Physio and Psychopharm Flashcards
Creation of new neurons is called
Neurogenesis
Where does neurogenesis occur
Hippocampus and caudate nucleus
Three parts to a neuron
Dendrite - receives info
Soma - nucleus, mitochondria, ribosomes, summate signals
Axon - transmits info from cell body to other cells, myelinated
Purpose of the golgi complex in neurons
Prepares neurotransmitters and other substances for secretion
Conduction
The travel of a message within a neuron
Electrical charge of a neuron at resting state
Negative
Action potential
An electrical signal that travels through the neuron once the dendrites receive a threshold amount of energy
All-or-none principle
Regardless of the amount of stimuli to a neuron, the action potential will always be the same strength
(It will fire, or it won’t)
Synaptic transmission
Transmission of information fo one nerve cell to another
Chemically mediated, involves the release of neurotransmitters into the synapse, and uptake by neighboring neurons
Neurotransmitters
Chemical substances that transmit signals from one neuron to another
Seven major: Ach, dopamine, serotonin, glutamate, GABA, norepinephrine, endorphins
Seven major neurotransmitters
Acetylcholine - muscle contraction
Dopamine - reward, movement, mood
Serotonin - sleep, arousal, aggression, mood
Norepinephrine - mood, attention, dreaming, learning
GABA - anxiety, mood control, sleep
Glutamate - learning and memory and LTP
Endorphins - analgesic properties
Acetylcholine
Found in the PNS - responsible for muscular contraction
Found in the CNS - REM sleep, memory
Acetylcholine is implicated in what major disease
Alzheimer’s - memory deficits
Drugs for tx reduce the breakdown of Ach: cognex, aricept, reminyl, exelon
Drugs used to slow the breakdown of Ach
Alzheimer’s
Aricept
Reminyl
Exelon
Cognex
Dopamine
Catecholamine (along with E and NE)
Personality, mood, memory, sleep, regulation of movement
Dopamine hypothesis
Predicts schizophrenia is a result of elevated dopamine levels or oversensitivity of dopamine receptors
Oversensitivity or excessive dopamine in the caudate nucleus causes…
Tourette’s
Degeneration of dopamine receptions in the substantia nigra and nearby areas
Parkinson’s symptoms
Elevated levels of dopamine in the mesolimbic system have been implicated in…
Reinforcement that comes with stimulant drugs
Norepinephrine
Mood, attention, dreaming, learning
Catecholamine hypothesis
Some forms of depression are due to lower than normal levels of norepinephrine
Serotonin
Mood, hunger, temperature, sex, arousal, sleep, aggression
Elevated levels of serotonin are implicated…
Schizophrenia
Autism
Food restriction associated with AN
Low levels of serotonin are implicated…
Aggression Depression Suicide Bulimia nervosa PTSD OCD
GABA
Eating, seizures, anx, motor control, sleep
Low levels of GABA have been associated with…
Anxiety disorders
Benzos and other drugs used to treat anx enhance the effects of GABA
Degeneration of cells that secrete GABA in the basal ganglia contribute to symptoms of…
Huntington’s disease
Glutamate
Learning, memory, long term potentiation
Excessive glutamate can lead to…
Seizures, Huntington’s, Alzheimer’s
The central nervous system consists of…
The brain and spinal cord
Five segments of the spinal cord
Cervical Thoracic Lumbar Sacral Coccygeal
Quadriplegia v paraplegia
Paraplegia - damage to the thoracic spinal area
Loss of sensory and voluntary functioning in the legs
Quadriplegia - damage at the cervical spinal area
Loss of sensory and voluntary functioning in the arms and legs
(Incomplete transection means some sensory or motor function may still remain)
Three layers of the meninges
Dura matter
Arachnoid space (full of CSF)
Pia matter
Cerebral ventricles
Four hollows in the Brian full of CSF
Hydrocephalus
Larger than normal cerebral ventricles
Caused by an obstruction in CSF flow
Job of the peripheral nervous system
Relay messages between the central nervous system and the body’s sensory organs, muscles, and glands
The divisions of the PNS
Somatic
- skeletal muscle control (voluntary)
Autonomic
- smooth muscle control (involuntary)
- sympathetic and parasympathetic divisions
Somatic nervous system
Part of the PNS
Carry information from body’s sensory receptors to the CNS and our to the skeletal muscles
Voluntary movement
Autonomic nervous system
Part of the PNS
Handle signals from the receptors in the body’s viscera, to the CNS, and out to the smooth muscle, cardiac muscle, and glands
(Involuntary stuffs)
Contains sympathetic and parasympathetic divisions
Sympathetic nervous system
