THE TEMPORAL

LOBE
Dr. Karmanya Vatwani
JR1 Psychiatry
19/09/2022
 Contents
◦Anatomy
◦Functional Areas
◦Blood Supply & Venous Drainage
◦Functions
◦Structures
◦Connections
◦Temporal Lobe dysfunction tests
◦Disorders of Temporal Lobe
 INTRODUCTION

◦One of the 4 major lobes of the cerebral cortex.

◦22% of the cerebral cortex belongs to the temporal

lobe.

◦Temporal lobe involves auditory, olfactory, language

& visual functions.
 ANATOMY
◦ Lies below the lateral cerebral fissure of Sylvius & anterior to the Occipital lobe.

◦ The Temporal lobe occupies the area inferior to the lateral sulcus.

◦ The lateral surface of the temporal lobe is divided into three gyri by two sulci.

◦ The superior and middle temporal sulci run parallel to the posterior ramus of the
lateral sulcus and divide the temporal lobe into the superior, middle, and inferior
temporal gyri.

◦ The Inferior temporal gyrus is continued onto the inferior surface of the hemisphere.
Temporal
Lobe
Tempor
al Lobe
Temporal
Lobe
 ANATOMY
 The anterior commissure is the first commissure to
develop. It runs in the lamina terminalis and connects
the olfactory bulb and the temporal lobe of the cortex
on one side with the same structures of the opposite
hemisphere.

 The lateral ventricle may be divided into a body,

which occupies the parietal lobe, and from which
anterior, posterior, and inferior horns extend into
the frontal, occipital, and temporal lobes, respectively.
 BROADMANN AREAS ON LATERAL
SURFACE OF TL.

◦ Auditory areas: Areas 41, 42

◦ Auditory association cortex: Area 22

◦ Ventral visual stream areas: Area 20, 21, 37 & 38

 Primary Auditory Area
The primary auditory area (Brodmann areas 41 and 42) includes the gyrus of
Heschl and is situated in the inferior wall of the lateral sulcus.
Projection fibers to the auditory area arise principally in the medial
geniculate body and form the auditory radiation of the internal capsule.
Anterior part - Reception of sounds of low frequency
Posterior part - Sounds of high frequency.
A unilateral lesion - Partial deafness in both ears, the greater loss being in the
contralateral ear. This can be explained on the basis that the medial geniculate
body receives fibers mainly from the organ of Corti of the opposite side as
well as some fibers from the same side.
 Secondary Auditory Area
The secondary auditory area (auditory association cortex) is situated posterior to the primary auditory area in the
lateral sulcus and in the superior temporal gyrus (Brodmann area 22).
It receives impulses from the primary auditory area and from the thalamus.
Interpretation of sounds and for the association of the auditory input with other sensory information.
The sensory speech area of Wernicke is localized in the left dominant hemisphere, mainly in the superior temporal
gyrus, with extensions around the posterior end of the lateral sulcus into the parietal region.
The Wernicke area is connected to the Broca area by a bundle of nerve fibers called the arcuate fasciculus.
It receives fibers from the visual cortex in the occipital lobe and the auditory cortex in the superior temporal gyrus.
The Wernicke area permits the understanding of the written and spoken language and enables a person to read a
sentence, understand it, and say it out loud
 BLOOD SUPPLY
[Link] Carotid System
Anterior choroidal artery Middle cerebral artery
Supplies Uncus, Amygdala, Anterior Branches into the temporopolar artery,
Parahippocampal gyrus. Anterior, middle & posterior temporal
artery.
Supplies the temporal pole as well as the
superior & inferior portions of the
temporal gyri.
2. Vertebrobasilar System
Supplies the inferior surface of the temporal lobe from the tempero-occipital artery.
 VENOUS DRAINAGE
1ST ROUTE 2ND ROUTE

