Neuropsychology Flashcards
Central Nervous System (CNS)
Brain → hindbrain, midbrain, forebrain
Spinal cord → 31 segments, 5 groups: cervical, thoracic, lumbar, sacral, coccygeal
Peripheral Nervous System (PNS)
Somatic nervous system → regulates sensory/voluntary motor activity by relaying info from senses (sight, hearing, smell, taste, touch) to CNS + controls skeletal muscles
Autonomic nervous system → regulates activities that are involuntary, e.g., HR, breathing, blood pressure, skin temps; maintain balance/homeostasis
- Sympathetic nervous system – active during “flight-or-flight,” blood pressure, slow down HR, restorative functions (digestion/elimination)
- Parasympathetic nervous system – helps body relax/conserve energy, controls normal daily functioning, e.g., digestion
Sensory neurons (afferent)
Carry info to the CNS
Motor neurons (efferent)
Carry info away from CNS to muscles and glands
Conduction
Neural impulses transmitted w/ in neuron by electrochemical process; begins w/ dendrites, stimulated by adjacent cells
All-or-none law
Any charge that the cell fires above the threshold does not increase the magnitude of the action potential
Synaptic transmission
Transmission of neural impulses from 1 neuron to the next; occurs when action potential reaches axon’s terminal buttons, which causes release of neurotransmitter in synapse
Acetylcholine (ACh)
Neurotransmitter
Control of voluntary movement, memory/cognition
(depletion of ACh = memory loss w/ Alzheimer’s)
Think about ACE card flexing/contracting muscles
Dopamine
Neurotransmitter
Controls movement, learning, and reinforcing effects of stimulants, nicotine, and opiates (abnormal levels linked w/ depression, schizophrenia, Tourette’s, ADHD, Huntington’s, and Parkinson’s)
Think about small dwarf “dopey” is parking a car (low dopamine associated w/ Parkinson’s); tall dopey is skiing (high dopamine associated w/ schizophrenia)
Norepinephrine
Neurotransmitter
MOOD, pain, sleep
depression – low NE
mania – excesses NE
Serotonin (5HT)
Neurotransmitter
regulate anxiety, mood, memory, aggression, pain, sleep, appetite, sexuality
Deficiences in mood disorders (medications used to treat anxiety, depression)
Low S and low N = depression
Low S and high N = mania
Think about “Sir Rotten,” he’s always in a rotten mood (low levels of serotonin associated w/ depression)
GABA
Neurotransmitter
inhibitory control for motor control and regulates anxiety, CALMING EFFECT
Abnormal levels linked to insomnia, anxiety, Huntington’s, and Parkinson’s disease
Too little GABA → anxiety and seizure disorders
Benzodiazepine (Xanax, valium) = GABA antagonists
Glutamate
Neurotransmitter
excitatory neurotransmitters, role in learning and memory
Abnormal levels linked to Huntington’s, Parkinson’s, Alzheimer’s (high levels); implications → OCD, ASD, depression, schizophrenia (w/ high dopamine)
Endorphins (“endogenous morphine”)
“endogenous morphine”
neuromodulators that reduce feelings of pain/producing feelings of pleasure
runners high
Think of “runner’s high” → running door w/ fins looks happy
Thyroxine
Hormone
Released by thyroid, regulates metabolism
hyperthyroidism – oversecretion; speeds up metabolism and causes increased appetite, accelerated heart rate, nervous/agitation, impaired attention
*symptoms can mimic anxiety symptoms, manic episode
** most common type = Graves’ Disease
hypothyroidism –undersecretion; causes slows down metabolism and causes reduced appetite
*symptoms can mimic depression
Insulin
Harmone
Released by pancreas to help body use glucose and amino acids
Undersecretion causes diabetes mellitus, leads to high blood glucose level, which causes increased appetite w/ weight loss, frequent urination, thirst, infections, and eventually heat attacks, strokes, kidney failure
Oversecretion causes hypoglycemia,
which involves intense hunger, headaches, visual disturbances, anxiety, depression, confusion
Cortisol
Hormone
secreted by adrenal gland and helps regulate blood glucose levels
Undersecreton –> causes Addison’s Disease
- characterized by fatigue, decreased appetite/weight loss irritability, depression, darkening of skin pigmentation
Oversecretion –> causes Cushing’s disease, which involves obesity, hypertension, impaired memory, depression, decreased libido
Medulla
Hindbrain
Controls breathing, heart rate, digestion