Part of the autonomic nervous division in the PNS
Associated with arousal and expenditure of energy
Parasympathetic nervous system
Part of the autonomic division of the PNS
Involved in conservation of energy and relaxation
Five stages of CNS development
Proliferation - new cells produced inside neural tube (2.5wks)
Migration - neurons move to final destination and aggregate (8wks)
Differentiation - neurons develop axons and dendrites
Myelination - glial cells insulate neurons (postnatal)
Synaptogenesis - formation of synapses (postnatal)
Structural neuroimaging techniques
CAT - xray of the brain
MRI - uses magnets to display brain structures
CAT v MRI
MRI is $$$, CAT is cheaper
MRIs don’t use xrays, better resolution and more detail, can be 3D and provide images at any angle
Functional neuroimaging techniques
fMRI - best resolution, info on brain activity (blood oxygenation)
SPECT - similar to PET with lower resolution
PET - activity thru glucose metabolism, oxygen consumption, blood flow
Structures of the hindbrain
Medulla - life sustaining
Cerebellum - movement coordination and balance
Pons - integration of movement between left and right sides of the body
Medulla
Part of the hindbrain
Swallowing, coughing, life sustaining functions (breathing, heartbeat, blood pressure)
Damage causes death
Damage to the medulla causes
Death
Pons
Part of the hindbrain
Plays a role in the integration of movements in the left and right sides of the body
Cerebellum
Part of the hindbrain
Balance, posture, coordinated movement (when with basal ganglia)
Damage results in ataxia (slurred speech, tremors, loss of balance)
What part of the hindbrain is substantially impacted by alcohol
Cerebellum
Structures of the midbrain
Inferior and superior colliculi - routes for visual and auditory info
Substantia nigra - motor activity and reward systems
RAS - consciousness, arousal, wakefulness
Interior and superior colliculi
Part of the midbrain
Paths for the transmittal of visual and auditory information (respectively)
Substantia nigra
Part of the midbrain
Involved in motor activity and reward systems
Reticular activating system
Part of the reticular formation in the midbrain
Consciousness, arousal, wakefulness
Damage = coma
Damage to the reticular activating system could result in…
Disruption in sleep-wake cycles
Can produce permanent, coma-like sleep
Structures of the forebrain
Thalamus - sensory switchboard Hypothalamus - homeostasis and 4 Fs Basal ganglia - planning, organizing, coordinating voluntary movement Amygdala - emotion and memory Hippocampus - learning and memory
Limbic system
Located in the forebrain
Contains amygdala and hippocampus
Learning, memory, emotion
Thalamus
Located in the forebrain
Acts as a relay station for the processing of sensory information
Wernike-Korsakoff Syndrome and the thalamus
Thiamine deficiency causes atrophy in areas of the thalamus
(Usually the result of chronic alcoholism)
Begins with Wernicke’s symptoms - confusion, dysfunctional eye movements, ataxia
End with Korskoff symptoms - amnesias and confabulation
Hypothalamus
Structure in the forebrain
Vital functions (4 Fs and homeostasis)
Contains the suprachiasmatic nucleus (SCN) - sleep wake cycles and circadian rhythms
Suprachiasmatic nucleus
Located in the hypothalamus of the forebrain
Responsible for regulating sleep-wake cycles and circadian rhythms
Basal ganglia
In the forebrain
Planning, coordination, and execution of voluntary movement
Consists of: substantia nigra, caudate nucleus, puts men
Amygdala
Located in the limbic system of the forebrain
Takes care of motivational activities, and attaches memory and emotion
Flashbulb memories
Kluver-Bucy Syndrome
Damage to the amygdala and temporal lobes
Reduced rear and aggression
Altered eating habits
Hypersexuality
Psychic blindness - inability to recognize meanings of events or objects
Hippocampus
Located in the limbic system of the forebrain
Learning and memory
Consolidation of declarative memories into LTM
Corpus callosum
Bundle of fibers that connects the right and left hemispheres
(If severed, the two hemispheres operate as separate, independent brains)
Contralateral representation
Left hemisphere controls the functions of the right side and vice versa
(Exception of olfaction)
Brain lateralization
Each hemisphere of the brain is specialized for a specific function
R - dominant - spatial processing (geometry), neg emos, nonverbal memory, nonlanguage sounds
L - dominant - language, verbal memory, positive emotions, speech, reading, writing
How was the function of each cerebral hemisphere initially discovered and researched?
