TEMPORAL LOBE

•H.H. –40 years old, successful lawyer–Left wife of 15 years to join a religious group–Experienced a seizure and a left temporal lobe tumor was found –Tumor removed and H.H. was able to return to his job–Left with word-finding difficulties

• ANATOMY(parts)

• FUNCTIONAL AREAS

• LOOPS & PATHWAYS

• FUNCTIONS

• DISORDERS

3

0VERVIEW

ANATOMY OF TEMPORAL LOBE

Directionally, the temporal lobes are anterior to the occipital lobes, inferior to the frontal lobes and parietal lobes, and lateral to the Fissure of Sylvius, also known the lateral sulcus

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Occurs only in primates and is largest in man

Approximately 17% of the volume of cerebral cortex16% in the right and 17% in the left hemisphere

Temporal cortex includes auditory, olfactory, vestibular, and visual senses ,prception of spoken and written language

Addition to cortex, its contains white matter, part of the lateral ventricle, the tail of the caudate nucleus, the stria terminalis, the hippocampal formation, and the amygdala

• SUPERIOR AND INFERIOR TEMPORAL SULCI DIVIDE TEMPORAL LOBE INTO 3 LOBES

• SUPERIOR TEMPORAL LOBE

• MIDDLE TEMPORAL LOBE

• INFERIOR TEMPORAL LOBE

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Involves areas 41,42,22Primary auditory area (area 41)On the left side of the brain this area helps

withgeneration and understanding of individual

words. On the right side of the brain it helps tell the

differencebetween melody, pitch, and sound intensity

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SUPERIOR TEMPORAL LOBE

The region encompasses most of the lateral temporal

cortex, a region believed to play a part in auditory

processing and languageLanguage function is left lateralized in most

individualsBrodmann area 21

10

MIDDLE TEMPORAL LOBE

Its corresponds to the inferior temporal gyrus. Brodmann area 20The region encompasses most of the ventraltemporal cortex, a region believed to play a partin high-level visual processing and recognitionmemory

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INFERIOR TEMPORAL LOBE

Auditory areas Brodmann’s areas 41,42, and 22

Ventral Stream of Visual Information -Inferotemporal cortex or TE, Brodmann’s areas 20, 21,37, and 38

Relations of the temporal lobe coronal section passing through the temporal pole, anterior to the amygdala, hippocampus, and temporal horn

Relations of the temporal lobe coronal section passing through the amygdala and the head of the hippocampus

Relations of the temporal lobe, horizontal section in the plane of the pituitary gland

The hippocampus is a scrolled structure located in the medial temporallobe The hippocampus can be divided into at least five different areas.The dentate gyrus is the dense dark layer of cells at the "tip" of thehippocampus. Areas CA3 and CA1 are more diffuse; the small CA2 ishard to distinguish between them. (CA stands for cornu ammonis,from its ram's horn shape.) The subiculum sits at the base of the hippocampus, and is continuouswith entorhinal cortex, which is part of the parahippocampal gyrus.

The Hippocampus

Dentate gyrus represents the free edge of the pallium and associated white matter, the alveus, fimbria, and fornix.

The cortex adjacent to the hippocampus is known as the entorhinal area, it present along the whole length of the parahippocampal gyrus

The hippocampal formation has indirect afferent connections from the whole of the cerebral cortex, funneled through the adjacent temporal cortex and the subiculum

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(1) inputs from the entorhinal region, which include the perforant and alvear pathways; (2) internal circuitry, which includes the connections of the mossy fibers and Schaffer collaterals; and (3) efferent projections of the hippocampal formation through the fimbria-fornix system of fibers. CA1-CA4 denote the four sectors of the hippocampus

The hippocampus is vulnerable to ischemia, which is any obstruction of blood flow or oxygen deprivation, Alzheimer's disease, and epilepsy.

These diseases selectively attack CA1, which effectively cuts through the hippocampal circuit

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Diseases of the Hippocampus

Amygdala

Amygdala

Amygdala located in the medial part of the temporal pole, anterior to and partly overlapping the hippocampal head

Its receives fibres of the olfactory tract

The ambient and semilunar gyri consist of periamygdaloid cortex receives fibres from the olfactory tract

The larger lateral part of the amygdala, like the hippocampal formation, receives direct and indirect input from most of the cerebral cortex

Inputs: The association areas of visual, auditory, and somatoSensory cortices are the main inputs to the amygdala

Outputs: The main outputs of the amygdala are to theHypothalamus and brainstem autonomic centers, including thevagal nuclei and the sympathetic neuronsThe amygdala is also involved with mood and the consciousemotional response to an eventThe amygdala is also extensively interconnected with frontalcortex, medio dorsal thalamus, and the medial striatum

Amygdala

The deep group, which includes thelateral, basal, accessory basal

nucleic

Func: collects input from sensorycortex.

