By: Anagha Deshmukh

Chairperson: Ms. Sahana Madhyastha

 Introduction
• Motivation is defined as “the reasons
underlying behavior”
(Guay et al., 2010)

• Gredler et al., 2004 broadly define motivation

as “the attribute that moves us to do or not to
do something”
• Motivation is purposeful and includes the
processes that guide the general strength and
direction of an organism’s activity over time
(Reeve et al., 2004)

• Sense of duration is important  orientation

is toward the future
(Larry et al., 2005)
• Guided and directed by putative cognitive
structures  motives

• Stable conscious motivational processes

depend on a large neocortex

(Dawson & Bill, 2007; Monaise, 2003; Gole et al., 2000)

Motives are hypothesized to guide behaviors and interests within
one of five social domains related to ever larger systems
• Motivation is purposeful and includes the
processes that guide the general strength and
direction of an organism’s activity over time

• Although motivated behavior takes place only

in the present, its orientation is toward the
future
• Motives, emotions, and self-control  trans
conscious process  modular brain structures
 adaptive mental mechanisms

• Stable conscious motivational processes

depend on a large neocortex.
• Interest in neural basis of motivation

– The increasing interest in human behaviour to

identify the underlying biological correlates in
order to formulate comprehensive theories of
functioning

(Deci, 2005; Rolls et al, 2004; Becker & Stance, 2001; Wills et al.,
1998)
– The emergence of multiple non-invasive methods
of studying the functions of the brain

– Understanding of the contributions of the various

brain areas towards these unifying behaviours

(Morrison et al., 2000; Bill, 2003; Mall & Deci., 2000; Tucker et al.,
1995)
 Instincts
• An instinct is an innate biological force that
predisposes the organism to act in a certain
way under appropriate circumstances

• William McDougall, maintained that all our

thoughts and behavior were the result of
inherited instincts
• Instead of choosing goals and actions, a
person was at the mercy of innate forces,
which determined-or motivated-behavior

• Psychoanalytical  Life & Death instincts

 Drives & Motives
• 1920  instinct  drive

A drive is an aroused state

Results from some biological need

(food/water/sex/pain avoidance)
• The organism attempts to reduce the drive by
doing something  satisfy the need

• “Need" and “Drive" are used interchangeably

– Need  physiological state of tissue deprivation

– Drive  psychological consequences of a need

 Motivational Control System

Optimal State
Error Signal
Search memory to
select appropriate
Comparator
response to
restore balance

State Monitor

Execute Response

Biological State
• Behavioral neuroscience  homeostasis

– Usually means a specific type of regulatory system

that uses a setpoint, or built-in goal value, to
maintain a stable physiological state

(Berridge, 2004)
Homeostatic Mechanism, Berridge (2004)
 Intrinsic & Extrinsic
• Intrinsic motivation refers to initiating an
activity for its own sake because it is
interesting and satisfying in itself, as opposed
to doing an activity to obtain an external goal
(extrinsic motivation)

(Deci & Ryan, 1971)

 Approach/ Withdrawal
• A large body of research has postulated the
existence of two overarching motivational
systems that organize behavior

– Involves behavior prompted by a possible

desirable outcome (approach)

– Involves behavior prompted by a possible aversive

outcome (aviodance)
 Liking/ Wanting

• Liking  immediate pleasure one gets from

contact with a stimuli

• Wanting  “magnet quality” of something

that makes it desirable

(Berridge, 2009; Berridge, Robinson, & Aldridge, 2009)

• The building blocks of these psychological
constructs correspond to two general systems
for orchestrating adaptive behaviour

(Carver & White, 1994; Fowles, 1980)

– Behavioral Inhibition System

(Gray, 1975, 1990; Lang, Bradley, & Cuthbert, 1990)

– Behavioral Activation System

(BAS; Fowles, 1980, 1988)
 Two Systems
• Behavioural inhibition

– Attentional system

– Sensitive to punishment/treat cues

– Tendency to halt on-going behaviour

 – Strong BIS: anxiety disorders
(Fowles, 1988; Quay, 1988)

– Weak BIS: primary psychopathy

(Newman et al., 2005)

• Corresponds to a conflict-monitoring
mechanism and its associated activity in the
ACC
(Pizzagalli et al., 2005)
• Behavioural activation

