, by detecting changes in blood oxygenation & flow in response to neural activity.
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23
Q

3 Divisions of the Brain (Structures)

A

Structure of the Brain categorized into 3 divisions:

  1. Hindbrain: From an evolutionary perspective, the hindbrain is the oldest part of our brain & is located deep w/in our head & on top of our spinal cord. This is the 1st & most basic brain it controls most of our most basic Fx’s. There are 3 structures of the hindbrain:
  • Medulla Oblongata: Helps control our heart rate, blood pressure & breathing. Located above the spinal cord.
  • Pons: Located just above the medulla & it helps coordinate the hindbrain w/the midbrain & forebrain; also involved in facial expressions.
  • Cerebellum: Located at the bottom rear of brain & looks like a little version of our whole brain (like mini me). Helps coordinate balance & fine muscle movements.
  1. Midbrain: Located in the middle of ther brain, the midbrain does a lot, but primary Fx’s are to coordinate sensory info. w/simple movements. Any sensory inputs, all 5 senses. There are 2 structures:
    • Substantia Nigra: Involved in motor activity & plays a role in the brains reward system. Reticular Formation: Control respiration, coughing, posture, locomotin, vomiting & REM sleep.
    • Reticular Activating System (RAS): Controls wakefulness, arousal & consciousness.
  2. Forebrain: The most important part of the brain & contains the newest structures in the brain. There are 3 structures:
    • ​​​​**Thalamus: The operator/switchboard of brain. Any sensory info. that comes into the body (sight, hearing, touch & taste) go thru the Thalamus 1st & sends the info. to the right parts of the brain to get processed (except for smell).
    • Hypothalamus: Size of a pea & the most important structure in the brain. Controls thirst, hunger, body temperature, sexual arousal & the endocrine system.
      • ​​Suprachiasmatic Nucleus (SCN)​
    • Limbic System: aka the emotional control center of the brain bc it contains structures that control raw emotions. It is made up of 3 structures:
      • Hippocampus: Involved in memory processing (not stored here), but it does helps put memories in the right parts of brain. Ex: Think of a librarian that does not store the info. of all the books in the library in her head, but can tell you where to find that info.
      • Amygdala: Controls some memory processing, but for the most part handles basic emotions like anger & jealousy.
      • Septum
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24
Q

Hindbrain

A

Hindbrain: From an evolutionary perspective, the hindbrain is the oldest part of the brain & is located deep w/in the head & on top of the spinal cord. This is the 1st & most basic brain it controls most of the most basic Fx’s. There are 3 structures of the hindbrain:

  1. Medulla Oblongata: Helps regulate automatic responses & helps control our heart rate, blood pressure & breathing. Located above the spinal cord.
    • Damage can be fatal (Ex: SIDS)
  2. Pons: Located just above the medulla & it helps coordinate the hindbrain w/the midbrain & forebrain; also involved in facial expressions.
  3. Cerebellum: Located at the bottom rear of brain & looks like a little version of our whole brain (like mini me). Helps coordinate voluntary motor movements & is responsible for balance & posture & motor skills.
    • Abnormalities have been linked to Autism, Schizophrenia &ADHD.
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25
Q

Medulla

A

Hindbrain: There are 3 structures of the hindbrain:

  1. Medulla Oblongata: Helps control flow of info. btwn the spinal cord & brain & regulates a number of vital Fx’s such as heart rate, blood pressure & regulate breathing. Located above the spinal cord. (Reflexes/Unconscious)
  2. Pons
  3. Cerebellum
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26
Q

Pons

A

Hindbrain: There are 3 structures of the hindbrain:

  1. Medulla Oblongata
  2. Pons: Located just above the medulla & it helps coordinate the hindbrain w/the midbrain & forebrain. Plays a role in integration of movement in right & left side of body, sleep & facial expressions.
  3. Cerebellum
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27
Q

Cerebellum and Ataxia

A

Hindbrain: There are 3 structures of the hindbrain:

  1. Medulla Oblongata
  2. Pons
  3. Cerebellum: A large structure on the dorsal aspect of the hindbrain.
    • Located at the bottom rear of brain & looks like a little version of our whole brain (like mini me).
    • It is involved in the extrapyramidal control of motor activities (e.g., timing & coordination of movements, balance, posture).
    • STM, following rules & carry out plans

Damage can result in:

  • Ataxia: Which is characterized by slurred speech, severe tremors, & a loss of balance
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28
Q

Midbrain

A

Midbrain: Located in the middle of ther brain, the midbrain does a lot, but primary Fx’s are to coordinate sensory info. w/simple movements. Any sensory inputs, all 5 senses. There are 2 structures:

  1. Substantia Nigra: Involved in motor activity & plays a role in the brains reward system. Reticular Formation: Control respiration, coughing, posture, locomotin, vomiting & REM sleep.
  2. Reticular Activating System (RAS): Controls wakefulness, arousal & consciousness.
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29
Q

Reticular Activating System

A

Midbrain: There are 2 structures:

  1. Substantia Nigra
  2. Reticular Activating System (RAS): A network of nerve fibers involved in wakefulness, arousal, and consciousness.​​
    • ​​Damage = Disrupts sleep-wake cycles & can produce permanent coma like state of sleep.
    • Reticular Formation: Plays a role in arousal & consciousness & includes the:
      • Ascending Reticular Activating System (ARAS): Which is involved in selective attention & arousal.
      • Ex: A mother being awakened in the middle of the night by a babies cry but not other background noises.
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30
Q

Forebrain

A

Forebrain: The most important part of the brain & contains the newest structures in the brain. There are 3 structures:

  1. ​​​​Thalamus: The operator/switchboard of brain. Any sensory info. that comes into the body (sight, hearing, touch & taste) go thru the Thalamus 1st & sends the info. to the right parts of the brain to get processed (except for smell).
  2. Hypothalamus: Size of a pea & the most important structure in the brain. Controls thirst, hunger, body temperature, sexual arousal & the endocrine system.
    • Suprachiasmatic Nucleus (SCN)​
  3. Basal Ganglia: Involved in control of voluntary movement.
  4. Limbic System: aka the emotional control center of the brain bc it contains structures that control raw emotions. It is made up of 3 structures:
    • Hippocampus: Involved in memory processing (not stored here), but it does helps put memories in the right parts of brain. Ex: Think of a librarian that does not store the info. of all the books in the library in her head, but can tell you where to find that info.
    • Amygdala: Controls some memory processing, but for the most part handles basic emotions like anger & jealousy.
    • Septum
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31
Q

Hypothalamus and Suprachiasmatic Nucleus

A

Forebrain: There are 3 structures:

  1. ​​​​Thalamus
  2. Hypothalamus: The hypothalamus consists of a cluster of nuclei (size of a walnut) that maintain the body’s homeostasis thru it’s influences on the autonomic nervous system & endocrine glands.
  • Mediate metabolic processes, temperature, hunger & thirst & regulate emotional expression.
  • Generates physiological reactions assoc. w/rage, fear 7 other stron emotions
  • Control the release of hormones from the pituitary & other endocrine glands
    • Suprachiasmatic Nucleus (SCN)​: Which is located in the hypothalamus, is involved in regulation of the body’s circadian rhythms.
      • ​Controls the release of melatonin
  1. Basal Ganglia
  2. ​Limbic System: 3 Structures:
    • ​​Hippocampus
    • Amygdala
    • Septum
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32
Q

Thalamus and Wernicke-Korsakoff Syndrome

A

Forebrain: There are 3 structures:

  1. ​​​​Thalamus: The thalamus is a “relay station” for all the sense except olfaction & is also involved in language & memory.
    • The operator/switchboard of brain.
    • Integrates any sensory info. that comes into the body (sight, hearing, touch & taste) go thru the Thalamus 1st & sends the info. to the right parts of the brain to get processed (except for smell).
    • Plays a role in declarative memory, & damage to certain areas can produce severe memory impairment.
  2. Hypothalamus:
    • Suprachiasmatic Nucleus (SCN)​
  3. Basal Ganglia
  4. Limbic System: 3 Structures:
    • ​​Hippocampus
    • Amygdala
    • Septum

Wernicke-Korsakoff Syndrome: Due to a thiamine deficiency that is often the result o long-term alchololism, that causes atrophy of neurons in certain areas of the thalamus & the mammillary bodies of the hypothalamus & is usually the result of chronic alcoholism.