The more dorsal group, whichincludes the central & medial

nuclei

Func: receives projections from thedeep group and sends the signal

outto autonomic centers.

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The amygdala is the heart of the emotional system. It

processes and interprets all sensory data

It modulates the flow of emotional information between

the cerebral cortex and the hypothalamus, and in doing

that, it modulates autonomic, endocrine, and affective

responses

Lesions in amygdala lead to-- agitation, irritability,

anxiety, mood disorders, paranoia, and psychosis

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Kluver-Bucy syndrome results due to a bilateral destruction ofthe amygdaloid body and inferior temporal cortex It is characterized by Visual agnosiaPlacidityHypermetamorphosisHyperorality Hypersexuality causes: cerebral trauma; infections including herpes andother encephalitides; Alzheimer's disease and other dementias,Niemann-Pick disease and cerebrovascular disease

Kluver-Bucy syndrome

White MatterSubcortical white matter comprises three populations of axons Association fibres connect cortical areas within the same cerebral hemispherelargest bundle is the arcuate fasciculusbetween frontal cortex, including Broca’s expressive speech area, and Wernicke’s receptive language area in the posterior part of the superior temporal gyrus. The condition of conduction aphasia is traditionally attributed to a destructive lesion that interrupts the arcuate fasciculusAnother frontotemporal association bundle is the uncinate fasciculus hook like shape Visual association cortex extends from the occipital lobe to the middle and inferior temporal and fusiform gyri

Commissural fibres connect mainly but not exclusively symmetrical cortical areas Largest group of commissural fibres is the corpus callosum Projection fibres connect cortical areas with subcortical nuclei of grey matter

Its afferent to the temporal cortex include medial geniculate body to the primary auditory area

Connected with the amygdala, hypothalamus, hippocampal formation, and parahippocampal gyrus

Thalamocortical pathway that passes through the temporal lobe is Meyer’s loop of the geniculocalcarine tract

This loop carries signals derived from the upper quadrants of the contralateral visual fields to the corresponding primary visual cortex of the anterior half of the inferior bank of the calcarine sulcus

FUNCTIONAL AREAS OF TEMPORAL LOBE

AUDITORY – primary & Association

OLFACTORY - primary & Association

VISUAL (Recognition & association)

MEMORY

EMOTIONAL & SOCIAL

Link past and present sensory and emotional experiences into a continuous self

LANGUAGE AREAS Wernicke's area is found in posterior temporal lobe of onehemisphere (usually the left),called the "speech area, " Wernicke'sarea surrounds& encompasses part of the auditory associationArea

AFFECTIVE LANGUAGE AREAS Involved in the nonverbal emotional components ,present non dominanthemisphere opposite Brocas's and Wernickes's areasThese "mirror images" allow tone of our voice and our gestures toexpress our emotions when we speak, and permit us to comprehendthe emotional content of what we hear Lesions to this cause aprosodia, in which speech is flat and

emotionsess,lacking the intonations that modify the meaning of our spoken words

LANGUAGE & COMPREHENSION

PRIMARY AUDITORY AREA (area 41) Essential to detect changes in frequency , & to know thedirection from which sounds originate.

AUDITORY ASSOCIATION AREA (area 42)

HIGHER AUDITORY ASSOCIATION AREA (area 22)

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AUDITORY SENSES

Processing of our recognition of objects occurs in a path on the lower, dorsal stream in the temporal lobe; here you find areas sensitive to faces vs. objects,

Area MT (right) performs processing on motion. Subjects without an area MT describe seeing motion as discontinuous pictures – eg. having to rely on sound before crossing a street

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VISUAL SENSES

OLFACTORY SENSES

The rightmost green spots are the location in cortex where smell is processed

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The sensation of taste is

processed in insular cortex

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GUSTATORY SENSES

connections of the Temporal Lobes

Five main types:Hierarchical sensory pathwayDorsal auditory pathwayPolymodal pathwayMedial (mesial) temporal pathwayFrontal lobe projection