Thru split-brain patients (had corpus callosum removed for seizure control)
Show object in left visual field - right hem - can pick the object out from behind screen with left hand (can’t say item or pick with right hand)
Show object in right visual field - left hem - can name and select image with right hand (can’t select with left hand)
Four lobes of the cerebral cortex
Frontal
Parietal
Temporal
Occipital
Important structures of the frontal lobe
Primary motor cortex - motor humunculous, execution of movement, damage results in loss of muscle tone
Supplementary motor area - planning and control of movement
Premotor cortex - control of motor movement in response to external sensory stimuli
PFC - executive function, emotion
Broca’s area - expressive language center
Function of the primary motor cortex
Involved in the execution of movement
Contains motor homunculous
(Damage is determined by where on the homunculous it is - weakness occurs on the opposite side of the body)
Damage to the primary motor cortex results in…
Loss of reflexes and flaccid hemiplegia (loss of muscle tone) in areas of the body that are contralateral to the damage
Purpose of the supplementary motor area
Planning and control of movement
Learning new motor sequences, mental representation of movement (includes other areas)
Function of the premotor cortex
Control of movement in response to external, sensory stimuli
Broca’s Area
Located in inferior left frontal lobe
Major motor speech area - responsible for expressive language
Function of the prefrontal cortex
Involved in a variety of complex behaviors - emotion, attention, self-awareness, executive function
Damage to each region of the prefrontal cortex…
Dorsolateral area - dorsal convexity dysexecutive syndrome
(Impaired judgement, insight, planning, and organization)
Orbitofrontal area - orbitofrontal disinhibition syndrome
(Pseudopsychopathy, poor impulse control, emo lability, aggression, lewd comments and inappropriate sexual behavior)
Mediofrontal area - mesial frontal apathetic syndrome
(Pseudodepression, reduced emo range, diminished verbal and motor output, extremity weakness, sensory loss, impaired spontaneity)
Damage to the dorsolateral area of the prefrontal cortex
Dorsal convexity dysexecutive syndrome
Impaired insight, judgement, planning, and organization
(Concrete, perseverative, trouble learning from experience, neglect hygiene, reduced sexual interest, apathetic)
Damage to the orbitofrontal area of the prefrontal cortex
Orbitofrontal disinhibition syndrome
(Pseudopsychopathy)
Emotional lability, distractibility, poor impulse control, impaired social insight
(Explosive aggressive outbursts, inappropriate humor, lewd comments, engage in inappropriate sexual behavior)
Damage to the mediofrontal area of the prefrontal cortex
Mesial frontal apathetic syndrome
(Pseudodepression)
Impaired spontaneity, reduced emotional reaction, diminished motor and verbal behavior, lower extremity weakness and sensory loss
(Bored, lack motivation, may seem dep without neg cognitions and dysphoria)
Important structures of the parietal lobe
Somatosensory cortex
Governs sensation of temperature, pressure, pain, proprioception, gustation
Common symptoms of parietal lobe damage
Apraxia (inability to perform motor movements despite no issues with motor functioning)
Somatosensory agnosia
Anosognosia (inability to recognize ones own symptoms or disorders)
Damage to the right (non-dominant) parietal lobe
Contralateral neglect (loss of knowledge or interest in the left side of the body)
Damage to the left (dominant) parietal lobe
Ideational apraxia - inability to carry out sequences of actions
Ideomotor apraxia - inability to carry out a single action in response to a command)
Gerstmann’s Syndrome - finger agnosia, right-left confusion, agraphia, acalculia
Agraphia
Aka dysgraphia
Inability to write
Acalculia
Inability to perform simple calculations
Important structures of the temporal lobe
Auditory cortex - processes auditory information
Wernicke’s Area - comprehension of language
Damage to the auditory cortex of the temporal lobe
Results in auditory agnosia
Auditory hallucinations
Other disturbances in auditory sensation and perception
Important structures of the occipital lobe
Visual cortex - responsible for visual perception, recognition, and memory
Damage to the occipital lobe (generally)
Visual agnosia
Visual hallucinations
Cortical blindness
Psosopagnosia
Caused by lesions at the junction of occipital, parietal, and temporal lobes
Inability to recognize familiar faces
Left occipital lobe damage
Simultagnosia (inability to see more than one aspect of an object at a time)
Two theories of color vision
Trichromatic color theory - red, grn, blu receptors that form all other colors
Opponent-process theory - bipolar receptors (r-g, b-y, b-w) stimulated (and inhibited) in different ways produce the colors we see
Trichromatic theory of color vision
Young-Helmholtz
There are three types of color receptors (r, b, g) that are activated in different intensities to produce all the colors we perceive
Opponent-process theory of color vision
Hering
Three types of bipolar cells are stimulated and inhibited in different ways to account for all the colors we perceive (r-g, b-y, b-w)
What phenomenon supports opponent-process theory
Negative after-images
Color blindness
Often the result of a genetic deficiency
(Recessive x-linked trait)
Most common in men
Most common type of color blindness is inability to distinguish between red and green
Achromatopsia
Color blindness