Think of an Olympic athlete wearing medals around his/her heart and lungs
Pons
Hindbrain
Relay sensory and motor info + regulates states of arousal
add a D to the end of pon = ponds, think about ponds (and walking) being relaxing
Cerebellum
Hindbrain
balance, coordinates movement, controls posture
Reticular activity system (RAS)
Midbrain
screens incoming sensory info especially during sleep and arouses higher center of brain when it is important info should be paid attention to
reTICULar formation – if you were TICKLED while asleep your re-TICKLE-ular formation would ALERT you
Substania nigra
Midbrain
helps control movement (degeneration of dopamine-producing neurons contribute to PARKINSON’S); also plays a role in REWARD-seeking and addictive behaviors
*damage to substantial nigra in basal ganglia produces excessive motor activity
Hypothalamus
Forebrain – subcortical structures
maintaining body’s homeostasis, eating/drinking, sexual behaviors
Think of 5 F’s (fever, feeding, fight/flight, falling asleep, sex (F***)
Think of a hypo-the-llamas (picture a hypo spraying 2 thirsty lamas w/ water to quench their thirst and cool them down)
Cingulate gyrus
SATISFACTION CENTER – mediates the feelings of satisfaction that follow eating and sex
Mammillary bodies
Forebrain – subcortical structures; in the hippocampus
play a role in memory
Thalamus
Forebrain – subcortical structures
(“central relay station”) – relays incoming sensory info to (except for olfactory info) to cortex + involved in language, memory, and motor activity
Think about Hal and Amos (traffic cops) relaying information to different areas of brain for processing
Basal ganglia
Forebrain – subcortical structures
includes caudate nucleus, globus pallidus, and putamen – all involved in control of voluntary movement (muscle and fine motor movements)
inhibited movement (brake), EF, motor learning
Dysfunction:
Huntington’s – abnormalities in CAUDATE NUCLEUS and PUTAMEN in BASAL GANGLIA
Parkinson’s – degeneration of dopamine-producing cells in SUBSTANTIA NIGRA (part of BASAL GANGLIA)
Limbic system
Forebrain – subcortical structures
(“emotional brain”) – mediates emotional component of behavior + includes amygdala and hippocampus
Amygdala - (AGGRESSION) integrates/directs emotional reactions and attaches emotion to info receives from senses
Septum (SIMMER DOWN) – inhibits emotionality
Cingulate cortex – attention, emotion, perception, and subjective experience of pain
Hippocampus (MEMORY) – involved w/ memory than emotion + facilitates transfer of info from short to long-term memory
Contralateral representation
Forebrain – hemisphere of the cerebral cortex
Right hemisphere controls functions on the left side of body and vise versa
Left hemisphere of brain
Left (dominant) hemisphere → ( language + logic) verbal functions, written/spoken language, rational/analytical thinking, expression of positive emotions
Right hemisphere of brain
Right (nondominant) hemisphere → visual-spatial, holistic/creative thinking, expression of negative emotions
Frontal lobe (of cerebral cortex)
Frontal lobe – motor behavior, expressive language, high-order cognitive functions
1) Primary motor cortex
2) Broca’s area (production of written or spoken language)
- Damage produces expressive aphasia
3) Prefrontal cortex
- Damage cases cognitive impairment/personality change
Temporal lobe (of cerebral cortex)
Temporal lobe – auditory processing (including receptive language) and memory
1) Auditory context
- Damage can produce auditory agnosia or hallucinations
2) Wernicke’s area (comprehension of language)
- Damage produces receptive aphasia
Parietal lobe (of cerebral cortex)
Parietal lobe – contains the somatosensory cortex + involved in processing info related to touch-pressure, kinesthesia, pain, temperature
Damage might cause anosognosia, ideomotor apraxia, contralateral neglect, or Gerstmann’s syndrome
Occipital lobe (of cerebral cortex)
Occipital lobe – contains visual cortex + involved in processing visual info
Damage can cause cortical blindness, loss of dept perception, or visual agnosia
- Damage at the junction of the occipital, temporal, and parietal lobes can cause prosopagnosia (inability to recognize familiar faces)
Split Brain Patients
Corpus callosum has been severed
- think of corPLUS calloSUM – connects (and bridges the gap between) the left/right hemispheres
