Cerebral Localisation
Prof.Dr. S. Naz Yeni
Objectives
• To learn functional areas of the brain and
the brain stem
• To learn how to localise the neurologic
symptoms and signs to particular areas in
the brain.
• Although the brain functions are integrated as
one unit some certain areas are specialised on
particular functions.
• Brain lobes
• Cerebellum
• Brain stem
– Mesencephalon
– Pons
– Medulla oblangata
Frontal lobe
Frontal lobe is the greatest lobe. Its boundaries are parietal
lobe posteriorly and temporal lobe under slyvian sulcus.
Areas of major clinical importance
Motor cortex (area 4)
Suplementary motor cortex (area 6)
Frontal eye fields (area 8)
Cortical centre for micturation
Broca’s speech area (dominant hemisphere)
Prefrontal cortex
Neighboring structures of clinical interest: olfactory bulb
optic nerve
Motor cortex
• Contralateral weakness usually limited to a
body part e.g. Hand, foot, mouth,
commisure
• Epileptic seizures: focal motor seizures
with or without jacksonien march
• Parasagittal motor strip lesions may cause
bilateral paraplegia.Sphinctary control may
be lost in these patients.
Eye and head deviation center
• Vulpian’s rule: a destructive lesion may
cause the head/eye deviate towards the
side of the lesion ipsilaterally
• Adversive fit: an excitation ( an epileptic
seizure) may cause contralateral deviation
of eye/head
Prefrontal cortex
• Frontal lobes play a major role in acquired social
behavior: executive functions, abstraction, reasoning,
attention. Lesions in prefrontal cortex causes personality
change.
• Personality change may present in two diferrent ways:
inhibitory, dysinhibitory type
• Inhibitory type: patient becomes apathic. Executive
dysfunction is the prominent feature.
• Loss of drive, apathy occurs. Decrease in personal
hygiene, loss of concern about personal, social and
famıly, business affairs.
• Dysinhibitory type: manic-like behavior occurs. Patient
doesn’t obey social rules. he may well urinate in public
without any feeling of ashame. Such a patient can use
inproper language and slang words.
Extrafrontal signs
• Foster Kennedy syndrome : tumors
growing at the base of frontal lobe such as
a meningioma of sphenoid bone may
cause:
Ipsilateral anosmia
Ipsilateral optic nerve atrophy
Contralateral papilla edema
Additional signs
• If the lesion is in the dominant hemisphere
Broca’s type of dysphasia (expressive
type) may occur.
• Grasp reflex: indicates contralateral frontal
lobe damage.If there is bilateral grasp
reflex this may indicate bilateral damage in
the frontal lobes.
Temporal lobe
• Anteriorly frontal lobe, posteriorly there is
occipital lobe. It is folded on itself .Temporal lobe
has two distinct part: medial and lateral.
• Medial: hippocampus amygdala, uncus,
parahippocampus etc..
• Lateral: primary auditory and vestibular cortex,
associated visual cortex, central representation
of receptive language (Wernicke) area.
• Deep in the layers passes the visual pathways
forming Meyer’s loop.
Functions
• Hippocampus: memory formation (recall of
the recent memory) visceral motility
functions
• Uncus: smell and taste represantation
• Amygdala: autonomic activity via the
connections with hypothalamus sexual
behavior
• A part of limbic system. Connections with
frontal lobe have implications on behavior
personality
Clinical features
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Epileptic seizures
Wernicke’s type of receptive dysphasia
Upper homonym quadrantanopsia
Emotional facial asymmetry
Epileptic seizure
Auras implying temporal lobe epilepsy;
Hippocampus: epigastric rising sensation,
deja vu, jamais vu like feelings..
Amygdala: fear, palpitation, autonomic
symptoms (piloerection, sweating,
mydriasis)
Uncus: gustatory, olfactory hallucinations
Lateral temporal lobe: Vestibular, auditory
hallucinations, complicated visual
hallucinations
Parietal lobe
• Extending from rolandic sulcus posteriorly
to the parieto-occipital junction. Below
there is temporal lobe.
Critical zones
• Somato-sensory cortex: 3,1,2
• Receptive language area of Wernicke (at
the junction with temporal lobe: opercular area)
• Visual pathways
Signs and symptoms
• Lower quadrantanoptic homonym
hemianopsia
• Wernicke’s (receptive) type of dysphasia
in the dominant hemisphere
• Cortical sensory loss : astereoagnosia,
loss of two point discrimination, extinction
phenomenon.
