Narkeesh

M.P.T (Neuro)
SBSPGI

Dysfunction or disease of the cerebral hemispheres

can be organic (ie, of known structural, chemical, or
metabolic mechanism) or nonorganic (of unknown
cause). The latter includes the major psychoses and
many behavioral disorders.

The cerebrum (supratentorial or front of brain) - composed

of the right and left hemispheres.
Functions : initiation of movement, coordination of
movement, temperature, touch, vision, hearing, judgment,
reasoning, problem solving, emotions, and learning.
Brodmann divided into 52 areas
Cerebral cortex 6 layers
The frontal cortex dominated by pyramidal rather than
granular. Agranular cortex
The parietal cortex dominated by granular layers
Granular cortex

 30% of cerebrum
Area 4, 6, 8 & 44-motor activity
Area 4-primary motor cortex- directly
connected
with somatosensory neurons of
the anterior part
of post central gyrus &
also parietal, thalamic
and red nuclei
and reticular formation of the brainstem.
Area 8 turning the head and eyes to
contralaterally.
Area 44 dominant hemisphere (brocas
area) lips
tongue pharynx larynx bilat
lesion cause
paralysis of phonation,
articulation and
deglutition.

The medial-orbital gyri and ant parts of

cingulated
gyri which are the frontal
components of limbic system- take part in
control of respiration, blood pressure,
peristalsis, and
autonomic functions.
The most ant parts 9-12 and 45-47prefrontal
areas-designated functionsinitiation of
planned action and executive
control of all
mental operations including
emotional expression
Pyramidal cells at area 4 & 6
Blood supply ACA and Sup div of MCA

Cat

Monkey

Dog

Human

C/F
motor abnor
Speech and language disorders
Impairment of cognitive function
Akinesia & lack of initiative and spontaneity (apathy
& abulia)
changes in personality, change in mood and self
control
incontinence of bladder and bowel

Motor Abnormalities
posterior part - spastic paralysis of the contralateral
face, arm and leg.
anterior and medial parts of the motor cortex -(area 6
& supplementary motor area of 8 the premotor
cortex) results in less paralysis and more spasticity as
well as a release of sucking, & grasping reflexes
Brocas area - loss of motor speech, agraphia, and
apraxia of the face, lips and tongue
Lesions of motor parts - quadriplegia/paresis-will be
severe and affecting the cranial nerves as well as
spine

Motor Abnormalities (cont.)

Gait Disorder:
medial part of frontal lobe - connections
with basal ganglion, then weakness, loss of
sensation, incoordination with cerebellum
results in gait disorders.

Posture of slight flexion

Turning with one foot
Difficulty in stepping
unable to move his feet forward
feet were glued to the floor (slipping Clutch)
unable to stand and to sit
difficulty in turn over in bed
(Cerebral paraplegia in flexion)

Incontinence involvement of posterior part of sup.

Frontal and ant. Cingulate gyri & intervening white
matter result in loss of control of micturition and
defecation.(no warning of fullness of bladder)
Speech and Language: Brocas Aphasia

laconic speech (concise)

Lack of spontaneity of speech

telegraphic speech (agrammatism)

Loss of fluency (verbal stereotypes)

Perseveration of speech

tendency to whisper instead of speaking aloud

dysarthria

Cognitive and Intellectual Changes

organ of Civilization
Changed personalities
Decreased initiative
Lack of concern (relation)
Freedom of anxiety
Difficulty in problem solving
Frontal lobe memory defect will be general
disturbance in thinking
Loss of volition (willing)

Problem solving proceeds in four steps (perceptual,

constructive, arithmetical and logical)
1. specification of a problem
2. a plan of action for the solution of the problem
3. execution, including implementation and
control of the plan
4. checking or comparison of the results against
the original plan

Summary of Frontal lobe disease

I.Effects of unilateral frontal disease
a.Contralateral spastic hemiplegia
b. Slight elevation of mood, increased talkativeness,
tendency to joke, lack of tact, difficulty in adaptation,
loss of initiative
c. it entirely prefrontal-no hemiplegia; grasp and
suck reflexes may be released.
d. Anosmia (loss of sense of smell) with involvement
of orbital parts
II. Effects of right frontal disease
a. Left Hemiplegia
b. changes in I- b, c and d

Summary of Frontal lobe disease (cont.)

III. Effects of left frontal disease
a.Right Hemiplegia
b. Motor speech disorder with agraphia, with or
without apraxia of the lips and tongue
c. loss of verbal associative fluency; preservation
d. changes as in I-b, c and d

Summary of Frontal lobe disease (cont.)