Hierarchical sensory pathway connections from primary(sensory neuron) and secondary

auditory and visual cortical

through the lateral temporal cortex

terminate in the temporal pole

visual travels inferior temporal gyrus auditory travels e suprior temporal gyrusMajor destinations:amygdala and hippocampusThis results in the integration of information into:

memory, retrieval of stored information, emotional tone

Ultimate effect stimulus recognitionThe familiar conscious experience of knowing,

assimilating, and feeling

Dorsal auditory pathway

Forms important functional connections with the posterior parietal cortex

Enables location of sounds in space Promotes orienting and initiation of movements

relative to sound location

Polymodal Pathway connections emerging from the auditory and visual

hierarchical pathways Directed towards the neurons enfolded within the

superior temporal sulcus Polymodal nature of neurons Assigns stimuli to specific category of classes,

linked to and can be retrieved by memory

Medial Temporal Projection

Medial Temporal Projection Projections from auditory and visual areas into the

limbic regions E.g., amygdala and hippocampus Directions of projectionsPeripheral cortex entorhinalcortex

amygdala/hippocampus Perforant pathway forms the main projection to the hippocampus Damage in this region severely affects memory

formation

Medial Temporal Projection

Frontal-lobe Projection

Neurons from the temporal lobe have strong connections with the frontal lobe

Posterior temporal cortex Projects to the dorsolateral prefrontal

cortex anterior temporal cortex Projects to the orbital frontal cortex Damage leads to terrible life decisions

Frontal-lobe Projection

Frontal-lobe Projection

The prefrontal cortex (PFC) divided into anterior (APFC, Brodmann area (BA) 10), dorsolateral (DLPFC, BA 46 and 9), ventrolateral (VLPFC, BA 44, 45 and 47) and medial (MPFC, BA 25 and 32) regions BAs 11, 12 and 14 are commonly referred to as orbitofrontal cortexThe medial temporal lobe comprises the hippocampus and amygdala, as well as the entorhinal, perirhinal and parahippocampal neocortical regions.There are large cortico-cortical direct reciprocal connections between the PFC and the medial temporal lobe, passing through the uncinate fascicle, anterior temporal stem and anterior corpus callosum. The orbitofrontal and dorsolateral cortices have strong reciprocal connections with the perirhinal and entorhinal corticesUnidirectional projections exist from the CA1 field to the caudal region of MPFCThe subicular complex and neocortical medial temporal regions have reciprocal connections with caudal MPFC

Arterial Blood Supply and Venous DrainageThe temporal lobe receives blood from both the carotid and the

vertebrobasilar systems.

Anterior choroidal artery are the anterior end of the parahippocampal

gyrus, the uncus, the amygdala, and the choroid plexus in the temporal

horn of the lateral ventricle

Middle cerebral artery giving off branches that supply the cortex of

the superior and middle temporal gyri and the temporal pole.

Posterior cerebral artery gives off two to four temporal branches,

before it divides into the calcarine and parieto-occipital arteries, which

supply the occipital lobe.

The temporal branches of the posterior cerebral artery supply the

inferior surface of most of the temporal lobe, but not the temporal pole.

The venous drainage of the temporal cortex

Venous drainage Temporal cortex and white matter into the superficial middle cerebral vein,in the cistern of the lateral sulcus and inferior anastomotic vein (vein of Labbé)Interior of the lobe, including amygdala, hippocampus, and fornix, flows into the posterior choroidal vein. The left and right internal cerebral veins joined by the basal veins and unite to form the great cerebral vein, a midline structure that continues into the straight sinus. The basal vein (vein of Rosenthal), which carries blood from the cortex and the interior of the frontal lobe, traverses the subarachnoid space in the cisterna ambiens, medial to the temporal lobe.

