one of the important topic in neurology...veryyy helpful

2. Anatomy
• Anatomy of cerebral connections
• 3 major types of fiber connections of
the neocortex:
A. Association fibers,
B. Projection fibers,
C. Commissural fibers
A. Association fibers- unite different parts of the same cerebral hemisphere
1. long fiber bundles that connect distant neocortical areas
2. Short subcortical U-fibers that connect adjacent neocortical areas
B. Projection fibers- consist of efferent and afferent fibers uniting the cortex with the
lower parts of the brain and with the spinal cord
C. Commissural fibers- function primarily to join the two hemispheres and include
principally the corpus callosum, the anterior commissure, and the the fornix, and
the habenular commissure.

6. Corpus callosum – Anatomy
• The corpus callosum also known as the colossal commissure, is a wide, flat bundle of
neural fibers beneath the cortex in the brain at the longitudinal fissure.
• It connects the left and right cerebral hemispheres and facilitates interhemispheric
communication.
• It is the largest white matter structure in the brain, made up of dense myelinated
fibers that usually interconnect homologous territories of the two cerebral
hemispheres.
• The dense compact nature of the white matter tracts, relative to the adjacent
hemispheric white matter, makes it a barrier to the flow of interstitial edema and
tumor spread.

7. 1. Splenium
2. Body
3. Genu
4. Rostrum
5. Isthmus

8. Corpus callosum – Anatomy
• The posterior portion of the corpus callosum is called the
splenium; the anterior is called the genu ; between the two
is the truncus, or "body", of the corpus callosum.
• The part between the body and the splenium is often
markedly thinned and thus referred to as the "isthmus".
• The rostrum is the part of the corpus callosum that projects
posteriorly and inferiorly from the anterior most genu, as
can be seen on the sagittal image of the brain.
• The rostrum is so named for its resemblance to a bird's
beak.

9. Blood supply
• The corpus callosum (CC) has a rich blood supply, relatively constant
and is uncommonly involved by infarcts.
• The majority of the CC is supplied by the pericallosal arteries (the
small branches and accompanying veins forming the pericallosal
moustache) and the posterior pericallosal arteries, branches from
the anterior and posterior cerebral respectively.
• In 80% of patients additional supply comes from the anterior
communicating artery, via either subcallosal artery or median
callosal artery.
• Subcallosal artery (50% of patients) is essentially a large version of a
hypothalmic branch, which in addition to supplying part of the
hypothalamus also supplies the medial portions of the rostrum and
genu
• Median callosal artery (30% of patients) can be thought of as a
more extended version of the subcallosal artery, in that it travels
along the same course, supplies the same structures but
additionally reaches the body of the corpus callosum
• Posterior pericallosal artery (also known as splenial artery) supplies
a variable portion of the splenium. Its origin is inconstant, arising
from P3 or branches thereof.

10. Age-Specific Growth of the Corpus Callosum
Region Age (yrs)
Relevant
Connections
Associated Cognitive
Functions
Anterior 3–6 Frontal lobes Attention, organization, and
planning behavior
Posterior 6–15 Temporal and
parietal lobes
Language and associative
thinking, social cognition
The development of the corpus callosum occurs between the 12th and 16-20th weeks of
gestation

11. Corpus callosum - function
• Genu connect the prefrontal cortex
between the two halves of the brain.
• Midbody and splenium interconnect
areas of the premotor and
supplementary motor regions and
motor cortex
• Posterior body of the corpus
communicates somatosensory
information between the two halves
of the parietal lobe and visual center
at the occipital lobe.

