Temporal Lobes

Function:

 Emotional Responses
 Hearing
 Memory
 Speech

Location:

 The temporal lobes are anterior to the occipital lobes and lateral to the Fissure of Sylvius.

The temporal lobe is a region of the cerebral cortex that is located beneath the Sylvian fissure on both the left
and right hemispheres of the brain.

The temporal lobe is involved in auditory processing and is home to the primary auditory cortex. It is also
important for the processing of semantics in both speech and vision. The temporal lobe contains the
hippocampus and plays a key role in the formation of long-term memory.

The superior temporal gyrus includes an area (within the Sylvian fissure) where auditory signals from the
cochlea (relayed via several subcortical nuclei) first reach the cerebral cortex. This part of the cortex (primary
auditory cortex) is involved in hearing. Adjacent areas in the superior, posterior and lateral parts of the temporal
lobes are involved in high-level auditory processing. In humans this includes speech, for which the left temporal
lobe in particular seems to be specialized. Wernicke's area, which spans the region between temporal and
parietal lobes, plays a key role (in tandem with Broca's area, which is in the frontal lobe). The functions of the
left temporal lobe are not limited to low-level perception but extend to comprehension, naming, verbal memory
and other language functions. Sound processing is controlled by the temporal lobes- in the Broca’s area and
Wernicke’s area.

The underside (ventral) part of the temporal cortices appear to be involved in high-level visual processing of
complex stimuli such as faces (fusiform gyrus) and scenes (parahippocampal gyrus). Anterior parts of this
ventral stream for visual processing are involved in object perception and recognition.

The medial temporal lobes (near the Sagittal plane that divides left and right cerebral hemispheres) are thought
to be involved in episodic/declarative memory. Deep inside the medial temporal lobes, the hippocampi seem to
be particularly important for memory function - particularly transference from short to long term memory and
control of spatial memory and behavior.

Decreased fluid volume in the temporal lobe of schizophrenic patients manifests the positive signs of
schizophrenia namely:

* hallucinations and illusions

Hallucinations are perceptions that occur without connection to an appropriate source. Although hallucinations
can occur in any sensory form - auditory (sound), visual (sight), tactile (touch), gustatory (taste) and olfactory
(smell) - hearing voices that other people do not hear is the most common type of hallucination in
schizophrenia. Voices are usually thoughts that are in the mind of the person. They can describe activities
taking place, carry on a converation, warn of dangers, or even issue orders to to person. The thoughts can
appear to be so loud that the person may believe that people nearby will also be able to hear them. The mind
usually adjusts to this very rapidly and as a result the thoughts then appear to come from some external source.
It is possible, using a medical imaging technique, to see changes in the speech area of the brain at the time when
a person says that he is hearing the voices. This is a real experience, it is not imaginary.

Illusions, on the other hand, occur when a sensory stimulus is present but is incorrectly interpreted by an
individual.

* delusions

Delusions are false personal beliefs that are not subject to reason or contradictory evidence and are not
explained by a person's usual cultural beliefs. Delusions may take on different themes. For example, people
suffering from paranoid-type symptoms - roughly one-third of people with schizophrenia - often have delusions
of persecution, or false and irrational beliefs that they are being cheated, harassed, poisoned or conspired
against. These people often believe that a member of their family or someone close to them is making them
happen. Delusions of grandeur, in which a person believes he or she is a famous or important person, mnay also
occur in schizophrenia. Sometimes the delusions experienced by people with schizophrenia are quite bizarre;
for instance, believing that a neighbour is controlling thier behaviour with magnetic waves; that people on
television are directing special messages to them; or that their thoughts are being broadcast aloud to others. A
person experiencing delusions may try to keep them secret, knowing that others would not understand. Other
individuals are gradually overwhelmed and begin to act strangely according to the content of the delusional
explanations.

Frontal lobe
The frontal lobe is an area in the brain of mammals. It is located at the front of each cerebral hemisphere and
positioned anterior to (in front of) the parietal lobes and above and anterior to the temporal lobes. It is separated
from the parietal lobe by the primary motor cortex, which controls voluntary movements of specific body parts
associated with the precentral gyrus.

In humans, the frontal lobe reaches full maturity around age 25[citation needed], marking the cognitive maturity
associated with adulthood. Arthur Toga, UCLA, found increased myelin in the frontal lobe white matter of
young adults compared to that of teens. A typical onset of schizophrenia in early adult years correlates with
poorly myelinated and thus inefficient connections between cells in the fore-brain.