Venous drainage

Venous drainage

Processing auditory input ◦ sends ventral and dorsal streams (object identification and for

movement planning)

Visual object recognition◦ Ventral visual stream

Biological motion perception◦ Superior Temporal Sulcus

Long-term storage of information◦ Memory (limbic system, hippocampus)

Temporal Lobe Function

Sensory ProcessesIdentification and Categorization of StimuliCross-Modal Matching

Process of matching visual and auditory information

Affective ResponsesEmotional response is associated with a particular stimulus

Spatial NavigationHippocampus – Spatial Memory

Temporal Lobe Function

Special face processing pathway

Faces

Asymmetry of Temporal Lobe Function

Left temporal lobeVerbal memory Speech processing

Right temporal lobeNonverbal memoryMusical processingFacial processing

DISORDERS OF TEMPORAL LOBE

Symptoms of Temporal-Lobe Lesions

Disturbance of auditory sensation and perceptionDisturbance of selective attention of auditory and visual inputDisorders of visual perceptionImpaired organization and categorization of verbal materialDisturbance of language comprehensionImpaired long-term memoryAltered personality and affective behaviourAltered sexual behaviour

8 principal symptoms of temporal lobe damage

Disorders of auditory perception:Lesions of the left superior temporal gyrus produce problems ofspeech perception with difficulty in discriminating speech and thetemporal order of sounds is impaired

Lesions of the right superior temporal gyrus can produce disorders ofperception of music with inability to discriminate melodies and produceprosody

The inferior temporal cortex is responsible for visual perception andlesions produce inability to recognise faces, called prosopagnosia.

There may be disturbance of visual and auditory input selection. Thispresents as impairment of short term memory, also called workingmemory and judgement about the recency of events.

Manifestations of temporal lobe lesions

Disorders of memory The medial and inferior temporal cortex and hippocampus are

responsible for memory. There is complete anterograde amnesia following bilateral removal of

medial temporal lobes, including hippocampus & amygdala. The left side is responsible for verbal material and the right for non-

verbal memory such as faces, tunes and drawings.

• Temporal lobe personality. There is egocentricity, pedantic speech, perseveration of speech, paranoia, religious preoccupations and a tendency to aggressive outbursts, especially after right temporal lobectomy

• temporal lobe lesions can present with visual field defects in the form of superior quadrant loss, sometimes called the "pie in the sky defect"

• Stroke normally reduces libido but temporal lobe lesions can increase it

• Any disturbance in the comprehension or expression of language caused by a brain lesion.

• NONFLUENT APHASIA, i.e. in lesion to Broca's area results in slow speech, difficulty in choosing words, or use of words that only approximate the correct word.e.g., a person may say "tssair" when asked to identify a picture of a chair.

• A lesion to Wernicke's area may result in FLUENT APHASIA, in which a person speaks normally, and sometimes excessively, but uses jargon and invented words, that make little sense (e.g., "choss" for chair). The person also fails to comprehend written and spoken words.

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APHASIA

Middle cerebral artery in farct:Aphasia or non-dominant hemisphere findings depending onthe side.“Partial” middle cerebral artery syndromes, almostalways of embolic origin, may include a) sensorimotor paresiswith little aphasia b) conduction aphasia c) Wernicke’s

aphasiawithout hemiparesis

Wernicke's aphasia, caused by occlusion of the lower divisionof the MCA bifurcation or one of its branchesThe infarct responsible for a classic Wernicke's aphasiaincludes the dominant posterior temporal, inferior parietal,

andlateral temporo-occipital regions

Posterior cerebral artery syndrome:

Recent memory loss may be present (involvement of hippocampus) 68

CVA-TEMPORAL LOBE

Bilateral temporal lobe hyperintensity

Infective diseases (herpes simplex virus, congenital cytomegalovirus infection)Epileptic syndrome (mesial temporal sclerosis) Neurodegenerative disorders (Alzheimer's disease, frontotemporal dementia, Type 1 myotonic dystrophy)Neoplastic conditions (gliomatosis cerebri)Metabolic disorders (mitochondrial encephalopathy, lactic acidosis and stroke-like episodes, Wilson's disease, hyperammonemia) Dysmyelinating disease (megalencephalic leukoencephalopathy with subcortical cysts)Vascular (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy) Paraneoplastic (limbic encephalitis) disorders

Diagnosis (n) Percentage of total cases (n=65) Age or age range (years) Sex distribution

Infective diseases

 Herpes encephalitis (15) 23 34–55 10M, 5F

 Congenital CMV infection (2) 3 8–11 1M, 1F

Epileptic syndrome

 Mesial temporal sclerosis (10) 15.3 8–27 6M, 4F

Neurodegenerative

 Alzheimer's disease (7) 10.7 58–65 5M, 2F

 Frontotemporal dementia (2) 3 61–64 2F

 Myotonic dystrophy (1) 1.5 27 1M

Neoplastic

 Gliomatosis cerebri (9) 13.8 33–64 6M, 3F

Metabolic

 MELAS (7) 10.7 10–22 5M, 2F

 Wilson's disease (1) 1.5 10 1M

 Hyperammonemia (1) 1.5 61 1F

Dysmyelinating disease

 MLC (6) 9.2 6–20 5M, 1F

Vascular

 CADASIL (2) 3 31–35 1M, 1F

Paraneoplastic disorder

 Limbic encephalitis (2) 3 25–32 2M

CADASIL, cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy; CMV, cytomegalovirus; F, female; M, male; MELAS, mitochondrial encephalopathy, lactic acidosis and stroke-like episodes; MLC, megalencephalic leukoencephalopathy with subcortical cysts.