Split brain pts have no communication between left and right hemispheres
Broca
Expressive language, produce speech
- Location: left frontal lobe
Broca’s broken language
Wernicke
Receptive language, comprehend speech
- Location: left temporal lobe
Wernicke’s comprehension is crappy
Aphasia
loss of language – ability to speak
Broca’s aphasia (damage to dominant [left] hemisphere, frontal lobe)
“Broken Broca’s”
- choppy speech, dysarthria (difficulty speaking, short phrases, lengthy pauses, telegraphic speech, leave out words)
- CAN comprehension
- EXPRESSIVE, MOTOR APHASIA
Wernicke’s aphasia (damage to left temporal lobe)
“Wernicke’s comprehension is crappy”
- they don’t understand language (can’t comprehend)
- CAN speak fluently but does not make sense (you can’t comprehend them)
- unaware of their problems (anosognosia)
- RECEPTIVE, SENSORY APHASIA
Conduction aphasia (damage to area that connects Broca’s and Wernicke’s)
- rare
- can understand (comprehension intact)
- impaired ability to repeat phrases
Global aphasia
- global = large
- all language difficulty
Anomic aphasia
- difficulty recalling words/names
Transcortical aphasia (damage outside of main lang centers of Broca’s or Wernicke’s)
- can repeat language but can’t do it spontaneously
Dementia
impairment in memory + at least 1 of the following
- aphasia, language problem, agnosia, apraxia or disturbance of EF (abstracting, planning, sequencing)
- interferes w/ work, social activities, and declines earlier than other functioning
- impairment due to medical process
HINT: memory + (if you just had a memory problem it would be amnestic/amnesia disorder)
equally found in men and women
Alzheimer’s = most common type of dementia
- other types of dementia = Vascular Dementia, Dementia with Lewy Bodies, Mixed Dementia
Alzheimer’s
- memory problems, apathy/depression
- disorientation, confusion, problems with motor movements, and ADL
- widespread damage to hippocampus/amygdala
- decrease in neurotransmitter acetylcholine (ACh) – learning an memory
- more common in women (b/c they live longer)
Vascular Dementia
Dementia with Lewy Bodies
Mixed Dimension
Vascular dementia
-more common in men
- caused by mini strokes – seen in people w/ high blood pressure
- more abrupt, stepwise (plateau, decline, plateau, decline)
- die w/ in 2-3 years
Dementia w/ Lewy Bodies (abnormal clumps)
- looks like Alzheimer’s but people experience sleep/vision issues
- changes in attention, EFs, ritualistic behavior
- found in Parkinson’s
Mixed Dimension
- coexists w/ another dimension
- more common than it was believed to be before
Korsakoff’s syndrome
memory disorder associated w/ alcohol abuse
Korsakoff’s is an amnestic disorder
- Have antegrade amnesia
- May have severe retrograde amneisa too
Another key factor = confabulations in speech (emergence of memories for experiences that never really took place)
James-Lange Theory
Theory of emotion
Emotions represent interpretations of body reactions and behavior (e.g., we’re afraid bc we tremble)
E.g., stimulus: sight of a bear → pounding heart [physiological arousal] → fear [emotional response]
Cannon-Bar Theory
Theory of emotion
Emotions reflect simultaneous activity in the sympathetic nervous system and cortex in response to stimuli in environment (sympathetic nervous system produces physical arousal, while cortex produces emotional feelings)
E.g., stimulus: sight of a bear → physiological arousal [pounding heart] + emotional response [fear]
Schachter and Singer’s cognitive-arousal theory
Theory of emotion
views emotions as related to physical arousal and cognitive attribute for the cause of the arousal
E.g., sight of oncoming car → pounding heart [arousal] + cognitive label [I”m afraid”] together = fear [emotion]
Lazarus’s Cognitive Appraisal Theory
“Lazarus label’s first”
cognitive label –> physiological response + emotion
Sleep
5 Stages of Sleep
- Non-REM sleep = Stages 1-4
1) Theta stage – transitional stage to being awake to going to asleep
2) Body decreases in temp and slows down – Sleep Spindles
3, 4) Delta stage – deep sleep (Delta Deep Sleep)
- REM sleep (rapid eye movements) = Stage 5
- dreams occur during REM and non-REM but dreams are more vivid/bizarre during REM sleep
Beta waves – state of alertness (beta - better be alert)
Alpha waves – relaxation (ahh relax!)