Binocular depth perception cues
Convergence (eyes turn inward the closer an object gets)
Retinal disparity (each eye sees a different, the closer the image the more disparate the two images)
Convergence
Binocular cue
Turning inward of the eyes as an object gets closer (and vice versa)
Retinal disparity
Binocular cue
Our two eyes see the world from two different views…the closer an object, the greater the disparity of the two images
Monocular depth perception cues
Relative size
Interposition of objects (overlap)
Linear perspective
Motion parallax
Purpose of monocular cues
See depth perception for objects at greater distances
Location of the primary olfactory cortex
Orbitofrontal cortex
Processing of olfactory memory
Amygdala
Dermatomes
The area of the body that is innervated by a dorsal root of a given segment of the spinal cord
Damage to nerves (as it relates to dermatomes)
Adjacent dermatomes overlap so that damage to a nerve causes diminished sensation, rather than complete loss of sensation in the corresponding dermatome
Gate-control theory of pain
The nervous system can only process a limited amount of sensory information at any given time
When too much information is being received, cells in the spinal cord act as a gate that blocks some incoming pain signals
Ex. Massaging injured area, applying ice, engaging in distraction mental activities
Coping with pain
Pain is very susceptible to placebos
Active strategy - exercise, physical therapy, distraction, ignoring pain
Passive strategy - taking it easy, relaxing, wishful thinking, medication, limiting activity
Research on active v passive coping strategies
Lower levels of reported pain, greater improvement in psychological and physical functioning associated with active strategies
Synesthesia
Stimulation of one sensory modality triggers a sensation in another sensory modality
Absolute threshold to detecting a stimulus
The minimum stimulus needed to produce a sensation
Difference threshold in stimulus detection
Smallest increment of a stimulus intensity needed to recognize the discrepancy between two stimuli (JND)
Weber’s Law
The more intense a stimulus, the greater the increase in stimulus intensity required for the increase to produce a JND
(JND)
Fetchner’s Law
Physical stimulus changes are logarithmically related to their psychological sensations
(Logs)
Steven’s Power Law
Sensation is an exponential function of stimulus intensity
Power and exponents
Three primary laws of psychophysics
Weber’s law - JND
Fechner’s law - logs
Steven’s power law - exponents
Impact of the temporal lobes on learning and memory
Encoding, storage, and retrieval of declarative LTMs
Damage to the brain as a result of Alzheimer’s
Amyloid plaques in hippocampus, amygdala, and entorhinal cortex
Relation of learning and memory to the amygdala
Responsible for connecting strong emotions to memories
(Flashbulb memories)
Fear conditioning
Implicated in PTSD
How the prefrontal cortex assists in learning and memory
Episodic memory
Prospective memory
Constructive memory and false recognition
Damage to the prefrontal cortex can impact learning and memory in what way…
People may incorrectly claim that new information is familiar
What part of the brain is response for working memory
Dorsolateral prefrontal cortex
Role of the thalamus in leaning and memory
Processing incoming information and transferring to to the cortex
Long-term potentiation
Refers to the greater responsivity of a postsynaptic neuron to low-intensity stimuli, after the neuron has been barraged by high-frequency stimuli
(First studied in aplysia)
Impact of protein synthesis on learning and memory
Learning and memory are dependent on increased protein synthesis and the presence of RNA (which is required for protein synthesis)
Reduced RNA or protein synthesis leads to the prevention of forming long term memories
Broca’s aphasia
Damage to Broca’s area (left side of frontal lobe)
Dysprosidy - poorly articulated speech, lacks normal intonation and stress
Anomia - inability to name common or familiar objects or people
Difficulty repeating phrases
Typically aware of their impairment, and experience frustration, anx, dep
Wernicke’s aphasia
Caused by damage to Wernicke’s area in left temporal lobe
Trouble understanding written and spoken language
Difficulty generating meaningful language
Speech is rapid, effortless, fluent, but meaningless
Typically do not realize their speech is meaningless
Conduction (associative) aphasia
Caused by damage to the arcuate fasciculous (area where Broca’s and Wernicke’s area connect)
Doesn’t impact language comprehension, but does result in anomia, paraphasia, and impaired repetition
Transcortical aphasia
Occurs when damage disconnects Broca’s and or Wernicke’s areas from the rest of the brain
Transcortical motor (isolates Broca’s), transcortical sensory (isolates Wernicke’s, mixed transcortical (both areas isolated)
Transcortical motor aphasia
Damage to the brain isolates Broca’s area from the rest of the brain
Nonfluent, effortful speech, lack of spontaneous speech
Transcortical sensory aphasia
Caused by damage that isolates Wernicke’s area from the rest of the brain
Deficits in comprehension, anomia, fluent and meaningless speech
Mixed transcortical aphasia
Caused by damage that separates Broca’s and Wernicke’s areas from the rest of the brain
Able to talk but have nothing to say
Unable to understand spoken and written language
Can sing familiar songs, repeat phrases spoken by others
Global aphasia