The clinical features, location and distribution of temporal lobe hyperintensity, additional and advanced MRI findings with relevant laboratory results ↓, decreased; ↑, elevated; −, negative; +, positive; A, anterior; CADASIL, cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy; Cho, choline; CMV, cytomegalovirus; CPS, complex partial seizure; CSF, cerebrospinal fluid; DWI, diffusion-weighted imaging; EC, external capsule; EEG, electroencephalogram; Gd, gadolinium; GM, grey matter; HSV, herpes simplex virus; L, lateral; Lac, lactate; LOC, loss of consciousness; M, medial; MELAS, mitochondrial encephalopathy, lactic acidosis and stroke-like episodes; ML, myoinositol; MLC, megalencephalic leukoencephalopathy with subcortical cysts; MRS, MR spectroscopy; NA, not applicable; NAA, N-acetylaspartate; ND, not done; P, posterior; R, restriction; S. no., serial number; SWI, susceptibility-weighted imaging; WM, white matter; VR, Virchow–Robin spaces.

Bilateral temporal lobe hyperintensity Advanced MRI findings

S. no.

DiagnosisClinical features

Lobe GM WM Additional MRI findings DWISWI

MRSGd-enhancement

Laboratory result

1Herpes encephalitis

Fever, seizure, altered sensorium

A, M + −Orbital gyri involvement, gyriform haemorrhages

R + ND GyriformHSV antibodies in CSF

2Mesial temporal sclerosis

Complex partial seizure

M + +Hippocampal, mamillary body, fornix and collateral WM atrophy

− − ND NDTemporal lobe localisation on EEG

3Gliomatosis cerebri

Headache, recurrent seizures

A, M + +Expansion of parenchyma, multilobar involvement

− − ↑MLAbsent / patchy

 Non-contributory

4 MELASEpisodes of LOC, seizure

P, M + +Fleeting hyperintensity, basal ganglia involvement

R − ↑lac Patchy↑Serum and CSF lactate

5Alzheimer's disease

Personality changes, memory loss

A, M − +Hippocampal atrophy, enlarged parahippocampal fissures

− − ↑ML − Non-contributory

6 MLCDevelopmental delay, seizure

Whole − +Temporal lobe cysts, subcortical WM, external capsule

− −↓NAA ↑cho

− Non-contributory

7Congenital CMV

Seizure P − +Periventricular cysts, pachygyria-agyria complex

− − ND − Non-contributory

8 CADASILMigraine, hemisensory loss

A, M − +

Lacunar infarcts, subcortical WM, external capsule and insula

− − ND −Non-contributory

9Frontotemporal dementia

Dementia A,M − +Fronto-temporal atrophy

− − ↓NAA ↑cho −Non-contributory

10Limbic encephalitis

Memory disturbance

M + −Cingulate gyrus, subfrontal cortex and inferior frontal WM

− − ND −

Pleocytosis, lymphoma antibodies in CSF

11 HyperammonemiaConfusion, altered sensorium

A + −Posterior cingulate gyrus

R − ND ND↑Blood ammonia

12 Wilson's disease

Weakness, extrapyramidal symptoms

A, P, L + +Fronto-parietal lobes, dorsal midbrain, deep grey nuclei

R − ND −↑Serum and urine copper, ↓ceruloplasmin

13Myotonic dystrophy

Developmental delay, facial and distal limb weakness

A − +Periventricular and deep WM, prominent VR spaces

− − ND ND

Myotonic discharges in electromyography

 A 34-year-old male with herpes encephalitis (a) Coronal T2weighted image shows bilateral symmetric cortical swelling and hyperintensity involving the anteromedial temporal lobes including the insular cortex (white arrows) with characteristic sparing of basal ganglia (open arrows). (b) AxialT2 weighted image shows additional involvement of orbital gyri (black arrows). (c) Axial diffusion-weighted image depicts restricted diffusion in the involved areas (white arrows).