12. AGENESIS OF CORPUS CALLOSUM

13. AGENESIS OF CORPUS CALLOSUM
• Agenesis of the corpus callosum (ACC) is a rare birth defect (congenital
disorder) in which there is a complete or partial absence of the corpus
callosum.
• The development of the fibers that would otherwise form the corpus
callosum become longitudinally oriented within each hemisphere and
form structures called Probst bundles.
• In addition to agenesis of the corpus callosum, other congenital callosal
disorders include
1. hypogenesis (partial formation),
2. dysgenesis (malformation) of the corpus callosum,
3. hypoplasia (underdevelopment) of the corpus callosum.
• Diagnosis
– Callosal disorders can be diagnosed only through a brain scan
– They may be diagnosed through an MRI, CT scan, prenatal ultrasound,
or prenatal MRI

14. AGENESIS OF CORPUS CALLOSUM

15. AGENESIS OF CORPUS CALLOSUM
• Cause
– Agenesis of the corpus callosum is caused by disruption to
development of the fetal brain between the 3rd and 12th
weeks of pregnancy.
– Research suggests that some possible causes may include
• chromosome errors,
• inherited genetic factors,
• prenatal infections or injuries,
• prenatal toxic exposures,
• structural blockage by cysts or other brain abnormalities
• metabolic disorders.

16. AGENESIS OF CORPUS CALLOSUM
• Signs and symptoms
• Vary greatly among individuals
• Some characteristics common in individuals with callosal disorders include
• Research : shown to have some cognitive disabilities (difficulty in complex problem
solving) and social difficulties (missing subtle social cues), even when their
intelligence quotient is normal.
• Other characteristics sometimes associated with callosal disorders include
seizures, spasticity, early feeding difficulties and/or gastric reflux, hearing
impairments, abnormal head and facial features, and mental retardation.
1. Poor motor coordination,
2. Delays in motor milestones such as sitting and walking,
3. Delayed toilet training,
4. Chewing and swallowing difficulties
5. Vision impairments,
6. Hypotonia
7. Low perception of pain, .

17. AGENESIS OF CORPUS CALLOSUM
• Associated syndromes
– ACC can occur as an isolated condition or in combination with other cerebral
abnormalities, including
• Arnold-chiari malformation,
• Dandy-walker syndrome,
• Andermann syndrome(motor and sensory neuropathy)
• Schizencephaly (clefts or deep divisions in brain tissue)
• Holoprosencephaly (failure of the forebrain to divide into lobes.)
– Girls may have a gender-specific condition called Aicardi's syndrome, which
causes severe mental retardation, seizures(infantile spasms), abnormalities in
the vertebra of the spine, and lesions(lacunae) on the retina of the eye.
– ACC can also be associated with malformations in other parts of the body,
such as midline facial defects.
– The effects of the disorder range from subtle or mild to severe, depending on
associated brain abnormalities.

18. AGENESIS OF CORPUS CALLOSUM
• Treatment
• There are currently no specific medical treatments for callosal disorders, it usually
involves management of symptoms and seizures if they occur.
• Patients may benefit from a range of
– developmental therapies,
– educational support, and services.
• Prognosis
• Prognosis varies depending on the type of callosal abnormality and associated
conditions or syndromes.
• ACC does not cause death in the majority of children.
• Mental retardation does not worsen.
• Although many children with the disorder have average intelligence and lead
normal lives, neuropsychological testing reveals subtle differences in higher
cortical function compared to individuals of the same age and education without
ACC.

19. Tumors

20. Tumours
• Tumors of the corpus callosum, especially those involving the
anterior portion, frequently cause psychiatric and behavioral
symptoms.
• These include
– Catatonia,
– Depression
– Psychotic symptoms
– Personality changes.
• Definitive brain imaging studies are indicated in psychiatric
patients with
– new or pre-existing psychiatric and behavioral symptoms
– accompanied by focal neurological findings
– atypical presentation

21. Lipoma
• Intracranial lipomas are rare developmental lesions of the central
nervous system,which are usually asymptomatic and discovered
incidentally.
• They mainly occur in the region of the corpus callosum and the
pericallosal cistern, accounting for up to 65% of all intracranial
lipomas and frequently associated with callosal dysgenesis.
A 2-year-old boy with lipoma of corpus callosum.
Coronal T1-weighted MR image shows large well-
defined homogeneous midline mass lesion in region
of corpus callosum with characteristic bright signal of
lipoma.
Note associated dysgenesis of corpus callosum.