Caused by widespread brain injury involving Broca’s area, Wernicke’s area, and other areas of the Brian
Extensive disruption in language comprehension and production
May be able to produce emotional explanations
Often accompanied by right hemisensory loss, right hemiplegia, and right hemianopia
Four major theories of emotion
James-Lange - physiological sensations lead to emotion
Cannon-Bard - the cortex and PNS receive thalamic stimulation which produce emotion and physiological sensations simultaneously
Two-Factor - physiological arousal plus cognitive interpretation results in specific emotions
Cognitive-appraisal - appraisal of the environment determines the emotion
James-Lange theory of emotion
Emotions represent perspectives of bodily reactions to sensory to stimuli
Ex. You area afraid because your knees are shaking and your heart is racing
Supported by studies of quadriplegics and paraplegics who receive limited info from their bodies and report feeling fewer emotional sensations after their injuries
Cannon-Bard theory of emotion
Thalamic stimulation of the cortex and PNS produce simultaneous bodily sensations/reactions and emotions
Supported by research showing that bodily reactions for all emotions are fairly similar (suggests the nature of emotional experience does not just depend on bodily arousal)
Schachter-Singer Two-Factor theory of emotion
Physiological arousal and cognitive interpretation of that arousal (and the environmental context) produce your subjective emotional experience
Supported by Schachter and Singer’s “epinephrine study”
Cognitive-Appraisal theory of emotion
Lazarus
Emotions are universal but there are differences in how emotion-arousing events are interpreted or appraised
So the appraisal of a situation leads to the emotion
(Ex. Two people with the same cognitive appraisal will feel the same emotion)
Lazarus’s cognitive-appraisal theory of emotion distinguishes between what three types of cognitive appraisal…
Primary appraisal - evaluating a situation as irrelevant, benign, or stressful with regard to their OWN WELLBEING
Secondary appraisal - evaluation of the resources they have to cope with a situation that has been identified as stressful
Re-appraisal - monitors a situation and modifies their primary or secondary appraisals
Papez’s circuit
The neural circuit that mediates the experience and expression of emotion
Areas of the brain key for emotion
Cerebral cortex
Amygdala
Hypothalamus
Emotion and the left hemisphere
Governs happiness and other positive emotions
Damage = depression, anxiety, aggression, paranoia
Emotion and the right hemisphere
Mediates sadness, fear, and other negative emotions
Damage = indifference, apathy, emotional lability, undue cheerfulness or joking
The role of the hypothalamus in emotions
Involved in the translation of emotions into physical responses
Damage = uncontrollable rage behaviors or laughter
General Adaptation Syndrome
Broadly
Mediated by the adrenal and pituitary glands
The response everyone experiences to stress
Three stages: alarm reaction, resistance, exhaustion
Alarm reaction phase of general adaptation syndrome
First phase of GAS - response to stress
Hypothalamus signals the production of adrenaline, which increases energy, heart rate, and respiration
Resistance phase of the general adaptation syndrome
Second stage of the GAS - reaction to stressful situations
Breathing and heart rate returns to normal
Hypothalamus signals the production of ACTH which activates cortisol production (which maintains high blood glucose levels for energy)
Exhaustion state of the general adaptation syndrome
Third stage of the GAS - response to stress
Adrenal and pituitary production of stress hormones tires, and physiological processes begin to break down (results in depression, fatigue, and illness)
Type A Behavioral Pattern
First studied to link emotion and illness
Type A persons are often high-achieving, competitive, easily irritated, urgent, and impatient
Higher incidence of health problems and (in men predominantly) coronary heart disease
Sexual dimorphism
There are sex-related, structural, physical differences in the brain
Related to differential exposure to androgens during prenatal and early postnatal development
Hypothalamic-pituitary-gonadal axis
HPGA releases testosterone or estrogen, which signal the onset of puberty and the development of secondary sex characteristics
Menopause
Cessation of menstruation
Late 40s or early 50s
Reduction of estrogen - vaginal dryness, moodiness, fatigue, hot flashes, nausea, reduced skin elasticity
Hormone replacement therapy
Used to treat negative effects of menopause
Largely helpful, but may not improve sex drive and may increase risk for blood clots and breast cancer
Four types of brainwaves associated with sleep
Beta - awake and alert
Alpha - awake and relaxed
Theta - deep relaxation, light sleep
Delta - deep sleep
Five stages of sleep
Stage 1 - NREM - starts when you fall asleep, alpha become theta
Stage 2 - NREM - theta with sleep spindles and K complexes
Stage 3 - NREM - theta becomes long and slow delta waves
Stage 4 - NREM - delta waves
Stage 5 - REM - beta and theta, physiologically look awake, flaccid paralysis, rapid eye movement
Changes in sleep with age
Infants begin with REM…the transition to beginning sleep with NREM occurs around three months of age
Total sleep, stage 4, and REM decrease with age
Traumatic brain injury
Injury to the brain that is caused by external force that involves temporary or permanent impairments to cognitive, emotional, behavioral, and/or physical functioning
