Exam 1

Question 1

Two conditions to be qualified as mental illness

Answer 1

1.) the syndrome results from an inability of some internal mechanism, or process to perform its natural function. (cognitive, behavioral, emotional)

2.) the syndrome is associated with significant distress or impairment in social, occupational, or other important activities.

Question 2

1800s classification system of mental illness

Answer 2

• 1840s: idiocy/insanity
• 1880s: seven mental illnesses: mania, melancholia, monomania, paresis, dementia, dipsomania, and epilepsy

Question 3

1900s classification of mental illness

Answer 3

1.) 1918: statistical manual for the use of institutions for the insane— 22 disorders

2.) 1933: standard classified nomenclature of disease— 24 major categories

3.) 1940s: the VA system created the diagnostic and statistical manual (DSM)

Question 4

Which DSM overhaul was motivated by an attempt to legitimize the field of psychiatry and psychiatric diagnosis?

Answer 4

DSM III

Question 5

Revisions following the DSM III REFLECTED WHAT TREND IN PSYCHIATRY?

Answer 5

Medicalization, including clinical significance criterion, and culture bound syndromes

Question 6

Three issues with the DSM IV

Answer 6

1.) basic definition of mental illness.
2.) use of categorical rather than dimensional criteria for certain diagnosis
3.) the need to address various expressions of mental illness across the lifespan, genders and culture.

Question 7

DSM 5 is:

Answer 7

• a living document- scientific advances are rapidly Inc.
• focus on neurobiological etiology
• dimensional diagnoses would be favored over categorical

Question 8

Two Major differences in the DSM5

Answer 8

1.) additional attention to culture racism and discrimination incorporated information on cultural influences on disorder characteristics.

2.) ethical, racial equity, and inclusion work group. Alter the language to avoid perpetuating stereotypes.

Question 9

Most prevalent 12 month mental disorders in adults

Answer 9

Anxiety > depression> somatic symptom disorders > PTSD > dual diagnosis > suicidal ideation

Question 10

What percent of patients with mental illness have a comorbid medical condition?

Answer 10

68%

Question 11

The average delay between the onset of mental illness, and the treatment is

Answer 11

11 years

Question 12

Depression screenings

Answer 12

PHQ9, PHQ2

Question 13

Anxiety screenings

Answer 13

GAD7, GAD2

Question 14

Psychiatric interview— review of systems

Answer 14

1. Identifying information
2. History of present symptoms
3. Social and behavioral history
4. Medical history/substance use history
5. Family medical in psychiatric history
6. Assessment measures
7. Formal DSM5 diagnosis

Question 15

Components of a mental status examination

Answer 15

1.) general observations (appearance, speech, behavior)
2.) thinking
3.) emotion (mood/affect)
4.) cognition (orientation, attention, memory)

Question 16

Mini mental state exam MMSE

Answer 16

One of the most common cognitive screening tests used by physician in office settings
— 30 point screening tool, including orientation, language, functions, registration, attention, visuospatial

Question 17

Scoring for MMSE

Answer 17

24-30: normal
18-23: mild cognitive impairment
0-17: severe cognitive impairment

Question 18

What is another cognitive assessment used in clinic?

Answer 18

Montreal cognitive assessment (moCA)

Question 19

Neuropsychological examinations

Answer 19

1.) intelligence tests.
2.) neurocognitive test and batteries
3.) personality tests

Most common: Halstead-Reitan neuropsychological test battery

Question 20

Alfred Binet

Answer 20

French psychologist who developed the first practical intelligence test in order to identify elementary students in need of academic assistance

Question 21

Lewis Terman and William Stern

Answer 21

• Expanded Binet’s work, Stanford-Binet intelligence test
• Stern came up with the intelligence quotient score (IQ)

Question 22

Early intelligent quotient calculation

Answer 22

MA/CA x 100

• mental age/chronological age

Question 23

Common intelligence tests

Answer 23

1.) Wechsler adult intelligence scale
2.) Wechsler intelligence scale for children
3.) wechsler preschool in primary scale of intelligence
4.) Bayley scales of infant and toddler development
5.) Stanford-Binet fifth edition

Question 24

Bell curve for IQ score

Answer 24

• 1SD: 68.2% (34.1%)
  -2 SD: 95.4% (13.6%)
  -3 SD: 99.6% (2.1%)
  -4 SD: 99.8% (0.1%)

Question 25

Problem with intelligence testing

Answer 25

They are racially and culturally biased to the white middle class — Larry P versus Riles case

Question 26

Projective personality test

Answer 26

Design to reveal hidden emotions and internal conflicts through a persons responses to ambiguous stimuli (Rorschach test— ink blot)

Question 27

Objective personality assessment

Answer 27

Use a restricted response format like true/false and contain extensively tested validity skills to determine whether the person taking the test is truthful — Minnesota multiphasic personality inventory (MMPI)

Question 28

Rorschach test administration

Answer 28

1.) free association phase 2.) inquiry phase — interpretation is complex and based on several aspects of the subjects response

Question 29

MMPI

Answer 29

• current version is MMPI-3, containing 335 true/false items • 52 scales (10 validity scales)

Question 30

MMPI is frequently used for;

Answer 30

1. Aid in clinical diagnosis 2. Police selection process. 3. Compensation and pension cases for veterans 4. Legal disputes (custody battles)

Question 31

Upper motor neurons

Answer 31

Motor cortex: planning initiating and directing voluntary movement Brainstem: postural control, locomotion, basic voluntary movement

Question 32

Lower motor neurons

Answer 32

Spinal cord and brain stem circuits: reflexes Skeletal muscles: contraction

Question 33

Corticobulbar tract

Answer 33

Origin: M1, premotor, SMA, somatosensory cortex Target: medullary pyramids (cranial nerve nuclei, reticular formation, red nucleus)

Question 34

Corticospinal tract

Answer 34

Origin: M1, premotor, SMA, somatosensory cortex At caudal medulla: 90% decussate (lateral innervates distal limb muscles, ventral, innervates, axial, and proximal limb muscles) Target: lower motor neurons with collaterals to the red nucleus and reticular formation

Question 35

Alpha motor neuron:

Answer 35

Contracts the muscle

Question 36

Rubrospinal tract

Answer 36

Origin: red nucleus Decussates immediately and travels in the lateral medulla Target: motor neurons near the lateral corticospinal tract in the upper spinal cord (cervical, thoracic) — control of the arms

Question 37

Rubrospinal tract, Parvocellular

Answer 37

Input: cerebellum Output: inferior olive

Question 38

Rubrospinal tract, magnocellular

Answer 38

Input: motor cortex Output: spinal cord

Question 39

Medial vestibulospinal tract

Answer 39

• terminates bilaterally in the medial ventral horn of the spinal cord, to regulate the head position

Question 40

Lateral vestibulospinal tract

Answer 40

• terminates bilaterally in the medial ventral horn of the spinal cord, and activates the antigravity muscles in limbs when deviations from stable posture are detected

Question 41

The two nuclei of the reticulospinal tract

Answer 41

1. Pontine reticular formation 2. Medullary reticular formation • both terminate in the medial ventral horn of the spinal cord— they coordinate bilateral movements of the trunk and proximal limbs • postural control, locomotion

Question 42

The goal of posture control

Answer 42

Keep the center of mass above the support surface. This is done by muscle tone providing force in the opposite direction of the shift in order to maintain balance.

Question 43

Definition of postural tone:

Answer 43

1.) tonic activity in the muscles, physiological extensors 2.) tonic firing of alpha motor neurons providing the mechanism

Question 44

Two ways to increase alpha motor neuron activity

Answer 44

1.) directly increase, alpha motor, neuron input from descending tracts 2.) indirectly increase gamma motor, neuron activity to create a feedback loop

Question 45

Feedback

Answer 45

• vestibulospinal tract • sense, environmental disturbance of body position, and stability

Question 46

Feedforward (anticipatory)

Answer 46

• reticulospinal tract • stabilized posture during ongoing movements through inputs from cerebral cortex, hypothalamus, brainstem

Question 47

Vestibulocolic reflex

Answer 47

Acts on neck muscles to adjust the head and stabilize it in space

Question 48

Vestibulospinal reflex

Answer 48

Adjust axial and proximal limbs

Question 49

Inputs and outputs of the vestibulospinal tract in postural control

Answer 49

Input: vestibular end organs: otoliths and semicircular canals, cerebellum Output: alpha and gamma motor neurons

Question 50

Responsible descending systems for anticipatory maintenance of body posture

Answer 50

1.) reticulospinal - proximal and axial muscle control 2.) corticospinal - voluntary motor function 3.) Rubrospinal - moves arms — feedforward adjustment example: proximal leg muscles contract before by serves to ensure posture stability

Question 51

What does the cortex inhibit in order to modulate tone?

Answer 51

Gamma motor neurons

Question 52

Lesion of the corticospinal tract results in:

Answer 52

Loss of fine voluntary movements of the hand

Question 53

Upper motor neuron syndrome

Answer 53

• spinal shock: loss of find voluntary movements, flaccidity • alpha and gamma motor neurons lose their excitatory inputs from the central nervous system

Question 54

Symptoms of upper motor neuron syndrome

Answer 54

+ Babinski sign, spasticity: increased muscle tone, hyperreflexia, clonus, loss of fine limb movements

Question 55

Causes for spasticity in the upper motor neurons

Answer 55

1.) removal of cortical inhibition on postural centers (vestibular, nuclei, and reticular formation) 2.) sprouting, local axon collaterals to make more synapses (homeostatic plasticity) 3.) increased receptor sensitivity of motor neurons do to denervation (homeostatic plasticity)

Question 56

Decorticate

Answer 56

• damage above the red nucleus, loss of cortical modulation • posture: upper extremities in flexion, lower extremities in extension

Question 57

Decerebrate

Answer 57

• damage below red nucleus, loss of Rubrospinal tract. No modulation of reticulospinal tract, vestibulospinal tract still intact • posture: all limbs in extension

Question 58

Loss of all of the descending motor tracks will result in:

Answer 58

Flaccidity and death

Question 59

Spinal cord transection

Answer 59

• more severe- spinal shock • loss of fine voluntary movements, flaccidity, but preserved trunk muscles caused from the shock • persistent effect: + Babinski, spasticity, loss of fine limb movements

Question 60

Lower motor neuron syndrome

Answer 60

• flaccid paralysis with little or no muscle tone • muscle atrophy • fasciculation and fibrillations on EMG

Question 61

Withdrawal reflex

Answer 61

• polysynaptic reflex that occurs in response to nociceptive stimulation • response is contraction of flexor muscles and inhibition of extensor muscles so that stimulated part is withdrawn from the stimulus

Question 62

Reciprocal inhibition

Answer 62

Collateral branches of the afferent fibers activate inhibitory interneurons that suppress the activity of alpha motor neurons that innervate antagonist muscles

Question 63

Stretch (muscle spindle) reflex

Answer 63

• patellar reflex • typically seen as monosynaptic (alpha motor neurons) must have reciprocal inhibitory and gamma motor neurons

Question 64

Gamma motor neurons purpose

Answer 64

Keep appropriate amount of tension in the intrafusal fibers to maintain spindle sensitivity, a.k.a. maintain tone

Question 65

Inverse stretch (Golgi tendon) reflex

Answer 65

• inverse = inhibitory interneuron • load is dropped because muscle relaxes instead of flexing

Question 66

Lengthening reaction

Answer 66

1.) stretch reflex = contraction, light weight 2.) inverse stretch reflex = relaxation, heavy weight — typically coordinated, so that adjustment of muscle tension occur seamlessly

Question 67

Spasticity

Answer 67

LMN lesion: flaccid paralysis UMN lesion: reduced inhibitory inputs to gamma motor neurons (fine motor function) —> hypertonic, spastic paralysis

Question 68

Clasp knife reflex— UMN lesion

Answer 68

As a limb is moved passively and rapidly, there is rigidity (catch) followed by activation of the inverse stretch reflex (relax)

Question 69

Rigidity

Answer 69

• increase in excitatory, or decrease in inhibitory signals to Alpha motor, neurons, leading to contraction of extrafusal fibers and generation of force independent of stretch reflex pathways

Question 70

Lead pipe rigidity

Answer 70

Constant rigidity, slow and stiff in every direction all the time

Question 71

Cogwheel rigidity

Answer 71

Resembles clasp knife, it is lead pipe, rigidity, coupled with a tremor

Question 72

Central pattern generators

Answer 72

Groups of neurons, who is activation result in stereotyped movements (fixed action patterns— once started you get the same movement every time) Ex: blinking, vomiting, locomotion

Question 73

Spinal locomotor center

Answer 73

• proprioceptive feedback initiates bilaterally in lower thoracolumbar spine, resulting in rhythmic activation of lectures and extensors in order to walk • stepping reflex in babies— not born with this

Question 74

Mesencephalic locomotor center

Answer 74

• proposed converging structure • regulates, duration (pace) of stepping as well as initiation and cessation

Question 75

Pontomedullary reticular formation locomotor center

Answer 75

• coordination of movements on one side of the body with postural control on the other— opposite compensation

Question 76

Actions of the brain stem locomotor centers are modified by descending control originating in:

Answer 76

• primary motor cortex • supplementary motor area • basal ganglia

Question 77

What is the purpose of gamma motor neurons in a person was normal upper motor neuron function?