– Motivational system

– Assess rewards and non-threat cues

– Helps escape from punishment

– Important for engaging behavior toward a reward

or away from a threat
• Strong BAS:

– Impulsivity disorders
(Wallace, Newman, & Bachorowski, 1991)

– Bipolar disorder
(Depue & Iacono, 1989)

– Attention-deficit/hyperactivity disorder
(Mitchell & Nelson-Gray, 2006)
• BAS  dopaminergic neurotransmitter system
 promote goal-related behavior in response
to anticipated reward or punishment

• Corresponds to a regulative mechanism and

its associated activity in the PFC

(Gray & McNaughton, 2000; Schultz, Dayan, & Montague, 1997)

• Models:
 Drive Reduction Theory
• Bases motivation on bodily needs that create
a state of tension or drive

• Organism then seeks to reduce the drive by

doing something to satisfy the need

• The body tends to maintain a constant

internal environment, or homeostasis
• Any psychological imbalance will also
motivate behavior designed to restore
equilibrium (Lorenz, 1981)

• Hull (1943) suggested that events that reduce

drive are positively reinforcing

• The hormone leptin  eating 

hypothalamus (Elmquist et al., 1998; 1999).
• Some of the researched motives/needs in
terms of neurobiology include:

– Affiliation

– Aggression

– Implicit power (n Power)

 Affiliation
• Behaviors that foster the development and
maintenance of social relationships (or bonds)
are known as affiliative social behaviors

(Steklis and Kling, 1985)

• Amicable behaviors  important components
of sociality in many species

(Sussman et al., 2005, 2006)

• Past research has largely been limited to
studies of individuals with brain damage or
disorders of social cognition
(Adolphs, 1999)

• More recently functional imaging

approaches

(Zink and Meyer-Lindenberg, 2012; Guastella and MacLeod, 2012)

• Two related neuropeptides critical to the
regulation of affiliative behaviors:

– Oxytocin
(Crowley and Armstrong, 1992; Ivell and Russell, 1996)

– Vasopressin
(Insel, 2010; Albers, 2012)
• Two brain areas involved in processing rewards:

– Anteroventral striatum

– Ventromedial/orbitofrontal cortex

– Receive midbrain dopamine projections and are rich

in neurons that respond to dopamine

(Rolls, 1999; Schultz, 1998)

 Aggression
• Normal component of mammalian behavior
(Huntingford, 1987)

• Neurobiology:

– Serotonin neurotransmission (reduces aggression)

– Vasopressin (increases aggression)

(Ferris, 2005)
• Subsets of interconnected neurons conveying
sensory and motor information to and from
sites of integration

• Normal aggressive behavior and aggression

characterized by impulsivity and violence

(Albert & Walsh, 1985)

• fMRI  Specific brain areas that have a key
role in the control of aggressive responding :

– lateral hypothalamus

– cortical and medial amygdala

– bed nucleus of the stria terminalis

(Recci et al., 2006)

 Implicit Power (n Power)

• Denotes, power-motivated individuals as

concerned with having impact over others,
and derive reward and reinforcement from
having this impact

(Schultheiss, 2008; Winter, 1973)

• Steele (1973) produced the first research on the
biological components of n Power

• Activation of the sympathetic nervous system as

a function of n Power arousal
(McClelland, 1987)

• Positively correlated with baseline testosterone

 high baseline levels of testosterone manifest
themselves in aspects of an individual’s
personality
(Schultheiss, 2007; Winter, 1973)
• In n Power significant increases in epinephrine
and norepinephrine have been seen

(Wells, 1999; Tom et al., 2001; Becker & James, 2007)

 Incentive Theory
• Emphasizes the importance of external
conditions as a source of motivation

• Conditions may be
– positive incentives  approach
– negative incentives  avoid

• Incentives – arouse behavior and direct it

 Important Brain Ares
• Lateral hypothalamus
• Ventromedial hypothalamus
• Ventral tegmental area
• Dorsal striatum
• Dopamine

(Hikosaka, 2007; Haber et al., 2007 Robinson et al., 2006)

 Self Determination Theory
• Most influential theories to explain the nature
of human motivation (Deci & Ryan, 1985;
Ryan & Deci, 2000)

• First conceptualized by Edward L. Deci based

on studies of the over-justification hypothesis
(Deci, 1971)
• Over-justification hypothesis