May be open or closed head injury
Closed-head injury
Nonpenetrating blow
Includes the initial blow (coup) and when the brain knocks against the opposite side of the skull (contrecoup) - can also include hemorrhage (bleeding) or edema (swelling)
Typically results in alterations or loss of consciousness and amnesia
Open-head injury
Penetrating blow through the skill (eg. gunshot)
Does not usually cause loss of consciousness, but results in more localized damage and highly specific symptoms based on where the damage was
Three factors for assessing the level of severity in a traumatic brain injury
Score on the GCS
Duration of posttraumatic amnesia
Duration of loss of consciousness
Classifications for TBI severity
Mild (GCS 13-15, less than one hour PTA, less than 30min LOC)
Moderate (GCS 9-12, PTA 1-24 hours, LOC 30min-24 hours)
Severe (GCS 0-8, PTA more than 24 hours, LOC more than 24 hours)
Mild classification of TBI
GCS: 13-15
PTA: less than one hour
LOC: less than 30 minutes
Moderate severity of TBI
GCS: 9-12
PTA: 1-24 hours
LOC: 30min-24hr
Severe classification of TBI
GCS: 0-8
PTA: more than 24 hours
LOC: more than 24 hours
Memory impairment s a result of TBI
Posttraumatic (anterograde) amnesia is a good predictor of the persistence of the symptoms caused by injury (loss of ability to form new memories after an event/injury)
Retrograde amnesia (forgetting past memories) can also occur, however it’s typically “shrinking retrograde amnesia” where memories gradually return
Postconcussional Syndrome
Occurs in up to 50% of persons with mild TBI
Initial sx: nausea, drowsiness, headache, dizziness
Then: cognitive impairment in attention, concentration, processing speed
Finally: depression, anxiety, irritability
Most recover within 3 months
Cerebrovascular accident
Aka stroke
Refers to a sudden or gradual onset of neurological symptoms resulting from a disruption of the blood supply to the brain
Three major causes of stroke/CVA
Thrombosis (blood clot)
Embolism (sudden blockage of an artery)
Hemorrhage (brain bleed)
Symptoms of stroke/CVA
Contralateral hemiplegia
Contralateral hemianesthesia (face, arm, leg)
Contralateral visual field loss
Neuropsychiatric symptoms that often follow a stroke/CVA
Depression! Typically occurs immediately, but can also occur several months later
Anxiety, mania, apathy, psychosis, dementia, pathological crying or laughter
Two major disorders of movement
Huntington’s - emo and cog sx, fidgeting, facial grimaces, clumsiness, jerky involuntary movements (chorea), eventually dementia
Parkinson’s - positive sx (resting tremor, rigidity), negative sx (slowed movement, speech difficulty, postural disturbance), depression
Seizure
Abnormal electrical signals in the brain that causes one or more of:
1 - aura that signals the onset of a seizure
2 - loss of consciousness
3 - some type of abnormal movement
How to diagnose seizures
Medical hx and physical exam
EEG to observe abnormal electrical signals in the brain
MRI/CT to determine if the seizures are due to a lesion or other abnormality in the brain
Tonic-clonic (grand mal) seizure
Includes tonic stage (muscle contract) and clonic stage (muscle shaking or jerking)
Postictal depression, confusion, or amnesia for the ictal event may occur after the seizure
Absence (petit mal) seizures
Brief attacks including loss of consciousness (no prominent motor symptoms)
May look like a blank stare, or have fluttering eyes
Thalamus may be indicated in absence seizures
Partial seizures
Usually have a focal starting point
Affects usually only one side of the body - sx depend on where the seizure activity is in the brain
Simple partial (no loss of consciousness), complex partial seizures (loss of consciousness)
Partial seizure sxs by brain lobe
Temporal (most common) - stereotyped movements, hallucinations, changes in personality
Frontal - jerky motor sx, inability to talk, olfactory sx
Parietal - unusually physical sensations on the opposite side of the body
Occipital - rapid eyeblinking, unusual visual phenomena
Cause of Huntington’s disease
Autosomal dominant gene
50% chance of inheriting if if your parent is a carrier
Cause of Parkinson’s disease
Progressive degeneration of dopamine-containing cells in the substantia nigra
Cause of multiple sclerosis
Demyelination of the nerve fibers of the brain and spinal cord
Issues may stem from autoimmune response where body attacks its own myelin
Two types of MS
Relapsing-remitting type - alternating periods of relapse (sx) and remission (partial or complete recovery)
- many relapsing-remitting pts eventually get secondary progressive
Secondary progressive type - gradual worsening periods without periods of relapse and remission
Relapsing-remitting type of MS
Experiences periods of symptoms (relapse) and periods with complete or partial symptom remission (remission)
Most patients eventually progres to secondary progressive type
Secondary progressive type of MS
Gradual worsening of symptoms without periods of remission or relapse
Symptoms of MS
Initial - eye pain or blurred vision, fatigue that worsens in afternoon, motor impairment (weakness, clumsiness, balance issues)
Progressive - tremor, speech and swallowing problems, hearing loss, dep, anx, cog sx
Psychophysiological Disorders
Used to describe physical symptoms that are caused, maintained or exacerbated my emotional factors
Hyperventilation, hypertension, fibromyalgia, migraines, PMS
Hyperventilation
A psychophysiological disorder
Panic attack - chest pain, numbness, dizziness, impaired concentration, tinnitus, etc.
