ol and tl presentation

7/30/2019 OL and TL Presentation

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Temporal &Occipital Lobe

Dr Anjali Nagpal


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TEMPORAL LOBE


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Superior Temporal Gyrus Receives inputs from auditory,

visual and somatic regions as well as from Frontal, Parietal

and paralimbic cortex.

Middle Temporal Gyrus (Limbic Cortex) includes amygdala,uncus, hippocampus, subiculum, entorhinal& prirhinal

cortices and fusiform gyrus

Inferior Temporal Gyrus (Visual regions)Includes Fusiform

gyrus

Anatomy of Temporal Lobe


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Connections

Sensory pathwayVentral stream

From primary and secondary visualand auditory areas. For stimulus recognition

Dorsal auditorypathway

From auditory areas to PPC. For detectingspatial localization of auditory inputs

Polymodal Pathway Parallel projections from the visual andauditory association areas into the STS. Forstimulus categorization

Medial Temporalprojection

The visual and auditory associationareas into the medial temporal or limbic.Called: perforant pathway.For long term

memory.

Frontal lobe projection The visual and auditory association areasinto the FL. For movement control and shortterm memory


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Major Temporal Lobe Dysfunctions

Impaired auditory sensation Impaired visual and auditoryperception Disordered perception of music Impaired language comprehension

Impaired selection of visual and auditory input Impaired ability to organize and categorizeinformation

Poor use of contextual information Impairment in long-term memory Changes in personality and affect


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Anatomy of language areas

The primary brain areas concerned with language are

Arrayed along and near the sylvian fissure (lateral cerebral

sulcus) of the categorical hemisphere.

A region at the posterior end of the superior temporal gyrus

called Wernickes area is concerned with comprehension ofauditory and visual information.

It projects via the arcuate fasciculus to Brocas area (area 44)

in the frontal lobe.


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The probable

sequence

of eventswhen a

subject

names

a visualobject

)


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ANOMIC

NON FLUENT

GLOBAL

APHASIA

FLUENT

BROCA'S AREA

WERNICKES AREACONDUCTION APHASIA

ANGULAR GYRUS

WIDESPREAD DAMAGE

TO SPEECH AREAS

EXPRESSIVE RECEPTIVE


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AREA LESION FAETURES

auditory associationareas

word deafness

visual associationareas

word blindness

Wernicke's Aphasia

Global Aphasia

unable to interpret the thought

Sensory Aphasia

Broca's Area Causes Motor Aphasia

Speech Disorder


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Lesion in the wernickes area

Speech itself is normal and sometimes the patients talk excessively.

However, what they say is full of jargon and neologisms that make little sense.

The patient also fails to comprehend the meaning of spoken or written words.

Fluent Aphasia - RECEPTIVE APHASIA,

POSTERIOR APHASIA

Conduction aphasia

Lesion in the auditory cortex (areas 40, 41 &42)

Patients can speak relatively well and have good auditory comprehensionbut cannot put parts of words together or conjure up words.

This is called conduction aphasia because it was thought to be due to

lesions of the arcuate fasciculus connecting Wernickes and Brocas areas.


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GLOBAL APHASIA (CENTRAL APHASIA)

This means the combination of the expressive problems of Broca's

aphasia and the loss of comprehension of Wernicke's.

The patient can neither speak nor understand language.

It is due to widespread damage to speech areas and is the

commonest aphasia after a severe left hemisphere infarct.

Writing and reading are also affected.


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Selection of Visual and Auditory Input

Not a conscious process

Selectivity in auditory perception- eg., attending to two different conversations or different

elements of a musical piece

Selectivity in visual perception- eg., watching a football game: where is the attention - the

quarterback or the runners?

Temporal lobe damage impairs selection- Dichotic listening task

Two words simultaneously presented in each ear- Normal result: Right ear words are recalled more (left temporal

lobe selectivity)- Patient: drop in correct recall of words, due to loss of selectivity(brain tries to simultaneously process information delivered toboth ears)

- Visual tasks involve simultaneous flashing of stimuli that are notcorrectly recalled


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Schizophrenia

Auditory hallucinations

- Perception of sound that is not externally present

- Patient hears fully formed verbal passages

Statements typically hostile and accusatory; feelings

engendered are of extreme paranoia

Spontaneous neural activity in the auditory cortex gives rise to

such hallucinations, interacting with the languageareas of thetemporal lobe


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Dierks et al (1999)

Conducted fMRI on schizophrenic patients duringauditory hallucinations

Compared results to neural activity in response toacoustic stimuli

Results: activation seen in Brocas area, primary auditory

cortex, and speech zone in posterior temporal cortex- Additional limbic areas also recruited (amygdala andhippocampus)- This probably was due to the engagement of memoryas well as emotional responses to hallucinatorycontent


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Temporal lobe epilepsy

Kluver-Bucy syndrome

Imposter syndrome / Capgras

syndrome

The Temporal Lobes Disorders


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Sensory/Thought: Emotional: Physical

dj vu or

Jamais vuFear/Panic Dizziness

Lightheadedness

Racing thoughts Pleasant feeling Headache

Smell

Sound

Taste

Stomach feelings

Nausea

Numbness

Visual loss or blurring

Strange feelings

Tingling feeling

Auras

Ph i l S t


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Seizure symptoms

Sensory/Thought Emotional

Black outConfusion

Deafness/Sounds

Fear/Panic

Electric Shock FeelingLoss of consciousnessSmellSpacing out

Out of bodyexperienceVisual loss or blurring

Physical Symptoms

Chewing movements

Convulsion

Difficulty talking

DroolingEyelid fluttering

Eyes rolling up

Falling down

Foot stomping

Hand waving

Inability to move

IncontinenceLip smacking

Making sounds

Shaking

Staring

Stiffening

Swallowing

Sweating

Teeth clenching/grinding

Tongue biting

Tremors

Twitching movements

Breathing difficulty

Heart racing


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After-seizure symptoms (post-ictal)

Thought EmotionalMemory loss Confusion

Writing difficulty Depression and sadness

Fear

FrustrationShame/Embarrassment


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(time between seizures)

A distinct syndrome of inter-ictal behaviorchanges occurs in many patients withtemporal lobe epilepsy.