IV. Effect of bifrontal disease
a. Bilateral hemiplegia
b. spastic bulbar palsy
c. If prefrontal, abulia(will power) or akinetic
mutism, lack of ability to sustain attention and
solve complex problems, rigidity of thinking,
behavioral disinhibition, inability to anticipate,
labile mood, decomposition of gait and sphinteric
incontinence.

 there is no definite anatomical boundary between

the temporal lobe and the occipital or parietal lobe
the sylvian fissure separates the superior surface
of each temporal lobe from the frontal and anterior
part of parietal lobe

the temporal lobe includes:

Superior, middle and inferior temporal
Lateral occipitotemporal
Fusiform
Lingual
Parahippocampal and hippocampal

Disorders of temporal lobe divided into

disorders of special senses
time perception
language
memory
emotion
behaviour

Visual Disorders
lesion of white matter of the central and posterior
part of temporal characteristically involve the lower arching
fibres of the geniculocalcarine pathway this results in
upper homonomous quadrantanopia
the middle (area 21) and inferior (area 37) temporal
gyri receive a massive fibres from the striate cortex (area
17) and parastriate visual (area 18 and 19) cortex
bilateral lesions results in psycically blind (can see
and pick up the objects but cant able to recognise)
Visual hallucinations appear too large (macropsia)
and too small (micropsia)

Cortical Deafness
Localization of primary auditory cortex (area 41 and 42) in
the transverse gyri lesions in this area results in
deafness/ effect on hearing
Auditory agnosia
lesions in the secondary cortex area 22 and part
of 21 results in perception of combinations of sound is
impaired.
auditory agnosia takes several forms - inability to
recognize sounds and differrent musical notes (amusia)
appreciation of music is impaired by nondominant
temporal lobe

Auditory Verbal Agnosia

- Wernickes aphasia
- left temporal lobe fails in its function of
decoding the acoustic signals of speech and converting
them into appropriate expressions.
Auditory illusions
- sounds are perceived more loudly or less loudly
than normal (paracusia)
- words may seem strange or disagreeable

Auditory Hallucinations
- murmurs, blowing, sound of running water,
whistles, sirens
Vestibular Disturbance
- Superior and posterior part of temporal
(posterior to the primary auditory cortex)
- inducing vertigo
- sense of disequilibrium
Time Perception
- seem to stand still or to pass with great speed
- repeatedly look at the clock

Smell and Taste

- medial part of temporal lobe
- gustatory and olfactory hallucinations
Disorders of Memory, emotion and behavior
- retentive memory
- hyper sexuality

Summary of Temporal lobe disease

I.

Effects of unilateral disease of the dominant lobe

a. Homonymous upper quadrantanopia
b. Wernickes aphasia
c. Amusia (loss of ability to recognize music)
d. Impairments in tests of verbal material
presented through the auditory sense
e. amnesic aphasia
f. Visual agnosia

Summary of Temporal lobe disease (cont)

II. Effects of unilateral disease of the nondominant lobe
a. Homonymous upper quadrantanopia
b. Inability to judge spatial relationships
c. Agnosia for sounds and musics
III. Effects of disease of either lobe
a. auditory, visual, olfactory and gustatory
hallucinations
b. Dreamy states with unicinate seizures
c. Emotional and behavioral changes
d. Delirium

Summary of Temporal lobe disease (cont)

IV. Effects of bilateral disease
a. Korsakoff amnesic defect (hippocampal formation)
(unable to place event in their proper time
relationship)
b. apathy and placidity
c. increased sexual activity
d. Sham rage

Kluver Bucy Syndrome

Areas in the Parietal Lobe play a role in somatosensory

processes.
Areas 3, 2, and 1 are located on the primary sensory
strip, - primary sensory areas for touch and
kinesthesia.
Areas 5, 7, and 40 - posterior to the primary sensory
strip and correspond to the presensory to sensory
association areas.
Area 39 - angular gyrus.