TEMPORAL LOBE INFERIOR TEMPORAL LOBE

Anteriorly

SUPERFICIAL MIDDLE CEREBRAL VEIN POSTERIOR CHOROIDAL VEIN

Pairs with
INFERIOR ANASTAOMOTIC VEIN (VEIN THALAMOSTRIATE VEIN
OF LABBE)

INTERNAL CEREBRAL VEIN

TRANSVERSE SINUS
Joins Basal vein
GREAT CEREBRAL VEIN
 FUNCTIONS OF THE TEMPORAL
LOBE
◦ Visual memory.
◦ Memory formation and storage.
◦ Processing sensory input:
a) Auditory perception.
b) Visual perception
c) Gustatory perception
d) Olfactory perception
e) Language recognition
f) Identification & Categorization of stimuli.
g) Emotional response
Structures enclosed in the
Temporal Lobe
◦Limbic Cortex

◦Amygdala

◦Hippocampal Formation
 LIMBIC CORTEX
CINGULATE GYRUS PARAHIPPOCAMPAL GYRUS

Lies dorsal to & follows the Corpus Cingulate gyrus travels posteriorly and
Callosum. becomes continuous with the
Parahippocampal gyrus.

Consists of various nuclei. The PHC Gyrus contains a

cytoarchitectonic region known as the
ENTRORHINAL CORTEX which funnels
highly processed cortical information to
the Hippocampal formation.
 AMYGDALA
◦ Group of nuclei located anterior to the hippocampal formation in the Median Temporal
Lobe.

◦ Basolateral complex: Largest nuclei. CB1(cannabinoid) receptor immunoreactivity on

Nissl stains.

◦ Centromedial amygdaloid group: Part of a larger structure continuous through the

sublenticular substantia innominate with the bed nucleus of the stria terminalis (BNST).

◦ Olfactory group: Includes cortical amygdaloid nuclei.

◦ Emotional learning and Memory Modulations.

 HIPPOCAMPAL FORMATION
Located in the floor of the temporal horn of the lateral ventricle.

Has 3 distinct zones : a) Dentate Gyrus

b) Hippocampus
c) Subicular complex
Function: Responsible for processing of long term memory,
emotional responses & memory of location of objects or people.
CONNECTIONS OF THE TEMPORAL
LOBE.
1) Ventral Sensory Pathway.

2) Dorsal Auditory Pathway.

3) Visual & Auditory projections to polymodal temporal regions.

4) Median Temporal Projections.

5) Frontal Lobe Projections.

1. VENTRAL
SENSORY
PATHWAY

Hierarchical
connections from
the primary and
secondary auditory
and visual areas to
the temporal pole.
(Stimulus
Recognition)

Auditory Stream
Visual Stream
2. DORSAL
AUDITORY
PATHWAY

Projects from
auditory cortex
to posterior
parietal cortex.
(Detection of
spatial
location/
movement)
 3.
POLYMODAL
PROJECTIONS
Parallel
projections from
visual and
auditory
association
SUPERIOR areas to
TEMPORA
L SULCUS polymodal areas
of the superior
temporal sulcus
(stimulus
categorisation).
4. MEDIAL TEMPORAL
PROJECTIONS

Auditory and visual

projections into medial
temporal regions (MTL),
finally arriving in the
hippocampus (Perforant
pathway, long-term
memory) and amygdala
(emotional tone).
5. FRONTAL
LOBE
PROJECTIONS
Projections to
the frontal
lobe
(movement
control,
emotion,
short term
memory).
ASSESSMENT OF TL DYSFUNCTION

◦Word List Learning (RAVLT).