– Extrinsic rewards exert detrimental effects on

intrinsic motivation

– Extrinsic rewards are given when people perform

a task intrinsically motivated to perform
without any extrinsic rewards

– Intrinsic motivation to do the task decreases once

extrinsic rewards are removed
 Behavioural Theory
• Thorndike (1911)

– Changed the focus of motivation from the internal

to the external

– Modified by environmental consequences

– Law of Effect
 – Environment has a causal role in motivation

– Motivation is an automatic and reflexive process

• Holt (1931) criticized this approach as

descriptive rather than explanatory

– faulted as mechanistic

(Neilsen & Day, 2000; Tinbergen, 1951)

• Tolman (1932)

– Notion of “purposive behaviorism”

– Purposeful behavior  obtain a desired goal

– Allowed cognitive intervening variables to reenter

the behavioral equation as antecedents
Cognitive Theory
• Motivation is caused by a more rational and
deliberative process

• Suffer from the same criticism that Holt (1931)

• Best equipped to:

– Describe thoughtful processes and their outcomes

– Less able to provide explanations for the existence of

these thoughtful processes in the first place

(Robins, 2010)
 Dopamine
• Growth of interest in the cognitive
neuroscience of motivation and reward

• Neurophysiology studies of the response

properties of dopamine-containing midbrain
neurons in primates receiving reward (Schultz,
1998).
• Dopamine was first identified with
motivational function  Ungerstedt’s report
(2011, 2009)

– feeding and drinking deficits that are similar to

those caused by lesions of the lateral
hypothalamus can be induced by selective
damage to the dopamine fibers that traverse this
region
• Reinforcement learning  computational
framework for trial and error learning from
reward

(Houk, Adams, & Barto, 1995; Montague, Dayan, & Sejnowski, 1996;
Schultz, Dayan, & Montague, 1997)
• Important functional role for dopamine and its
targets in:

– Stimulus-response learning
(Gabrieli, 1998; Knowlton, Mangels, & Squire, 1996; White, 1997)

– Addiction
(Everitt & Robbins, 2005; Hyman, Malenka, & Nestler, 2006)

– Movement
(Albin, Young, & Penney, 1989; DeLong, 1990)
• Damage to nigrostriatal dopamine fibers 
feeding and drinking deficits

• Selective damage to the mesolimbic

dopamine fibers  decreases the forward
locomotion  common to most reward
seeking

(Wills & Conner, 2009; Dollar et al., 2005; Solomon et al., 2001;
Bells, 1995)
 Dopamine and Reinforcement
Learning

•Neuromodulator dopamine  Straitum

•Key point at the nexus of motivation and action

(Wallis, 1985; Chester et al., 1999; Grace et al., 2001)

• Activity of dopamine neurons recorded in
primates receiving reward appears  similar
to those used for reinforcement learning
(prediction error)

(Houk et al., 1995; Montague et al., 1996; Schultz et al., 1997; Sutton
and Barto, 1998)
(Faure et al., 2005; Parkinson et al., 2002)
• fMRI studies  signals in striatum 
prediction error  dopaminergic activity

(McClure, Berns, & Montague, 2003; O’ Doherty, Dayan, Friston,

Critchley, & Dolan, 2003)

• Evidence for the involvement of midbrain

dopamine in learning in humans comes from
studies examining learning in individuals with
Parkinson’s disease

(Graybiel, Hirsch, & Agid, 1990)

• Disease causes  profound loss of dopamine-
containing neurons in the midbrain
dopamine depletion in the striatum

• Prominent symptoms
– Motoric
– Cognitive deficits
• Reward
• Learning

(Frank, Seeberger, & O’Reilly, 2004)

 Dopamine Hypothesis of Reward
• Four main DA systems

– Tuberoinfundibular system

• Location: hypothalamus

• Function: this regulates the pituitary hormone

prolactin, involved in the control of lactation
– Nigrostriatal system

• Location: projecting from the substantia nigra pars

compacta (SNc) in the midbrain to the dorsal striatum,
part of the basal ganglia

• Function: regulates the initiation of movement and

goes wrong in Parkinson’s disease
– Mesocortical system

• Location: projecting from the ventral tegmental area

(VTA) near the SNc in the midbrain to the prefrontal
cortex

– Mesolimbic system

• Location: projecting from the VTA to the nucleus

accumbens (Acb) in the ventral striatum

• Function: mediated pleasure (Wise, 1982)