Parietal lobes - two functional regions

1 - sensation and perception (cognition).
2 - sensory input, primarily with the visual
system. (a spatial coordinate system to represent
the world around us)

Visual Disorders
Deep to the inferior part of parietal
- involving geniculocalcarine radiations
- results in homonomous hemianopia
Posterior parietal lesion
- defect in localization of visual stimuli
- inability to compare the sizes of objects
- failure to avoid objects when walking
- inability to count objects
- striking disorder of motor behavior of eyelids

Cortical sensory syndrome

- friendship between thalamus and sensory cortex
Pseudo thalamic syndrome
- burning pain (identical to thalamic pain
syndrome)
- resulted from vascular lesions restricted to
cortex
Pseudo cerebellar syndrome
- hypotonia
- incoordination of movement
- intention tremor

Verger-Dejerine Syndrome
- loss of position sense
- astereognosis
- impairment in two point descrimination
- impairment to recognize figures written on the
skin
Parietal sensory deficit
- inconsistency of response to painful stimuli
- difficulty in distinguishing more than one contact
at a time
- occurrence of hallucination of touch

Asomatognosias
- perception of ones own body and of the relation
of bodily parts to one another
- depends upon the visual and labyrinythine
impulses
Unilateral asomatognosia (Anton Babinski Syndrome)
- anosognosia (asked to raise the paralyzed arm,
patient will raise the intact arm)
- pt may fail to shave one side
- fail to apply lipstick or comb the hair on one side
- impossible to wear eyeglasses
- dressing on one side

Bilateral Asomatognosia
"Gerstmann's Syndrome
Right-left confusion
Agraphia
Acalculia / Dyscalculia
Aphasia
Agnosia
Ideomotor and ideational apraxia

Summary of Parietal lobe disease

I.

Effects of unilateral disease of the parietal lobe

a. Cortical senory syndrome (total hemianaesthesia
with large acute lesions of white matter)
b. mild hemiparesis, unilateral muscular atrophy in
children, hypotonia, poverty of movement,
hemiataxia
c. homonomous hemianopia, visual inattention,
anosognosia, neglect of one half of the body

Summary of Parietal lobe disease (cont)

II Effects of unilateral disease of the dominant lobe
a. disorders of language
b. Gerstmann syndrome
c. tactile agnosia
d. Bilateral ideational and ideamotor apraxia

Summary of Parietal lobe disease (cont)

III Effects of unilat. disease of nondominant lobe
a. Visual spatial disorders
b. Topographic memory loss
c. Anosognosia and dressing apraxia
d. Confusion
e. Tendency to keep the eyes closed & resist to
opening
IV. Effects of Bilateral disease
a. Visual spatial imperceptions, optic ataxia, spatial
disorientation and severe forms of constructional
apraxia

The Occipital Lobe contains areas that process visual

stimuli.
Area 17 is the primary visual area.
Areas 18 and 19 are the secondary visual areas.
But approximately 20 other visual areas, but not well
defined
The Island of Reil or Insula is a cortical area which
lies below the fissure of Sylvius and is considered by
some anatomists to be the fifth lobe of the cerebrum.
It can only be seen by splitting the lateral fissure

Visual Field Defects

- homonomous hemianopia
- Hemiachromatopsia (loss of color vision)
- bilateral lesion result in bilateral central
hemianopia
Cortical Blindness
- loss of sight
- loss of reflex closure of eye lids to a bright light
- cause occlusion of PCA
- Recovery stage- complaints of visual fatigue,
difficulties in fixation and fusion

Visual Anosognosia (Anton syndrome)

- blindness act like normal
- can see small objects - act like blind
Visual illusions (metamorphosias)
- fail to arouse visual memories
- Micropsia (seems too small)
- Macropsia (seems too large)
- inverted vision
- Achromatopsia (disappearance of color)
- erythropsia (illusion coloring)
- polyopia (appearing as two or more)

Visual Hallucinations (sensory as well as cognitive)

- flashes of light

- colors

- stars

- multiple lights

- geometric forms
lesion indication of visual associative area
Visual agnosia
- Object agnosia
- simultagnosia
- Balint syndrome (hand eye incoordination)
- Prospognosia (face ID)
- Visual disorientation
- color agnosia

Damage to the subcortical structures results to

Behavioral and Cognitive disturbance
Dominant thalamic lesions results in Dysphagia and
Dyspraxia
Amygdala is importance in behavior if bilateral
damage to the amygdalae results in
disturbance of memory as well as social behavior
impaired recognition of emotional facial
recognition

 Disease of Basal ganglia results in prominent cognitive

and conative dysfunction
Bilateral Thalamic infarcts results in disturbance of
attention
Right thalamic infarcts results in left Neglect syndrome
Caudate lesions are commonly with behavioral
disturbances, usually abulia than with motor syndromes
Dominant head of caudate infarcts resultsin dysphagia
with dysarthria and orofacial dyspraxia.
Bilateral infarction of head of caudate had resulted in
severely aggressive and criminal behavior

References

Snells Neuro Anatomy

Poddars Anatomy of Central Nervous System
Adams Principles of Neurology
Lindsays Clinical Neurology
Gilroys Basic Neurology
Brains Diseases of the Nervous system
John Pattern Neurological Differential Diagnosis