The frontal lobe contains most of the dopamine-sensitive neurons in the cerebral cortex. The dopamine system
is associated with reward, attention, long-term memory, planning, and drive. Dopamine tends to limit and select
sensory information arriving from the thalamus to the fore-brain. A report from the National Institute of Mental
Health says a gene variant that reduces dopamine activity in the prefrontal cortex is related to poorer
performance and inefficient functioning of that brain region during working memory tasks, and to slightly
increased risk for schizophrenia.

Anatomy
On the lateral surface of the human brain, the central sulcus separates the frontal lobe from the parietal lobe.
The lateral sulcus separates the frontal lobe from the temporal lobe.

The frontal lobe can be divided into a lateral, polar (frontalmost), orbital (above the orbit; also called basal or
ventral), and medial part. Each of these parts consists of particular gyri:

 Lateral part: Precentral gyrus, lateral part of the superior frontal gyrus, middle frontal gyrus, inferior frontal gyrus.
 Polar part: Transverse frontopolar gyri, frontomarginal gyrus.
 Orbital part: Lateral orbital gyrus, anterior orbital gyrus, posterior orbital gyrus, medial orbital gyrus, gyrus
rectus.
 Medial part: Medial part of the superior frontal gyrus, cingulate gyrus.

The gyri are separated by sulci. E.g., the precentral gyrus is in front of the central sulcus, and behind the
precentral sulcus. The superior and middle frontal gyri are divided by the superior frontal sulcus. The middle
and inferior frontal gyri are divided by the inferior frontal sulcus.

Function
The executive functions of the frontal lobes involve the ability to recognize future consequences resulting from
current actions, to choose between good and bad actions (or better and best), override and suppress
unacceptable social responses, and determine similarities and differences between things or events. Therefore, it
is involved in higher mental functions.
The frontal lobes also play an important part in retaining longer term memories which are not task-based. These
are often memories associated with emotions derived from input from the brain's limbic system. The frontal
lobe modifies those emotions to generally fit socially acceptable norms.

Psychological tests that measure frontal lobe function include finger tapping, Wisconsin Card Sorting Task, and
measures of verbal and figural fluency.[1]

Theories of function

Theories of frontal lobe function can be differentiated into four categories:

 Single-process theories. Posit "that damage to a single process or system is responsible for a number of different
dysexecutive symptoms” (Burgess, 2003, p. 309).
 Multi-process theories. Propose “that the frontal lobe executive system consists of a number of components that
typically work together in everyday actions [(heterogeneity of function)]“ (Burgess, 2003, p. 310).
 Construct-led theories. Assume “that most if not all frontal functions can be explained by one construct
(homogeneity of function) such as working memory or inhibition” (Stuss, 1999, p. 348; cf. Burgess & Simons,
2005).
 Single-symptom theories. Suggest that a specific dysexecutive symptom (e.g., confabulation) is related to the
processes and construct of the underlying structures (cf. Burgess & Simons, 2005)

Stuss (1999) suggests a differentiation into two categories according to homogeneity and heterogeneity of
function.

Further theoretical approaches to frontal lobe function include:

 Grafman's managerial knowledge units (MKU) / structured event complex (SEC) approach (cf. Wood &
Grafman, 2003)
 Miller & Cohen's integrative theory of prefrontal functioning (e.g. Miller & Cohen, 2001)
 Rolls's stimulus-reward approach and Stuss's anterior attentional functions (Burgess & Simons, 2005; Burgess,
2003; Burke, 2007).

It may be highlighted that the theories described above differ in their focus on certain processes/systems or
construct-lets. Stuss (1999) remarks that the question of homogeneity (single construct) or heterogeneity
(multiple processes/systems) of function “may represent a problem of semantics and/or incomplete functional
analysis rather than an unresolvable dichotomy” (p. 348). However, further research will show if a unified
theory of frontal lobe function that fully accounts for the diversity of functions will be available.

Damage
Damage to the frontal lobes can lead to a variety of results:

 Mental flexibility and spontaneity are impaired, but IQ is not reduced.

 Talking may increase or decrease dramatically.
 Perceptions regarding risk taking and rule abiding are impaired.
 Socialization can diminish or increase.
 Orbital frontal lobe damage can result in peculiar sexual habits.
 Dorsolateral frontal lobe damage reduces sexual interest.
 Creativity is diminished or increased as well as problem solving skills.
 Distraction occurs more frequently.
 Loss of smell and/or taste.