Answer 77

Maintain tension in intrafusal muscle fibers

Question 78

What is most likely to be uniquely exhibited in a patient with an upper motor neuron lesion?

Answer 78

Clasp knife reflex

Question 79

What are the locomotor centers?

Answer 79

1.) spinal 2.) mesencephalic 3.) Pontomedullary reticular formation

Question 80

Cerebellum

Answer 80

- Sensory motor coordination - Connects with UMNs and primary motor cortex to create feedback loops

Question 81

Cerebellar cortex includes

Answer 81

Vermis, paravermis (in the medial cerebellum), hemispheres

Question 82

Cerebellar nuclei includes

Answer 82

Fastigial, interposed, dentate

Question 83

Cerebellar peduncles

Answer 83

Superior, middle, and inferior

Question 84

Three cerebellar layers

Answer 84

1.) Molecular: contains stellate cells, parallel fibers, and basket cells 2.) Purkinje: purkinje cells 3.) Granule: Granular cells, golgi cells, mossy fibers, purkinje cell axons, and climbing fibers

Question 85

Purkinje cells

Answer 85

the only output neuron, inhibit (GABA) cerebellar nuclei/vestibular nucleus

Question 86

Granule cells

Answer 86

origin of parallel fibers, excitatory (glutamate) with three interneurons: Stellate, basket, and golgi cells

Question 87

Golgi cells

Answer 87

inhibitory (GABA), all excited by parallel fibers

Question 88

Mossy fiber circuitry

Answer 88

Mossy fibers--> granule cells --> parallel fibers (+) --> purkinje cells

Question 89

Climbing fibers (+) excite:

Answer 89

purkinje cells

Question 90

Basket cells (-) inhibit:

Answer 90

purkinje cells

Question 91

stellate cell s(-) inhibit:

Answer 91

purkinje cells

Question 92

Purkinje cells (-) inhibit:

Answer 92

cerebellar nuclei and vestibular nucleus (medial and lateral) cerebellar nuclei --> central nervous system

Question 93

Mossy fibers

Answer 93

- from multiple spinal and brainstem sites - synapse on granule cells (excitatory) - produce simple spikes (discrete, individual) - high frequency discharge -encode temporal and intensity of sensory and motor information

Question 94

Climbing fibers

Answer 94

- Solely from contralateral inferior olive - monosynaptic excitation to purkinje cells - generate complex spikes in purkinje cells - low frequency discharge - encode teaching signals for motor learning

Question 95

Cerebellar cortex is:

Answer 95

- Ipsilaterally organized - The output of cerebellar circuitry inhibits movement

Question 96

Function of spinocerebellum

Answer 96

output to motor cortex, medial and lateral descending systems: motor execution to produce adaptive smooth motor coordination

Question 97

Function of Cerebrocerebellum

Answer 97

output to motor and premotor cortex: motor planning, cognition and affective function

Question 98

Function of Vestibulocerebellum

Answer 98

Output to vestibular nuclei: balance and eye movements and postural maintenance (receives a huge amount of input)

Question 99

Disorders of vestibulocerebellum

Answer 99

- disturbances of equilibrium and balance- fall towards side of lesion - nystagmus - loss of smooth pursuit eye movements

Question 100

Disorders of spinocerebellum

Answer 100

- Disturbance of gait of vermis - Hypotonia - action tremor - limb ataxia/dysmetria - dysdiadochokinesia (disorder of timing) - decomposition of movements

Question 101

Disorders of cerebrocerebellum

Answer 101

- ataxia of finest movements (hand shaping, writing) - cognitive deficits

Question 102

Decomposition of movement

Answer 102

The breakdown of movements down into their component parts in order to execute the desired trajectory- sequence movements

Question 103

Intention tremor

Answer 103

Produce involuntary tremor that increases when approaching the target (back and forth movement)

Question 104

Dysdiadochokinesia

Answer 104

Difficulty in performing rapidly alternating movements (ex. palm up, palm down on hands)

Question 105

Deficits in motor learning

Answer 105

example: VOR- lesions to the cerebellum prevent the adjustment of VOR

Question 106

Inherited spinocerebellar ataxia (hypermetria)

Answer 106

prevents proper termination of movements, patient overreaches and comes back to target

Question 107

Associative learning system

Answer 107

- receives a huge amount of sensory and motor input - learns to associate sensory feedback from actual movements with the intended motor output - modulates motor output to match expected sensory input - plays a role in non-motor cerebellar fxn

Question 108

Reafference

Answer 108

sensory information from the periphery about motions actually occurring

Question 109

Efference copy (corollary discharge)

Answer 109

Neural copy of the intended action (motor commands)

Question 110

Cerebellar cognitive affective syndrome (CCAS)

Answer 110

1. Execution: planning, set-shifting, verbal fluency, abstract reasoning, working memory 2. Spatial cognition: visual spatial organization and memory 3. Personality: blunt affect, disinhibited and inappropriate behavior 4. Language: agrammatism, aprosodia SOCIAL BEHAVIOR CHANGES

Question 111

Decreased firing of purkinje cells results in:

Answer 111

autistic-like behaviors (ex. Tsc1 protein deletion causing autism)

Question 112

Movement disorders definition

Answer 112

excess or slow movements, unrelated to weakness or spasticity-- different from neuromuscular disorders

Question 113

Hypokinetic

Answer 113

Akinesia, hypokinesia, bradykinesia, and rigidity Example: Parkinson's, Parkinsonism, ataxias

Question 114

Hyperkinetic

Answer 114

Dyskinesias: excessive, often repetitive involuntary movements that intrude into the normal motor activity Example: Huntington's disease, dystonia, essential tremor, restless leg syndrome, Wilson's disease, Tourette syndrome, myoclonus

Question 115

If the basal ganglia is affected:

Answer 115

involuntary or decreased movements, but not weakness or changes in reflexes. Basal ganglia = smooths out muscle movements

Question 116

If the cerebellum is affected:

Answer 116

Loss of coordination. Cerebellum helps limbs smoothly and accurately, helps maintains balance

Question 117

MPTP-induced Parkinson's

Answer 117

- impurity found in synthetic heroin - transforms into MPP+ - selective degeneration of dopaminergic neurons in SNc - similar findings in intoxication from Rotenone

Question 118

Atypical Parkinson's

Answer 118

- Shares Parkinson's triad + other symptoms such as autonomic dysfunction (incontinence), eye involvement, frontal cortex (cognitive, psychiatric), bulbar involvement (speech) - Synucleinopathy and tauopathy

Question 119

Ataxias

Answer 119

- Neuronal loss in cerebellum and brainstem - autosomal dominant (spinocerebellar ataxias) - autosomal recessive: Friedrich's ataxia, Niemann Pick, ataxia-telangiectasia - treatment: symptomatic, PT

Question 120

Chorea (choreiform movement)

Answer 120

Rapid controllable movements such as tics or jerks commonly seen in Huntington's

Question 121

Dystonia

Answer 121

- Sustained muscle contractions frequently causing twisting and repetitive movements, or abnormal postures - Primary: dystonia only clincal sign - Secondary: hereditary, acquired (head trauma, stroke, tumor, drugs), parkinsonian disorders

Question 122

Treatment of dystonia

Answer 122

1. Anti-cholinergic drugs 2. GABA agonists 3. dopaminergic agents 4. Botulism toxin 5. DBS (GPi)

Question 123

Essential Tremor

Answer 123

- Common, kinetic tremor of the arms > head > postural instability - Benign, however complex and progressive - 50% inherited, 4% prevalence - Treatment: propanolol, and primidone (anticonvulsant)

Question 124

Restless leg syndrome

Answer 124

- Throbbing, pulling, creeping, or other unpleasant sensations in the legs and uncontrollable urge to move them - Primarily at night, moving legs relieves symptoms - Exhaustion and daytime fatigue - 10% prevalence, associated with loss of DA and basal ganglia dysfunction - Treatment: dopamine agonists, benzodiazepines, anti-convulsants

Question 125

Tourette syndrome

Answer 125

- Motor and phonic tics, onset in childhood or adolescence that can be voluntarily suppressed - Comorbidities: ADHD, OCD - decreased activity of inhibitory neurons in cortico-striato-thalamo-cortical circuit (disinhibition)

Question 126

Treatment of tourettes

Answer 126

- alpha2-agonists like guanfacine (ADHD) - 5-20% pts experienced sustained/worsened symptoms - 30-50% pts experience reduced tics - 50% pts experience complete tic remission

Question 127

Wilson's disease

Answer 127

- Accumulation of Cu+ in the liver and brain - Autosomal recessive, loss of fxn of ATP7B - causes hepatitis, parkinsonism, psychiatric symptoms, SI, homicidal ideation, depression, and aggression - Treatment: diet changes and chelating agents

Question 128

Myoclonus

Answer 128

Sudden, involuntary jerking of a muscle or group of muscles. Myoclonic twitches or jerks: sudden muscle contractions or relaxation -- uncontrolled twitching (hiccups) - treatment: Clonezepam (anticonvulsant), and barbiturates (sedatives)

Question 129

Somatic Symptom disorder

Answer 129

- one or more somatic symptoms that are distressing and/or result in disruption of daily activities and function leading to excessive thoughts, feelings, or behaviors that are related to the somatic symptoms. - Somatic states lasts > 6 months

Question 130

Risk factors of SSD

Answer 130

- anxiety or depression - alexithymia - history of trauma, abuse, or neglect (esp in childhood) - Lower SES

Question 131

Clinical features of SSD

Answer 131

- large number or outpatient visits - frequent hospitalizations - repetitive subspecialty referrals - large number of diagnoses - multiple medications

Question 132

Treatments of SSD

Answer 132

• schedule, regular follow up visits • perform physical exams on the focus area of discomfort each visit • avoid unnecessary tests, invasive treatments, referrals, and hospitalization • set limits on contact outside of schedule visits

Question 133

Illness anxiety disorder

Answer 133

• preoccupation with having or acquiring a serious illness. Somatic symptoms are not present typically • specific illness that is feared may change, preoccupation must be present for > 6 months • excessive health related behaviors or exhibit maladaptive, health related avoidance

Question 134

Treatment for illness anxiety disorder

Answer 134

• General: establish trust, history, taking and physical exam, identification of stressors, education • CBT • supportive therapy • pharmacotherapy: serotoninergic meds, benefit 70 to 80% of patients

Question 135

Conversion disorder (functional neurological symptom disorder)

Answer 135

• one or more symptoms of altered voluntary motor or sensory function • clinical findings provide evidence of a mismatch between the symptom and recognized neurological condition • clinically significant distress or impairment in functioning likely to occur following stress

Question 136

Conversion disorder, clinical subtypes

Answer 136

• motor symptoms or deficits: involuntary movements, seizures, paralysis, weakness • sensory symptoms or deficits: anesthesia, blindness or tunnel, vision, deafness

Question 137

Astasia abasia

Answer 137

No neurological gait (bouncing) typically resulting from conversion disorder

Question 138

What area of the brain shows increased activity in conversion disorder?

Answer 138

The limbic system

Question 139

Treatment of conversion disorder

Answer 139

• general/conservative: reassurance, addressing stressors, protective environment • physical therapy • neurologist/psychiatrist and mental health study • psychotherapies/hypnosis

Question 140

Good prognosis of conversion disorder

Answer 140

• onset following a clear stressor • prompt treatment • symptoms of paralysis, aphonia, and blindness

Question 141

Poor prognosis of conversion disorder

Answer 141

• delayed treatment • symptoms of seizures or tremors

Question 142

Psychological factors affecting other medical conditions

Answer 142

Psychological and/or behavioral factors adversely affect a separate medical condition: influence the course, interfere with the treatment, constitute health risks, influence the underlying pathophysiology Example: anxiety increasing asthma exacerbation

Question 143

Factitious disorder

Answer 143

• intentionally exaggerates or induces signs and symptoms of illness • motivation is to assume the sick role • other incentives for the illness inducing behavior is absent Example: contaminating, PICC line with stool

Question 144

Self-enhancement model of factitious disorder

Answer 144

• a means of increasing or protecting self-esteem • a way to blame failures on illness • can be brave/heroic with medical illness/sophisticated with knowledge

Question 145

Munchhausen syndrome

Answer 145

• most severe form of factitious disorder • impostership, generally prestigious • pseudologia Fantastica (exaggeration of symptoms stories)

Question 146

Factitious disorder by proxy

Answer 146

A person intentionally produces physical signs or symptoms in another person under the first person’s care. Most commonly mothers of young children.