◦Figure Reproduction (Rey Complex figures task).
◦Sequence Tapping (Corsi Blocks).
◦Mirror drawing task - Procedural Memory (Route
learning).
◦Dichotic Listening Task
 RAVLT
Rey Auditory Verbal
Learning Test is a
measure of a person’s
ability to encode,
combine, store and
recover verbal
information in different
stages of immediate
memory. Therefore, the
effect of interference
stimulus, delayed
memory and
recognition are
evaluated with this
assessment tool.
 RAVLT

Rey's auditory
verbal learning test
(RAVLT) is a well-
known measure of
episodic memory,
and in previous
studies it has had a
significant role in
early diagnosis of
AD.
RAVLT
Figure Reproduction (Rey
Complex figures task)
REY-
OSTERREITH
COMPLEX
FIGURE
 FINGER
TAPPING
CORSI BLOCKS

The patient's task

is to reproduce the
sequence of
spatial positions
pointed to by the
examiner.
Sequences of
increasing length
are presented. In
the actual board,
the numbers are
on the examiner's
side.
 MIRROR
DRAWING
TASK
Helps in
analyzing &
observing the
nature of the
learning process
and also in
studying the
relationship
between visual-
spatial and
motor learning.
DICHOTIC
LISTENING
TASK
It is a psychological test
used to assess selective
attention within the
auditory system.
It is used as an auditory
processing disorder test.
The DWLT stimuli are
common words varying
in length from one to
three syllables. The test
is in two equivalent parts
with 10 practice items
and 30 test items in
each part.
 DISORDERS OF TEMPORAL LOBE
◦ Prosopagnosia
◦ Visual Agnosia
◦ Auditory Agnosia
◦ Topographagnosia
◦ Kluver Bucy Syndrome
◦ Temporal Lobe Epilepsy
◦ ADHD
◦ Alzheimer’s Disease
◦ Frontotemporal Dementia
◦ Aphasia
◦ Memory Dysfunction
◦ Schizophrenia
 1. PROSOPAGNOSIA
Patients with prosopagnosia, although able to recognize faces as faces, able to describe
accurately the facial features of others, are yet unable to identify the other person. Although
unable to identify others by their facial features, may be able to identify them by other features,
such as their voice, dress, or characteristic gaitperson.
ETIOLOGY:
• Prosopagnosia generally occurs secondary to bilateral lesions of the inferior occipitotemporal
area. Rarely prosopagnosia may occur secondary to a unilateral occipitotemporal lesion on the
right.
• Prosopagnosia may also occur on a paroxysmal basis as a simple partial seizure: in one case, a
patient with left occipitotemporal scarring had seizures characterized by a sense of ‘flickering
lights’ followed by a brief episode of prosopagnosia.
TREATMENT:
Speech/language and occupational therapy may assist the patient in developing compensatory
strategies.
 2. VISUAL
ETIOLOGY: AGNOSIA
 Apperceptive visual agnosia has been noted Visual agnosia, or the inability
with bilateral infarction of the occipital lobes, to recognize and name objects
by sight, is a rare disorder.
which spare the striate cortex but involve the Interestingly, however, if
secondary visual cortices; the adjacent patients are given the object
temporal lobes are often also involved but only and allowed to handle it, they
are able to recognize it by
in their more posterior extent.
touch.
 Associative visual agnosia may occur Apperceptive and Associative.
secondary to bilateral infarction of the medial In apperceptive visual agnosia
occipitotemporal cortex and subcortical white patients can neither make a
drawing of the object nor can
matter, especially involving the lingual,
they pick it out of a group of
fusiform, and parahippocampal gyri. objects. In associative visual
TREATMENT: agnosia, however, patients are
able to perform these tasks.
Speech/ Language & Occupational therapy.
 3. AUDITORY
Auditory agnosia, or, more explicitly, AGNOSIA
environmental auditory agnosia, is a very
rare condition characterized by an inability ETIOLOGY:
to recognize such environmental sounds as Auditory agnosia has been
the ringing of a telephone or the honking reported with an infarction
of the posterior portion of
of a horn, despite normal hearing and a the right temporal lobe.
normal ability to understand the spoken
word. TREATMENT:
Bedside testing may be accomplished by Speech/ Language therapy.
standing behind the patient and ringing a
bell or perhaps snapping your fingers, and
then asking the patient what he heard.
 4. TOPOGRAPHAGNOSIA
Topographagnosia refers to a ETIOLOGY:
condition in which patients, Infarction involving the medial
despite adequate memory and occipitotemporal area (primarily the
vision, are unable to find their fusiform and lingual gyri, with some
way in surroundings that had not involvement of the parahippocampal
gyrus), either unilaterally on the right
previously caused any difficulty.
or bilaterally.
Landmark Agnosia &
TREATMENT:
Topographical Disorientation.
Speech/language and occupational
therapy
ETIOLOGY:
1. Bilateral damage or dysfunction of the temporal lobes.
5. KLUVER
2. Bilateral destruction of the amygdaloid body &
BUCY
Inferior temporal cortex. SYNDROME
3. Herpes simplex viral encephalitis classically involves
both temporal lobes.
 Characterized by:
4. Rare cases of infarction of both temporal lobes (as for
1. Visual Agnosia
example secondary to a vasculopathy of systemic
lupus erythematosus). 2. Placidity
3. Hypermetamorphosis
TREATMENT:
(excessive tendency to take
a) No controlled studies of the treatment of the Kluver– notice of and to attend and
Bucy syndrome. react to every visual stimulus)
b) Improvement has been noted with Carbamazepine, 4. Hyperorality
Sertraline. 5. Hypersexuality
c) Hypersexuality can be reduce by Leuprolide(GnRH
receptor superagonist).
6. TEMPORAL LOBE TUMOURS