Brain: Frontal lobe

Frontal lobe

Temporal lobe
 Parietal lobe

Occipital
lobe

Principal fissures and lobes of the cerebrum viewed laterally.

(Frontal lobe is blue.)

Orbital surface of left frontal lobe.

Latin lobus frontalis

Gray's subject #189 821

Part of Cerebrum

Anterior cerebral
Artery
Middle cerebral

Acronym(s) FL

NeuroNames hier-37

MeSH Frontal+Lobe

NeuroLex ID birnlex_928

Decreased fluid volume in the frontal lobe causes negative signs of schizophrenia, namely:

In some cases, especially with hindsight, families may realise that their relative's behaviour has been changing
over a period of time in subtle ways. He may for instance have become slower to think, talk and move, and may
have become indifferent to social contact, his sleeping patterns may have changed so that he is happy to remain
up all night and sleep all day. Body language may also be affected. These are the so-called 'negative symptoms':
they will affect the person in a different way from the positive symptoms. The overall result is a reduction of
motivation, the effect of which varies from minor to severe. Negative symptoms are much less dramatic than
positive, but they then to be more persistent. Recognising these changes can be particularly difficult if the
illness develops during teenage years when it is quite acceptable for changes in behaviour to occur, particularly
where the young person is experimenting with new freedoms and lifestyles.

Dopamine hypothesis of schizophrenia

Some researchers have suggested that dopamine systems in the mesolimbic pathway may contribute to the
'positive symptoms' of schizophrenia (whereas problems with dopamine function in the mesocortical pathway
may be responsible for the 'negative symptoms', such as avolition and alogia.)

Recent evidence on a variety of animal models of psychosis, such as sensitization of animal behaviour by
amphetamine, or phencyclidine (Angel Dust)[citation needed], or excess steroids[citation needed], or by removing various
genes (COMT, DBH, GPRK6, RGS9, RIIbeta), or making brain lesions in newborn animals, or delivering
animals abnormally by Caesarian section, all induce a marked behavioural supersensitivity to dopamine and a
marked rise in the number of dopamine D2 receptors in the high-affinity state for dopamine.[1] This latter work
implies that there are multiple genes and neuronal pathways that can lead to psychosis and that all these
multiple psychosis pathways converge via the high-affinity state of the D2 receptor, the common target for all
antipsychotics, typical or atypical.
Evidence for the dopamine hypothesis

Some of the most obvious evidence for this theory is from the effects of drugs such as amphetamine and
cocaine. These drugs (and others like them) increase levels of dopamine in the brain and can cause symptoms
which resemble those present in psychosis, particularly after large doses or prolonged use. This is often referred
to as "amphetamine psychosis" or "cocaine psychosis," but may produce experiences virtually indistinguishable
from the positive symptoms associated with schizophrenia. Similarly, those treated with dopamine enhancing
levodopa for Parkinson's disease can experience psychotic side effects mimicking the symptoms of
schizophrenia. Up to 75% of patients with schizophrenia have increased signs and symptoms of their psychosis
upon challenge with moderate doses of methylphenidate or amphetamine or other dopamine-like compounds,
all given at doses at which control normal volunteers do not have any psychologically disturbing effects.[2][3]
Some functional neuroimaging studies have also shown that, after taking amphetamine, patients diagnosed with
schizophrenia show greater levels of dopamine release (particularly in the striatum) than non-psychotic
individuals. However, the acute effects of dopamine stimulants include euphoria, alertness and over-confidence;
these symptoms are more reminiscent of mania than schizophrenia.[4]

Another important development was the serendipitous discovery that a group of drugs called the
phenothiazines, including antipsychotics such as chlorpromazine, antagonized dopamine binding (particularly at
receptors known as D2 dopamine receptors) and reduced positive psychotic symptoms. This observation was
subsequently extended to other antipsychotic drug classes, such as butyrophenones including haloperidol. This
link was strengthened by experiments in 1970s which suggested that the binding affinity of antipsychotic drugs
for D2 dopamine receptors seemed to be inversely proportional to their therapeutic dose. This correlation,
suggesting that receptor binding is causally related to therapeutic potency, was reported by two laboratories in
1976.[5][6]

Genetic evidence has suggested that there may be genes, or specific variants of genes, that code for mechanisms
involved in dopamine function, which may be more prevalent in people experiencing psychosis or diagnosed
with schizophrenia. Dopamine related genes linked to psychosis in this way include COMT, DRD4, and AKT1.
[7]