Question 147

Ganser’s syndrome

Answer 147

Characterized by the use of approximate answers. Example: 5+5= 9 or 11

Question 148

Predisposing factors of factitious disorder

Answer 148

• true, physical disorders in childhood, leading to extensive medical treatment • employment as a medical paraprofessional • severe personality disorder (especially cluster B)

Question 149

Factitious disorder comorbidities

Answer 149

• anxiety • depression • personality disorders • borderline personality disorder/ antisocial

Question 150

Malingering

Answer 150

• the intentional production of feigning illness • motivated by external incentives (obtain drugs, financial compensation, avoid work/school/military service, evade criminal prosecution)

Question 151

The basal ganglia:

Answer 151

Gates proper initiation of movement. At rest, the basal ganglia suppress all movement.

Question 152

The basal ganglia circuit: direct pathway

Answer 152

1. The striatum receives excitatory glutamatergic input from cortex 2. Striatum sends inhibitory GABA signal to internal Globus pallidus 3. Internal Globus pallidus produces less of its own GABA—> Les GABA reaches the thalamus 4. Increased excitatory outflow from the thalamus to the cortex 5. Selected/desired motor activity increases.

Question 153

The basal ganglia circuit: indirect pathway

Answer 153

1. Striatum receives excitatory, glutamatergic input from cortex 2. Striatum sends inhibitory GABA signal to external Globus pallidus 3. External Globus pallidus produces less of its own GABA 4. Less GABA reaches the subthalamic nucleus 5. Subthalamic nucleus produces more glutamate 6. More glutamate reaches the internal Globus pallidus 7. Intro Globus pallidus produces more of its own GABA 8. More GABA reaches the thalamus 9. Reduced excitatory outflow from the thalamus to cerebral cortex 10. Competing motor activity decreases

Question 154

Substantia nigra

Answer 154

Innervates the striatum, and has tonic dopamine release that promotes movement in a graded fashion by activating the direct pathway and inactivating the indirect pathway

Question 155

Striatum’s dopamine receptor for the direct pathway

Answer 155

D1

Question 156

Striatum’s dopamine receptor for the indirect pathway

Answer 156

D2

Question 157

Hyperdirect pathway

Answer 157

• quickest route through the basal ganglia • cortex excites subthalamic nucleus before it reaches the striatum • stops current movements immediately— interrupts signal

Question 158

Hypokinetic disorders

Answer 158

• direct pathway, inhibited, and/or indirect pathway active • thalamus = more inhibited, less motor activity • bradykinesia, Parkinson

Question 159

Hyperkinetic disorders

Answer 159

• direct pathway active, and/or indirect pathway inhibited • thalamus = less inhibited, more motor activity • dyskinesia, ballismus, Huntington’s

Question 160

Parkinson’s disease

Answer 160

• progressive loss of dopaminergic neurons in substantia nigra pars compacta • Less DA in the striatum • decreased direct pathway, increased, indirect pathway—> inhibition the thalamus • symptoms: bradykinesia, muscle, rigidity, resting, tremor, impaired postural balance

Question 161

Degenerated areas in Parkinson disease

Answer 161

• substantia nigra • locus coeruleus • NE and DA decrease

Question 162

Levodopa (L- DOPA)

Answer 162

• a pro drug, transported across the blood brain barrier buy an amino acid transporter • enzymatically converted to dopamine by L aromatic amino acid decarboxylase (Dopa decarboxylase)

Question 163

Carbidopa

Answer 163

• inhibits, L aromatic amino acid decarboxylase— does not cross the BBB so it only inhibits AAAD in the periphery • can reduce l-dopa those by 75%

Question 164

Mechanism of levodopa

Answer 164

• restores dopaminergic activity in the striatum • activation of D1 receptors—> activation D1, direct pathway • activation of D2 receptors—> inhibits D2, indirect pathway

Question 165

Diphasic dyskinesia

Answer 165

• appears at the onset and offset of the levodopa effect, coinciding with rising and falling plasma levodopa levels • often repetitive, slow movement of the lower limbs off and coinciding with tremors in the upper limbs

Question 166

On- off phenomenon

Answer 166

Sudden and rapid loss of clinical affect. Can last 30 minutes-4 hours, occur up to 10 times per day.

Question 167

Where do we find DA receptors?

Answer 167

• CNS- limbic system and frontal cortex (schizophrenia), other areas • brainstem- chemoreceptor trigger zone outside of the BBB • pulmonary arteries • kidneys

Question 168

Adverse non-motor effects of levodopa

Answer 168

• confusion/anxiety/agitation • psychotic reactions due to high concentrations of dopamine in the CNS • peripheral dopamine effects: orthostatic hypotension, nausea, vomiting, anorexia

Question 169

COMT inhibitors

Answer 169

• entacapone, tolcapone • decrease peripheral metabolism of L-DOPA by catechol-O-methyltransferase (COMT) to 3-OMD • smoother response, more prolonged “on” time

Question 170

Monoamine oxidase inhibitors (MAOIs)

Answer 170

• Selegiline, Rasagiline (more potent) • MAO-A: primarily metabolizes NE and 5-HT • MAO-B: primarily metabolizes dopamine (useful for PD treatment)

Question 171

MAOIs interact with what?

Answer 171

Antidepressants and meperidine. Can cause serotonin syndrome.

Question 172

Dopamine receptor agonist

Answer 172

• pramipexole (D3), ropinirole (D2) • bypass conversion of l-dopa to dopamine • more nausea, hallucinations, peripheral DA symptoms • help with “on-off” fluctuations

Question 173

Amantadine

Answer 173

• antiviral drug acting as a MDMA receptor antagonist • used in early PD patients, benefits are short-lived • adverse effects: agitation, confusion, excitement, hallucinations, psychosis with OD • can cause livedo reticularis- blotchy, netlike red/purple discoloration of the skin

Question 174

Muscarinic antagonist (anti-cholinergics) for PD

Answer 174

• benztropine, trihexyphenidyl • ACh used as neural transmitter for striatal interneurons • mechanism: loss of DA innervation of striatum leads to relative excess of ACh activity

Question 175

Tissue transplantation for Parkinson’s treatment

Answer 175

Human fetal adrenal medullary tissue into caudate nucleus

Question 176

Electrical stimulation for Parkinson’s treatment

Answer 176

Stereotaxic surgical implantation of electrodes into subthalamic nucleus to reduce motor symptoms and smooth out clinical response

Question 177

Surgery treatment for Parkinson’s

Answer 177

• pallidotomy- alleviates akinesia, rigidity and drug induced dyskinesia • thalamotomy- ameliorates tremor

Question 178

Huntington’s disease

Answer 178

• hyperkinetic disorder associated with basal ganglia degeneration (degeneration of striatal neurons projecting to external Globus pallidus) • loss of thalamic inhibition leading to increased excitatory drive and spastic movements

Question 179

Huntington’s disease treatment

Answer 179

• tetrabenazine, Reserpine— inhibit vesicular monoamine transporter (VMAT) • antipsychotics (haloperidol)— dopamine receptor blocking agent • benzodiazepine— helps control anxiety/stress, which can make involuntary movements worse

Question 180

Genetics of Huntington’s disease

Answer 180

• expanded CAG polyglutamine repeats in the Huntington • > 40 repeats = affected full penetrance • autosomal, dominant—> causes death within 10 to 20 years

Question 181

4 tools in the physical exam for UMN versus LMN

Answer 181

1. Tone: muscle tension 2. Strength: amount of force the person can exert 3. Deep tendon reflexes: muscle stretch 4. Gait: walking, combining strength tone and reflexes.

Question 182

Decorticate rigidity

Answer 182

abnormal flexure response, destruction of corticospinal tracts in/very near cerebral hemispheres

Question 183

Decebrate rigidity

Answer 183

Abnormal extensor response, lesion in diencephalon, midbrain, bonds, or severe hypoxia/hypoglycemia

Question 184

Paratonia

Answer 184

• Velocity dependent resistance in response to passive movement, inability to relax. Impacts frontal lobes, can be diffuse cerebellar damage. • seen in late dementia— stiffen and arch back response to touch

Question 185

Special reflexes

Answer 185

• cutaneous, or superficial stimulation reflexes 1. Abdominal reflex- light stroke, T9-11, T11-12 2. Cremasteric reflex: stroke to inner thigh, L1 branches 3. Anal reflex, S2-4

Question 186

Spasticity clinical findings

Answer 186

• UMN, corticospinal tract • hypertonia, clasp knife • common from strokes, or cerebral palsy

Question 187

Rigidity clinical findings

Answer 187

• basal ganglia, extrapyramidal • lead pipe or cogwheel rigidity • Lewy, body disease, supernuclear palsy, Parkinson’s

Question 188

Flaccidity clinical findings

Answer 188

• LMN, from anterior horn cell to peripheral nerves, or UMN in cerebellar disease • hypotonia, loose floppy limbs • Guillian Barre, initial spinal cord injury, or initial stroke symptoms

Question 189

Paratonia clinical findings

Answer 189

• both hemispheres, usually frontal lobe • sudden change in tone with passive ROM (+/-) • dementia

Question 190

Spastic hemiparesis

Answer 190

• stroke • affected arm flexed, at side • affected leg extensors, spastic • circumduction of leg or lean trunk to contralateral side

Question 191

Scissor gate

Answer 191

• cerebral palsy • stiff gait, rigidity • excessive, add duction, internal rotation of leg in the swing movement • short steps • walking through water

Question 192

Steppage gait

Answer 192

• foot drop/radiculopathy at L4/L5 • drag foot or compensate by lifting high • cannot heel walk • tibialis anterior, toe extensor weakness

Question 193

Parkinsonian gate

Answer 193

• stooped posture and poor posture control • slow initiation of movement • short steps and shuffling gait • arm swing decreased • turning is slow and wide based

Question 194

Cerebellar ataxia

Answer 194

• gait broad-based, staggering, unsteady • difficulty with turns • cannot stand steadily with feet together • paired with: dysmetria, nystagmus, intention tremor • cannot stand with feet together

Question 195

Sensory ataxia

Answer 195

• gait broad-based, unsteady • throw feet forward and out with gait, heel first • can stand with feet together, positive Romberg

Question 196

Antalgic gait

Answer 196

It hurts to walk, or use body parts used to walk

Question 197

Types of tremors

Answer 197

Resting, postural, intention (senile)

Question 198

Clinical findings UMN lesion

Answer 198

• weakness • increased reflexes/tone • positive Babinski • spastic paralysis NO: • atrophy • fasciculations/fibrillations • flaccid paralysis

Question 199

Clinical findings of a LMN lesion

Answer 199

• weakness • atrophy • fasciculations/fibrillations • decreased, or absent reflexes/tone • flaccid paralysis NO: • Babinski present • spastic paresis

Question 200

Apraxia

Answer 200

Damage to the motor cortex and association cortex can result in impairments in motor planning and strategies and an inability to perform complex motor tasks— seen in upper motor neuron lesions

Question 201

Hyperkinetic

Answer 201

1. Dyskinesia: abnormal, involuntary movements. 2. Athetosis: slow chorea, riding movements, seen in cerebral palsy/Huntington’s 3. Ballismus: rare, involuntary ballistic movements, most common in stroke and severe hyperglycemia

Question 202

Hypokinetic

Answer 202

1. Akinesia: abnormal, involuntary postures, freezing (Parkinson’s) 2. Rigidity: cogwheel 3. Dystonia: agonist/antagonist muscles, both contract, twisting muscles, abnormal posture 4. Bradykinesia: slow movements, Parkinson’s

Question 203

Cerebrum diseases of UMN

Answer 203

1. Stroke 2. Cerebral palsy 3. Space occupying/structural lesion 4. Degenerative diseases

Question 204

Sub cortex/brainstem diseases of UMN

Answer 204

1. Stroke 2. Degenerative 3. Space occupying/structural lesion— lacunar syndromes, midbrain/brainstem syndromes

Question 205

Spinal cord diseases of UMN

Answer 205

1. Acute transverse myelitis 2. Spinal cord infarct 3. Spinal epidural, or subdural hemorrhage 4. Central intravertebral disc herniation 5. Spinal cord tumors- metastatic or primary

Question 206

Anterior horn disease of LMN

Answer 206

1. Amyotrophic lateral sclerosis 2. Poliomyelitis

Question 207

Spinal nerve root disease of LMN

Answer 207

1. Intravertebral disc herniation

Question 208

Polyneuropathies disease of LMN

Answer 208

1. Guillian Barre syndrome 2. Toxins- puffer fish, shellfish 3. Porphyria 4. Lead/heavy metal poisoning 5. Alcohol/drug induced 6. Diabetic

Question 209

Plexipathies diseases of LMN

Answer 209

1. Brachial 2. Lumbar

Question 210

Peripheral neuropathies diseases of LMN

Answer 210

1. Nerve compression syndromes

Question 211

Spinal nerve issues

Answer 211

L1: hip flexion, groin sensation L2: hip flexion, thigh sensation L3: knee extension, patellar, reflex, knee sensation L4: ankle dorsiflexion, patellar reflex, medial calf sensation L5: first toe dorsiflexion, medial, hamstring reflex, posterior thigh/leg and dorsum of the foot sensation S1: foot movements, Achilles reflex, posterior side, and lateral foot sensation S2: knee, flexor/hamstring, Achilles reflex, back of thigh sensation S2-4: external anal sphincter, anal reflex, perianal area sensation

Question 212

Neuralgia

Answer 212

An intense, typically intermittent pain along with the course of a nerve, especially in the head or face — often described as stabbing, burning, usually severe and can disrupt function (trigeminal neuralgia, shingles, MS, diabetes)

Question 213

Neuropathy

Answer 213

A diffuse situation affecting a region, often peripheral. Can also be described as stabbing, but more commonly is burning or itching. It can be severe (Guillian Barre, chronic demyelinating syndromes, diabetes)

Question 214

ALS vs MS

Answer 214

ALS: combination of upper and lower motor on signs and symptoms MS: can involve upper and lower motor neurons, though is primarily upper motor neurons

Question 215

The difference between a stroke (UMN) and Bell’s palsy (LMN)

Answer 215

Stroke victims can lift their eyebrows on the affected side, while Bell’s palsy cannot

Question 216

The three deadly withdrawal substances

Answer 216

1. Alcohol 2. Barbiturates 3. Benzos

Question 217

Tolerance

Answer 217

Decreased effective drug with repeated administration. Increasing doses of a drug needed to produce a specific affect. — can create cross tolerance to similar drugs, or unequal rate of tolerance development for different drugs

Question 218

Pharmacodynamic tolerance

Answer 218

Cellular response to a Drug, reduced with repeated use

Question 219

Pharmacokinetic tolerance

Answer 219

Decreased quantity of the substance, reaching the site it affects (change in metabolism, transport, etc.)