• Anhedonia hypothesis
Dopamine Pathways
Insular Cortex
• Most influential theories about human
motivation and reward-related decision

Somatic marker hypothesis

• Proposes that emotional processing greatly

influences human decision making processes,
including reward-related decision-making

(Bechara & Damasio, 2005; Bechara et al., 2005; Damasio et al., 1996).
• Important brain regions for human motivation
and reward-related decision making

– Insular cortex  somatosensory map

– Amygdala  primary reinforcer for somatic states

– Ventromedial prefrontal cortex  catalyzes

functions of insular and amygdala

(Bechara & Damasio, 2005)

 Ventral Striatum

Ventral striatum is a part of the mesolimbic system

• Motivationally-relevant findings from human
clinical patient studies with those from animal
studies:

– Ventral striatum (nucleus accumbens) mediates

the associative knowledge to guide actions or
behaviors

– Amygdala works for associative learning among

stimuli and outcomes

(Cardinal et al., 2002)

• fMRI studies

– Ventral striatum works more as a ‘critic’ while the

dorsal striatum works more as an ‘actor’ in reward
processing

– Ventral striatum is recruited when people learn

the reward-related information regardless of the
existence of action selections

(Haruno et al., 2004; O’Doherty et al., 2004)

• Ventral striatum (nucleus accumbens)
mediates the associative knowledge to guide
actions or behaviors.

• Processing of social stimuli activates

associated reward circuitry via MPFC and
anterior cingulated cortex, as well as the
ventral striatum

(Grace et al., 2007)

• Compromised functioning of the ventral
striatal  to the inability to use positive
reinforcement to motivate behavior

(Grace et al., 2007)

Prefrontal Cortex
Orbitofrontal Cortex (OFC)
Dorsolateral Prefrontal Cortex (DLPFC)
• The prefrontal cortex is less involved in

– Establishing whether a stimulus is positive or

negative (valence)

– It regulates the overall motivational salience and

determines the intensity of behavioral responding

(Jentsch & Taylor, 1999; Bush et al., 2002)

• Drug seeking:

– Glutamanergic projection  prefrontal cortex 

nucleus accumbens  drug seeking behaviour

(Robinson & Berridge 2000; Everitt et al. 2001)

• The medial prefrontal cortex (mPFC)

– Processing of both reward cues and social

cognition tasks such as theory of mind

(Brunet- Gouet and Decety, 2006; Harris et al., 2007)

• Involved in the BAS system

– Striatal dopamine projections

(Lehe´ ricy et al., 2004; Rolls, 2000)

– Mesocortical system

– Decision making  holding information

(Schultz, 2000)
Nucleus Accumbens (Nacc)
• The activities of the nucleus accumbens
involve:

– monitoring the gap between the expected values

and the real values
– directing behavior appropriately

– Malfunction  motor and cognitive deficits

(Parkinson’s Disease)
• Role of Nacc  debatable

– Prediction error theory : people learn from

previous decision errors to make subsequent
decisions

(Hare, O’Doherty, Camerer, Schultz, & Rangel, 2008; McClure et

al., 2004; O’Doherty et al., 2004)

– Identified from a connection with reward-

motivated behaviors
(Olds & Milner, 1954)
• Part of mesolimbic pathway

– Liking & wanting

– Reward deception and perception
– Goal directed behaviour

• Important in reward processing  addiction

(McClure et al., 2004; O’Doherty et al., 2004)

Thalamus/ Hypothalamus
• Thalamus

– Major relay center for all information

– Part of major neural pathways

– Helps in initiation and maintenance of behaviour

– Helps in activation of behavioural systems

(Wilkens et al., 1957; Domasio, 1985; Walsh, 1999; Craig &

Moore, 2004; Dollar et al., 2008; Freeman et al., 2010)
• Hypothalamus: involved in a large number of
behaviourally significant activities

– Eating can be suppressed  lesions of the lateral

hypothalamus
(Anand & Brobeck, 1951)

– Enhanced  lesions of the ventromedial

hypothalamus
(Hetherington & Ranson, 1939)
• Stellar (1954) suggested that the LH and VMH
were ‘hunger’ and ‘satiety’ centers,
respectively