22. Glioblastoma Multiforme
• extremely aggressive diffuse astrocytic tumor
• commonly found in the supratentorial white matter of the cerebral
hemispheres.
• It is the most common primary brain tumor in adults, accounting
for 25% of all cases.
• Glioblastomas most commonly spread via direct extension along
white matter tracts, including the corpus callosum, although
hematogenous, subependymal, and cerebrospinal fluid spread can
also be seen.
• When the corpus callosum is affected, glioblastoma multiformes
commonly display a characteristic bihemispheric involvement,
resulting in a classic butterfly pattern.

23. • Because the corpus callosum is relatively resistant to infiltration,
glioblastoma multiforme should be considered for any lesion crossing the
corpus callosum
A, Axial T1-weighted MR
image shows hypointensity
(arrow) of left parietal white
matter extending across
corpus callosum.
B, Axial T2-weighted MR
image shows hyperintensity
(arrow) in left parietal white
matter extending across
corpus callosum with mass
effect on lateral ventricle.
C, Enhanced axial T1-weighted
MR image shows glioblastoma
(arrow) of left parietal white
matter that extends across
corpus callosum, classic for
glioblastoma multiforme
or lymphoma

24. Lymphoma
• Primary central nervous system lymphomas are rare aggressive
neoplasms of the brain, accounting for less than 2% of malignant
primary brain tumors.
• They are almost always of the B-cell non-Hodgkin’s type.
• Common locations include the corpus callosum, deep gray matter
structures, and the periventricular region.
• Lymphomas differ from glioblastoma multiformes because they
usually have less peritumoral edema, are more commonly
multiple, are less commonly necrotic, are highly radiosensitive,
and fre-quently temporarily respond dramatically to steroid
administration producing “vanishing lesions.”

25. Lymphoma
A, Axial T1-weighted MR
image shows hypointense
lesion (arrow) in deep left
parieto–occipital white
matter extending into
splenium of corpus
callosum.
B, Axial T2-weighted MR
image shows hyperintense
lesion involving corpus
callosum surrounded by
high-signal-intensity
edema.
C, Enhanced axial T1-
weighted MR image shows
markedly enhancing lesion
(arrow) of left parieto–
occipital white matter,
crossing corpus callosum in
classic butterfly pattern.
79-year-old nonimmunocompromised woman with primary central nervous system
lymphoma who presented with disorientation

26. Juvenile Pilocytic Astrocytoma
• Juvenile pilocytic astrocytomas are a distinct low-grade variant of
astrocytoma.
• They are usually well-circumscribed unencapsulated masses, with
frequent cyst formation, either microscopic or macroscopic.
• Most lesions commonly involve the cerebellar vermis, cerebellar
hemispheres, optic chiasm, hypothalamus, or floor of the third
ventricle.
• The corpus callosum is an uncommon location.
• The solid portion of the tumor usually enhances, in contrast to most
low-grade infiltrative astrocytomas, which tend not to enhance

27. Demyelinating Diseases

28. Multiple Sclerosis
• Multiple sclerosis is a demyelinating that more commonly affects young women.
• Lesions characteristically involve the periventricular white matter, internal capsule,
corpus callosum, and pons, although plaques can be found anywhere in the white
matter and less commonly even in gray matter.
• The lesions of the corpus callosum can be focal or confluent nodular lesions and
tend to affect the callosal–septal interface, which is the central inferior aspect of
the corpus callosum.
• On MR imaging, the prevalence of lesions in the corpus callosum has been
reported to be up to 93% in the radiology literature.
• Atrophy of the corpus callosum can coexist in long-standing multiple sclerosis,
making the diagnosis of corpus callosum lesions difficult.
• Enhancement is common in the acute stage.
• Differentiation should be made from ischemia, trauma, and other demyelinating
processes on the basis of morphology, location, and the presence of concurrent
multiple sclerosis plaques in the periventricular region

29. Multiple Sclerosis
A, Axial T2-weighted MR
image shows multiple
hyperintense somewhat
ovoid lesions of corpus
callosum and periventricular
white matter, classic for
multiple sclerosis.
B, Sagittal T2-weighted MR
image shows multiple
hyperintense lesions (arrows)
in corpus callosum.
C, Sagittal fluid-attenuated
inversion recovery
paramedian image obtained
through corpus callosum
shows multiple ovoid
hyperintense lesions (arrow).
A 24-year-old woman with multiple sclerosis who
presented with visual complaints.