Hypertension
A psychophysiological disorder
Primary - no physical cause
Secondary - related to a known physical cause
Treatment for hyperventilation
Relaxation
Breathing into a paper bag
Sedation
Treatment for hypertension
Lifestyle modification
Blood pressure medication
Blood pressure biofeedback
Fibromyalgia
A psychophysiological disorder
Muscle aches, tenderness, stiffness, fatigue, sleep disturbances
More common in females
Treatment of fibromyalgia can include
Psychological treatments
Especially behavioral methods
Migraines
A psychophysiological disorder
Throbbing headache limited to one side of the head, includes nausea, vomiting, diarrhea, sensitive to light/noise/smells
General (no aura) and classic (contains aura)
Treatments for migraines
NSAIDS
SSRIs
Beta-blockers
Precipitates or aggravating factors for migraines
Stress
Alcohol
Changes in barometric pressure
Menstruation
Foods
Connection between migraines and personality
(More common in females)
Perfectionism Orderliness Neuroticism Inflexibility Ambitious ness
Differential dx for migraines
Cluster headaches - occur behind one of the eyes, burning
Tension headache - nonthrobbing, one or both sides of neck and head
Sinus headache - occur over the eyes, felt worse when bending over
Three major components to the endorcrine system
Pituitary gland - master gland - acts in the kidneys and important for growth
Thyroid gland - metabolism (secretes thyroxine)
Pancreas - involved in uptake and use of glucose (releases insulin)
Hyposecretion of ADH from pancreas causes…
Dwarfism
Hyperscreation of ADH from pancreas causes…
Gigantism
In adulthood - acromegaly (large hands, feet, facial features)
Purpose of pancreas
Secrete growth hormones (ADH)
Job of the thyroid gland
Regulate metabolism thru the release of thyroxine
Job of the pancreas
Regulate the uptake and use of amino acids and glucose (releases insulin)
Hypersecretion of thyroxine…
Hyperthyroidism
Sx: weight loss, fast metabolism, increased appetite, high body temperature, heat intolerance, irritability, emotional lability, impaired attention span
Hyposecretion of thyroxine results in…
Hypothyroidism
Sx: weight gain, decreased appetite, low body temperature, depression, apathy, lethargy, concentration and memory deficits
Hyperinsulinism results in
Hypoglycemia (low blood glucose)
Hunger, dizziness, headaches, palpitations, anx, dep, confusion
Hypoinsulinism results in
Diabetes mellitus (excessive blood glucose)
Increased susceptibility to infection, increased appetite, mental dullness
Psychoactive drugs
Ideals that interact with the CNS in a way that produces a change in mood, consciousness, perception, and/or behavior.
Agonist drugs
Produce similar effects to those of neurotransmitters
Direct - mimic the NT
Indirect - bind and facilitate NT action
Antagonist drugs
Reduce or block the effects of a neurotransmitter
Direct - attach to a receptor site and block
Indirect - attach elsewhere and interfere with the action of the NT
Inverse agonist
Produce an effect that is opposite that of the neurotransmitter
Partial agonist
Produces effects that are similar but less than the effects of the neurotransmitter
Types of agonists
(Agonists bind and increase effects of a neurotransmitter)
Direct - bind and mimics the NT
Indirect - bind elsewhere and facilitate action of the NT
Inverse - produces opposite effect of the NT
Partial - binds an produces a similar but less effect than the NT
Factors that contribute to medication-related problems in people over age 65
The use of multiple medications
Medication noncompliance
Decreased or increased sensitivity to drug effects
Changes in renal fxning (poor functioning means medications process through more slowly, increasing their half-lives and the risk of toxicity)
Cross-ethnic differences in responses to psychotropic medication
Higher proportions of Asians and African Americans are poorer metabolizers of some psychotropic medications
So start at a lower dose and titrate up to avoid a sudden presentation of harsh side effects that lead to discontinuation or meds
What symptoms do traditional (conventional) antipsychotics treat
Positive symptoms (delu, halu) associated with psychosis, organic psychosis, or psychotic symptoms associated with MDD
Generic names for traditional antipsychotic drugs
Chlorpromazine
Fluphenazine
Thiothixene
Haloperidol
Traditional antipsychotic mode of action
Blocking D2 dopamine receptors
Dopamine hypothesis - schizo sx due to increased sensitivity to DA or overproduction of DA
Side effects to traditional antipsychotics
Anticholinergic effects - dry mouth, water retention, blurred vision
Extrapyramidal symptoms - tardive dyskinesia
Neuroleptic malignant syndrome - MATH, can be fatal
Anticholinergic effects
Side effect of antipsychotic medication
Dry mouth, blurry vision, water retention/constipation, tachycardia, delayed ejaculaton
Mechanism for extrapyramidal symptoms
Result of the antipsychotic drug on DA receptors in the caudate nucleus
Most common extrapyramidal side effects
Parkinsonism
Akathisia (extreme restlessness)
Acute dystonia (muscle spasms in mouth, face, and neck)
Most severe extrapyramidal symptom
Tardive dyskinesia
Six similar to Huntington’s, involuntary movements of limbs and face
May be reversible if medication is gradually withdrawn
Neuroleptic malignant syndrome
MATH
Muscular rigidity
Altered consciousness
Tachycardia
Hyperthermia
Can be fatal if drug is not discontinued right away if these symptoms develop
Types of atypical antipsychotic medications
Clozapine
Risperidone
Olanzapine
Quetiapine
Use for atypical antipsychotics
Psychosis and schizophrenia