• LH & Basolateral hypothalamus: key role in

– Organization and initiation of aggressive

behaviour
– Aggressive responding

(Wolff, 2006; Jenkins et al., 2005; Hamani et al., 2004; Mitchell et

al., 2000)
• Lateral hypothalamus  extensive efferent
connections to a majority of the brain areas

– Constitute the putative neural circuit of aggressive

motivation identified with fMRI

(Ogawa, 1990; Logothetis, 2005; Smith et al., 2005)

Hypothalamus part of the tuberoinfundibular

 regulates the pituitary hormone prolactin,
involved in the control of lactation)
Ventral Tegmental Area (VTA)
• fMRI studies  rewards processing network

• Part of mesocortical system

– Projections from the VTA release dopamine

throughout the circuit in response to a
motivationally relevant event

(McLure et al., 2003)

Ventral Pallidum
• Mechanism of reward and incentive
motivation

– Stimulated activation  sufficient to cause

reward and motivation enhancements

– Activation patterns  specifically encode reward

and motivation signals via phasic bursts of
excitation to incentive and hedonic stimuli

(Smith et al., 2009)

• Motivation is essential to adaptive functioning
and quality of life

• Motivational loss handicaps physical

rehabilitation and coping skills  major
source of burden for families

• Ever-present, essential determinant of

behavior and adaptation

• Motivation is not a single function of the brain

(Finset and Andersson, 2000)
Disorders of Diminished Motivation
(DDM)
• Most important structures for establishing and
maintaining the current motivational state:

– Anterior cingulum (AC),

– Nucleus accumbens (NAcc),
– Ventral pallidum (VP),
– Medial dorsal nucleus of the thalamus (MD),
– Ventral tegmental area (VTA)

• Comprise a cortico-striatal-pallidal thalamic

circuit
(Kalivas, 1993; Marin, 1997)
Cortico-striatal-pallidal thalamic circuit
(Marin, 1997)
• Motivation is the psychological domain
concerned with goal-directed behavior

• Recognition of diminished motivation requires

examining goal-related aspects of:

– Overt behavior

– Thought content

– Emotion
American Congress of Rehabilitation Medicine,
2005 (Fisher, 2005; Marnin, 2007) places DDM
on a continuum of motivational loss
Minor pole of severity Major pole of severity

• Result from dysfunction of the neural machinery

that mediates motivation.
 Akinetic Mutism
• Essentially characterized by

– Total absence of spontaneous behavior and speech

– Occurring in the presence of preserved visual tracking

(Marnin, 2007)
 Abulia
• Originally denoting a disorder of will

• Characterizes patients with symptoms less severe

than but qualitatively identical to akinetic mutism

– poverty of behavior and speech output

– lack of initiative
– loss of emotional responses
– psychomotor slowing
– prolonged speech latency

(Mega, 1997; Berrios, 1995)

 Apathy
• Characterized by:

– Diminished motivation
– Presence of normal consciousness, attention,
cognitive capacity, and mood
– Generally able to initiate and sustain behavior
– Describe their plans, goals, and interests
– React emotionally to significant events and
experiences
• These features are:

– Less extensive
– Less common
– Less intense
– Shorter in duration

• Apathy differs from normality quantitatively

rather than qualitatively

(Mega, 1997; Berrios, 1995)

(Benson, 1990)
 Addiction
• Researchers have identified cellular
mechanisms underlying the acute and chronic
effects of drugs of abuse in animal models

(Nestler & Aghajanian 1997; Everitt et al. 2001; Robinson &

Berridge 2003).
• WHO (1969)  drug dependence
• Acute administration of most drugs of abuse
increases dopamine transmission in the basal
ganglia (Wise, 1989)

• Essential for these drugs to reinforce

behavior, and thereby promote addiction
(Koob & Moal, 2001; Robinson & Berridge,
2007)

• Dopamine projections to the basal ganglia and

cortex are important in facilitating the
encoding of learned associations necessary for
the development of addiction (Jay, 2005)
• Motivated behavior classically implies both an
activation of the organism by environmental
or interoceptive stimuli and a directed
behavioral output (Lashley, 1938)

• Neurobiological search for the antecedents of

motivated behavior involves defining these
neural substrates
Neurobiology has focused on three brain regions in the
activation of behavior:
(Kalivas and Volkow, 2005)
(Kalivas and Volkow,
2005)
 Schizophrenia
• Neurocognition and functional outcome are
associated in schizophrenia (Gottesman, 1994;
Green, 1996; Green et al., 2000)

Brekke et al., 2005

• Motivation likely plays an important role in
the cognitive dysfunction of schizophrenia,
with important associations to functioning
(Barch, 2005; Barch et al., 2008; Docherty et
al., 2001; Gold et al., 2008; Heerey and Gold,
2007).