Question 220

Mesolimbic dopamine system

Answer 220

• prime target of addictive drugs, originating at the ventral tegmental area—> nucleus, accumbens, amygdala, hippocampus, PFC

Question 221

Drugs with higher capacity to cause addiction typically involve:

Answer 221

Dopamine release

Question 222

Sedative hypnotics

Answer 222

1. Benzodiazepine- prolonged activity and decreased immediate reward. Makes it less abusable 2. Short acting barbiturates- high addiction potential 3. Ethanol

Question 223

Effects of sedative hypnotics

Answer 223

• reduce inhibitions, suppress, anxiety, and produce relaxation • respiratory depression at higher doses, facilitation of the effects of GABA • enhance brain DA pathways- related to the development of addiction • flumazenil is an antidote for benzodiazepines

Question 224

Date rape drugs fall into what category?

Answer 224

• sedative hypnotics • flunitrazepam (rohypnol): rapid onset benzodiazepine with marked amnesic properties • gamma- hydroxybutyrate: renders victim incapable of resisting

Question 225

Sedative hypnotic withdrawal symptoms

Answer 225

• excessive CNS simulation: anxiety, tremor, nausea and vomiting, delirium • seizures- life-threatening

Question 226

Sedative hypnotics withdrawal treatments

Answer 226

• administration of a long acting sedative hypnotic— diazepam to suppress acute withdrawal syndrome • clonidine ( alpha-2 adrenergic agonist)and propanolol (beta-adrenergic antagonist) suppress, sympathetic overactivity • naltrexone- treatment alcoholism

Question 227

Nicotine

Answer 227

Effects: rewarding involving the VTA, where the nicotinic acetylcholine receptors are expressed on dopamine neurons Withdrawal: anxiety and mental discomfort- treatment may include varenicline (Chantix) which is a partial agonist of the nicotinic acetylcholine receptors in the VTA

Question 228

Amphetamine- stimulant

Answer 228

Effects: alter transporters of CNS amines (DA, NE) occasionally increasing their release. Euphoria and self-confidence, chronic high-dose abuse, typically treated with benzodiazepines. Withdrawal: abstinence syndrome, increased appetite, sleepiness, exhaustion, mental depression

Question 229

Cocaine- stimulant

Answer 229

Effects: inhibits, the CNS monoamine reuptake. Amphetamine-like effects - overdose: arrhythmias, seizure, respiratory depression. Treatment is benzodiazepines and alpha blockers. Withdrawal: abstinence syndrome, depression. Antidepressant drugs may be indicated.

Question 230

Marijuana

Answer 230

• cannabinoids, backwards, signaling, so Endocannabinoids are retrograde messengers. Signal to the CB1 receptors on presynaptic neurons to increase release of neurotransmitter • effects: euphoria, disinhibition, uncontrollable, laughter, changes, and perception— withdrawal in heavy users

Question 231

Phencyclidine: PCP

Answer 231

• NDMA antagonist - sedative effects, neural impulses cannot travel • violence, impulsivity, psychomotor agitation, analgesia, nystagmus, hypertension, tachycardia, psychosis, seizures • ketamine is also an NDMA antagonist

Question 232

Lysergic acid diethylamide (LSD)

Answer 232

• 5-HT receptor agonist • significant visual and auditory distortion, anxiety, paranoia, psychosis, possible flashbacks in sober state

Question 233

MDMA (ecstasy)

Answer 233

• inhibits/reverses 5-HT transporters affecting NE and DA receptors as well • disinhibition, hyperactivity, hypertension, tachycardia, hyperthermia, serotonin syndrome

Question 234

Opioids- Mu agonists (highest misuse)

Answer 234

• morphine • oxycodone • meperidine • fentanyl • heroin • methadone • Hydromorphone • oxymorphone

Question 235

Opioids- week/partial mu agonists

Answer 235

• codeine • hydrocodone

Question 236

Opioids- mixed agonist-antagonist

Answer 236

• buprenorphine (agonist at mu) • Pentazocine (agonist at kappa) • Nalbuphine (agonist at kappa, antagonist at mu) • butorphanol (agonist at kappa)

Question 237

Opioids- antagonists

Answer 237

• naloxone • naltrexone

Question 238

Dextromethorphan

Answer 238

OTC, anti-tussive, weak mu agonist, Limited abuse potential

Question 239

Loperamide

Answer 239

OTC, anti-diarrheal, mu agonist, action mostly limited to gut, Limited abuse potential

Question 240

The three waves of opioid epidemics

Answer 240

1.) 1990s: increased prescribing of opioids 2.) 2010: rapid increase in overdose deaths involving heroin 3.) 2013: synthetic opioids- illicitly manufactured fentanyl

Question 241

The two ways to decrease the opioid crisis

Answer 241

1.) supply reduction strategies 2.) harm reduction strategies

Question 242

First order kinetics of elimination

Answer 242

Clearance depends on the amount of drug, taking longer as the amount of drug decreases

Question 243

Zero order kinetics of elimination

Answer 243

Clearances linear until the drug is completely gone— independent of amount

Question 244

What do alcohol dehydrogenase & MEOS (CYP2E1) do?

Answer 244

Convert ethanol to acetaldehyde (hangover feeling) — alcohol, dehydrogenase: NAD+—> NADH — MEOS: NADPH + O2—> NADP+ + H2O

Question 245

What does alcohol dehydrogenase do?

Answer 245

Convert acetaldehyde to acetate for elimination (NAD+—> NADH)

Question 246

Alcohol dehydrogenase

Answer 246

• mainly in the liver and gut • metabolizes low to moderate doses of ethanol • zero order kinetics: 7-10 g/hr • ADH1B2: gene that rapidly converts alcohol to acetaldehyde

Question 247

Microsomal ethanol oxidizing system (MEOS)

Answer 247

• CYP2E1 activity is a major component • in the liver only • metabolizes hi ethanol levels (>100mg/dL) • upregulated with chronic alcohol consumption • it converts acetaminophen to a hepatotoxic metabolite

Question 248

Aldehyde dehydrogenase is inhibited by what?

Answer 248

Disulfiram, metronidazole, cephalosporins

Question 249

Ethanol acute effects based on BAC

Answer 249

50-100: sedation, subjective high, slower reaction time 100-200: impaired motor function, slurred speech, ataxia 200-300: emesis, stupor 300-400: coma >400: respiratory depression, death Other effects: depression of myocardial contractility, vasodilation, uterine relaxation

Question 250

Ethanol molecular mechanism

Answer 250

• facilitates the action of GABA at GABA-A receptors • inhibits the ability of glutamate to activate NMDA receptors (black out) • modifies the activities of adenylyl cyclase, phospholipase C, and ion channels

Question 251

Ethanol withdrawals

Answer 251

• hyperexcitability, seizures, toxic psychosis, Delerium tremens (DTs) • DTs: delirium, agitation, ANS instability, low-grade fever, diaphoresis— can cause death • intensity determined by dose, rate, and duration of alcohol consumption

Question 252

Effects on the liver and G.I. tract of alcohol

Answer 252

liver: fatty liver disease—> hepatitis—> cirrhosis—> liver failure GI: irritation, inflammation, bleeding, scarring, increased risk of pancreatitis

Question 253

Effects on the CNS with alcohol

Answer 253

• peripheral neuropathy • Wernicke Korsakoff syndrome: ataxia, confusion, paralysis of extraocular muscles—> coma, death

Question 254

Treatment of alcoholism

Answer 254

• correction of electrolyte imbalances, administration of thiamine, substitute a long acting sedative hypnotic drug such as diazepam • naltrexone • diazepam (causing hangover, feeling because it is an aldehyde dehydrogenase inhibitor)

Question 255

Methanol consumption

Answer 255

• metabolized to formaldehyde and formic acid, causing severe acidosis, retinal damage, blindness • found in windshield, cleaners, and bootleg ethanol

Question 256

Ethylene glycol consumption

Answer 256

• antifreeze, industrial inhalation/skin absorption, or intentional ingestion • metabolized to toxic aldehydes and oxalic acid, causing severe acidosis, renal damage

Question 257

Fomepizole

Answer 257

Inhibits alcohol dehydrogenase to reduce the conversion of methanol to formaldehyde in formic acid, or to reduce the conversion of Ethylene glycol to toxic aldehydes and oxalic acid

Question 258

The hypothalamus is limited at:

Answer 258

The anterior: optic chiasm, and anterior commissure The posterior: the mammillary bodies Medial and lateral regions: fornix

Question 259

Regulation of basic physiological needs by the hypothalamus

Answer 259

1.) controls, blood pressure and electrolytes. 2.) regulates body temperature. 3.) regulates, energy, metabolism, through feeding, digestion, and metabolic rate. 4.) regulates circadian rhythms, and sleep wake cycles. 5.) directs responses to stress 6.) regulates reproduction through hormonal control.

Question 260

Paraventricular nucleus of the hypothalamus

Answer 260

Water balance/stress— oxytocin/vasopressin

Question 261

Anterior hypothalamic area of the hypothalamus

Answer 261

Body temperature— cooling center

Question 262

Supraoptic nucleus of the hypothalamus

Answer 262

Water balance— vasopressin

Question 263

Suprachiasmatic nucleus of the hypothalamus

Answer 263

Biological clock, circadian rhythms, sleep/wake cycles

Question 264

Posterior hypothalamic area

Answer 264

Heating center, responsible for shivering

Question 265

Ventromedial nucleus of the hypothalamus

Answer 265

Satiety— Leptin

Question 266

Mammillary bodies

Answer 266

Under the hypothalamus, responsible for memory. Part of the limbic system.

Question 267

Parvocellular paraventricular nucleus

Answer 267

• medially: secretes hypothalamic releasing hormones, such as CRH and CRF • dorsally and ventrally: neurons project to the medulla and spinal cord to exert autonomic control

Question 268

Magnocellular paraventricular nucleus of the hypothalamus

Answer 268

• two distinct populations, control endocrine function by secreting oxytocin and vasopressin directly into the posterior pituitary

Question 269

Hypothalamic control of endocrine function

Answer 269

• secretes oxytocin and vasopressin into the general circulation from the posterior pituitary (neurohypophysis) • secretes regulatory hormones into the local portal circulation that drains into the anterior pituitary (adenohypophysis) • some hypothalamic neurons influence, peptidergic neurons—> synapsing at those neurons’ cell bodies or axon terminals

Question 270

Lateral hypothalamus

Answer 270

• hunger, activated by ghrelin, lesion causes anorexia

Question 271

Ventromedial hypothalamus

Answer 271

Satiety- activated by leptin, lesion causes over eating, and obesity/ rage

Question 272

Arcuate nucleus

Answer 272

• Thermostat of feeding in the hypothalamus. Responsible for integrating information, and providing inputs to other nuclei in the hypothalamus. • may be regulated by glucose, insulin, Leptin

Question 273

Long-term changes in body fat causes:

Answer 273

• changes in levels of leptin • paraventricular nucleus of the hypothalamus activated • TSH & ACTH secretions are changed from anterior pituitary • sympathetic, and parasympathetic tones change • metabolic rate changes • feeding behavior is regulated

Question 274

Circuitry of the hypothalamus and limbic system

Answer 274

Essential for the normal expression in control of emotions and motivated behavior

Question 275

Circuitry of the hypothalamus and sensory/autonomic system

Answer 275

Provide visceral and somatic sensory input to the hypothalamus and output of the hypothalamus to the control of the ANS

Question 276

Neuro humoral connections

Answer 276

Both sends and receives information by the way of bloodstream (endocrine system) • the pituitary • circumventricular organs

Question 277

Hypothalamus controls ANS function by:

Answer 277

• control of autonomic preganglionic neurons at the parabrachial nucleus, nucleus of the solitary tract, and neurons in the ventrolateral medulla • posterior hypothalamus: heating and sympathetic • anterior hypothalamus: cooling and parasympathetic

Question 278

Circumventricular organs

Answer 278

• several sites I wish the blood brain barrier is highly permeable 1.) organa vasculosum of the lamina terminalis (OVLT) (IL-1, TNF, body temperature, setpoint) 2.) area postrema (vomiting) 3.) pineal gland: melatonin secretion

Question 279

Hypothalamus: neural output and neural input

Answer 279

Controls the autonomic nervous system, emotions

Question 280

Hypothalamus: Neural input, humoral output

Answer 280

Controls release of oxytocin for milk lactation

Question 281

Hypothalamus: humoral input, neural output

Answer 281

Used for drives and motivated behavior

Question 282

Hypothalamus: humoral input, humoral output

Answer 282

Controls release of vasopressin for fluid regulation

Question 283

What contain the magnocellular neurons that secrete oxytocin into the general circulation in the posterior pituitary?