• Apraxia (dominant hemisphere lesions)
• Anosagnosia (nondominant hemisphere
lesions)
Gerstman syndrome (angular
gyrus/dominant side)
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Loss of right/left discrimination
Acalculia
Finger agnosia
Alexia with agraphia
Some definitions
• Apraxia: loss of ability of learned motor
skills
Ideomotor apraxia: when asked “as if to brush teeth” patient can not
perform. However in daily life spontaneous acts are performed.
Ideational apraxia: the patient can not program, plan multistep
activities. Daily life may be problematic.
• Agnosia:is a loss of ability to recognize
objects, persons, shapes, etc. while the
specific sense is not defective.
Some definitions
• Dyslexia(word blindness): loss of ability to
reading
• Anosagnosia: denial, hemineglect
• Asteroagnosia: inability to identify an
object by touch without visual input.
Occipital lobe
• Primary visual cortex(area 17) is located
behind parietal and temporal lobes.
Signs and symptoms;
• Epileptic seizures
• Homonymous hemianopsia (unilateral
disease)
• Cortical blindness (in bilateral lesions)
• Agnosia
• Dyslexia
Epileptic seizures
• occipital lobe seizures start with auras of
elemantary visual hallucinations,
scotomas, amourosis, homonoym
hemianopsia.
Bilateral occipital lobe damage
• Cortical blindness with macular sparing
• If there is widespread damage to the
occipital lobes without sparing macular
vision, cortical type of blindness occurs.
The question is how can we differ such a
blindness from a blindness as a result of a
bilateral optic nerve disease; importance
of light reflex
Definitions
• Prosopagnosia: Loss of ability to recognize
familiar faces. Such a patient can recognize a
familiar person by using mimics, emotional
clues. The lesion is usually located in the
periphery of occipital lobe bilaterally(not in the
primary visual cortex).
• Visual agnosia: loss of ability to recognise visual
stimuli; may describe all details of a picture but
still can not understand the picture as a whole
(lesions in the bilateral visual association areas).
Cerebellum
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Coordination of movement
Control of gait, posture (Balance )
Control of muscle tone (Motor control )
Cognitive functions
– Attention
– Emotions
– Language
Features with regard to lobes
Posterior lobe
(neocortex)
Anterior lobe
(paleocortex)
Flocculonodulus
(archicortex)
Ataxia
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Nystagmus
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Intentional tremor
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Hyptonia
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Rebound
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Dysmetria..
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Mesencephalon
Midbrain is located above pons and below
diencephalon(thalamus).
Critical structures:
Edinger westphal nuclei
4 th nerve nuclei
Substantia nigra
Crus cerebri
Well-known vascular syndromes
Weber’s syndrome
• Ipsilateral 3rd nerve palsy
• Contralateral hemiparesis
Benedikt’s syndrome
• İpsilateral tremor(nucleus ruber)
• Cerebellar signs
• 3rd nerve palsy
Pons
• Location: below midbrain, above medulla
oblangata and in front of cerebellum
• Spinothalamic tract
• Corticospinal tract
• Cerebellar peduncles
Pons; important structures
• mid-pons: The chief or pontine nucleus of
the trigeminal nerve sensory nucleus (V)
• mid-pons: the motor nucleus for the
trigeminal nerve (V)
lower down in the pons:
• abducens nucleus (VI)
• facial nerve nucleus (VII)
• vestibulocochlear nuclei
Well-known vascular and
nonvascular syndromes
• Millard-Gubler syndrome
• Locked-in syndrome
• Cerebello-pontine angle tumors
Crossed motor deficits
• Ipsilateral 6th nerve palsy
• Ipsilateral 7th nerve palsy
• Contralateral hemiparesis
Locked-in syndrome
• Occlusion of basilary artery may cause this syndrome.
The signs consist of quadriplegia and the inability to
speak in otherwise cognitively intact individuals.
Consciousness is preserved.Those with locked-in
syndrome may be able to communicate with others
through coded messages by blinking or moving their
eyes, which are not affected.
Cerebello-pontine angle tumours
• This is usually a schwannoma of 8 th
nerve.
• One sided sensorineural hearing loss may
last many years before diagnosis.
Additional features may be;
• 5th nerve (loss of cornea reflex) palsy
• 6, 7th nerve palsies
• Cerebellar features
Medulla oblangata
• It is the lower half of brain stem below
pons.
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Corticospinal tract and the decussation
Spinothalamic pathway and the leminiscus
Cerebellar peduncles (inferior)
9,10,11,12 cranial nerves and the nuclei
Autonomic fibers
Wallenberg syndrome
(lateral medullary syndrome)
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A vascular syndrome
Vertigo
Nausea, womiting
Ipsilateral cerebellar findings, ataxia
Difficulty in swallowing
Horner’s syndrome
Crossed sensory deficit (one sided facial,
contralateral-sided body)