• Causal relationships unclear between

motivation, neurocognition and social
cognition  Role of mediation
• Behavioral neuroscience research 
distinction between in-the moment pleasure
and anticipated pleasure
(Berridge and Robinson, 1998; Schultz, 2007; Wise, 2002)

• Researchers have shown that schizophrenia

patients appear to have a deficit in the more
cognitively complex aspects of motivation – or
anticipating that things will bring them
pleasure
(Gard et al., 2007)
• Anhedonia and other motivationally relevant
deficits to problems with working memory
(Burbridge and Barch, 2007)

• The medial prefrontal cortex (mPFC) is an

important neural correlate for the processing
of both reward cues and social cognition
(Brunet- Gouet and Decety, 2006; Harris et al., 2007)

• Associated reward circuitry via MPFC and

anterior cingulated cortex, as well as the
ventral striatum
(Grace et al., 2007)
• Deficient neural activity in the ventral
striatum in response to reward anticipation 
severity of negative symptoms
(Kapur, 2003)

• Striato-thalamo-cortical circuits

– Striatal dopamine-mediated (DA) input from the

pars compacta of the substantia nigra (SNpc) and
ventral tegmental area (VTA) play a fundamental
role in regulating these circuits

(Alexander et al., 1990)

Cortical-Striatal-Thalamic-Cortical Loop
Andrew et al., 2003
• Apathy  cortical hypo-function of various
circuits

• Crucial component is the limbic-ventral-

striatopallidal system, or ‘motive circuit’,

– Suggested as the key to the translation of

motivation into action

(Mogenson et al., 1980; Alexander et al., 1990)

• A role for dopamine within this circuitry,
particularly at the levels of the dorsal and
ventral striata signaling of primary rewards
and reward-predicting events

(Schultz, 1993)
 Motivation and Assessment
• Important prerequisite
– Assess baseline level function/motivation prior to
assessment

• Motivation continues process  regular

monitoring

• Deficits  poor performance

(Walsh, 2001)
 Neuropsychological Assessment
• Motivation : Cause or Effect or Mediator?

• Reaserched in:
– Traumatic brain injury (TBI)
– Schizophrenia
– Addiction
– Mood disorders (depression)

(Beck et al., 1985; Tucker & Bear, 1999; Donald, 2000; Whales &
Samuel, 2001; Bill et al., 2005; Grace et al., 2009)
• Motivation is not directly related to / affects
performance on neuropsychological tests

• It plays an important “mediating role”

(Wilper, 2011, Walsh & Kumar, 2010, Ross et al., 2000)

 Tests of Attention
• Schizophrenia & Traumatic Brain injury

– Letter cancellation
(Doles et al., 2001; Becks, 2009)

– Digit symbol substitution

(Gram & Winter, 2002; Ross et al., 2000; Mills, 2000)

 Executive Function Tests
• Schizophrenia & Addiction

– WCST
– Trail making (A and B)
– Tower of London
– Colour trails
– Stroop test

(Wilper, 2011, Walsh & Kumar, 2010, Ross et al., 2000)

 Language & Memory Function Tests
• Schizophrenia & Addition

– AVLT – Paired associates

– COWAT – RCFT
– Free association – Digit span

(Miller & Wells, 2007; Grace et

al., 2005) (Bell, 2004; Down et al., 2001)
• Main findings:

– Performance of individuals with schizophrenia was

worse as compared to those with alcohol dependence

– Response inhibition improved more rapidly in the

alcohol group as compared to schizophrenia

(Wilper, 2011, Walsh & Kumar, 2010, Ross et al., 2000; Wells, 2007; Bell,
2004; Down et al., 2001)
• Motivation important driving force

• Most widely researched areas in the field of

psychology