A 46-year-old male with herpes encephalitis (a) Axial susceptibility-weighted image demonstrates haemorrhages (black arrows) in both temporal lobes. (b) Axial T1weighted post-gadolinium image shows gyriform enhancement (white arrows) in the involved temporal lobes.

An 11-year-old female with cytomegalovirus infection(a) Axial fluid-attenuated inversion-recovery image shows bilateral periventricular cysts with gliosis of white matter (white arrows) in both temporal lobes. (b) Axial T2weighted image demonstrates gyral abnormality in the form of pachygyria–agyria complex (open arrows) bilaterally involving the temporo-occipital lobes in addition to the periventricular cysts (white arrows). Combination of these imaging findings along with periventricular calcifications are in favour of congenital cytomegalovirus infection

 A 17-year-old male with complex partial seizure(a) Oblique coronal fluid-attenuated inversion-recovery image reveals bilateral hippocampal atrophy, hyperintensity indicating gliosis (white arrows) with loss of internal architecture consistent with a diagnosis of bilateral mesial temporal sclerosis. (b) Oblique coronalT1 weighted image demonstrates bilateral mamillary body atrophy (white arrows).

A 64-year-old male with memory loss and personality changes (a) Axial fluid-attenuated inversion-recovery image shows hyperintensity in both anteromedial temporal lobes (white arrows). (b) Axial T2weighted and (c) coronal T1weighted images depict marked atrophy of temporal lobes with preferential volume loss of hippocampi and parahippocampi gyri and corresponding enlargement of parahippocampal fissures including choroidal (downwards arrows on c) and hippocampal fissures (black arrows), and temporal horns (white arrow). Temporal lobe hyperintensity indicates non-specific gliosis because of marked atrophy; however, the selective mesial temporal atrophy with enlarged parahippocampal fissures are diagnostic of Alzheimer's disease

A 64-year-old female with frontotemporal dementia(a) AxialT2 weighted image shows hyperintensity with volume loss in bilateral temporal lobes (black arrows). (b) Axial fluid-attenuated inversion-recovery image demonstrates predominate volume loss in both frontal and temporal lobes with associated increased signal in white matter indicating underlying gliosis (white arrows)

A 34-year-old male with myotonic dystrophy Type 1 (a) Axial fluid-attenuated inversion-recovery image shows bilateral anterior temporal white matter hyperintensity (black arrows). (b) Coronal T2weighted image shows hyperintensity in periventricular white matter (white arrow) and prominent perivascular spaces (open arrows) disproportionate to the age.

A 61-year-old male with gliomatosis cerebri (a) Axial T2weighted image demonstrates cortical expansion and hyperintensity (white arrows) in both medial temporal lobes. (b) Axial T2 weighted image shows multifocal brain parenchymal involvement with expansion and relative preservation of architecture. Involvement of frontotemporal lobes (white arrows), basal ganglia (open arrows) and thalami (black arrows) are seen. (c) MR spectroscopy shows markedly elevated myoinositol peak at 3.45 parts per million.

A 17-year-old male with mitochondrial encephalopathy, lactic acidosis and stroke-like episodes (MELAS)(a) Axial fluid-attenuated inversion-recovery (FLAIR) image shows bilateral asymmetric cortical and subcortical temporal lobe hyperintensity (white arrows), right more than the left and (b) axial FLAIR image 4 months later shows resolution of previous hyperintensity and new area of involvement on left side (white arrow) indicating the fleeting nature of the lesions. (c) MR spectroscopy demonstrates elevated lactate peak at 1.3 parts per million. These findings are consistent with a diagnosis of MELAS

A 61-year-old female with hyperammonemic encephalopathy. Axial fluid-attenuated inversion-recovery images show (a) bilateral peripheral cortical temporal lobe (white arrows) and (b) right posterior cingulate gyrus (open arrow) hyperintensity. Diffusion-weighted images show corresponding restricted diffusion (white arrows) in (c) the bilateral peripheral cortical temporal lobe and (d) the right posterior cingulate gyrus. The typical distribution of lesions with elevated blood ammonia level suggests this diagnosis.