Answer 283

Supraoptic and paraventricular nuclei (Neural input and hormonal output)

Question 284

What is sensitive to osmotic pressure changes?

Answer 284

The supraoptic nucleus containing vasopressin (humoral input, and humoral output)

Question 285

Diabetes insipidus

Answer 285

Caused by lack of or insensitivity to vasopressin = excessive thirst, excessive urination

Question 286

The DSM-V defines a substance use disorder as:

Answer 286

The presence of at least 2 to 11 criteria which are clustered in 4 groups 1.) general impaired functioning— impaired control, taking more drugs for longer than intended, etc 2.) social impairment— failure to fulfill major obligations to to use, etc. 3.) risky behavior/pattern of use— recurrent use in hazardous situations, despite physical or psychological problems 4.) pharmacological dependence— tolerance, and withdrawal

Question 287

Defining severity of SUD

Answer 287

2-3 criteria: mild SUD 4-5 criteria: moderate SUD 6+ criteria: severe SUD • can also indicate remission status (early, sustained, maintained therapy, control environment)

Question 288

Substance related disorders are distinguished from nonpathological substance used by the presence of:

Answer 288

1. Tolerance. 2. Withdrawal. 3. Compulsive use. 4. Substance related problems.

Question 289

Compulsive use in SUD

Answer 289

• drugs, taken in larger amounts, or for longer periods • development of substance centered lifestyle • neglect of significant personal or social interest or obligations • persistent desire to, or unsuccessful attempts at controlling use of a substance

Question 290

Vulnerability phenotypes for SUD

Answer 290

• starting drug use • liking drugs more • continuing drug use • specific to a particular drug (faster high= more addictive)

Question 291

Inheritability for drug abuse ranges from:

Answer 291

40 to 60%

Question 292

Medications for SUD

Answer 292

1.) opioid use disorder: buprenorphine, methadone, naltrexone 2.) opioid, overdose prevention medication: naloxone 3.) medication’s for alcohol use disorder: acamprosate, disulfiram, naltrexone

Question 293

Papez circuit involves (limbic system):

Answer 293

cingulate cortex, hippocampus, fornix, hypothalamus, anterior nuclei of the thalamus, mamillary bodies, amygdala, olfactory bulbs

Question 294

The functions of the limbic system are:

Answer 294

1. Homeostasis 2. Olfaction 3. Memory 4. Emotion and drives

Question 295

Papez circuit:

Answer 295

Hippocampus --fornix--> Mamillary nuclei--mamillothalamic tract--> anterior thalamic nucleus--internal capsule-->cingulate gyrus--cingulum-->parahippocampal gyrus-->entorhinal cortex--alvear/perforant pathways-->Subiculum (hippocampus)

Question 296

Cingulate gyrus

Answer 296

-- Receives input from the thalamus and the neocortex, and projects to the entorhinal cortex via the cingulum -- Involved in emotion formation and processing, learning and memory -- Important in depression and schizophrenia

Question 297

Amygdala

Answer 297

-- Large nuclear group in the temporal lobe -- Integrative center for emotions, emotional behavior, and motivation -- Functions include: Fear, learned fear, anger, and aggression

Question 298

Pathway of amygdala response

Answer 298

input from auditory thalamus/cortex, somatosensory thalamus/cortex --> Lateral nucleus of the amygdala --> central nucleus of the amygdala, central gray, lateral hypothalamus, and paraventricular hypothalamus

Question 299

Fornix and mamillary bodies

Answer 299

--Fornix: major output tract of the hippocampus -- Mammillary bodies: act as relay center for impulses coming from the amygdala and hippocampus. Involved in the processing of memory

Question 300

Korsakoff's syndrome

Answer 300

A chronic memory disorder (loss) caused by a severe deficiency of thiamine (B1). Most common in alcohol misuse, causing damage to the Thalmus and to the mammillary bodies of the hypothalamus

Question 301

Hippocampus

Answer 301

Pathways: entorhinal cortex and fornix, cingulate cortex, temporal lobe cortex, amygdala, orbital cortex, and olfactory bulb all have inputs to the hippocampus via the entorhinal cortex. Functions: Learning and memory, associated with Alzheimer's disease

Question 302

Learning

Answer 302

The ability of previous experiences to modify the inborn reactions or create new ones. It is also the acquisition of knowledge or skills as a result of experiences and can alter behavior.

Question 303

Associative learning

Answer 303

-Classical conditioning: Pavlov, unconditioned stimulus --> conditioned stimulus--> conditioned response -Operant conditioning: Performing a voluntary action in order to receive a reward (positive reinforcement, negative reinforcement, punishment, extinction)

Question 304

Non-associative learning

Answer 304

Habituation: repeated stimulation --> decreased response Sensitization: repeated stimulation --> increased response

Question 305

Learning has 3 stages

Answer 305

1. acquiring: mastering a new activity/concept 2. retaining: keeping the new acquisition for a period of time 3. Remembering: enables one to reproduce the learned act or memorized material

Question 306

Encoding phase of memory

Answer 306

Within the association cortex, information for each memory is assembled from different sensory systems and translated into a form to be remembered

Question 307

Consolidation phase of memory

Answer 307

Converting the encoded information into a form that can be permanently stored. The hippocampal and surrounding areas do this

Question 308

Storage phase of memory

Answer 308

The actual deposition of memories into the final resting places- this is at the association cortex level.

Question 309

Retrieval phase of memory

Answer 309

Memories are of little use if they cannot be read out for later use. Where at is unknown

Question 310

Declarative memory

Answer 310

1. Semantic: Facts 2. Episodic: Events -- Conscious, depend on the medial temporal lobes

Question 311

Non-declarative memory

Answer 311

1. Skills: motor, perception, cognition 2. Priming: perceptual, semantic, judgement 3. Dispositions: classical conditioning, operant conditioning 4. Non-associative: habituation, sensitization

Question 312

Procedural memory

Answer 312

Improving some perceptual or motor skill-- in humans this is not associated with conscious awareness of what is being learned

Question 313

Short term memory

Answer 313

-- Duration: mins-hrs -- Formation of temporary memory traces (newly developed pathway of signal transmission resulting from facilitation of new synapses (new circuits in the brain)

Question 314

How does short term memory occur?

Answer 314

1.) Long term potentiation of synapses 2.) Changes in physical properties of post-synaptic membrane--> increasing sensitivity to chemical transmitters

Question 315

Long term memory

Answer 315

-- Duration: hrs-yrs -- From practice, punishment, or reward -- memory engrams (long-lasting memory traces) -- Formation of new engrams requires protein synthesis

Question 316

Memory engrams are made up by:

Answer 316

1. increase in number of vesicles 2. increase in number of presynaptic terminals 3. increase in release sites of chemical transmitters 4. generation of new receptor sites 5. long term potentiation

Question 317

Brain regions involved in the consolidation of memory

Answer 317

1. hippocampus 2. anterior and lateral temporal lobe 3. Medial temporal lobe 4. Amygdala

Question 318

Patient H.M.

Answer 318

-removed the medial temporal lobe bilaterally to reduce seizures, resulted in inability to form new memories

Question 319

Kluver-Bucy Syndrome

Answer 319

- results from temporal lobe damage, amygdala damage - Caused by herpes encephalitis, and trauma - Characterized by: Amnesia, docility, hyperorality, hypersexuality, and visual agnosia

Question 320

Urbach-Wiethe disease

Answer 320

-lipoid proteinosis - recessive genetic disorder - dermatological symptoms related to general thickening of the skin and mucous membranes, scarring on the skin, easily damaged skin with poor wound healing, dry wrinkly skin - Neurological symptoms related to bilateral symmetrical calcification on the medial temporal lobes

Question 321

Implicit bias

Answer 321

the process of associating stereotypes or attitudes toward categories of people without conscious awareness. It affects behavior

Question 322

Fatphobia

Answer 322

Fear of/aversion to fatness

Question 323

Weight bias

Answer 323

Negative attitudes towards and beliefs about others because of their weight

Question 324

Internalized weight bias

Answer 324

Holding negative beliefs about oneself due to weight or size

Question 325

Weight stigma

Answer 325

The social rejection and devaluation that accrues to those who do not comply with prevailing social norms of adequate body weight and shape

Question 326

What is obesity?

Answer 326

a prevalent, complex, progressive and relapsing chronic disease characterized by abnormal or excessive body fat that impairs health (BMI>30)

Question 327

BMI categories

Answer 327

underweight: <18.5 normal weight: 18.5-25 overweight: 25-30 obesity: >30

Question 328

Weight cycling is correlated with a higher risk of:

Answer 328

Cardiovascular disease and type 2 diabetes

Question 329

When people experience weight stigma:

Answer 329

- eating increases - self-regulation decreased - cortisol levels were higher than controls (cortisol is obesogenic) - increase in all-cause mortality

Question 330

Anorexia nervosa

Answer 330

- BMI < 17.5 - Restriction of energy intake leading to a significantly low body weight - intense fear of gaining weight or being fat, disturbed body inmage - Denial, or pride of control of eating SUBTYPES: Restrictive, binge-eating/purging

Question 331

Atypical anorexia

Answer 331

All of the symptoms of anorexia except a BMI <17.5

Question 332

Bulimia nervosa

Answer 332

- Binge eating and repeated unhealthy behaviors to prevent weight gain ( vomiting, misuse of laxatives or diuretics, food restriction, or excessive exercise) - self-worth based on body shape and weight - weekly behaviors for at least 3 months

Question 333

Bulimia of low frequency and/or limited duration

Answer 333

- purging disorder (no binge eating)

Question 334

Binge eating disorder

Answer 334

- Recurrent episodes of binge eating - associated with eating faster than normal, eating until feeling uncomfortable, eating large quantities of food when not hungry, feeling bad or embarrassed about eating behaviors, - No compensatory behaviors to prevent weight gain - weekly behaviors for at least 3 months

Question 335

Other specified feeding and eating disorder

Answer 335

An eating disorder that does not meet full criteria for one of the main categorized but has specific disordered eating behaviors such as restricting intake, purging/ binging - unclassified disorders

Question 336

Avoidant/restrictive food intake disorder

Answer 336

-avoidance of food intake because of one of the following: lack of interest, sensory characteristics of food, concern about consequences of eating (choking) - associated with weight loss, nutritional deficiencies, and interference with psychosocial functioning - avoidance NOT about weight - Autism SD comorbidity

Question 337

Rumination disorder

Answer 337

- repeated regurgitation of food for at least one month - not attributable to GI or medical condition - No weight concerns

Question 338

Rumination disorder

Answer 338

- repeated regurgitation of food for at least one month - not attributable to GI or medical condition - No weight concerns

Question 339

PICA

Answer 339

- Eating non-nutritive, nonfood substances for at least one month - Eating behavior is developmentally inappropriate that is not culturally supported or socially normative

Question 340

Orthorexia

Answer 340

- not official DSM5-TR diagnosis - Fixation and obsession with eating healthy - Warning signs: compulsive checking of nutrition facts, cutting out food groups, inability to eat anything that is not "pure" or "clean" - high levels of distress when healthy foods are unavailable - obsessive following of food and lifestyle accounts on Social media - body image concerns may or may not be present

Question 341

Bodies affected by eating disorders

Answer 341

- less than 6% of eating disorder people are underweight - 1/3 is male - 42% of men with EDs are gay - Trans students 4x more likely to have disordered eating - Black teenagers 50% more like to binge/purge - Asian americans report more restrictive eating - pregnancy is associated with increased binge eating