It beings w/Wernicke’s encephalopathy, which is characterized by mental confusion, abnormal eye movements, & ataxia; & is then followed by Korsakoff’s syndrome, which involves severe anterograde amnesia, retrograde amnesia, and confabulation

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33
Q

Basal Ganglia

A

The basal ganglia are subcortical structures (caudate nucleus, putamen, globus pallidus, & substantia nigra) that are involved in planning, organizing, & coordinating voluntary movements.

Damage may cause Akinesia (Reduced movement or paralysis) or Hyperkinesia (Excessive movement).

Basal ganglia pathology has been linked to:

  • Huntington’s disease,
  • Parkinson’s disease,
  • Tourette’s Disorder,
  • OCD, and
  • ADHD
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34
Q

Amygdala and Kluver-Bucy Syndrome

A

Forebrain: There are 3 structures:

  1. ​​​​Thalamus
  2. Hypothalamus
    • Suprachiasmatic Nucleus (SCN)
  3. Basal Ganglia
  4. Limbic System: 3 Structures
    • Hippocampus
    • Amygdala: A substructure of the limbic system & is involved in the control of emotional activities, including the mediation of defensive-aggressive behaviors & the attachment of emotions to memories.

Bilateral lesions in the amygdala & temporal lobes of primates produces:

  • Kluver-Bucy Syndrome: Which is characterized by emotional blunting, excessive hunger, reduced fear & aggression, increased docility & compulsive oral exploratory behaviors, altered dietary habits, hypersexuality, and “psychic blindness” (an inability to recognize the significance or meaning of events or objects)
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35
Q

Flashbulb Memory

A

Refers to a vivid recollection of an emotionally-charged event.

Attributed to activity in the limbic system & the amygdala which is part of the limbic system. It is believed to add the emotional component to our memories & active in the formation of flashbulb memories.

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36
Q

Hippocampus

A

Forebrain: There are 3 structures:

  1. ​​​Thalamus
  2. Hypothalamus
    • Suprachiasmatic Nucleus (SCN)
  3. Basal Ganglia
  4. Limbic System: 3 Structures
    • ​​Hippocampus: A limbic system structure that is important for visual, spatial & verbal info., explicit memory & the consolidation of declarative memories.
      • Involved in converting shot-term declarative memories to long-term memories & temp. storage for new decalrative memories.
      • ​Controls emotion & degeneration has been linked to depression
    • Amygdala
    • Septum

A person w/damage (lesions) to the hippocampus & adjacent areas in the temporal lobe wil most likely demonstrate an inability to form long-term memories about facts & events.

Ex: H.M.’s epilepsy, he was unable to form new memories of facts & events.

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37
Q

Corpus Callosum

A

The right & left hemisphere are connected by several bundles of fibers, the largest of which is the corpus callosum.

If the corpus callosum is severed, the two hemispheres operate essentially as separate, independent brains.

Damage to one side = Opposite Side Response

Left Dominant Hemisphere:

  • Language & Verbal Abilities
  • Math
  • Logical Thought/Analytical
  • Positive Emotional States (Happiness)

Right non-Dominant Hemisphere:

  • Visuo-Spatial abilities
  • Face recognition
  • Visual imagery
  • Creative & holistic/intuitive Thinking
  • Music
  • Non-verbal Memory
  • Negative Emotional States (Anger)
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38
Q

Contralateral Representation

A

For most sensory & motor Fx’s, the cortex exhibits contralateral representation, which means that the left hemisphere controls the functions of the right side of the body and vice-versa

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39
Q

Brain Lateralization/Split Brain Patients

A

Although the left and right hemispheres are both involved to some degree in most Fx’s, they tend to specialize.

Left (dominant) hemisphere:

  • Dominates in verbal activities (spontaneous speaking and writing, word recognition, memory for words and numbers);
  • analytical, logical thought; and
  • positive emotional states.

The right (non-dominant) hemisphere:

  • dominates in visual-spatial activities such as facial recognition, spatial interpretation and
  • memory for shapes and in
  • negative emotions.

The specialization of the two hemispheres is referred to as brain lateralization and was initially studied in split-brain patients, whose corpus callosums had been severed to control severe epilepsy.

  • This had some unusual consequences. When a picture of an object was presented so that it was processed by the right hemisphere only, the CT could not use language to name or describe the object.

Damage to one side = Opposite Side Response

In about 95-99% or Right-handed ppl & 50-60% of Left-handed ppl, the left hemisphere is dominant for written & spoken language.

Exception: Olfactory signals from the right nostril go to the right hemisphere & vice vers w/ the left side.

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40
Q

Primary Functions of Each Lobe of the Cerebral Cortex

A
  1. Frontal Lobe: Mediates motor Fx, language production, personality & executive cognitive Fx’s, attention, planning.
  2. Parietal Lobe: Recieves tactile input & mediates visuospatial Fx, reading & calcualtion.
  3. Occipital Lobe: Responsible for vision & visual perception.
  4. Temporal Lobe: Responsible for auditory perception, language comprehension & memory,.
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41
Q

Frontal Lobe and Broca’s Area/Prefrontal Cortex

A

The frontal lobe occupies the major portion of the cortex & includes the primary motor cortex, supplementary motor area, premotor area, Broca’s area, & prefrontal cortex.

Prefrontal Cortex: Playsa role in emotion, memory, self-awareness, attention & higher-order cog. Fx’s (initiative, planning ability, abstract thinking) & other executive functions.

  • Damage to the prefrontal cortex produces personality changes and deficits in higher-level cognitive abilities.
  • Damage to Dorsolateral Area causes impaired judgement, planning, insight, org., inflexibility & perseverative responses. Indiv that has trouble learning from exp. will repeat the same response over & over.
  • Damage to Orbitofrontal area causes Psudopsychopathy: which involves to emotional liability, distractibility, poor impule control, & impaired social insight.
  • Damage to Mediofrontal Area produces Psudodepression: Which involves impaired spontaneity, reduced emptional reactions, & diminished motor behavior & verbal output.

Primary Motor Cortex: Part of the pyramidal motor system & different areas control muscle in different parts of the body & involved in execution of voluntary movement & damage includes impaired motor Fx in corresponding area of brain.

Broca’s Area: The major language area, & damage to Broca’s area produces Broca’s (expressive) aphasia: Involves deficits in the prod. of written & spoken lang. while comprehension remains relatively intact; ppl w/this D/O speak slowly & w/great difficulty & have ltd vocab.

  • Often includes Anomia (Inability to ID familiar objects by name) & difficulty repeating phrases spoken by another person espescially phrases that contain many prepositions & conjunctions.
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42
Q

Parietal Lobe and Apraxia/Anosognosia/Gerstmann’s Syndrome

A

The parietal lobe contains the somatosensory cortex: which processes sensation related to touch, pressure, pain, temperature & propiocertion.