30. Progressive Multifocal Leukoencephalopathy
• Progressive multifocal leukoencephalopathy is an uncommon progressive fatal
demyelinating disease that affects immunocompromised patients.
• The cause is a papovavirus—the Creutzfeldt-Jakob virus.
• The lesions are usually multifocal and asymmetric, most commonly affecting the
subcortical white matter and corpus callosum.
• In the corpus callosum, focal lesions can occur that enlarge and become confluent
as the disease progresses.
• Progressive multifocal leukoencephalopathy should be considered in the
differential diagnosis of space-occupying lesions in HIV patients.
• The lack of enhancement and mass effect can act as features differentiating this
entity from others such as lymphoma or glioblastoma

31. A, T2-weighted axial MR image shows asymmetric
white matter lesion of frontal lobes with
involvement of corpus callosum.
B, Enhanced axial T1-weighted MR image shows no
enhancementof lesion.
Biopsy of lesion (not shown) confirmed progressive
multifocal leukoencephalopathy.
A 44-year-old man with HIV presented with behavioralchanges and facial droop
caused by progressive multifocal leukoencephalopathy

32. Marchiafava-Bignami Disease
• Marchiafava-Bignami disease is a rare demyelinating neurologic
disorder, primarily affecting the corpus callosum.
• It was first described in Italian wine drinkers and is thought to be due
to chronic and massive alcohol use.
• The central layers of the corpus callosum are affected, with sparing of
the dorsal and ventral layers (sandwich sign).
• The disease can follow one of three clinical courses, a fulminate, acute
form or subacute and chronic forms.
– acute = genu and splenium,
– chronic = body.

33. Marchiafava-Bignami Disease
A, Axial T2-weighted MR image shows signal
abnormality of corpus callosum and
periventricular white matter.
B, Sagittal T1-weighted MR image shows corpus
callosum atrophy (short arrow), which is
characteristic of chronic form.
Involvement of central layers of corpus callosum,
indicated by hypointensity, with sparing of dorsal
and ventral layers results in the sandwich sign
(long arrow).

34. Vascular

35. Infarction
• Infarcts involving the corpus callosum are rare, in part because the corpus
callosum is a dense white matter tract and therefore is less sensitive to
ischemic injury than gray matter.
• The anterior and posterior cerebral arteries provide the major blood
supply of the corpus callosum via the pericallosal artery and small
penetrating vessels that run perpendicular to the parent artery.
• On MR imaging, infarcts have the same characteristics as strokes elsewhere,
with similar enhancement patterns.
• Differentiation of lacunar infarcts from other entities such as trauma and
demyelinating processes can be made by the presence of concurrent
infarcts in characteristic sites (centrum semiovale, basal ganglia).
• With large-vessel ischemic events, the corpus callosum is usually involved as
part of a large vascular distribution

36. Arteriovenous Malformations
• Arteriovenous malformations of the corpus callosum comprise 9–11% of all
cerebral arteriovenous malformations.
• Clinically, 84% of patients with these malformations present with
intracranial hemorrhage, most with intraventricular hemorrhage.
• Most are supplied by both the anterior and posterior cerebral arteries, and
many have a bilateral blood supply.
• Drainage is mainly into the internal cerebral vein or interhemispheric
superficial veins.
• The MR imaging characteristics are those of arteriovenous malformations
elsewhere, with serpentine flow voids noted through the corpus callosum
and the ventricle and frequently with evidence of intraventricular
hemorrhage.

37. Arteriovenous Malformations
• A, Sagittal T1-weighted MR image shows
hemorrhage (arrows) and multiple flow
voids in corpus callosum.
• B, Axial T2-weighted MR image shows
hyperintense lesion (arrow) with flow voids.

