2Objectives 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.
3Although the brain functions are integrated as one unit some certain areas are specialised on particular functions.Brain lobesCerebellumBrain stemMesencephalonPonsMedulla oblangata
4Frontal lobeFrontal lobe is the greatest lobe. Its boundaries are parietal lobe posteriorly and temporal lobe under slyvian sulcus. Areas of major clinical importanceMotor cortex (area 4)Suplementary motor cortex (area 6)Frontal eye fields (area 8)Cortical centre for micturationBroca’s speech area (dominant hemisphere)Prefrontal cortexNeighboring structures of clinical interest: olfactory bulb optic nerve
5Motor cortexContralateral weakness usually limited to a body part e.g. Hand, foot, mouth, commisureEpileptic seizures: focal motor seizures with or without jacksonien marchParasagittal motor strip lesions may cause bilateral paraplegia.Sphinctary control may be lost in these patients.
6Eye and head deviation center Vulpian’s rule: a destructive lesion may cause the head/eye deviate towards the side of the lesion ipsilaterallyAdversive fit: an excitation ( an epileptic seizure) may cause contralateral deviation of eye/head
7Prefrontal cortexFrontal 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 typeInhibitory 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.
8Extrafrontal signsFoster Kennedy syndrome : tumors growing at the base of frontal lobe such as a meningioma of sphenoid bone may cause:Ipsilateral anosmiaIpsilateral optic nerve atrophyContralateral papilla edema
9Additional signsIf 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.
10Temporal lobeAnteriorly 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.
11FunctionsHippocampus: memory formation (recall of the recent memory) visceral motility functionsUncus: smell and taste represantationAmygdala: autonomic activity via the connections with hypothalamus sexual behaviorA part of limbic system. Connections with frontal lobe have implications on behavior personality
12Clinical features Epileptic seizures Wernicke’s type of receptive dysphasiaUpper homonym quadrantanopsiaEmotional facial asymmetry
13Epileptic 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 hallucinationsLateral temporal lobe: Vestibular, auditory hallucinations, complicated visual hallucinations
14Parietal lobeExtending from rolandic sulcus posteriorly to the parieto-occipital junction. Below there is temporal lobe.Critical zonesSomato-sensory cortex: 3,1,2Receptive language area of Wernicke (at the junction with temporal lobe: opercular area)Visual pathways
15Signs and symptoms Lower quadrantanoptic homonym hemianopsia Wernicke’s (receptive) type of dysphasia in the dominant hemisphereCortical sensory loss : astereoagnosia, loss of two point discrimination, extinction phenomenon.Apraxia (dominant hemisphere lesions)Anosagnosia (nondominant hemisphere lesions)
16Gerstman syndrome (angular gyrus/dominant side) Loss of right/left discriminationAcalculiaFinger agnosiaAlexia with agraphia
17Some 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.
18Some definitions Dyslexia(word blindness): loss of ability to reading Anosagnosia: denial, hemineglectAsteroagnosia: inability to identify an object by touch without visual input.
19Occipital lobePrimary visual cortex(area 17) is located behind parietal and temporal lobes.Signs and symptoms;Epileptic seizuresHomonymous hemianopsia (unilateral disease)Cortical blindness (in bilateral lesions)AgnosiaDyslexia
20Epileptic seizuresoccipital lobe seizures start with auras of elemantary visual hallucinations, scotomas, amourosis, homonoym hemianopsia.
21Bilateral occipital lobe damage Cortical blindness with macular sparingIf 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
22DefinitionsProsopagnosia: 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).
23Cerebellum Coordination of movement Control of gait, posture (Balance )Control of muscle tone (Motor control )Cognitive functionsAttentionEmotionsLanguage
24Features with regard to lobes Posterior lobe(neocortex)Anterior lobe(paleocortex)Flocculo-nodulus(archicortex)Ataxia+++Nystagmus-+/_Intentional tremor_HyptoniaReboundDysmetria..
25Mesencephalon Midbrain is located above pons and below diencephalon(thalamus).Critical structures:Edinger westphal nuclei4 th nerve nucleiSubstantia nigraCrus cerebri
27PonsLocation: below midbrain, above medulla oblangata and in front of cerebellumSpinothalamic tractCorticospinal tractCerebellar peduncles
28Pons; 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
29Well-known vascular and nonvascular syndromes Millard-Gubler syndromeLocked-in syndromeCerebello-pontine angle tumors
31Locked-in syndromeOcclusion 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.
32Cerebello-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) palsy6, 7th nerve palsiesCerebellar features
33Medulla oblangata It is the lower half of brain stem below pons. Corticospinal tract and the decussationSpinothalamic pathway and the leminiscusCerebellar peduncles (inferior)9,10,11,12 cranial nerves and the nucleiAutonomic fibers