Sleep patterns
- Total time in stages 3 and 4 and REM sleep decrease from childhood to adulthood
- Older adults exhibit advanced sleep phase – they fall asleep and awaken earlier
- People deprived of REM sleep, display REM rebound when permitted to sleep normally
- older adults have increased non-REM sleep in stages 1 and 2, and decreased absolute amounts of REM
Brain structures (for Memory)
- Amygdala (attaches emotions to memories)
- Hippocampus (memory consolidation)
- Prefrontal cortex (working memory + ability to do something in future)
- Temporal lobes (storage of long-term declarative memories)
Neural mechanisms (for Memory)
- Long-term potentiation (change in sensitivity of neurons and structures of their dendrites as a result of high-frequency stimulation)
- Protein synthesis (important in the formation of long-term memories)
Vision – rods vs. cones
Rods – responsible for seeing black and white
Cones – responsible for seeing colors
Young-Helmholtz trichromatic theory
1 of the 2 main theories of color vision
Proposes 3 types of cones that respond to
- red
- blue
- green
It applies to the 1st level of processing in the retina
Hering’s opponent-process theory
1 of the 2 main theories of color vision
Proposes that there are 3 types of opponent-process cells
- red-green
- yellow-blue
- white-black
It applies to the 2nd level of processing that occurs as visual signals pass from retina to visual cortex
(e.g., why after starting at a green square and then a blank piece of paper we see a red image)
Color Blindness
Usually caused by genetic defect on the X chromosome, so men are more likely than females to be color blind (most common cant tell difference btwn red/green)
can also be caused by an injury that affects the retina, optic nerve, or other part of visual system
Gate-control theory
How we experience feel pain/how we feel it is not directly related to activation of pain receptors (e.g., somebody steps on your toe, pain receptors are activated, but rather neural gates in spinal cord that medicate signal and either stop them or continue to brain)
pressure closes the gate
Neuropathic Pain
Caused by nervous system trauma, surgery, disease, and certain drugs
Phantom limb pain is an e.g., of this that can occur when a limb is amputated and is believed to be result of damage to neurons in central or peripheral nervous system – treated by antidepressants, opioids, anticonvulsant drugs, topical analgesics
Synesthesia
Synesthesia (“joining senses”) is an involuntary perceptual condition in which stimuli in 1 sensory modality spontaneously elicit a sensation in another sensory modality
Most common = grapheme synesthesia – numbers or letters are associated w/ specific colors
Eg man giving numbers and letters attributes — different sensory signals get crossed
Weber’s Law
1 of 3 psychophysical laws proposed to explain relationship btwn magnitude of physical stimuli and psychological sensations
“just noticeable difference” for any stimulus increases in size in direct proportion to magnitude of the stimulus
when in a noisy place, must shout to be heard, while when in a quiet place a whisper works
Fechner’s Law
Law proposed to explain relationship btwn magnitude of physical stimuli and psychological sensations
Fechner’s Law predicts that psychological sensation is logarithmically related to the magnitude of the physical stimulus
Stevens’s power law
Law proposed to explain relationship btwn magnitude of physical stimuli and psychological sensations
Stevens’s power law proposes that there is an exponential relationship between psychological sensation and the magnitude of a physical stimulus, with the exponent varying for different kinds of stimuli
Structural vs. functional brain imaging techniques
Structural techniques
- determine structural changes due to blood clots, tumors, strokes, infection, etc.