38. Trauma

39. Trauma
• The classic triad of diffuse axonal injury is that of diffuse damage to axons at
1. The gray–white matter interface of the cerebral hemispheres,
2. The dorsolateral aspect of the rostral brainstem,
3. The corpus callosum.
• The callosal lesions most commonly involve the splenium, are usually eccentric in
location, and can involve a focal part or the full thickness of the corpus callosum.
• On MR imaging, spin echo T2-weighted images and FLAIR sequences during the
sagittal plane are most sensitive in detecting small nonhemorrhagic lesions.
• Hemorrhagic lesions are best seen on T2- weighted images during the first 4 days
after injury and, after 4 days, are better seen on T1- weighted images.
• Differentiation from other lesions such as ischemia should be made on the basis of
history and the location of the lesions in the corpus callosum

40. A, Sagittal T1-weighted MR image shows nonhemorrhagic
hypointense lesion (arrow) of corpus callosum.
B, Axial proton density–weighted MR image shows
hyperintense lesion of corpus callosum.
C, Sagittal T1-weighted MR image on follow-up examination 10
days after B shows hemorrhagic lesion of corpus callosum.
D, Enhanced coronal T1-weighted MR image on follow-up
examination 10 days after B shows hemorrhagic lesion of
corpus callosum, with classic shearing-type lesion also seen at
gray–white junction, both indicative of diffuse axonal injury.
20-year-old man with diffuse axonal injury 1 week after motor vehicle crash.

41. Miscellaneous Lesions
• Lesions in the corpus callosum, both diffuse and focal, have been described
in patients with long-standing hydrocephalus after shunting.
• Callosal lesions and tectal neoplasms producing hydrocephalus have been
seen in patients with aqueductal stenosis.
• Patients with these lesions were thought to have long-standing
hydrocephalus before ventricular decompression.
• The exact mechanism responsible for the production of these callosal
lesions is unknown, although they may be the result of ischemia with
subsequent demyelination caused by prolonged severe stretching of the
corpus callosum from ventriculomegaly and subsequent rapid
decompression of the ventricles.

42. 45-year-old man with cystic lesions associated with long-standing hydrocephalus,
with multiple prior shunt revisions.
Patient is asymptomatic other than for headaches, which are probably due to mild
hydrocephalus.
A, Sagittal T1-weighted MR image
shows well-defined
cystic lesions (arrows) of corpus
callosum.
B, Axial T2-weighted MR image
shows abnormal signal
(arrow) throughout corpus
callosum, which has
persisted for many years.

43. Disconnection syndromes

44. Disconnection syndrome:
Introduction
• Defined as symptoms and sign, which are
arises due to white matter disconnection
• 1965 - Norman Geschwind, US neurologist
• Usually two types-
1) Interhemispheric disconnection syndrome:
due to involvement of commissural fibres
2) Intrahemispheric disconnection syndrome:
due to association fibres involvement

46. Disconnection syndrome
Fibre type Tract involved Symptoms
Association Arcuate fasciculus Conduction aphasia,
ideomotor apraxia
Inferior longitudinal
fasciculus
Visual object agnosia
Pure alexia
Prosopagnosia (B/L)
Commissural Corpus callosum Left hand apraxia, left hand
agraphia, pure alexia etc
Projection Corticospinal tract Locked in syndrome,
hemiparesis

48. Arcuate fibres
• Conduction aphasia,
• Ideomotor apraxia

49. Conduction aphasia

50. Conduction aphasia
• The lesions of conduction aphasia usually
involve either the superior temporal or
inferior parietal region.
1) Conduction aphasia plus limb apraxia:
parietal lesions
2) Conduction aphasia without apraxia:
temporal lesions

