1. Cerebral Localisation
Prof.Dr. S. Naz Yeni

2. 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.

3. 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

4. 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

5. 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.

6. 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

7. 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.

8. 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

9. 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.

10. 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.

11. 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

12. Clinical features Epileptic seizures
Wernicke’s type of receptive dysphasia
Upper homonym quadrantanopsia
Emotional facial asymmetry

13. 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

14. 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

15. 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)

16. Gerstman syndrome (angular gyrus/dominant side)
Loss of right/left discrimination
Acalculia
Finger agnosia
Alexia with agraphia

17. 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.

18. Some definitions Dyslexia(word blindness): loss of ability to reading
Anosagnosia: denial, hemineglect
Asteroagnosia: inability to identify an object by touch without visual input.

19. 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

20. Epileptic seizures
occipital lobe seizures start with auras of elemantary visual hallucinations, scotomas, amourosis, homonoym hemianopsia.

21. 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

22. 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).

23. Cerebellum Coordination of movement
Control of gait, posture (Balance )
Control of muscle tone (Motor control )
Cognitive functions
Attention
Emotions
Language

24. Features with regard to lobes
Posterior lobe
(neocortex)
Anterior lobe
(paleocortex)
Flocculo-nodulus
(archicortex)
Ataxia + ++
Nystagmus -
+/_
Intentional tremor _
Hyptonia
Rebound
Dysmetria..

25. Mesencephalon Midbrain is located above pons and below
diencephalon(thalamus).
Critical structures:
Edinger westphal nuclei
4 th nerve nuclei
Substantia nigra
Crus cerebri

26. 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

27. Pons
Location: below midbrain, above medulla oblangata and in front of cerebellum
Spinothalamic tract
Corticospinal tract
Cerebellar peduncles

28. 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

29. Well-known vascular and nonvascular syndromes
Millard-Gubler syndrome
Locked-in syndrome
Cerebello-pontine angle tumors

30. Crossed motor deficits
Ipsilateral 6th nerve palsy
Ipsilateral 7th nerve palsy
Contralateral hemiparesis

31. 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.

32. 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

33. Medulla oblangata It is the lower half of brain stem below pons.
Corticospinal tract and the decussation
Spinothalamic pathway and the leminiscus
Cerebellar peduncles (inferior)
9,10,11,12 cranial nerves and the nuclei
Autonomic fibers

34. Wallenberg syndrome (lateral medullary syndrome)
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)