- CT** or CAT scan, MRI
Functional techniques
- provide info on neural activity and movement and now the brain is functioning at the moment in time
- PET scan, SPECT, functional MRI (fMRI) - looks at blood flow
- EEG (useful for diagnosing seizer disorder)
Stroke
2 types of strokes (cerebrovascular accident)
1) Ischemic stroke – occurs when an artery that supplies blood to brain becomes blocked
2) Hemorrhagic stroke – occurs when a weakened blood vessel ruptures or leaks
Consequences of a stroke
A) MIDDLE CEREBRAL ARTERY (supplies blood to parts of frontal, temporal, and parietal lobes + basal ganglia) - contralateral hemiplegia (opposite side paralysis of body) and hemiparesis (weakness in one side of body) in face and arm
- visual field loss in both eyes
- aphasia if dominant hemisphere affected
- contralateral neglect/denial of deficits if non-dominant hemisphere affected
B) ANTERIOR CEREBRAL ARTERY (supplies areas of front and parietal lobes, corpus callosum, and caudate nucleus)
- contralateral hemiplegia, usually in the leg
- impaired judgment and insight
- personality change
- incontinence (loss of bladder control)
C) POSTERIOR CEREBRAL ARTERY (supplies blood to the thalamus, temporal lobe, and occipital lobe)
- cortical blindness (loss of vision)
- visual agnosia (loss of ability to identify visual objects/people by sight); visual and other visual deficits
- language impairment
- memory loss
depression more associated w/ strokes that cause damage to left hemisphere, damage to right hemisphere can cause indifference (or euphoria or mania)
greatest improvement in symptoms following a stroke ordinarily occurs during 1st 3-6 months
Traumatic Brain Injury (TBI)
2 categories of TBI
(1) Open Head Injuries (contusion)
- when skull IS penetrated, e.g., by gunshot or knife
- produce focal symptoms (related to the area of brain damage) + resolve rapidly
- do not cause a loss of consciousness
(2) Closed Head Injuries (concussion)
- when blow to head DOES NOT penetrate the skull
- cause more widespread damage
- usually followed by a loss of consciousness
- when regain consciousness, experience combo of emotional, behavioral, physical, and cognitive symptoms
(1) Concussions
- more common than contusions
- may cause short-term impacts such as consciousness (little injuries throughout the brain that tend to cause functional rather than structural damage), antegrade/retrograde amnesia (usually for events right before the incident not older events), etc.
(2) Contusions
- cerebral bruises by severe blows to head that cause bleeding and bruising
- spreads to the opposite side
- concern for cerebral swelling and life threatening
- frontal (EF) and temporal lobe (irritability) most common
Measures used to assess severity:
- Glasgow Coma Scale (GCS)
- Duration of Post-Traumatic Amnesia (PTA)
- Duration of Loss of Consciousness (LOC)
Mild:
- GCS = 13-15
- PTA = < 1 hr
- LOC = < 30 mins or none
Moderate:
- GCS = 9-12
- PTA = 1-24 hrs
- LOC = 30mins-24 hrs
Severe:
- GCS = < 8
- PTA = 24 hrs<
- LOC = 24 hrs<
Prognosis related to severity/location of injury; greatest recovery during first 3 months w/ significant additional improvement continuing during 1st year
Postconcussional Syndrome (PCS)
Many people w/ TBI (especially mild TBI) develop a postconcussional syndrome (PCS) that lasts for several months + involves multiple symptoms
- Symptoms = irritability, fatigue, headaches, dizziness [first 4 most common], memory impairment, and emotional instability
** apraxia not usually a symptom of PCS
Person w/ PCS would get DSM-5 diagnosis of Major or Mild Neurocognitive Disorder due to Traumatic Brain Injury
(a) Symptoms meet Major or Mild Neurocognitive Disorder
(b) Evidence of a traumatic brain injury w/ 1+ symptoms: loss of consciousness, posttraumatic amnesia, disorientation and confusion, neurological signs (e.g., a new onset of seizures, visual field cuts, hemiparesis)
(c) Neurocognitive disorder presents immediately after TBI or recovery of consciousness and persists past acute post-injury period
Huntington’s disease
- degenerative disease caused by autosomal dominant gene
- unwanted thursting movement in body (choreaform movements)
- combination of affective + personality changes
- abnormalities in the basal ganglia and cortex
Parkinson’s disease
- movement (degenerative brain) disorder
- involving abnormalities in movement – difficulties initiating movements, tremors, rigidity, postural instability, bradykinesia (slowness in initiating movement/speed)
- linked to a degeneration of dopamine-producing cells in substantia nigra (part of basal ganglia)
- too little dopamine in Parkinson’s so take an agonist like LDOPA which enhances dopamine in brain
Frontaltemporal dementia
affects frontal/temporal lobe of brain
change in personality/behavior, explosive temper, poor impulse control, difficulty w/ language
dementia caused by HIV/AIDS
ADC (aids dementia complex)
typically progressive, but punctuated by abrupt accelerations.