Depending on its location, damage to the parietal lobe can cause

  • apraxia (inability to perform skilled motor movements in the absence of impaired motor functioning),
    • Ideomotor Apraxia: Involves an inability to mimic a simple motor action in response to a request.
  • anosognosia (inability to recognize one’s own neurological symptoms or other disorder), or
  • Gerstmann’s syndrome, which involves a combination of finger agnosia, right-left confusion, agraphia, and acalculia (May occur after a stroke or in assoc. w/damage to parietal lobe.
  • Contralateral Neglect: Usually the result of damage to the right parietal lobe & involves neglect of the left side of the body & env.
  • Tactile Agnosia: Involves an inability to recognize familiar objects by touch.

L-R confusion is ordinarily caused by lesions in the L Angular Gyrus which is located near the boundary btwn the L Parietal & Temporal Lobes.

  • Finger Agnosia: Inability to distinguish btwn fingers on the hand.
  • Agraphia: Deficiency in the ability to write
  • Acalculia: Difficulty in learn/comprehend math.
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43
Q

Temporal Lobe and Wernicke’s Area

A

The temporal lobe contains the primary auditory cortex and Wernicke’s area.

Auditory Cortex: Responsible for auditory sensations, & perceptions.

  • Damage can result in auditory agnosia, cortical deafness, impairments in long-term memory, and/or

Wernicke’s (receptive) aphasia: A major language area & deficits in comprehension & production of speech.

  • Speech is rapid & seems effortless & has approp. syntax yet devoid of content & may include
    • anomia (probs. w/repitition) &
    • Paraphasia (Sub one word for another) & jumble words; unitelligible speech
  • Wernicke’s = Word Choice Probs. (What?)

Certain areas of the temporal lobe are essential for the encoding, storage & retrival of long-term declarative memories.

  • Damage to these areas, the Amygdala & Hippocampus produces anterograde & retrogrande amnesia.
  • Electrical stimulation of certain areas elicits complex, vivid memories that had been previously forgotten.
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44
Q

Occipital Lobe and Visual Agnosia/Prosopagnosia

A

The occipital lobe contains the visual cortex.

Visual Cortex: Responsible for visual sensations & perceptions.

Damage to the occipital lobe can result in:

  • Visual Agnosia (inability to recognize familiar objects),
  • Achromatopsia: An inability to distinguish btwn different colors.
  • Color Agnosia: An inability to pair particular colors w/specific object.
  • word blindness, and/or
  • scotomas (blind spots).
  • Lesions at the junction of the occipital, temporal, and parietal lobes can produce Prosopagnosia (inability to recognize familiar faces)
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45
Q

Theories of Color Vision (Trichromatic and Opponent Process)

A

There are 2 theories of color vision:

Trichromatic theory: There are 3 types of color receptors that are each a receptor to a different primary color (red, blue, or green).

  • All other colors are produced by variations in the activity of these 3 receptors.

​O​pponent-process theory: Postulates 3 bipolar receptors:

  1. red-green
  2. yellow-blue
  3. white-black.

According to this theory, some cells are excited by red & inhibited by green, & so on; & the overall pattern of stimulation of these cells produces the various colors that we perceive

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46
Q

Depth Perception/Retinal Disparity

A

Depth perception depends on a combination of binocular and monocular cues.

Retinal disparity is a binocular cue and refers to the fact that our two eyes see objects in the world from two different views; and the closer an object, the greater the disparity of the two images

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47
Q

Gate-Control Theory of Pain

A

According to the gate-control theory of pain, there are mechanisms (special cells) in the spinal cord that mediate (block) the perception of pain

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48
Q

Synesthesia

A

Synesthesia (“joining senses”) is a rare condition in which the stimulation of one sensory modality triggers a sensation in another sensory modality.

Ex: a person with synesthesia might hear a color or taste a shape

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49
Q

Psychophysical Laws (Weber’s Law, Fechner’s Law, and Stevens’s Power Law)

A

The psychosocial laws attempt to predict the relationship between perception & sensation.

  • Weber’s Law: States that the just noticeable difference in stimulus intensity is a constant proportion of the initial stimulus intensity.
  • Fechner’s Law: States that physical stimulus changes are logarithmically related to their psychological sensations.
  • Steven’s Power Law: Proposes that the magnitude of a sensation is equal to the physical magnitude of the stimulus producing the sensation raised to a certain power (exponent) which varies, depending on the specific sensation being measured
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50
Q

Learning and Memory- Temporal Lobe

A

Essential for the encoding, storage, and retrieval of long-term declarative memories

51
Q

Learning and Memory- Hippocampus

A

Responsible for the consolidation of long-term declarative memories (transferring information from short-term to long-term memory) but not for subsequent storage of those memories.

52
Q

Learning and Memory- Amygdala

A

Plays a key role in fear conditioning, learning about rewards and punishments, and adding emotional significance to memories

53
Q

Learning and Memory- Prefrontal Cortex

A

Has been implicated in short-term memory, episodic memory, and prospective memory

54
Q

Learning and Memory- Thalamus

A

Involved in processing information and transferring it to the neocortex

55
Q

Learning and Memory- Neural Mechanisms

A

Neural mechanisms that are believed to mediate long-term memory include long-term potentiation and protein/RNA synthesis.

  • Long-Term Potentiation (LTP): is a physiological process involving the modification of nerve synapses, especially at glutamate receptors in the hippocampus.
  • Protein/RNA Synthesis: Inhibiting the synthesis of protein or RNA at the time of learning prevents the formation of long-term memories
56
Q

Broca’s Aphasia

A

Produced by damage to Broca’s area.

  • Located on the frontal lobe of the left hemisphere
  • Damage to it typically results in Broca’s, or nonfluent, aphasia, (“expressive, motor, and nonfluent aphasia”)

It involves:

  • difficulty in producing written or spoken language
  • little or no trouble in understanding language
  • anomia
  • impaired repetition
  • Word-finding difficulty;
  • Diminished vocabulary;
  • slow speech w/ difficulty
  • poor articulation
  • omissions
  • comprehension of language OK
  • aware of deficits
  • frustration & depression
  • Impoverished grammar;
57
Q

Wernicke’s Area

A

Caused by damage to Wernicke’s area.

  • Located on the temporal lobe of the left hemisphere toward the rear
  • Damage typically results in Wernicke’s, or fluent, aphasia (“receptive, sensory, and fluent aphasia”)

It is characterized by:

  • Inability to comprehend written/spoken language
  • production of rapid, seemingly effortless speech
  • anomia,
  • paraphasia
  • impaired repetition.
  • Lack of self-monitoring;
  • Fluent production of speechlike phrases normal in length and intonational contour, but otherwise comprising an uninterpretable mix of random words plus freely invented nonwords.
  • probs understanding
  • speech devoid of content
  • unaware that speech is meaningless
58
Q

Conduction (Associative) Aphasia

A

Produced by damage to the arcuate fasciculus that connects Wernicke’s & Broca’s areas

It does not significantly affect language comprehension but does result in:

  • anomia,
  • paraphasia, and
  • impaired repetition
  • damage to structure
  • know what they want to say, but have difficulty
59
Q

Global Aphasia

A

Total or near-total loss of language

Some automatic speech

60
Q

Transcortical Aphasia

A

Lesion that isolates Broca’s leads to:

  • Transcortical MOTOR aphasia

Lesion that isolates Wernicke’s leads to:

  • Transcortical SENSORY aphasia
61
Q

Emotion- Amygdala

A

Plays a role in the perception and expression of anger, fear, sadness, happiness, and other emotions and attaches emotion to memories

Mediates the subjective exp. of emotion & the attachment of emaotion to memory.

62
Q

Emotion- Hypothalamus

A

Involved in the translation of emotions into physical responses

Generates physiological responses assoc. w/rage, fear, & other strong emotions

63
Q

Emotion- Cerebral Cortex

A

Mediates positive & negative emotions:

Left Hemisphere- governs happiness and other positive emotions.

  • Damage can cause catastrophic anxiety or depression.