A 10-year-old male with Wilson's disease. (a) Axial T2weighted and (b) fluid-attenuated inversion-recovery images demonstrate bilateral extensive cortical and subcortical temporal lobe hyperintensity (white arrows), dorsal midbrain involvement (open arrow), bilateral symmetric basal ganglia (yellow arrows) and anterolateral thalamic (black arrows) hyperintensity. Extensive grey and white matter lesions are less frequently in Wilson's disease however concomitant basal ganglia, thalamic and dorsal brainstem abnormalities point to the diagnosis.

A 22-year-old male with megalencephalic leukoencephalopathy with subcortical cysts. (a) Axial fluid-attenuated inversion-recovery and (b) axial T2weighted images reveal bilateral anterior temporal lobe cysts (white arrows), deep (black arrow) and subcortical (open arrow) white matter hyperintensity. Temporal lobe cysts with extensive white matter lesions involving the deep and subcortical white matter, and external capsule with sparing of basal ganglia, thalami and internal capsules are typical for this subtype of van der Knaap leukoencephalopathy.

 A 35-year-old female with cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy. (a) Axial T2weighted image shows confluent hyperintense lesions in both anterior temporal lobes (open arrows). (b) Axial fluid-attenuated inversion-recovery image shows patchy subcortical hyperintense areas (white arrows) and multiple lacunar infarcts (thin white arrow). (c) AxialT2 weighted image shows multiple patchy hyperintense areas involving the external capsule (open arrow), insular cortex (thin arrow) and basal ganglia (asterisk).

A 26-year-old male with paraneoplastic limbic encephalitis presenting with progressive memory disturbance. (a) Initial coronal T2weighted image demonstrates swelling and increase signal in both mesial temporal lobes (white arrows). (b) Follow-up coronal T2weighted image after 1 year shows significant decrease in the swelling and abnormal signal intensity (white arrows). (c) Axial contrast-enhanced CT section through the mid-abdomen shows ileocolic intussusception (black arrow) with marked concentric wall thickening of ascending colon (white arrows). Biopsy proven Burkitt's lymphoma of ascending colon is also shown.

Temporal and frontal lobe seizures differential semiological features.

Features Temporal Frontal

Sz frequancy Less frequent Often daily

Sz onset Slower Abrupt, explosive

Sleep activation Less common Characteristic

Progression Slower Rapid

Automatisms Common-longer Less common

Initial motionless stare Common Less common

Complex postures Late, less frequent, less prominent Frequent, prominent, and early

Hypermotor Rare Common

Bipedal automatisms Rare Characteristic

Somatosensory Sx Rare Common

Vocalization Speech (nondominant)Loud, nonspeech (grunt, scream, moan)

Seizure duration Longer Brief

Secondary generalization Less common Common

Postictal confusion More prominent-longer Less prominent, Short

Postictal aphasia Common in dominant hemisphere Rare unless spreads to temporal lobe

Feature Location

Automatism

Unilateral limb automatism Ipsilateral focus

Oral automatism (m)Temporal lobe

Unilateral eye blinks Ipsilateral to focus

Postictal cough Temporal lobe

Postictal nose wiping Ipsilateral temporal lobe

Ictal spitting or drinking Temporal lobe focus (R)

Gelastic seizures(m)Temporal, hypothalamic, frontal

(cingulate)

Dacrystic seizures (m)Temporal, hypothalamic

Unilateral limb automatisms Ipsilateral focus

Whistling Temporal lobe

Semiological Features (TLE) - Lateralizing or Localizing Value.

Autonomic

Ictal emeticus Temporal lobe focus (R)Ictal urinary urge Temporal lobe focus (R)Piloerection Temporal lobe focus (L)

Speech

Ictal speech arrestTemporal lobe (usually dominant hemisphere)

Ictal speech preservation Temporal lobe (usually nondominant)

Postictal aphasiaTemporal lobe (dominant

hemisphere)

Motor

Early nonforced head turn Ipsilateral focus

Late version Contralateral focus

Eye deviation Contralateral focus

Focal clonic jerking Contralateral perirolandic focus

Asymmetrical clonic ending Ipsilateral focus

Fencing (M2E)Contralateral (supplementary

motor)

Figure  4Contralateral to the extended limb

(temporal)

Tonic limb posturing Contralateral focus

Dystonic limb posturing Contralateral focus

Unilateral ictal paresis Contralateral focus

Postictal Todd’s paresis Contralateral focus

CORRESPONDENCE OF COGNITIVE FUNCTIONSEVALUATED BY MMSE TO SPECIFIC BRAIN AREAS