Question 342

Comorbidities with EDs

Answer 342

1. Anxiety disorders 2. Mood disorders 3. Impulse control disorder 4. substance use disorders 5. any mental disorders -- Highest comorbidities in Bulimia

Question 343

Anorexia treatments

Answer 343

1. Emergency procedures to restore weight 2. SSRI and atypical antipsychotics (Zyprexa/olanzapine) 3. family based therapy 4. CBT 5. NO WELLBUTRIN (BUPROPION)

Question 344

Family based therapy for anorexia

Answer 344

Phase 1.) empowers parents in promoting healthy eating behaviors and restore weight Phase 2.) autonomy in feeding gradually shifted back to pt Phase 3.) facilitates improved family communication and independence

Question 345

Treatment of Bulimia

Answer 345

- SSRIs (fluoxetine/prozac, escitalopram/lexapro, citalopram/celexa) - anticonvulsants (topiramate/Topamax) - Family based therapy - CBT -NO WELLBUTRIN

Question 346

Treatment of Binge eating disorder

Answer 346

-SSRIs, appetite suppressants, anticonvulsants (topomax), stimulant medication (vyvanse) - CBT -Interpersonal psychotherapy (Phases: 1. identify problems and relation to eating, 2. learn skills to promote interpersonal fxning and reduce disordered eating, 3. maintenance of gains and relapse prevention

Question 347

Physician's role in eating disorder care

Answer 347

1. screening for eating disorders at annual visits 2. medical surveillance/monitor for refeeding syndrome 3. Weigh ins (blind) 4. setting activity restrictions 5. reinforcement of treatment/goals/messages

Question 348

Screening tools for eating disorders

Answer 348

1. EAT-26 (AN) 2. BEDS-7 (BED) 3. SCOFF 4. EDE-Q 5. EDGE symptom survey

Question 349

refeeding syndrome

Answer 349

the potentially fatal shifts in fluids and electrolytes that may occur in malnourished patients receiving artificial refeeding (whether enterally or parenterally5). These shifts result from hormonal and metabolic changes and may cause serious clinical complications.

Question 350

Physiological and endocrine circadian cycles: higher in the day vs at night

Answer 350

Higher in the day: Core body temperature, Urine volume, systolic blood pressure, cortisol Higher at night: Cerebral blood flow, melatonin, thyrotrophin, growth hormone

Question 351

Cellular clock oscillation pathway

Answer 351

light-->retina--> suprachiasmatic nucleus (SCN)--> 2nd messengers--> kinases--> mRNA/DNA modification--> protein--> output signals for sleep/wake

Question 352

Entraining agents of circadian rhythm

Answer 352

- light - melatonin - activity

Question 353

Potential causes of chronic misalignment of circadian rhythm

Answer 353

- Chronotype - Social jet lag - Shift work - Circadian rhythm disorders - disrupted feeding rhythm - psychiatric disorders

Question 354

Circadian rhythm disorders

Answer 354

Jet lag, shift work sleep disorder, advanced sleep phase syndrome (ASPD), delayed sleep phase syndrome (DSPS), non-24 hour sleep wake disorder

Question 355

Circadian clock-related disorders

Answer 355

Cancer, neurological and psychiatric disorders, metabolic syndromes, cardiovascular diseases

Question 356

What disease has a strong alteration in the circadian rest-activity rhythms?

Answer 356

Alzheimer's

Question 357

Sleep is defined as:

Answer 357

A naturally recurring state of mind and body characterized by altered consciousness, relatively inhibited sensory activity, inhibition of nearly all voluntary muscles, and reduced interactions with surroundings

Question 358

What drives sleep?

Answer 358

Process-S (sleep drive) and Process-C (circadian wake drive). The greatest urge to sleep occurs when they are the greatest distance from one another (around 11pm)

Question 359

How is sleep studied?

Answer 359

1. EEG - gross brain wave activity, electroencephalogram 2. EMG - muscle tone measuring, electromyogram 3. EOG - eye movement measurement, electrooculogram

Question 360

Electroencephalogram

Answer 360

- reflects the summation of the synchronous activity of millions of neurons 1.) awake with mental activity: Beta, 14-30 Hz 2.) awake and resting: Alpha, 8-13 Hz 3.) Sleeping: Theta, 4-7 Hz 4.) Deep sleep: Delta, <3.5 Hz

Question 361

Three functional sleep stages of the brain

Answer 361

1.) Awake: beta waves, alpha when eyes closed 2.) Non-REM sleep: Stage 1: Theta waves (light sleep), Stage 2: spindles, K complexes (Slow, long), Stage 3-4: delta waves, highest amplitude, synchronized 3.) REM sleep: Beta waves (similar to awake) -- Movement only occurs in Wake, eye movement occurs in wake and REM

Question 362

Stage 1 sleep

Answer 362

-Drowsiness, eyes move very slowly and muscle activity decreases. - May experience sudden muscle jerks or have a falling sensation - 4-5% of the time

Question 363

Stage 2 sleep

Answer 363

- Light sleep, eye movements stop, and heart rate and breathing decreases, body temp decreases, bruxism - increase wave frequencies (sleep spindles) and increase in wave amplitude (K complexes) - 45-55% of the time

Question 364

Stage 3-4 sleep

Answer 364

- Deep sleep, no eye movements or muscle activity - Slow wave sleep (SWS) - waking would cause groggy feeling or disorientation - bedwetting, night terrors, and sleepwalking occur here - 3 = 4-6% of the time - 4 = 12-15% of the time

Question 365

Stage 5 sleep: REM

Answer 365

- rapid eye movements, heart rate and breathing increase, dreaming occurs, limbs paralyzed, clitoral/penile tumescence occurs - plays a role in memory consolidation, organization of cognition, and mood regulation - 20-25% of the time

Question 366

Neural mechanisms of sleep

Answer 366

1.) Norepinephrine, Locus coeruleus 2.) Serotonin, Raphe nucleus 3.) Acetylcholine, Basal forebrain 4.) Histamine, Midbrain 5.) Orexin, Hypothalamus -- Therefore, SSRIs and SNRIs inhibit REM sleep

Question 367

Ascending reticular activation system

Answer 367

Reticular core of the brain stem in processes that arouse and awaken the forebrain

Question 368

Sleep promoting factors

Answer 368

1. adenosine: inhibits awaking diffuse modulatory systems 2. Caffeine: antagonist of adenosine receptors 3. Melatonin: SCN-PVN-Pineal gland, inhibited by light 4. Nicotine: stimulant, can cause insomnia

Question 369

Orexin/hypocretin

Answer 369

- neuropeptide that regulates arousal, wakefulness, and appetite - Ex. narcolepsy comes from a lack of orexin in the brain in the lateral hypothalamus - orexin binds the two G-protein coupled orexin receptors (GPCR), OX1 and OX2

Question 370

Amine hypothesis (monoamine hypothesis)

Answer 370

Depression associated with changes in serotonin or NE signaling in the brain with significant downstream effects - other NTs/neuropeptides downstream

Question 371

Tricyclic antidepressants (TCAs)

Answer 371

Mech: blocks the reuptake of NE and/or 5-HT by nerve terminals resulting in higher concentration of NTs at the receptors Side effects: antimuscarinic effects, dry mouth, blurred vision, urinary retention, constipation Drugs: Amitriptyline, Desipramine, Imipramine

Question 372

Adverse effects of TCAs

Answer 372

1. orthostatic hypotension 2. Antimuscarinic effects 3. Weight gain 4. Tachycardia and arrhythmias Why? It blocks multiple receptors. Shotgun effect. Reuptake of 5-HT, block histamine H1 receptors, block muscarinic receptors, block alpha1 receptors, block Na channels

Question 373

TCAs are metabolized by

Answer 373

CYP2D6, which is inhibited by fluoxetine (prozac)

Question 374

Monoamine oxidase inhibitors (MAOIs)

Answer 374

- initially from isoniazid for TB (accident) Mech: Blocks the oxidative deamination of monoamines (MAOA, NE and 5-HT, and MAOB, DA) Drugs: Phenelzine (Nardil), and Isocarboxazid (Marplan)

Question 375

Adverse effects and drug interactions of MAOIs

Answer 375

- low therapeutic index (<5) - Contraindicated with other serotonergic drugs (meperidine, methadone, tramadol, dextromethorphan) which can lead to serotonin syndrome - reacts with Tyramine in the diet to increase adrenergic stimulation and increase blood pressure to dangerous levels (foods such as cheese, wine, beer, yogurt, avocados, bananas) and also sympathomimetic amines such as ephedrine, and pseudoephedrine

Question 376

Symptoms of serotonin syndrome

Answer 376

hyperthermia, muscle rigidity, tremors, seizures, autonomic instability, diarrhea, confusion, irritability, and agitation. Can progress to coma and death. Treatment: Cyproheptadine (5-HT2 receptor antagonist)

Question 377

SSRIs

Answer 377

Mech: selective inhibition of serotonin reuptake by CNS neurons- increases the serotonin in synapse Side effects: sexual dysfunction, DO NOT use alone with bipolar disorders (triggers mania), Suicide (black box warning) Drugs: Fluoxetine (Prozac), Sertraline (zoloft), Paroxetine (Paxil), Citalopram (Celexa), Escitalopram (Lexapro)

Question 378

Discontinuation syndrome

Answer 378

Occurs when stopping SSRIs without tapering: dizziness, flulike symptoms, nausea, insomnia, imbalance, and sensory disturbances

Question 379

SNRIs

Answer 379

Mechanism: block serotonin reuptake AND NE reuptake. Unlike TCAs, does not block adrenergic receptors, histaminergic receptors, and cholinergic receptors Side effects: GI distress, sexual dysfunction, discontinuation syndrome ( 5-HT). Increased BP, increased HR, insomnia, anxiety, agitation (NE). Higher dropout rates than SSRIs Drugs: Venlafaxine (Effexor), Duloxetine (cymbalta), Desvenlafaxine (Pristiq- active metab. of venlafaxine)

Question 380

Mirtazapine (Remeron)

Answer 380

Mech: blocks presynaptic alpha-2 receptors on adrenergic neurons and serotonergic neurons (alpha2 normally blocks NE release presynaptically) - Also acts on H1 antagonists (sedation, increased appetite, weight gain)

Question 381

Bupropion (Wellbutrin)

Answer 381

Mech: Enhances both NE and DA neurotransmission by both increasing presynaptic release and inhibiting reuptake Side effects: CNS stimulation (agitation, anorexia, and insomnia), NO sexual side effects Also: smoking cessation- Zyban

Question 382

Trazodone (Desyrel)

Answer 382

Mech: potent 5-HT2A receptor antagoninst and weak selective inhibitor of SERT while little effect on NET. Weak antagonist at alpha-adreneric and H1 receptors Side effects: sedation, GI disturbances, and fewer sexual side effects

Question 383

Ketamine

Answer 383

Mech: injectable anesthetic, potent N-methyl-D-aspartate (NMDA) receptor antagonist - growing evidence for glutamate in depression (post-mortem studies) - single dose improves symptoms of depression in less than two hours, lasting for a week Side effects: nightmares and hallucinations

Question 384

Esketamine

Answer 384

Mech: active S-enantiomer of ketamine, Nasal spray low dose. Needs supervision FDA warning: risk for sedation, difficulty with attention/judgement, abuse/misuse, and SI

Question 385

Brexanolone/Allopregnanolone

Answer 385

Metabolite of progesterone, increases during pregnancy, decreased considerably following childbirth. Potent positive allosteric modulator of GABAA receptors. HELPS WITH post-partum depression

Question 386

Lithium Carbonate (Lithobid, Eskalith)

Answer 386

Drug for Bipolar disorder. Renal clearance of lithium is reduced and 25-40% by THIAZIDE DIURETICS, which can be toxic. Monitor salt levels and renal clearance.