For psychosis that is not otherwise treated by traditional antipsychotics
Clozapine: Treatment-resistant bipolar, depression and suicidality, hostility
Mode of action for atypical antipsychotics
Act on D4 and other dopamine receptors
As well as some receptors for serotonin and glutamate
Advantages and disadvantages of atypical antipsychotics
Adv - much less chance of extrapyramidal symptoms and tardive dyskinesia, can be used when traditional antipsychotics have failed
Disadv - have slower therapeutic effects than transitional antipsychotics (takes longer for them to work)
Side effects of atypical antipsychotics
Anticholinergic effects - dry mouth, water retention, tachycardia
Neuroleptic malignant syndrome - MATH
Agranulocytosis - decrease of certain white blood cells
(Requires blood monitoring)
Agranulocytosis
A marked decrease in a certain type of white blood cell
Possible side effect of atypical antipsychotics
Why do atypical antipsychotics require blood monitoring
To monitor for the presence of agranulocytosis
Marked decrease of a certain type of white blood cell
Two types of antipsychotics
Traditional (chlorpromazine, haloperidol)
Atypical (clozapine, risperidone)
Three major types of antidepressants
TCAs - imipramine, amitriptyline
SSRIs - fluoxetine, sertraline, paroxetine
MAOIs - isocarboxazid phenelzine
Uses for tricyclic antidepressant medications
Depression with a lot of vegetative or somatic symptoms
Weight loss, sleep disturbance, psychomotor retardation, anhedonia
Mode of action for TCAs
Block reuptake of NE, serotonin, and/or dopamine
Support catecholamine hypothesis that depression is caused in part by low levels of norepinephrine
Primary side effects of TCAs
Cardiotoxicity (high or low blood pressure, tachycardia, arrhythmia)
Anticholinergic effects
Cognitive impairment
Weight gain
Overdose and TCAs
Can be lethal
Prescribe in small doses for those at increased risk for suicide
Indications for SSRIs
Melancholic depression
PTSD
Mode of action for SSRIs
Blocks reuptake of serotonin specifically
Side effects of SSRIs
Frequent unrination
Gastrointestinal issues (nausea)
Insomnia
Sexual dysfunction
Dizziness and headache
TCAs vs SSRIs
SSRIs are less cardiotoxic
Less toxic in overdose
Less likely to produce cognitive impairment
Most widely prescribed antidepressant
Fluoxetine (Prozac)
SSRI
BUT accompanied with black box warning about increased risk for suicide
SSRI combined with MAOI
Serotonin syndrome
Neurological effects, changes in mental state, cardiac arrhythmia
Can result in coma and death
Use of MAOIs is indicated in what cases…
Atypical depression
- hypersomnia, hyperphagia, interpersonal sensitivity
Method of action for MAOIs
Inhibit monoamine oxidase, which is involved in deactivating DA, serotonin, and norepinephrine
Side effects of MAOIs
Hypertensive crisis
- taken with barbiturates, certain foods or beverages that contain tyramine
Headache, stiff neck, rapid heart rate, nausea, sensitive to light
Seek emergency treatment
Two newer antidepressants
SNRI - serotonin norepinephrine reuptake inhibitor (venlafaxine)
(Used for pain, may act more quickly in the body)
NDRI - norepinephrine dopamine reuptake inhibitor (bupropion)
(No sexual dysfunction but could exacerbate psychosis or seizures)
Two main mood stabilizing drugs
Lithium
Carbamazepine
Indications for lithium salts
Classic bipolar disorder
- mania
- no rapid cycling episodes
Limits mania and reduces mood swings
Side effects of lithium salts
Gastrointestinal effects (nausea, vomiting, metallic taste) usually subside in a few weeks
Toxicity is the major danger (dose is too high) - slurred speech, tremor, confusion
Also, increases body’s salt - so watch sodium, alcohol, caffeine, and diuretics
Anticonvulsant drug indicated for the treatment of mania/mood swings
Carbamazepine
Indications for carbamazepine
Mania
Bipolar disorder that does not respond to lithium
Rapid cycling
Side effects of carbamazepine
Cardiovascular effects
Dizziness
Rash
Visual disturbance
Types of sedative-hypnotic drugs
Barbiturates (-barbitals)
Benzodiazepines (diazepam, alprazolam)
Alcohol
Barbiturates
Suppress activity in the RAS
Initially used for sedative properties but no longer prescribed that often due to the side effects and risk of death
SEs: dizziness, impaired cog fxn, poor REM sleep
Effect of low, moderate, and high doses of sedative-hypnotic drugs
Low doses - reduce arousal and motor activity
Moderate doses - sedation and sleep
High doses - anesthesia, coma, death
Types of benzodiazepines
Diazepam
Alprazolam
(Sedative-hypnotics)
Mode of action for benzodiazepines
Stimulate the inhibitory action of GABA
Why are benzodiazepines prescribed
Relief of anxiety
Sleep disturbances
Side effects of benzodiazepines
Drowsiness, dizziness, lethargy, slurred speech, ataxia, impaired psychomotor abilities
Rebound excitability
Psychological dependence, physical dependence
The clinical indications of beta-blockers
Physical sx of anxiety
Heart conditions
Tremors
High blood pressure
Primary beta-blocker used today
Propranolol
Most common psychostimulant
Methylphenidate
Purpose of psychostimulants
Treatment of ADHD
Side effects of psychostimulants
Restlessness
Depression/irritability
Tolerance and dependence
Stunted growth (hence “drug holidays”)
“Drug holidays”
When people (children, most commonly) are temporarily removed form their psychostimulants, usually over summer holidays.
Purpose: determine if drug is still needed, minimize growth suppression and other side effects
Naltrexone (fxn and SEs)
Used to reduce reinforcing effects and cravings for alcohol
SEs: abdominal cramps, nausea, vomiting, insomnia, joint and muscle pain