ICTAL INTERICTAL

50-55% of patients with TL tumors experience psychiatric, behavioural or

personality changes.
1. Patients with TL Tumours often have seizure associated schizophrenia
like symptoms like Auditory Hallucinations, Atypical dreamlike
episodes, depersonalization, blanking out & dazed feelings.

How to differentiate between interictal tumour & Primary

psychosis?
In interictal tumour, there is mood reactivity & variability, normal affect,
and retained ability to relate to others in a relatively normal fashion.
Olfactory, gustatory, visual & tactile hallucinations may occur in such
patients, with olfactory hallucinations being a part of the preictal aura.

2. A few patients may present with depression & frontal lobe like
apathy, irritability & features suggesting hypomania & mania.
3. Schizophrenia like symptoms are more frequently seen in left sided TL tumors
while affectiform symptoms, anxiety and panic attacks may be seen in right side TL
tumors.
4. Rarely: episodic rage & aggressiveness.
5. Amygdala: Paroxysmal acute fear reactions.
6. Neurocognitive changes: Memory deficits (verbal or non verbal), Receptive
aphasias.
7. Interictal personality changes (Norman Geshwind) are seen, and are one of
the earliest indicators of undiagnosed TL tumor.
a. Interpersonal stickiness & viscosity.
b. Hostility & aggressiveness.
c. Increased emotionality with depression, elation or irritability or a combination of these.
d. Humorlessness.
e. Hyperreligiousity.
f. Hyposexuality.
g. Hypergraphia.
h. Excessive Philosophical concerns.
 7.
Temporal lobe epilepsy may be preceded by an aura of acoustic
or olfactory experience. The olfactory aura is usually an TEMPORAL
unpleasant odour. The patient is often confused, anxious, and
docile and may perform automatic and complicated movements,
LOBE
such as undressing in public or driving a car, and then, following EPILEPSY
the seizure, may have no memory of what occurred previously.
Most common type of
epilepsy characterized by
ETIOLOGY: recurrent unprovoked
seizures originating from
1) Mesial Temporal Sclerosis.
the anteromedial aspect
2) Cavernous angiomas of the TL.
3) Gliomas Complex Partial Seizure.
4) Alcohol Withdrawal
5) Head Injury
6) Cortical Dysplasia and gliosis secondary to encephalitis or
meningitis.
COMPLICATIONS:
Post Ictal – Brief self limiting episodes of psychosis
that are of abrupt onset.
Mixed psychotic and affective features are seen with TREATMENT:
agitation being the most common.
Tends to recur and a few patients may develop chronic
1. Antiepileptics
interictal psychosis.
2. Surgery: Temporal
Lobectomy
Interictal – Depression
Anxiety
Schizophrenia like psychosis
Gastaut Geshwind Personality
Syndrome.
 8. ADHD
Disrupted connections between the amygdala &
OFC contribute to behavioural disinhibition in
children with ADHD.