Question 387

Valproic acid (Depakene), or sodium valproate (Depacon)

Answer 387

Anticonvulsant Drug for Bipolar disorder that has efficacy similar to lithium in many cases. Can combine with lithium

Question 388

Anticonvulsants for bipolar disorder

Answer 388

YES: Carbamazepine, Lamotrogine NO: Phenytoin, Phenobarbital

Question 389

Characteristics of psychosis

Answer 389

- impaired behavior - inability to think coherently - inability to comprehend reality - inability to understand disturbance - symptoms may include delusions and hallucinations

Question 390

Psychosis spectrum

Answer 390

mental retardation --> autism --> schizophrenia --> schizoaffective disorder --> bipolar/unipolar disorder

Question 391

Schizophrenia positive symptoms (gained when the disorder began)

Answer 391

- delusions - Disorganized speech - grossly disorganized behavior - catatonic - hallucinations (auditory)

Question 392

Schizophrenia negative symptoms (lost when the disorder began)

Answer 392

- lack of emotion/interest in life - social isolation - affective flattening (blank facial expression) - alogia (difficulty speaking) - inability to keep friends

Question 393

Schizophrenia cognitive symptoms

Answer 393

- disorganized thinking - slow thinking - poor concentration - poor memory - difficulty integrating thoughts, feelings, and behaviors

Question 394

DA dysfunction- goldilocks principle

Answer 394

Psychosis: DA in Limbic system, block D2 receptors for treatment--> leads to Parkinsonism Parkinsonism: DA in striatum, increase DA levels for treatment --> leads to psychosis

Question 395

First generation antipsychotics

Answer 395

- Block D2 receptors causing less downstream G-protein activation - Chlorpromazine (originally antihistamine) - Can make negative symptoms worse because of increase activation of 5-HT (which normally inhibits DA release) - FGAs block D2 in 4/4 pathways causing decrease in positive symptoms and increase in negative symptoms

Question 396

EPSE- extrapyramidal side effects

Answer 396

- drug-induced movement disorders (dystonia, akathisia, parkinsonism, tardive dyskinesia) - Because of the decrease of D2 receptor activation EVERYWHERE when giving first generation antipsychotic

Question 397

Mesolimbic pathway

Answer 397

- Tegmentum (midbrain) --> accumbens (limbic system) - mediated the positive symptoms of schizophrenia - Block D2 DA receptors--> decrease positive symptoms

Question 398

Mesocortical pathway

Answer 398

- Tegmentum (midbrain) --> frontal and limbic cortex - Area of the brain that mediates negative and cognitive symptoms of schizophrenia - Decreasing DA activity may produce or worsen negative symptoms

Question 399

Nigrostriatal pathway

Answer 399

- Substania nigra (midbrain) --> basal nuclei - regulates posture and voluntary movement - Blocking D2 receptors in receptors in striatum resulting in Parkinsonism like syndrome (EPSE) - imbalance of DA and ACh

Question 400

Tuberoinfundibular pathway

Answer 400

- Hypothalamus --> anterior pituitary - DA inhibits prolactin release - Blocking DA in this pathway may result in galactorrhea, amenorrhea, hypogonadism, infertility, erectile dysfunction

Question 401

Second generation antipsychotics

Answer 401

- Clozapine (Clozaril), blocks D2 receptors and 5-HT2A receptors (works on positive and negative symptoms) - Can cause life-threatening AE- agranulocytosis (only use clozapine with WBC monitoring) - Targeted block of 3/4 pathways to decrease negative symptoms

Question 402

Non-clozapine second generation antipsychotics

Answer 402

- risperidone (Risperdal) - Olanzapine (Zyprexa) - Ziprasidone (Geodon) - Aripiprazole (Abilify)

Question 403

Names of first generation antipsychotics

Answer 403

- Chlorpromazine (Thorazine) - Haloperidol (Haldol) - Thiorodazine (Mellaril) - Fluphenazine (Prolixin)

Question 404

second generation antipsychotics adverse effects

Answer 404

- weight gain (most common reason for poor compliance), less common in ziprasidone and aripiprazole - Type 2 diabetes

Question 405

Tardive Dyskinesia

Answer 405

- DA receptor disuse supersensitivity - occurs from discontinuation of of TGAs/SGAs, more common with FGAs (does not occur with clozapine)

Question 406

Other uses of antipsychotics

Answer 406

- Delirium - Dementia - ADHD - Severe depression - Eating disorders - PTSD - OCD - GAD

Question 407

When is a sleep study indicated?

Answer 407

Insomnia from limb movements, or a sleep related breathing disorder

Question 408

Actigraphy

Answer 408

- movement is detected using accelerometers - provides estimate of circadian rhythm, sleep and wakefulness - Helpful for: insomnia, circadian rhythm disorders, assessing insufficient sleep, paradoxical insomnia

Question 409

What is the most common sleep disorder?

Answer 409

Insomnia: Repeated difficulty with sleep initiation, duration, consolidation, or quality that occurs despite adequate time and opportunity for sleep and results in daytime impairment

Question 410

Primary insomnia

Answer 410

- pure insomnia - sleep difficulty is the core of the issue - Occurs > 3 times/week for at least 1 month

Question 411

Secondary insomnia

Answer 411

- Most prevalent - separate underlying factors have led to poor sleep (meds/stressors/etc)

Question 412

What is the most effective treatment for primary insomnia?

Answer 412

Cognitive behavior therapy- long term benefits of treatment response in 70-80% of patients (Sleep hygiene also helps)

Question 413

Medication for insomnia

Answer 413

- Benzodiazepines - non-benzos ( Zolpidem, Zaleplon) - Melatonin agonists - Orexin receptor antagonists (Suvorexant) - Antidepressants (Trazadone) - Diphenhydramine - Antipsychotics - OTCs

Question 414

Etiologies of excessive sleepiness

Answer 414

1.) inadequate sleep duration 2.) Narcolepsy 3.) Idiopathic hypersomnia 4.) post-traumatic hypersomnia

Question 415

Narcolepsy tetrad

Answer 415

1. Hypersomnia 2. Cataplexy (abrupt, transient loss of muscle tone)- type 1 has cataplexy, type 2 does not 3. Hypnagogic (hallucinations) 4. Sleep paralysis

Question 416

First line treatment of narcolepsy

Answer 416

Modafinil

Question 417

Parasomnia

Answer 417

- episodic, often undesirable behaviors that accompany sleep - disorders of NREM - Disorders of REM - sleep related dissociative disorders - sleep enuresis (bed wetting)

Question 418

Somnambulism- Sleep walking

Answer 418

- Eyes usually open - mumble/give inappropriate answers - happens in first few hours of the night (during SWS)

Question 419

Sleep terrors

Answer 419

- Dramatic events, crying, screaming, extreme agitation, fright - Sudden arousal from SWS - Autonomic and behavioral manifestations of intense fear

Question 420

Confusional arousals

Answer 420

-Confusion, disorientation, grogginess - sleep inertia: period of extreme grogginess lasting 15-30 minutes, significant agitation upon awakening

Question 421

Nightmare disorder

Answer 421

- Repeatedly being awakened by disturbing dream and recalling the details of the dream, causing distress - Occurs in REM sleep -Recalling the details is a KEY DIFFERENTIATOR of this and sleep terror disorder

Question 422

Sleep related eating disorder

Answer 422

- episodes of nocturnal eating with partial or complete amnesia - typically high calorie, and weird (cat food, raw coffee grounds, pancake mix, etc) - seen more with EDs - associated with sleep deprivation, substance use/abuse, hypnotic meds (Zolpidem)

Question 423

REM behavior disorder

Answer 423

- abnormal behaviors develop during REM - Act out dreams, eyes usually closed - episodes end with rapid awakening and full alertness, with dream recall - usually in the second half of the night - CAN BE ASSOCIATED WITH PARKINSON DISEASE, dementia with lewy body, and multiple system atrophy

Question 424

Sleep movement disorders

Answer 424

- restless leg syndrome - periodic limb movements - sleep leg cramps - sleep rhythmic movement - Bruxism

Question 425

Restless leg syndrome

Answer 425

- abnormal and unpleasant sensations (paresthesias or dysesthesias) involving lower extremities - worse at rest and at night (circadian pattern) - Check ferritin level for low iron - meds include FIRST LINE: gabapentinoids, and then lithium, sedating antihistamines, SSRIs, and TCAs

Question 426

Dementia

Answer 426

Decline in mental ability that interferes with daily life. Not a disease but a symptom, caused by damage to brain cells, interferes with ability of neurons to communicate (esp in the frontal and temporal lobes)

Question 427

Prevention factors of Dementia

Answer 427

- Top risk factors: age and genetics - Cardiovascular health: damage to brain blood vessels - Physical exercise: increases blood and O2 flow to brain - Mental exercise: stimulating life and social contacts (Nun study) - Diet: heart-healthy mediterranean diet

Question 428

Reversible dementias

Answer 428

1. infections and immunity (fever, autoimmune) 2. Metabolic and endocrine (thyroid, low blood sugar, low/high Na, Ca) 3. Nutrition (dehydration, low B1, B6, B12) 4. Medicational 5. Subdural hematomas 6. poisoning (heavy metals, pesticides, alcohol, rec drugs) 7. Brain tumors (add'l pressure) 8. Anoxia ( Asthma, MI, CO poisoning) 9. Normal-pressure hydrocephalus

Question 429

Delirium

Answer 429

Disturbance in mental abilities, confused thinking, reduced awareness of the environment ONSET: rapid, few hours or days.

Question 430

Differences between dementia and delirium

Answer 430

1. ONSET: delirium is sudden onset, dementia gradually worsens 2. ATTENTION: focus/attention impaired in delirium, not in early dementia 3. FLUCUATION: Delirium symptoms fluctuate throughout the day. In dementia memory and thinking stay fairly constant during the day.

Question 431

Vascular dementia

Answer 431

- Multi-infarct, or post-stroke dementia (10% of cases) - Sudden post-stroke changes in thinking and perception (vs memory loss in AD) - Co-existing stroke symptoms: HA, difficulty walking, numbness, paralysis on one side of face or body

Question 432

Cerebral amyloid angiopathy

Answer 432

amyloid deposition in block vessels causing blockage and decreased elasticity

Question 433

Mixed dementia

Answer 433

- abnormalities linked to more than one cause of dementia - Third most common cause of dementia (under AD and vascular) - Brain changes: hallmark abnormalities of more than one cause of dementia, AD + vascular is the most common, and then tau/amyloid, alpha-syn pathologies seen in atypical Parkinsonism

Question 434

Lewy body dementia

Answer 434

- coritcal alpha-synuclein, A-beta42 plaques, and Tau-NFT - 80% of PD pts develop dementia after 10 years - Familial forms: alpha-synuclein, and LRKK2 - ApoE4 increases the risk of sporadic LBD

Question 435

Lewy body dementia imaging shows:

Answer 435

1.) no hippocampal atrophy 2.) abnormal striatonigral activity (SPECT) 3.) visuospatial or constructional impairment (half or quarter clock)

Question 436

Lewy body dementia treatment

Answer 436

- acetylcholinesterase inhibitors: rivastigmine, donepezil - NDMA receptor blockers: Memantine

Question 437

Frontotemporal dementia (FTD)

Answer 437

- behavioral variant, semantic variant (primary progressive aphasia), and non-fluent variant PPA (Pick's disease)- starts with behavioral (AD starts with memory) - 40% + motor neuron disease, 20% + Parkinsonism, both are from the behavioral variant

Question 438

Behavioral variant FTD

Answer 438

-20% of early onset dementia is FTD - deterioration in behavior and personality, language disturbances, or alterations in muscle or motor functions

Question 439

Semantic PPA (primary progressive aphasia)

Answer 439

anomia for people, places, and objects. Word finding difficulties, and impaired word comprehension

Question 440

Non-fluent PPA (primary progressive aphasia)

Answer 440

slow, labored, and halting speech production and by omission or misuse of grammar

Question 441

Frontotemporal vs Alzheimer's disease

Answer 441

- AGE AT DIAGNOSIS: most FTD is early onset, 40-60s. Alzheimer's is more common with old age - BEHAVIOR/LANGUAGE: alterations in early FTDs vs memory loss in early AD - SPATIAL ORIENTATION: getting lost in familiar places, AD>FTD - HALLUCINATIONS/DELUSIONS: moderate-late AD> FTD

Question 442

Frontotemporal pathology and genetics

Answer 442

1. TDP-43 in 50%, increase FTD with MND 2. Tau <50%, Pick's 3. FUS 10%, rare Genetics: SOD1, Tau (MAPT), TDP-43 and FUS, C9orf72** present in 25% FTD and 25% ALS

Question 443

Chronic traumatic encephalopathy

Answer 443

- repetitive head trauma: boxers, football, hockey, soldiers - Dementia including depression, explosiveness, memory loss - Movement disorders: incoordination, slurred speech, slow movement, tremors, and rigidity - symptoms appear years after trauma. - Most common from Tau buildup and TDP-43

Question 444

Creutzfeldt-Jakob disease

Answer 444

- most common human form of transmissible spongiform encephalopathies or prion disease - Rapidly fatal disorder, months after onset that impairs memory and coordination and causes behavior changes

Question 445

Misfolding: seeded nucleation

Answer 445

oligomers are the most dangerous part of monomer--> mature fibrils. Seeding with oligomer avoids latent/nucleation phase for rapid transmission

Question 446

Neuroanatomy of Depression

Answer 446

1. elevated amygdala activity 2. elevated subgenual anterior cingulate activity 3. diminished hippocampus activity 4. Diminished dorsolateral prefrontal cortex during emotional regulation

Question 447

Depression includes a decrease of what NTs?