The Waxman and Geschwind Syndrome

Intrt-ictal Changes

Hyperemotionalism

hyperreligiosity

Hypersexuality

Viscosity

Aggression

Hypergraphia

Symptoms Waxman and Geschwind Syndrome

TLE inter-ictal changes-The Waxman-Geshwind syndrome


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HYPEREMOTIONALISM

Depression

Mania

liable to obsessions and fixed idea

HYPERSEXUALITY or HYPOSEXUALITY.


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VISCOSITY

Increased verbalization

Circumstantiality

Difficulty shifting topics in conversation.

Clingy Behavior

Restricted range of topics


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TLE and Aggression

Recurrent episodes with interictal affective

aggression area rare but well-recognized

problem in patients with temporallobe

epilepsy. They are referred to as episodicdyscontrol or,more precisely, as

intermittent explosive disorder (IED)

(Strauss, 1989).


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The Capgras Syndrome

(named for Jean Marie Joseph Capgras).

Delusion is that people have been replaced by an impostor, an

exact double. Key figure -Spouse

May see himself as his own double.

The person is conscious of the abnormality of these perceptions.There is no hallucination.

Capgras Syndrome :(a.k.aDelusional misidentification, illusion of doubles,misidentification syndrome, nonrecognition syndrome, phantom double

syndrome)


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Causes of Capgras Syndrome?

Conscious ability to recognize faces is intact but damage tothe system that produces the automatic emotional arousal tofamiliar faces.

Damage of the nerve pathways between the vision areas ofthe temporal lobe and emotional processing associated withthe amygdala, thus, patient sees his mother but feels noemotional familiarity and thinks she is an impostor


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Recognition of Faces has been associated with the FusiformGyrus of the Temporal lobes. Visual Info is relayed from thetemporal lobes to the Amygdala as well as other brain regions


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Kluver- Bucy SyndromeAssociated with damage to both of the anterior temporal lobes of

the brain

Hypersexuality (like TLE)

Hyperorality

Aggressive Behaviors ( like IED in TLE)

Loss of normal fear and anger responses (Psychic blindness aninability to recognize "the emotional importance of events

Other symptoms may include visual agnosia (inability to visuallyrecognize objects)

The temporal lobes project to the Amygdala

Temporal Lobe damage may also involve underlying neural tissue -specifically the Amygdala


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The anterior pole of the temporal lobe is adjacent to theunderlying amygdala


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OCCIPITAL LOBE


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Three Short Sulci- Lateral and transverse occipital sulciand lunate sulcus

1. Lateral Occipital Sulcus- Divides the lobe intosuperior and inferior gyri

2. Lunate Sulcus It is the C shaped sulcus withforward convexity in front of occipital lobe

3. Transverse Occipital Sulcus Runs downwards intothe uppermost part of OL from the superomedialborder of hemisphere, a little behind theparietooccipital sulcus

Occipital Lobe Anatomy


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Object Agnosias Apperceptive

Associative

Other Visual Alexia

Visual-spatial agnosia

Agnosias

Other Symptoms of OL Damage1. Monocular Blindness

2. Bitemporal Blindness

3. Nasal Hemianopia

4. Homonymous Hemianopia

5. Quadrantanopia

6. Scotoma

Symptoms of OL Damage


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Cortical Pathways for Visual Perception

Output from occipital lobe follows two major fiber tracts

Superior longitudinal fasciculus to parietal lobe

Inferior longitudinal fasciculus to temporal lobe

Two distinct processing systems

Dorsal (occipito-parietal) is the where system specialized forspatial analysis

Ventral (occipito-temporal) is the

what

system specialized forobject perception and recognition


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Pohl experiments reveal double dissociation

Landmark task: monkeys with bilateral parietal lesion havedeficit, but monkeys with bilateral temporal lesion can learntask

Object discrimination task: monkeys with bilateral temporallesion have deficit learning task, but monkeys with bilateralparietal lesion do not

Other bilateral lesion experiments show dissociation withintemporal lobe

Anterior temporal lesions disrupt visual memory posterior temporal lesions disrupt visual discrimination

OL


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OBJECT AGNOSIA

a) Apperceptive agnosia: Cant recognize an object although basicvisual functions (color, motion etc.) are preserved. Cant copy or

match simple objects. Can see one thing at a time:Simultagnosia.Diffuse bilateral lesion in the ventral stream in OL.

Agnosias2. Monocular Blindness3. Bitemporal Blindness

b) Associative agnosia: Cant recognize objects in spite of beingto perceive them. Subjects can describe the object, know what itis for, copy it, but cant identify it. Lesion in ventral stream in TL.

Symptoms of OL Damage

OL


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Function of OL is vision, perception of form movement and color.

Three major routes: ventrally into the temporal lobe, dorsally into

parietal lobe, and a middle route going to the STS.Ventral stream for stimulus recognition, dorsal stream for guidance

of movements in space.

Some occipital regions are functionally asymmetrical: word

recognition on left and facial recognition and mental rotation on

the right.

Summary:


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