cognitive (memory, attention, language), motor (weakness, gate, jerky movements), behavior/mood
Creutzfeldt-Jakob Disease (CJD)
- rare
- rapidly degenerative dementia diseases (4-6 months)
- characterized by rapid changes in orientation and cognition
Hydrocephalus
pathological accumulation of cerebral spinal fluid in braid ventricles – too much pressure in brain
cause urinary contents, gait, and leads to demensia
can sometimes be corrected with a shut to get fluid out of brain
Dementia due to head trauma
dementia secondary to head injury
head injury – post-traumatic amnesia right after trauma, issues with EF in frontal lobe, attention, mood, emotion regulation difficulty
(Epileptic) Seizers
- sudden disruption in brain’s electrical activity
- altered consciousness (person either goes unconscious) or behavior alteration (twitchy/ some sort of motor movement )
- lasts 2-3 mins
Generalized vs. Partial seizures
(1) Generalized seizures – throughout the entire brain – also always have a loss of consciousness
- Tonic-clonic seizures – involve a loss of consciousness and include a tonic stage that involves a stiffening of the muscles in the face and limbs followed by a clonic stage that involves jerky rhythmic movements in the arms and legs
- Absence seizures – are characterized by a brief loss of consciousness with a “vacant stare” but few or no other symptoms and occur 1-30 secs and more common in kids
2) Partial seizures – originate in 1 side of brain and affect 1 side of body and be in any lobes (although they may spread and become generalized)
- Simple partial seizures – do not cause loss of consciousness
- Complex partial seizures – include some alteration in consciousness
Headaches – Migraine, Tensions, Cluster, Sinus
(1) Migraine headaches – produce intense, throbbing pain, usually on o1 side of the head and may be accompanied by dizziness, nausea or vomiting, and sensitivity to sound, light, and odors
(2) Tension headaches –characterized by dull and diffuse mild to moderate pain that is experienced as a tight band around the head
(3) Cluster headaches – involve severe (often burning or piercing) nonthrobbing pain that is usually located behind 1 eye but may spread to face, cheek, and/or temple; last 15-90 minutes and recurs more than 1x each day over several weeks/months
(4) Sinus headaches – caused by sinusitis and produce a dull throbbing pain and pressure around eyes and in cheeks and forehead
Traditional antipsychotics
(chlorpromazine, thioridazine, and haloperidol)
- Alleviate positive symptoms of Schizophrenia
- Dopamine antagonist (want to reduce dopamine b/c Schizophrenia has too much dopamine, work by blocking postsynaptic dopamine receptors)
- Side effects = anticholinergic effects, extrapyramidal side effect, neuroleptic malignant syndrome, tardive dyskinesia (abnormal voluntary movements in face, tongue, jaw)
Atypical antipsychotics
(clozapine, risperidone, olanzapine, aripiprazole)
- Alleviate positive (and some negative ) symptoms of Schizophrenia
- Dopamine antagonist (want to reduce dopamine b/c Schizophrenia has too much dopamine, work by blocking postsynaptic dopamine receptors)
- Less likely to cause extrapyramidal side effects
- Side effects = anticholinergic effects, sedation, weight gain, and neuroleptic malignant syndrome (can be fetal, high fever, unstable blood pressure)
- Clozapine can also cause agranulocytosis (low white blood cell count)
TCAs
TCAs (e.g., imipramine and clomipramine) = Antidepressant
- Block the reuptake of norepinephrine and serotonin at synapses.