Answer 447

- NE -Serotonin - DA

Question 448

Depression sleep physiology changes

Answer 448

- decreased REM latency - repeated nighttime awakenings - decreased slow-wave sleep - increased total REM sleep

Question 449

Altered neurogenesis in depression

Answer 449

- decreased hippocampal volume - decreased neuronal complexity

Question 450

DSM-5 definition of mental disorder

Answer 450

a syndrome characterized by clinically significant disturbances in an individual's cognition, emotion, regulation, or behavior that reflects a dysfunction in the psychological, biological, or developmental processes underlying mental functioning. -- two mood disorder categories: depression, and bipolar

Question 451

Disruptive mood dysregulation disorder

Answer 451

- previously known as childhood bipolar disorder - first diagnosis can only be between 6-18 - Features: persistent irritability and frequent bouts of extreme, out of control behavior

Question 452

Premenstrual dysphoric disorder

Answer 452

- significant affective symptoms that arise in the week before menses and abate shortly after onset of menses - must have at least 5 symptoms: mood lability, irritability, tension, problems focusing, anhedonia, fatigue, problems sleeping - symptoms must be present for a year

Question 453

Major depressive disorder

Answer 453

- depressed mood or loss of interest lasting at least 2 weeks - must have at least 4 add'l symptoms: insomnia, hypersomnia, psychomotor retardation or agitation, significant weight loss or gain, increased/decreased appetite, loss of energy, feeling worthlessness, excessive guilt, difficulty concentrating, thinking, or making choices, recurrent thoughts of death or suicide

Question 454

SIGECAPS

Answer 454

- depression assessment evaluating: Sleep, interest, guilt, energy, concentration, appetite, psychomotor changes, suicidal ideation

Question 455

Major depressive disorder epidemiology:

Answer 455

- onset: 29 years - lifetime prevalence is 20.6% - 2-8% of children ages 4-18 meet criteria - prevalence and manifestation of MDD varies, across lifespan

Question 456

Grief

Answer 456

- affect is dominated by feeling of emptiness and loss - dysphoria comes in waves - capacity for positive emotional experiences - self-esteem remains intact - fleeting thoughts or joining decreased

Question 457

Dysthymia

Answer 457

- chronic depressive disorder for at least 2 years, 1 year for children/adolescents - must have two other symptoms: poor appetite or overeating, sleeping too much or too little, poor self-esteem, trouble concentrating/making decisions, feelings of hopelessness - lifetime prevalence is 6%

Question 458

Depression commonly is comorbid with

Answer 458

- anxiety - substance abuse - ADHD and conduct problems - dysthymia is highly comorbid with personality disorders

Question 459

First line treatment for depression

Answer 459

Therapy: cognitive behavior therapy, behavioral activation therapy SSRIs: Fluoxetine (prozac), Escitalopram (lexapro), sertraline (zoloft), Paroxetine (paxil), Citalopram (celexa)

Question 460

Interpersonal psychotherapy (IPT)

Answer 460

- short-term psychodynamic therapy focused on current relationships

Question 461

Acceptance and commitment therapy (ACT)

Answer 461

- teaches mindfulness, acceptance, and cognitive defusion skills to help individuals live in a psychologically flexible and values-consistent way

Question 462

Problem-solving therapy (PST)

Answer 462

- treatment is aimed at resolving barriers to effective social problem solving as the way in which people cope with stressors is believed to be predictive of the degree to which they will struggle

Question 463

Depression treatments for non-responders to first-line treatment

Answer 463

1.) electroconvulsive therapy (ECT)- intentionally induced brain seizures, side effects include memory loss, headaches, and musculoskeletal problems 2.) Ketamine 3.) Transcranial magnetic stimulation (TMS) 4.) Psychedelic assisted psychotherapy 5.) Deep brain stimulation

Question 464

General personality disorder

Answer 464

- a lasting and pervasive configuration of personality traits that strays from cultural norms, and is expressed inflexibly across a range of social settings, and leads to significant distress or impaired functioning. - Affects Cognition, affectivity, interpersonal functioning, and impulse control

Question 465

Cluster A personality disorders (Weird)

Answer 465

1. Paranoid PD 2. Schizoid PD 3. Schizotypal PD

Question 466

Cluster B personality disorders (wild)

Answer 466

1. Antisocial PD 2. Borderline PD 3. Histrionic PD 4. Narcissistic PD

Question 467

Cluster C personality disorders (worried)

Answer 467

1. Avoidant PD 2. Dependent PD 3. Obsessive PD 4. Compulsive PD

Question 468

Paranoid personality disorder

Answer 468

- Cluster A PD - needs 4 criteria to be met - Criteria include problems with trust, fidelty, reading into situations to make them demeaning or threatening - 0.5-2.5% of population - treatment: rarely seek treatment, lack insight to the disorder, anxiolytics and antipsychotics can be helpful

Question 469

Schizoid personality disorder

Answer 469

- Cluster A PD - needs 4 criteria to be met - criteria includes: choosing solitary activity, little/no interest in sexual experiences, lacks close friends, indifferent to praise or criticism - 1.8% of the population - may be genetically related to autism/ parents cold and aloof - prognosis is poor no effective treatments

Question 470

Schizotypal personality disorder

Answer 470

-Cluster A PD - 5 criteria must be met - Criteria includes: unusual perceptual experiences, bodily illusions, odd thinking and speech, behavior is eccentric or peculiar, they desire friendships but cannot make them - commonly associated with anxiety and depression - 3 % of the population - low dose antipsychotics might help

Question 471

Antisocial personality disorder

Answer 471

- Cluster B personality disorder - 3 criteria must be met - Criteria includes: performing acts that are grounds for arrest, lying, use of aliases or conning others, irritability or aggressiveness, lack of remorse - highly comorbid with substance abuse disorders, strong genetic association - individual therapy treatment plans (group work doesn't work)

Question 472

Borderline personality disorder

Answer 472

- Cluster B personality disorder - 5 criteria must be met - criteria include: frantic efforts to avoid real or imagined abandonment, unstable self-image, impulsivity, marked mood changes, chronic emptiness feelings - 1.4-2% of population - childhood sexual abuse is very common - Treatment: dialectical behavior therapy and low dose antipsychotics, antidepressants, or lithium

Question 473

Histrionic personality disorder

Answer 473

- Cluster B personality disorder - 5 criteria must be met - criteria include: dramatic, strong desire for attention, rapidly shifting and shallow emotional expression, uses physical appearance to draw attention to self, considers relationships to be more intimate than they actually are - 1-3% of the population - hyperresponsive noradrenergic system (heritable) - Treatment: may respond to psychotherapy if less impaired

Question 474

Narcissistic personality disorder

Answer 474

- Cluster B personality disorder - Criteria include: has a grandiose sense of self-importance, preoccupied with fantasies of success, power, beauty, or ideal love, requires excessive admiration, exploitative, envious - 2-16% of the population - more common among men, sometimes heritable - may respond to long-term psychotherapy

Question 475

Avoidant personality disorder

Answer 475

- Cluster C personality disorder - 4 criteria are required - Criteria include: avoids interpersonal contact for fear of criticism, disapproval, or rejection, views self as socially inept, personally unappealing, or inferior to others - 2.1-2.6% of population - modest genetic influence - group therapy might be helpful, unlikely to seek treatment

Question 476

Dependent personality disorder

Answer 476

- Cluster C personality disorder - Typically occurs from poor parental bonding - Criteria include: difficulty making decisions without excessive advice and reassurance, needs others to assume responsibility for major areas of their life, feels uncomfortable or helpless when alone, exaggerated fears of being unable to care for themselves - 2-4% of the population - commonly associated with anxiety and depression - no known treatment

Question 477

Obsessive compulsive personality disorder

Answer 477

- Cluster C personality disorder - criteria include: preoccupation with details, rules, lists, order, etc., perfectionism, excessively devoted to work and productivity, inflexible about matters of morality, ethics, or values, micromanages - 2-8% of the population - less common in younger adults, more common in higher education - treatment: psychotherapy

Question 478

Cognition

Answer 478

process of acquiring and understanding knowledge through our thoughts, experiences, and senses. Cognitive functions include all aspects of human culture and behavior (language, emotion, attention, memory, etc.). Both conscious and unconscious

Question 479

Reductionism

Answer 479

Complex brain fxns emerge from the biological properties of neuron and their interconnections

Question 480

Mind

Answer 480

Sum of operations in an information processing organ powered by a vast number and variety of neurons and the complexity of their interconnections

Question 481

Cortical layers and circuitry

Answer 481

- Connect laterally to other hemisphere or deep nuclei (signal integration - area dedicated to a function is proportional to computational columns involved - Cell types: pyramidal, local axon collateral , stellate, dendrites, descending axon (output)

Question 482

Serial organization of sensory information

Answer 482

- unimodal primary sensory cortex (vestibular, somatosensory, gustatory, olfactory, auditory, visual)--> unimodal secondary cortex (same name as primary) --> multimodal association areas that can select and integrate signals in a seamless perception fashion

Question 483

Association cortex has input from:

Answer 483

Thalamic sensory, motor input, subcortical input (DA from midbrain, NE from brainstem, 5-HT from brainstem, ACh from brainstem and basal forebrain nuclei)

Question 484

Parallel processing

Answer 484

1. Dorsal stream, (magnocellular), Parietal cortex, WHERE? processes motor and spatial information such as: position, motion, speed 2. Ventral, (Parvocellular), Temporal cortex, WHAT? processes objection recognition such as: color, shape, texture

Question 485

Where do the dorsal and ventral pathways converge to form planned behaviors?

Answer 485

Frontal cortex (Orb MVPFC, DLPFC)

Question 486

Lesion in the temporal cortex is associated with:

Answer 486

Agnosias: aware of objects but unable to recognize them

Question 487

Visual agnosia

Answer 487

Cannot recognize things but can draw

Question 488

Prosopagnosia

Answer 488

Cannot recognize faces

Question 489

Auditory agnosia

Answer 489

can hear, but cannot recognize sounds

Question 490

Wernicke aphasia

Answer 490

Left temporal injury: impaired understanding of spoken language, garbled speech

Question 491

Hemispatial neglect

Answer 491

Contralateral neglect syndrome of the WHERE? parietal. Patient ignores image contralateral to injury (half clock drawn, half house drawn, etc)

Question 492

Personal neglect hemispatially

Answer 492

Patient will not dress or wash contralateral side, disowning the arm or leg. They still respond and move to pinprick

Question 493

Parietal association cortex (PAC)

Answer 493

Left side contains the language center (specialization), and the right side supports the left. Object on the left: only R PAC activated Object on the right: L+R PAC activated

Question 494

Left side lesion of the PAC

Answer 494

leads to Right sided compensation (less deficits)

Question 495

Right side lesion of the PAC

Answer 495

Right side cannot be compensated by Left side leading to hemispatial neglect

Question 496

Ventrolateral parietal cortex vs. dorsomedial parietal cortex

Answer 496

VLP cortex: Visual fxn- spatial recognition DMP cortex: Motor fxn

Question 497

Lateral intraparietal area responds to

Answer 497

Retina-centered attention (eye fields)

Question 498

Ventral intraparietal area responds to

Answer 498

Head centered attention (Head turning + eye field)

Question 499

Hippocampal formation

Answer 499

- episodic memory, ability to remember past events regardless of emtional content. Long term memory consolidation - Complex functions related to emotion and episodic (autobiographical) memory - transfers information to neocortex by inducing replay in parietal, temporal, and frontal association cortices

Question 500

Frontal cortex

Answer 500

- Organizes behavior and working memory - executive fxn: selecting and planning appropriate behavioral responses - Phineas Gage :)

Question 501

Dorsolateral PFC (DLPFC)

Answer 501

- organization and planning - motor planning: active maintenance of information relevant to an ongoing behavior - Orb VMPFC --> DLPFC --> premotor cortex --> M1 --> appropriate behvior - LESION: working memory deficits, indifference

Question 502

Motor behavior

Answer 502

Perception --> meaning, purpose --> emotional processes in OVPFC --> influence cognitive processes in DLPFC --> act on premotor and primary motor neurons

Question 503

Premotor cortex is activated:

Answer 503

When the object is handling OR just observed. Presentation of an object translates its physical motor properties into a potential motor act -- Parietal cortex (WHERE) is interconnected with premotor, temporal (WHAT) is not

Question 504

Potential motor acts

Answer 504

1.) sight of object triggers all its properties in parietal (WHERE) cortex (pragmatic opportunities) 2.) temporal (WHAT) cortex extracts the meaning of the object based on the subject's intention 3.) Premotor cortex transforms and opportunity into an appropriate potential motor act (convergence of what and where)

Question 505

Blind sight

Answer 505

Lesion in primary visual cortex. subjects cannot see but can guess correctly (subconscious processing?)

Question 506

Unilateral neglect perception

Answer 506

Lesion in RPAC perceives two houses (one with Left fire) as the same, but still would prefer to live in the house that does not have the fire (even though they cannot see it)

Question 507

Left temporal cortex damage forming agnosia but patients still:

Answer 507

place cards in a slot accurately even though they cannot recognize the shapes-- sensory information is guiding them unconsciously.

Question 508

Injury to perception-forming association cortex results in:

Answer 508

Coma, vegetative state, etc. even if they are still able to receive individual information, they cannot put them together or perceive anything