Enlarged Hippocampus may contribute to

disturbances in the perception of time, stimulus
seeking & temporal processing
 9.
Most common form of Dementia,
ALZHEIMER’S
characterized by Cognitive,
DISEASE
Behavioural and Mood changes. ETIOLOGY:

Cognitive: Forgetfulness, difficulty Atrophy in the posterior

temporal cortex
thinking and understanding, inability Chromosome 21 mutation
to recognise common things, inability Amyloid Beta protein and
synapse loss
to create new memories. Old age & head trauma

Behavioural: Aggression, Agitation,

Irritability, Wandering. TREATMENT:
Cholinesterase Inhibitors:
Mood: Depressive, anger, mood Donepezil, Rivastigmine
Non Competitive NMDA
swings. Receptor Antagonist:
Memantine
 10. FRONTO
TEMPORAL DEMENTIA
AKA: Pick’s Disease
Autosomal Dominant
Progressive circumscribed atrophy of frontal and temporal lobe cortices.
1. Loss of inhibitions
2. Apathy
3. Loss of Empathy
4. Compulsive Behaviour
5. Changes in diet
6. Loss of Executive Functions
7. Primary Progressive Aphasia
 11. APHASIA
Any disturbance in the comprehension or expression of language.
NON-FLUENT APHASIA: Lesion in the Broca’s area resulting in slow speech, difficulty in choosing words
or use of words that only approximate the correct word. Comprehension is intact.
FLUENT APHASIA: Lesion in the Wernicke's area which results in the person speaking normally or
excessively, but also uses jargon and invented words that make little sense. The person fails to
comprehend written & spoken words.

WERNICKE’S APHASIA
AKA: Fluent/ Receptive/ Post Rolandic Aphasia
It is due to the destruction of the postero-superior temporal area (Area 22) of the dominant hemisphere
supplied by the inferior division of Middle Cerebral Artery.
1) Fluency is preserved with normal or increased word output.
2) But speech is devoid of meaningful content.
3) Neologism & defective sentence structure is seen.
4) Auditory comprehension is impaired.
5) Patient is unaware of his speech defect.
 12.
Declarative
Memory
It is the conscious
recollection of facts &
events.
Thus in Amnesia, only
one kind of memory is
affected which is
Declarative memory.
While Non Declarative
memory includes skill
learning, habit learning &
simple forms of
conditioning.
 13. SCHIZOPHRENIA
 There is dysfunction in Cognition & Emotion
 Abnormal activations in ventromedial & superior temporal lobe, PFC &
Limbic Structures.
 Verbal Learning deficits are present.
 Decreased activation of the hippocampus(reduced gray matter volume in
the left anterior hippocampus-amygdala complex and the left superior
temporal gyrus) and PHC gyrus is seen on fMRI.
 There is disruption in the frontotemporal connectivity(mainly the temporal
and DLPFC).
 Deficit in social cognition due to reduced activity of the amygdala.
 References
◦ Kaplan & Sadock’s Study Guide & Self Examination Review in Psychiatry 9 th Edition
(2011).
◦ Frank H. Netter, MD Atlas of Human Anatomy 6th Edition (2014).
◦ Richard S. Snell Clinical Neuroanatomy 7th Edition (2010).
◦ David P. Moore Textbook of Clinical Neuropsychiatry 2nd Edition (2008).
◦ Kevin Walsh AO Neuropsychology: A clinical approach 3rd Edition (1994).
◦ BD Chaurasia’s Human Anatomy Volume 3 6th Edition (2013).
◦ Neuroanatomy Temporal Lobe; Anand Patel, Fowler JB
[Link]
THANK YOU!