Right Hemisphere- mediates sadness, fear, and other negative emotions

  • Damage can produce apathy or undue cheerfulness & euphoria
64
Q

Theories of Emotion- James-Lange Theory

A

Stresses the importance of peripheral factors and proposes that emotions represent perceptions of bodily reactions to sensory stimuli.

Physiological response before exp. an emotion

Ex: You are afraid bc your knees are shaking & heart pounding

65
Q

Theories of Emotion- Cannon-Bard Theory

A

Places greater emphasis on the brain mechanisms that mediate emotion.

It proposes that emotional and bodily reactions to stimuli occur simultaneously as a result of thalamic stimulation of the cortex and the peripheral nervous system

Emotional exp. accompanied by physiological reaction.

66
Q

Two-Factor Theory of Emotion

A

(Schacter & Singer, 1962) Describes subjective emotional experiences as the consequence of a combo of of physiological arousal (physical reaction) & cognitive interpretation of that event & the env. context in which it occured especially when there is no clear explanation for the arousal.

Ex: Epinepherine Studies. Participants that had no explanation for their arousal & looked to the env. to determine it’s cause.

67
Q

Theories of Emotion- Lazarus’s Cognitive Appraisal Theory

A

Proposes that emotions are universal but that there are differences in how emotion-arousing events are interpreted and appraised.

Distinguishes between 3 types of cognitive appraisal:

  1. Primary: A persons eval. of a situation as irrelevant or stressful w/regard to his/her own well-being.
  2. Secondary: The person’s eval. of the resources he/she has to cope w/a situation that has been ID as stressful.
  3. Re-appraisal: Occurs when the person monitors the situation & as necessary modifies his/her primary &/or secondary appraisals.
68
Q

Papez’s Circuit

A

Papez’s circuit was proposed as a brain mechanism (circuit) that mediates the experience and expression of emotion. It includes the hippocampus, mammillary bodies, anterior nuclei of the thalamus, and cingulated gyrus

69
Q

General Adaptation Syndrome

A

According to Selye, the human response to stress is mediated by adrenal-pituitary secretions (e.g., cortisol) and involves 3 stages:

  1. *Alarm Stage/Reaction:* The hypothalamus responds to stress by activating the adrenal medulla to release adrenalin, which increases glucose levels & heart & respiration rates which boosts the bodies energy level ppl may feel excited or frightened.
  2. *Resistance Stage:* The hypothalamus signals the pituitary gland to release ACTH, which activates the adrenal cortex to release cortisol. Maintains the bodies high blood glucose levels & increase metabolism of fats & protiens; ppl may be irritable & angry, feel constantly tired & have trouble concentrating.
  3. *Exhaustion Stage:* Occurs as the pituitary & adrenal cortex lose the ability to maintain evelvated hormone levels. Physiological processes begin to break down, ppl exp. mental, emotional, & physical exhaustion & are at high risk for cold & flu as well as more serious conditions such as heart disease & cancer.

The model predicts that prolonged stress can result in illness or death

Human response to stress mediated by adrenal-pituitary secretions & involves 3 stages

  • alarm reaction
  • resistance (ACTH/cortisol)
  • exhaustion
70
Q

Type A Behavior Pattern

A

People exhibiting Type A behavior pattern are:

  • Highly competitive & achievement-oriented,
  • Have a sense of time urgency, &
  • Tend to be hostile, angry, easily irritated, & impatient.

A number of studies have confirmed that, of the Type A characteristics these are most strongly associated w/health probs, especially coronary heart disease in males:

  • Cynical or antagonistic hostility (Hostility & Anger)

This charateristic has also been linked to other stress related illnesses

71
Q

Sexual Dimorphism

A

Refers to systematic gender-related differences in physical appearance.

Research has confirmed that certain structures in the human brain are sexually dimorphic.

Studies using structural brain imaging techniques have found sex-related differences in the size of specific regions of the brain including:

  • Hypothalamus: The size & secretion of growth hormones differ for male & female.
  • Corpus Callosum,
  • Hippocampus,
  • SCN
72
Q

Secondary Sex Characteristics/Hypothalamic-Pituitary-Gonadal Axis

A

Puberty, can increase gonadal hormones & influences the emergency of secondary sex characteristics and the development of the reproductive system.

Although the mechanisms that trigger the development of the secondary sex characteristics are not well understood, it occurs when the hypothalamus secretes chemicals that stimulate the anterior pituitary gland, which then releases the gonadotropic hormones that stimulate testosterone and sperm production by the testes or ovulation and estrogen produced by the ovaries.

This system is referred to as the hypothalamic-pituitary-gonadal axis.

73
Q

Menopause/Hormone Replacement Therapy

A

The decreased estrogen levels that accompany menopause produce a variety of emotional and physical symptoms including hot flashes, fatigue, mood swings, nausea, vaginal dryness, and loss of bone mass.

Hormone replacement therapy (HRT) alters estrogen levels only or both estrogen and progesterone levels and is effective for eliminating hot flashes, mood swings, and vaginal dryness and reduces the risk for bone loss

74
Q

Sleep (Stages)

A

The sleep cycle: A sleep cycle lasts about 90 minutes & during that time we move through 5 stages of sleep.

The first 4 stages make up our non-rapid eye movement (NREM) sleep, and the 5th stage is when rapid eye movement (REM) sleep occurs.

Sleep is divided into 5 stages on the basis of EEG (electroencephalogram) pattern:

  1. Stage 1: Alpha brainwaves (8-14 Hertz) Occur during relaxed states such as daydreaming/fantasizing & are stimulated by sensory input. Serves as a bridge to Theta brainwaves (unconscious info.) & are repalced by these brainwaves.
  2. Stage 2: Theta brainwaves (4-7 Hertz) Is a slightly deeper stage of sleep but still can be awakened easily. Consists primarily of theta waves assoc. w/dreaming & REM sleep. Theta waves are interrupted by bursts of sleep spindles & K complexes.
  3. Stage 3: Delta brainwaves (0.5-3 Hertz) Theta waves begin to be replaced by delta waves. Large, slow delta waves appear during stage 3 and are assoc. w/deep sleep when occur in isolation.
  4. Stage 4: “Deep Sleep” Stage, delta waves dominate the EEG record. Very difficult to wake an indiv. in this stage & if awakened will be groggy & confused.
  5. Stage 5: REM Sleep, Characterized by the presence of rapid eye movements, REM, dream sleep. Not all dreams occur during this stage, but the most vivd dreams occur in this stage. EEG similar to Stage 1 &2, & physiological response similar to those of an awake indiv.
  • Paradoxical Sleep: Involves a combo of physiological arousal & deep sleep.

Sleep Stages (BATS Drink Blood):

  • Beta (Awake; highest frequency, lowest amplitude)
  • Alpha (Awake, eyes closed)
  • Theta (light sleep)
  • Sleep spindles and K complexes (bruxism)
  • Delta (Deepest; slowest frequency, highest amplitude; enuresis)
  • Beta (REM; same frequency as awake!)

Order: 1, 2, 3/4, 2, REM, 2, 3/4, 2, REM

75
Q

Gamma Brainwaves

A

Frequency of 38-100 Hertz, assoc. w/peak performance states, high attentional focus/concentration, & meditation.

These waves synchronize broad activites across brain regions.

Also assoc. w/schizophrenia, hyperactivity & anxiety.

76
Q

Beta Brainwaves

A

Frequency of 15-38 Hertz & are charateristic of “normal” waking states of consciousness.

Involved w/outward attention & conscious, logical & analytical thought.