51. Apraxia

52. Apraxia

53. Callosal Apraxia
• What distinguishes these patients is that their apraxia is
confined to the nondominant limb, usually the left arm or hand
in right-handed individuals.
• Liepmann and others described left-sided disconnection-variant
ideomotor apraxia due to Callosal lesions and strokes.
• These patients cannot pantomime with their left hand to verbal
command or imitate but can recognize and identify gestures.
• Various presentations:
 combination of both disconnection-variant ideomotor and
dissociative apraxia of their left arm and hand.
 callosal “alien limb”
 “diagonistic apraxia” or the intermanual conflict of the hands
(The classic example of this is the split-brain patient who has
undergone a corpus callosotomy )
 conceptual apraxia

56. Inferior longitudinal fasciculus
• Visual object agnosia
• Pure alexia
• Prosopagnosia (B/L)

57. Visual object agnosia
Inability to recognize object
by sight
• Based on lesion:
a) Lateral occipital cortex
(cortical): apperceptive
visual agnosia
b) Associative fibre
connections
(transcortical): associative
visual agnosia-
disconnection syndrome
DORSAL STREAM-VISUALY
GUIDED ACTION
VISUAL INFORMATION
VENTRAL STREAM-
VISUAL RECOGNITION

58. Visual object Agnosia

59. Alexia
Acquired inability to read
1) Alexia without agraphia /pure alexia / pure
word blindness/visual verbal agnosia -
disconnection syndrome
2) Alexia with agraphia- lesion at angular gyrus
3) Third alexia/ alexic agraphia- seen with
brocas aphasia

60. Pure Alexia
• Was described by Dejerine
• Left occipital lesion, usually an infarction
• Involve the commisural fibres in splenium
• Fibres from right occipital lobe are disconnected from language centres in the left parietal
lobe
• Patients are unable to read because of disruption the visual stimulus from the right occipital
lobe cannot be transferred to the region of the opposite angular gyrus

61. Callosal Disconnection Syndrome
Verbal Disconnection Motor Disconnection
Left visual anomia Crossed optic ataxia
Left hemialexia Left unilateral motor apraxia
Left auditory anomia Agraphia of the left hand
Left tactile anomia Right unilateral constructional apraxia
Right olfactory anomia Alien hand syndrome
Mainly due to-Posterior callosal lesion Mainly due to-Anterior callosal lesion

62. A) Verbal disconnection disorders
• Verbal output is exclusively sub served by the
left hemisphere
• So in callosal lesion patient have difficulty in
communicating from right hemisphere

63. 1. Left visual anomia
• Image seen in right visual field (left
hemisphere) are normally named or
described, while those shown in the left hemi
field (right hemisphere) cannot.
• Lesion site: Posterior and dorsal portion of
splenium

64. 2. Left hemialexia
• Special case of anomia for words shown in the
left visual field, patient unable to report aloud
or write down those presented on the left side
• Lesion site: Ventral and anterior portion of
splenium

65. 3. Left auditory anomia
• Repetition of verbal material (syllables, words
and numbers) or naming of auditory stimuli
(sound and voices) are normal when presented to
each ear separately- due to the bilateral
projection of cortical auditory pathway
• Bilateral simultaneous stimulation of both ear,
results in deficit from left ear i.e right hemisphere
• Lesion site: Posterior inferior trunk/isthmus

66. 4. Left tactile anomia
• Patient can describe and name objects
palpated with the right hand (without
vision)but not with the left hand
• Also k/a pseudoastereognosis
• Lesion site: posterior trunk

67. 5. Right olfactory anomia
• Odors presented to right nostril (right
hemisphere) are not named, while those
presented to left nostril (left hemisphere)
are—olfactory inputs project ipsilaterally.
• No anosmia: patient winces in response to
unpleasant odours

68. B) Motor disconnection disorders
• Difficulty in coordinating bimanual gesture
due to lack of sensory motor transfer,
• eg- difficulty in tie shoelaces in absence visual
inspection
• Rapid alternating movement of both hand
also impaired, eg-hand clapping/tapping
• Lesion: anterior corpus callosum

69. 1. Right unilateral constructional
apraxia
• Difficulty in drawing and constructive abilities
when using right hand
• Due to disconnection of the left motor cortex
from right hemisphere visuospatial skills