- b/c of toxicity in overdose prescribed w/ caution for those w/ heart disease or who are suicidal
SSRIs
SSRIs (e.g., fluoxetine, sertraline [Zoloft], and paroxetine) = Antidepressant
- Block the reuptake of serotonin at synapses
- SSRIs have a quicker onset of effectiveness
- Produce fewer and less severe side effects (especially anticholinergic ones)
-Safer in overdose than TCAs
MAOIs
MAOIs (e.g., phenelzine and tranylcypromine) = Antidepressant
- Block the action of an enzyme that breaks down norepinephrine and serotonin
- Use for atypical depression
- Can cause fatal hypertensive crisis when combined w/ certain other drugs or foods containing amino acid tyramine
Lithium
Lithium = Mood stabilizer
- Treatment-of-choice for classic Bipolar Disorder (euphoric mania without rapid cycling)
Anti-seizure drugs
Anti-seizure drugs = Mood stabilizer
- Include carbamazepine and valproic acid
- Treatment for dysphoric mania and mania w/ rapid cycling
Benzodiazepines
- Iclude diazepam (valium), alprazolam, and triazolam
- Treatment of anxiety, insomnia, muscle spasms, seizures, and symptoms of alcohol withdrawal
- Cross tolerance w/ alcohol
- Chronic use can lead to dependence, tolerance, and withdrawal symptoms
Barbiturates
- Include thiopental and amobarbital
- Use for general anesthetic and for management of agitated patients
- Regular use leads to dependence, tolerance, and withdrawal symptoms, and sudden withdrawal can cause seizures, delirium, and death
- Widely abused drugs and are often implicated in accidental deaths and suicide
Narcotic-analgesics
- Include natural opioids (opium, morphine) and synthetic and semi-synthetic opioids (heroin, methadone, oxycodone)
- Used as pre-operative drugs and to treat chronic pain
- Methadone is used in the treatment of heroin addiction
- Chronic use leads to dependence, tolerance, and withdrawal symptoms
- Widely abused drugs
Psychostimulants
- Include prescription drugs such as methylphenidate and pemoline and drugs-of-abuse such as cocaine and methamphetamine
- As prescription drugs, used to treat ADHD and narcolepsy
Beta-blockers
- Beta-blockers (e.g., Propranolol and others) been used to treat hypertension, cardiac arrhythmias, migraine headache, and essential tremor
- Also been found useful for alleviating palpitations, tremors, and other physical symptoms of anxiety
Anti-alcohol drugs
- Treat alcohol abuse and dependence
- Disulfiram inhibits alcohol metabolism and, when taken w/ alcohol, causes nausea. vomiting, shortness of breath, tachycardia, etc.
- Naltrexone is an opioid receptor antagonist and reduces pleasurable effects of and craving for alcohol
Aphasia
loss of language – ability to speak
Broca’s aphasia – damage to dominant hemisphere (usually left) front lobe damage; broken – choppy speech: dysarthria (difficulty speaking, short phrases, lengthy pauses, telegraphic speech, leave out words); comprehension intact; word finding, naming objects, repeating phrases
Wernicke’s aphasia – damage to left temporal lobe; lact comprehension (dont understand language), cant follow verbal commands, and can speak fluently but it does not make sense; sensory aphasia people with Wernicke’s are unaware of their problems (anosognosia)
Conduction aphasia – rare; can understand, comprehension intact
Global aphasia – large, all language
Anomic aphasia – difficulty recalling words or names
Transcortical aphasia – damage outside of main lang centers (outside of Broca’s or Wernicke’s)