77
Q

Sleep (Effects of Age)

A

Sleep patterns vary with age:

  • Newborns (1st 2-3 mos.): The sleep period begins with REM sleep which gradually changes to NREM sleep, but
  • 3 mos. the sequence of REM & NREM sleep begins to reverse. REM sleep accounts for 50% of a newborns total sleep period, but drops to 30% at 6 mos. of age & 20% in adulthood
  • Childhood to Adulthood, total sleep time, stage 4 sleep, and REM sleep all decrease.
  • Older adults awaken more often during the night, spend more time in Stage 1 & 2 sleep, & exp. a phase shift that involves going to sleep & waking up earlier.
78
Q

Traumatic Brain Injury (Post-Traumatic Amnesia, Retrograde Amnesia)

A

Traumatic Brain Injury (TBI): refers to an injury to the brain that is caused by an external force and involves temporary or permanent impairments in cognitive, emotional, behavioral, and/or physical functioning. It can be due to closed or open head injury:

  • Open Head Injury: Depends on its location & etent of the injury.
  • Closed Head Injury: usually causes an alteration or loss of consciousness followed by anterograde and retrograde amnesia.
    • Anterograde amnesia is referred to as post-traumatic amnesia, and its duration is a good predictor of recovery.
    • Retrograde amnesia affects recent memories more than remote memories and, when long-term memories begin to return, the more remote memories return first
79
Q

Postconcussional Disorder

A

Involves impaired cognitive functioning & certain neurobehavioral Sx’s followng a sever head trauma.

Begins shortly after the head trauma & requires:

  • A Hx of head trauma that caused significant cerebral concussion as evidenced by a loss of consciousness, post-traumatic amnesia, &/or post-traumatic seizures;
  • Disturbances in attention or memory; &
  • 3 or more Sx’s that have lasted for at least 3 mos. (e.g. fatigue, headache, irritability or anger w/out provocation)

​The majority of patients w/postconcussional D/O fully recover w/in 1-3 months of injury.

80
Q

Cerebrovascular Accident

A

Cerebrovascular accident (CVS) is referred to as cerebral stroke and refers to brain damage that occurs when a blood clot or other obstruction or hemorrhage disrupts the flow of blood to the brain involving the middle crebral artery.

Major risk factors are hypertension & atherosclerosis (thickening or hardening of the arteries)

Common Sx’s include:

  • contralateral hemiplegia/muscle weakness
  • conterlateral sensory loss,
  • hemianesthesia involving the face, arm, and leg, and
  • contralateral visual field loss
  • Aphasia
  • Apraxia & sensory neglect

Neuropsychiatric Sx’s are common w/Depression immediatly following stroke

81
Q

Parkinson’s Disease

A

Parkinson’s disease is a progressive degenerative disease characterized by prominent motor Sx’s:

  • Tremor: Often begins in hands & includes pill rolling
  • Muscular Rigidity: Causes muscle stiffness & pain & when affect the face produces a mask like facial expression.
  • Akathisia,
  • Bradykinesia: Slowed movement & can progress to akinesia
  • Akinesia: Marked reduction of spontaneous movement
  • speech difficulties; and it may eventually include dementia.
  • Linked to a degeneration of neurons that secrete dopamine in the substantia nigra, part of the basal ganglia

50% of patients exp. Sx’s of depression at some time during their illness (For 20% Dep. precedes motor Sx’s)

Symptoms are temporarily relieved by L-dopa in the early stages by increasing dopamine levels in the brain, a dopamine agonist.

82
Q

Huntington’s Disease

A

An inherited neurodegenerative disease that is transmitted by a single autosomal chromosome (refers to a chromosome that is not an X/Y sex chromosome) dominant gene & involves emotional, cognitive, & motor Sx’s.

For many patients, affective/emotional (mood Sx’s) appear 1st & cognitive Sx’s include:

  • Depression (40% of cases)
  • Irritability
  • apathy,
  • anxiety,
  • antisocial tendencies
  • forgetfulness
  • Cognitive deterioration begins w/forgetfulness & impaired attention & progresses to dementia.

Early motor Sx’s include:

  • fidgeting & clumsiness, followed by
  • facial grimaces & “piano-playing” movements of the fingers.

Huntington’s disease is believed to be due to a loss of GABA-secreting neurons & glutamate excitotoxicity in the basal ganglia, especially in the caudate nucleus, putamen, & globus pallidus

83
Q

Seizures (Tonic-Clonic, Absence, and Partial)

A

Caused by an abnormal discharge of electrical energy by nereve cells in the brain.

Dx includes a medical Hx & physical exam followed by an EEG

There are 2 main types of seizures:

  1. Generalized seizures: are bilaterally symmetrical (Involve abnormal electrical activity in both hemispheres) & do not have a focal onset. Caused by electrical impulses throughout the entire brain. Which include:
    • Tonic-Clonic (grand mal) seizures: include an itital tonic stage in which the muscles contract & clonic stage the body stiffens;
      • A clonic stage: that involves rhythmic shaking of the limbs; unconsciousness, convulsion & muscle rigidity and a postseizure depression or confusion with amnesia for the event.
    • Absence (petit mal) seizures: are brief attacks involving a brief loss of consciousness w/out prominent motor Sx’s.
    • Myoclonic Seizure: Primary Sx’s are brief jerky contractions of muscles in different parts of the body, most often the arms & legs.
  2. Partial seizures (aka Temporal Lobe Epilepsy): begins/limited to one side of the brain (Temporal Lobe) & affect one side of the body, at least initially but sometimes spread and become generalized seizures. Produced initally by electrical impulses in a specific area of the brain. Includes.
    • Simple Partial Seizure: Do not involve a loss of consciousness
    • Complex Partial Seizure: They impair consciousness
      • Sx’s depend on which part of the brain is affected
      • Temporal lobe seizures include hallucinations, illusions, sudden alteration in emotion, sense of deja vu, & automatisms (repetative movements such as lip smacking or chewing motion).
84
Q

Multiple Sclerosis (MS)

A

A progressive disease of the nervous system that involves a degeneration of the myelin that surrounds nerve fibers in the CNS.

Common initial Sx’s are:

  • optic neuritis,
  • motor impairments,
  • sensory abnormalities, &
  • fatigue.

Additional Sx’s that arise as the disease progresses include:

  • tremors,
  • speech problems,
  • mood symptoms, and
  • cognitive impairments.

It is est. that up to 70% of ppl w/MS devel. some type of cog. dysfx & most often involves impairments in attention, recent memory & info. processing sped.

85
Q

Hypertension

A

There are 2 types of hypertension:

  • Primary (essential) hypertension is Dx when high blood pressure is not due to a known physiological cause.
    • Primary hypertension accounts for about 85% & 90% of all cases of high blood pressure; untreated, it can lead to cardiovascular disease, and it is a major cause of heart failure, kidney failure, and stroke.
  • Secondary hypertension is Dx when elevated blood pressure is related to a known disease.

The prevalence of hypertension is related to age-related to age, race, and gender:

  • Older adults have higher rates than younger adults, and African Americans have higher rates than Whites.
  • The rates are generally higher for men, among older adults and African Americans, they are higher for women.
86
Q

Migraine Headache

A

A migraine headache is a recurrent vascular headache characterized by:

  • severe throbbing pain, usually on one side of the head.

riggers include:

  • certain foods,
  • alcohol,
  • bright lights, and
  • relaxation following physical or psychological stress.

A migraine may be preceded by an aura (classic migraine) or gastrointestinal or other symptoms (common migraine).