70. 2. Alien hand syndrome
• “Feeling that one limb is foreign or “has a will
of its own,” together with observable
involuntary motor activity
• Depending upon the site of lesion, 3 types of
alien hand syndrome described

71. Alien hand syndrome
Frontal variant Callosal variant Sensory variant
Clinical features Reflexive grasping, groping
and compulsive
manipulation of tools
Intermanual
conflict
Levitation
Lesion site Medial prefrontal cortex Anterior corpus
callosum
Parietal cortex
Affected side of
hand
Dominant hand Nondominant
hand
Nondominant hand
Associated finding Transcortical motor
aphasia,
Sensory ataxia,
Optic ataxia,
neglect
Cause ACA territory stroke
Callosal surgery in epilepsy
Head injury
CBGD
Posterior cortical
atrophy (AD)

72. Geschwind’s disconnection syndromes
Disconnections between
sensory areas and limbic
cortex
Disconnections between
sensory areas and Wernicke’s
area
Disconnections between
sensory areas and motor
cortex
Disconnection between
the hemispheres
Pain asymbolia (no
response to pain in the
presence of normal tactile
discriminatory function)
Tactile aphasia/anomia/agnosia:
(the inability to name a held
object in the presence of
preserved speech and naming
in other sense modalities
Conduction aphasia/central
aphasia: disconnections of
Broca’s area from
Wernicke’s area
Callosal disconnection
syndrome
Verbal learning impairment
examples- autism,
schizophrenia
Pure word deafness(auditory
verbal agnosia): inability to
understand spoken words in
the presence of preserved
hearing
Apraxia: disconnections of
the hand motor
cortex from posterior
sensory area
Pure word blindness: (visual
verbal agnosia or alexia)

74. Involvement of Total length of corpus
callosum
• Results in:
Unilateral verbal anomia
Hemialexia
Unilateral ideomotor apraxia
Unilateral agraphia
Unilateral tactile anomia
Unilateral constructional apraxia
Lack of somaesthetic transfer
Dissociative phenomena

75. Lesions in psychiatric diseases
• ADHD, Dyslexia: anterior part of corpus callosum
• Autism – posterior part of corpus callosum
• OCD – Rostrum – OrbitoFrontal Cortex
• In childhood sexual abuse between 9 to 10 years and
14 to 16 years was associated with maximal affects
on corpus callosum and frontal cortex, respectively.
• PTSD - smaller intracranial volume and corpus
callosum area.

76. Lesions in Schizophrenia
• Several observations are seen with the studies on the corpus callosum in schizophrenia
1. Callosal pruning and myelination as well as interhemispheric coherence continue to
develop into early adulthood, a factor that may be relevant to age of onset in
schizophrenia
2. Impairments in callosal transfer have been reported in patients , implicating alterations
in callosal connectivity;
3. Structural alterations in asymmetric perisylvian regions linked by the callosum have
been reported
4. Callosal myelination begins prenatally and is susceptible to malnutrition, asphyxia and
toxins of infectious origin; also, these same events are linked with aberrant
neurodevelopmental events in schizophrenia
5. The corpus callosum forms the roof of the superior horns of the lateral ventricles, which
are enlarged in schizophrenic patients.
• In spite of evidence linking callosal abnormality to schizophrenia, imaging studies assessing
alterations in callosal morphometry as well as in other cortical and subcortical structures
have produced surprisingly mixed results

77. Epilepsy and the Corpus
Callosotomy(split-brain surgery)
• Corpus callosum contributes to the spread of seizure
impulses from one side of the brain to the other.
• A corpus callosotomy is an operation that severs (cuts)
the corpus callosum, interrupting the spread of
seizures from hemisphere to hemisphere.
• Indication:-most extreme and uncontrollable forms of
epilepsy, those who do not respond to treatment with
antiseizure medications.
• Corpus callosotomy is successful in stopping drop
attacks, or atonic seizures in which a person suddenly
loses muscle tone and falls to the ground, in about 50%
to 75% of cases.