87
Q

Hyper- and Hypothyroidism

A
  • Hyperthyroidism: Due to higher than normal levels of thyroid hormones & is caused by hypersecretion of thyroxine by the thyroid gland. Characterized by a:
    • speeded-up metabolism,
    • elevated body temperature,
    • accelerated heart rate,
    • increased appetite with weight loss, nervousness, and
    • insomnia.
  • Hypothyroidism: Due to lower than normal levels of thyroid hormones & is caused by hyposecretion of thyroxine. Involves a:
    • slowed metabolism,
    • slowed heart rate,
    • lethargy,
    • owered body temperature,
    • impaired concentration and memory, and
    • depression,
    • confusion,
    • thought D/O,
    • hallucinations.
88
Q

Hypoglycemia & Diabetes Mellitus

A

Hypoglycemia (abnormally low blood sugar) Higher than normal levels of insulin is caused by excessive secretion of insulin by the pancreas and is characterized by:

  • hunger,
  • dizziness,
  • headaches,
  • blurred vision,
  • palpitations,
  • anxiety,
  • depression, and
  • confusion

Diabetes Mellitus: Due to lower than normal levels of insulin which produces excessive blood sugar & is charaterized by:

  • Increased thirst & urination
  • excessive hunger w/weight loss
  • increased susceptibility to infection
  • apathy &
  • confusion
89
Q

Post-Traumatic Amnesia (PTA)

A

Refers to post-injury amnesia, and its duration has been found to be a good predictor of the persistence of cognitive, motor, personality, and other types of symptoms caused by the injury

90
Q

Effects of Psychoactive Drugs

A

Terms used to describe the effects of the psychoactive drugs include the following:

  1. Agonists: (Mimick neurotransmitter & block re-uptake so neurons keep going firing; Parrot) Produce effects similar to those produced by a neurotransmitter.
    • Direct Agonist: Mimic effects of neurotransmitter at receptor site.
    • Indirect Agonist: Facilitates the action of a neurotransmitter by attaching to a binding site on a receptor cell, to a site other than one used by the neurotransmitter.
  2. Inverse Agonist: Produce an effect opposite the effect produced by a neurotransmitter or agonist (Some antipsychotics).
  3. Partial Agonist: produce effects that are similar to (but less than) the effects produced by a neurotransmitter or an agonist.
  4. _AnTAGonist:_ (Game ot tag to freeze & block receptors so neurons cant fire; frozen) Produce no activity in the cell on their own but, instead, reduce or block the effects of a neurotransmitter or agonist
    • Direct Antagonist: Attach to a neurotransmitter’s receptor site
    • Indirect Antagonist: Interfere w/ the action of a neurotransmitter by attaching to a binding site on a receptor cell.
91
Q

2 Types of Antipsychotic Drugs

A
  1. Traditional (conventional)
  2. Atypical (novel)
92
Q

Traditional (Conventional) Antipsychotic Drugs

A

Phenothiazine:

  • Chlorpromazine
  • Fluphenazine

Thioxanthene:

  • Thiothixene

Butyrophenone:

  • Haloperidol
93
Q

Traditional (Conventional) Antipsychotics

A

Work primarily by blocking dopamine receptors (D2) in the brain to reduce dopamine & are used for the management of Schizophrenia, Acute Mania & organic psychoses.

Supports the Dopamine hypothesis: Schizophrenia is due to overactivity at dopamine receptors either as the result of oversensitivity of the receptors or excessive dopamine levels.

Most effective: for positive symptoms (delusions, hallucinations, agitation, thought disorders) & Acute Mania (Less effective for negative Sx’s of Schizophrenia)

Side effects include:

  • Anticholinergic Sx’s: Blockage of ACh in CNS & PNS. Effects appear early & tolerance usually devel. w/in a few weeks of months. Sx’s include Dry mouth, blurred vision, tachycardia, urinary retention, constipation & other Sx’s.
  • Extrapyramidal Sx’s: Include parkinsonism, akathisia, dystonia & tardive dyskinesia
    • Tardive Dyskinesis: May be alleviated by slowly w/drawing the drug & can add benzo or other GABA agonist to treat. (Occurs esp. w/Haloperidol)
  • Neuroleptic Malignant Syndrome (NMS): Involves muscular rigidity, tachycardia, high fever, alterstate of consciousness & severe diarrhea, urinary incontinence.
    • When tese Sx’s occr the drug must be stopped immediatly

These drugs exert their beneficial effects primarily by blocking dopamine receptors, & their effectiveness provides support for the dopamine hypothesis which attributes schizophrenia to overactivity at dopamine receptors.

94
Q

Dopamine Hypothesis

A

According to the dopamine hypothesis, Schizophrenia is due to overactivity at dopamine receptors either as the result of oversensitivity of the receptors or excessive dopamine levels.

95
Q

Anticholinergic Effects

A

Caused by several drugs including the antipsychotics & tricyclic antidepressants.

Blockage of ACh in CNS & PNS. Effects appear early & tolerance usually devel. w/in a few weeks of months.

Sx’s include:

  • Dry mouth
  • Blurred vision
  • Tachycardia (rapid heart rate)
  • Urinary retention
  • Constipation
  • Memory impairment
  • Confusion.

In older adults the Sx’s are more severe due to decreased production of ACh as a result of age

96
Q

Extrapyramidal Side Effects (EPSE)

A

Believed to be caused by the effects of the drug on dopamine receptors especially in the caudated nucleus.

Sx’s Include:

  • Parkinsonism
  • Akathisia: Inability to remain motionless
  • Akinesia: Inability to initiate movement
  • Acute Dystonia: Muscle spasm in the mouth,face & neck.
  • Tardive Dyskinesis:
    • May be alleviated by slowly w/drawing the drug & can add benzo or other GABA agonist to treat.
    • Occurs esp. w/Haloperidol (most potent) & assoc. w/most severe side effects.
97
Q

Tardive Dyskinesia

A

A potentially irreversible extrapyramidal side effect associated w/long-term use of traditional antipsychotic drugs.

Symptoms include:

  • Involuntary rhythmical, stereotyped movements of the muscles of the face, limbs, and trunk (similar to Huntington’s chorea).
  • Late occuring Sx’s more common in females & older adults

Sx’s May be alleviated by slowly w/drawing the drug & can add benzo or other GABA agonist to treat (inital increase then decline in Sx’s)

  • Occurs esp. w/Haloperidol (most potent) & assoc. w/most severe side effects.
98
Q

Neuroleptic Malignant Syndrome (NMS)

A

Caused by dopamine blockage in the basal ganglia

A rare, but potentially fatal side effect of the antipsychotic drugs.

Sx’s Involve:

  • A rapid onset of motor, mental,& autonomic Sx’s including:
    • Muscle rigidity
    • Painful joints
    • Tachycardia,
    • Hyperthermia (High fever)
    • Altered consciousness
    • Severe diarrhea
    • Urinary incontinence
    • Phosphokinase: Elevated plasma creatine

To avoid a potentially fatal outcome, the drug must be stopped as soon as symptoms of NMS develop.

99
Q

Atypical (Novel) Antipsychotics

A

Dibenzodiazepine

  • Clozapine (Clozaril)

Benzisoxazole

  • Resperidone (Risperdal)

Thienobenzodiazepin

  • Olanzapine

Dibenzothiazapine

  • Quetiapine
100
Q

Atypical (Novel) Antipsychotics

A

Atypical (newer) antipsychotic drugs affect receptors for several neurotransmitters by blocking dopamine (D4 & 2), serotonin, & glutamate.

Drugs effective for:

  • Schizophrenia & other D/O’s w/Psychotic Sx’s: Both positive & negative Sx’s of Schizophrenia (slower onset of theraputic effects, use when traditional antipsychotics failed) & less likely to produce EPSE & Tardive Dyskinesia than the traditional antipsychotics.
    • Can produce Agranulocytosis & other blood dyscrasias (Clozapine)
    • Neuroleptic Malignant Syndrome (NMS)
  • Bi-Polar D/O: Clozapine found useful for treating D/O when have not responded to a mood stabilizer.
  • Alcohol & Drugs
  • Huntington’s, Parkinson’s & other Movement D/O’s: Treat hostility & motor Sx’s

Side Effects Include:

  • Anticholinergic Effects (Blurred vision, dry mouth/eyes, constipation, urinary retention)
  • Agranulocytosis (Blood D/O)
  • Lowered seizure threshold
  • Sedation
  • No Tardive Dyskenisia
101
Q

Agranulocytosis

A

Blood Disorder caused by Atypical Antipsychotic Drugs (especially Clozapine)

The use of these requires careful blood monitoring & may cause NMS.

102
Q

Tricyclic Antidepressants (TCA’s)

A
  • Amitriptyline
  • Doxepin (Sinequan)
  • Imipramine (Tofranil)
  • Clomipramine (Anafranil)
103
Q

Types of Antidepressants

A
  • Tricyclics (TCA’s)
  • Selective Serotonin Re-uptake Inhibitors (SSRI’s)
  • Monoamine Oxidase Inhibitors (MAOI’s)
  • Newer Antidepressants
104
Q

Tricyclic Antidepressant (TCA’s)

A

Are believed to work by blocking the reuptake of norepinephrine, dopamine, &/or serotonin at nerve synapses & increasing them in the brain.

Effects of TCA’s on Norepinepherine support the:

  • Catecholamine Hypothesis: Proposes that depression is caused by a deficiency of this neurotransmitter.

Most effective for:

  • “Typical” Depression: (Loss of interest in usual activities, decreased appetite, insomnia & other vegative Sx’s) Alleviating somatic & vegetative Sx’s
  • Panic Disorder
  • Agoraphobia,
  • Bulimia
  • OCD (Clomipramine)
  • Enuresis (Imipramine)
  • Neuropathic pain (Amitriptyline & Nortriptyline)

Takes 2-4 weeks for drugs to exert theraputic effects.

Side effects include:

  • Anticholinergic effects (Dry mouth, blurred vision & other rel. Sx’s)
  • Tremor
  • Confusion
  • Drowsiness
  • Memory Problems
  • Sexual Dysfx
  • Weight gain
  • Cardiovascular Sx’s
  • Cardiotoxic & can be fatal in overdose

Imipramine has also been found useful for treating enuresis

Clomipramine is an effective treatment for Panic Disorder, Agoraphobia, Bulimia, & OCD.

105
Q

Selective Serotonin Reuptake Inhibitors (SSRI’s)

A
  • Fluoxetine (Prozac)
  • Fluvoxamine (Luvox)
  • Paroxetine (Paxil)
  • Sertraline (Zoloft)
  • Citalpram (Celexa)
106
Q

Selective Serotonin Reuptake Inhibitors (SSRI’s)

A

Antidepressant drugs that exert their effects by blocking the reuptake of serotonin at nerve synapses & increases it in the brain.

Effective Tx for:

  • “Melancholic Depression”/Depression
  • OCD
  • PTSD
  • Bulimia
  • Panic D/O
  • Premature Ejaculation

Fairly rapid onset of theraputic effects & most indiv. exp. substantial improvments in dep. Sx’s w/in 2-4 weeks; in some indiv. may take 6-8 weeks.

Side effects include:

  • Gastrointestinal disturbances (Nausea, appetite loss, constipation, diarreha)
  • Sexual dysfunction,
  • Insomnia,
  • Anxiety,
  • Nausea
  • Dizziness
  • Headache,
  • Anorexia (Loss of appetite).

Many of the side effects are temp. but others may require a change in dosage

In comparison to the TCAs, the SSRIs are less:

  • cardiotoxic,
  • safer in overdose, and
  • less likely to produce cognitive impairments.

Fluoxetine (Prozac) is one of the most widely-prescribed antidepressants but its use is surrounded by controversy due to evidence linking it to an increased risk for suicide.

Administration of SSRI’s w/MAOI’s or other Serotonergenic agents may result in Serotonin Syndrome & Sx’s include:

  • Neurological Effects (Headaches, nystagums, tremor, dizziness, unstady gait)
  • Changes in Mental State (irratabiity, confusion, delirium)
  • Cardiac Arrhythmia
  • Can progress to coma or death.
107
Q

Monoamine Oxidase Inhibitors (MAOI’s)

A
  • Isocarboxazid
  • Phenelzine (Nardil)
  • Tranylcypromine (Parnate)
108
Q

Monoamine Oxidase Inhibitors (MAOI’s) & Hypertensive Crisis

A

Antidepressants that work by inhibiting the enzyme monoamine oxidase, which is involved in deactivating dopamine, norepinephrine, & serotonin. Blocks the action of enzymes that break down norepinepherine & serotonin & increase the avalibility of these neurotransmitters at nerve synapse.

Most effective for:

  • Non-Endogenous & Atypical Depression: (Phobic features, anxiety, reversed vegative Sx’s/Hypersomnia/Hyperphagia, Interpersonal sensitivity)

Side Effects:

  • Anticholinergic Effects (Dry mouth, blurred vision & other rel. Sx’s)
  • Insomnia
  • Headaches
  • Confusion
  • Tremor
  • Sexual Dysfx
  • Hypertensive Crisis: (Most dangerous side effect) Which occur when an MAOI is taken in conjunction w/barbiturates, amphetamines, antihistamines, or certain other drugs, or w/foods containing the amino acid tyramine (e.g. aged cheeses and meats, beer, red wine, chicken liver, avocados, bananas, fava beans). Sx’s include:
    • severe headaches,
    • stiff neck,
    • rapid heart rate,
    • nausea,
    • vomitting,
    • sweating, and
    • sensitivity to light.
109
Q

Newer Antidepressants

A

Norepinepherine Dopamine Reuptake Inhibitors (NDRI’s):

  • Bupropion (Wellbutrin)

Used to treat major Dep. & Dep. phase of Bi-Polar D/O

Has a few Anticholinergic side effects & is less cardio toxic than TCA’s; does not cause sexual dysfx

May aggravate pre-existing psychosis & seziures & often effective for indiv. that have not rsponded to other antidep.

Serotonin Norepinepherine Reuptake Inhibitors (SNRI’s):

  • Venlafaxine (Effexor)

Used to Tx major dep., gen. anxiety D/O (GAD), wocial anxiety D/O & OCD.

Has also beeb an effective drug for certain pain Sx’s includinf fibromyalgia, mixed headaches, back pain, perepheral neuropathic pain.

Less dangerous in overdoes than TCA’s & may have aster onset of theraputic effects; can increase blood pressure

Oter RX’s

  • nefazodone (serxone)
  • trazodone (desyrel)
110
Q

Mood Stabilizing Drugs (Lithium, Anticonvulsant Drugs)

A

Effects believed to be related to the reuptake of serotonin & norephinepherine

Used to Tx classic Bi-Polar D/O involving manic episodes w/elevated mood & w/out rapid cycling of moods. Not only reduces/eliminates manic Sx’s but also suppresses mood swings.

  • Lithium & anticonvulsants (carbamazepine).

Mood stabilizing drugs are used to Tx:

  • Bi-Polar D/O: Alleviate Mania & mood swings in & LIthium is usually the drug-treatment-of-choice for classic Bipolar Disorder.
    • Anticonvulsant drug may be more effective for patients who experience rapid mood swings or who have dysphoric mania.

Side Effects:

  • Gastrointestinal (usually subside w/in a few weeks) Include:
    • nausea,
    • vomitting,
    • diarreha,
    • mettalic taste,
    • increased thirst & urination
    • weight gain
    • fine hand tremmors
    • weakness & fatigue.

The retention of lithium is affected by the body’s sodium levels & ppl taking the drug must be careful to avoid fluctuations in salt intake & avoid caffinee, alcohol & other diuretics. Lithium levels must be monitored to avoid:

  • Lithium Toxicity: Includes diareah, ataxia, drwowsiness, slurred speech, confusion & trmor; can lead to coma or death.

Contraindicated for ppl w/cardiovascular, kidney, liver, thyroid or gastrointestinal probs.

Carbamazepin (Tegretol): Useful for Atypical forms of Bipolar D/O (mania w/dysphoric meed or frequent mood swings) & when lithium has not been effective.

Side Effects:

  • Dizziness
  • Tremor
  • Ataxia
  • Nausea
  • Visual Disturbances
    • Bc of the risk of agranulocytosis & aplastic anemia reg. blood monitoring req.
111
Q

Sedative-Hypnotics (Barbituates)

A

Drugs exert their effects by interrupting impulses to the Reticular Activating System (RAS).

The sedative-hypnotics include the:

  • Barbiturates
  • Anxiolytics (Benzodiazepines):
    • Diazepam (Valium)
    • Alprazolam (Xanax)
    • Lorazepam (Ativan)
  • Alcohol.

These drugs are generalized CNS depressants, & their effects are mostly dose dependent:

  • Low doses, these drugs reduce arousal & motor activity;
  • Moderate doses, they induce sedation & sleep;
  • High doses, can produce anesthesia, coma, & death.

Side effects:

  • Impaired motor & cog. perf.
  • Dizziness
  • Irritability
  • Slurred speech
  • Nystagums

When used to alleviate insomnia the soporific (Sleep inducing) effects gen. last when used only a few weeks & after that total sleep time may fall below pre-drug levels.

Use causes a decrease in REM sleep & abrupt cessation can prod. REM rebound & nightmares

  • Chronic use can result in tolerance, psych, & physical dependence
  • W/drawl Sx’s are sever & w/out medical supervision can be life threatening

Most abused class of drugs & frequently involves suicide & accidental death.

112
Q

Benzodiazepines (Anxiolytics)

A

The Benzodiazepines are a type of anxiolytic that are most commonly perscribed & stimulate an inhibitory action of the neurotransmitter GABA:

Anxiolytics (Benzodiazepines) - Minor Tranquilizers & anti-anxiety drugs:

  • Diazepam (Valium)
  • Alprazolam (Xanax)
  • Lorazepam (Ativan)

​Used to alleviate:

  • Anxiety
  • Acute
  • Stress Reactions
  • Insomnia
  • Seizure
  • Cerebral Palsy
  • Alcohol Withdrawl

The relaxation/euphoria effects promote psychological dependence & chronic use can result in tolerance & physical dependence.

Are addictive w/chronic use & have super addictive effect when taken w/another CNS depressant; which can be fatal.

Side effects include:

  • drowsiness,
  • ataxia,
  • Dizziness
  • Lethargy
  • slurred speech,
  • ther signs of CNS depression
  • Abrupt cessation can cause Rebound Hyperexcitability: A potentially serious side effect that involves insomnia & other Sx’s that were more intense prior to taking the drug.

They can also produce paradoxical agitation, impaired sexual functioning, confusion, and sleep disturbances.

113
Q

Beta-Blockers (Propranolol)

A

Propranolol and other beta-blockers block or diminish the cardiovascular excitatory response to the hormones epinephrine & norepinephrine.

Used to treat:

  • Hypertension
  • Angina
  • cardiovascular disorders,
  • glaucoma,
  • migraine headache
  • Essential tremor
  • reducing the physical symptoms of anxiety.

Common side effects include:

  • bradycardia,
  • nausea,
  • diarrhea,
  • dizziness,
  • decreased sexual ability
  • trouble sleeping
  • Hypotension
  • Numbness in fingers and toes

Overdose: Result in toxicity which prod. breathing difficulties, irregular heartbeat, blurred vision, confusion or coma.

Abrupt Cessation: Should be avoided bc doing so can cause heart palpitations, headaches, tremulousness, & cardiac arrhythmia.

114
Q

Narcotic-Analgesics (Opioids)

A

The drugs classified as narcotic-analgesics (opioids) have both sedative & analgesic properties.

Medically, the narcotic-analgesics are used for the same reasons they were used centuries ago- i.e. as analgesics, treatments for diarrhea, and cough suppressants.

Chronic use of a narcotic-analgesic results in tolerance and psychological and physical dependence.

Withdrawal symptoms resemble those associated with a base case of a flu.

115
Q

Methylphenidate

A

Methylphenidate (Ritalin, Concerta, Metadate) is a psychostimulant drug used to treat:

  • ADHD in children & adults: Most effective for alleviating the core Sx’s of D/O than for improving academic achievement & social FX.

Common side effects include:

  • decreased appetite,
  • insomnia,
  • dysphoria,
  • Abdomina Pain
  • Tachycardia
  • Growth suppression: Can occure w/high doses of the drug & can be min. w/drug holidays.

Contraindicated for indiv. w/anxiety, severe hypotension, recent Hx of drug/alcohol abuse, pre-existing tics, angina pectoris or recent Hx of psychosis.

116
Q

Disulfiram (anatbuse)

A

Inhibits alcohol metabolism which increases the accumulation of acetaldehyde & produces unpleasnt effects that deter drinking.

Sx’s include:

  • Nausea
  • Vomitting
  • Sweating
  • Throbing headache
  • Hyperventalation
  • Other unplesant effects
117
Q

Naltrexone

A

Naltrexone (ReVia, Vivitrol) is an opioid antagonist that blocks the craving for and reinforcing effects of alcohol and is used to treat Alcohol Abuse and Dependence.

Side effects include:

  • abdominal cramping,
  • nausea,
  • vomiting,
  • Dizziness
  • insomnia,
  • nervousness,
  • headache, and
  • joint and muscle pain.

An indiv. should not start this drug if they have consumed alcohol or taken an opioid drug in past 10 days bc doing so can cause severe w/drwl Sx’s

118
Q

Electroconvulsive Therapy (ECT)

A

Memory deficits following ECT are more common w/bilateral ECT that w/unilateral ECT to the nondominant hemisphere.

Anterograde amnesia does occur w/ECT but generally clears up w/in 6 mos.

ECT is most likely to produce permanent retrograde amnesia for autobiographical memories from the recent past.

Loss of memory for past events (events prior to ECT) can sometimes be permanent.

Prefered Tx for CT’s w/severe depression & high risk of suicide

119
Q

Lesions in the Dorsolateral Area of the Prefrontal Cortex will most likely produce?

A

Dysexecutive Syndrome is characterized by problems related to planning, prob.-solving, abstract thinking, insight, preservation, inapproporiate behaviors, & Apathy.

120
Q

Left-Handed Individuals

A

Approximately 50 to 60% of left-handed ppl are left-hemisphere dominant for language.

121
Q

Dysprosody

A

(Communication D/O) Characterized by difficulties in regulating the rate, rhythm, pitch & loudness of speech.

A characteristic of Broca’s aphasia & other nonfluent aphasias.

Has traditionally been linked to right hemisphere damage, it’s presence in Broca’s aphasia suggests that prosody is also governed to some degree by the left hemisphere.

The pattern of stress & intonation in speech is referred to as prosody.

122
Q

simultanagnosis

A

Inability to see more than one thing or one aspect of an object at a time

123
Q

Gonadotropic Hormones

A

estrogen (ovaries)
progesterone (ovaries)
testosterone (testes)
androstenedion (testes)

124
Q

Anticholinergic Syndrome

(Mnemonic)

A

Anticholinergic syndrome is the following:

  • Blind as a bat (dilated pupils)
  • Red as a beet (vasodilation/flushing)
  • Hot as a hare (hyperthermia)
  • Dry as a bone (dry skin)
  • Mad as a hatter (hallucinations/agitation)
  • Bloated as a Toad (ileus, urinary retention)
  • The heart runs alone (tachycardia)

EPPP shorter (29 decks)

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