higher brain functions., (physiology)
- 1. Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Dee Unglaub Silverthorn, Ph.D. HUMAN PHYSIOLOGY PowerPoint® Lecture Slide Presentation by Dr. Howard D. Booth, Professor of Biology, Eastern Michigan University AN INTEGRATED APPROACH T H I R D E D I T I O N Speech physiology Speech physiology DR. RAMADAN MOHAMED AHMED
- 2. The dominant & non dominant hemisphere The dominant & non dominant hemisphere The dominant hemisphere is the left hemisphere in - 96% of the right handed person. - 70% of the left handed persons. In the remaining 30% of the left handed persons. . 15% have right categorical hemisphere . 15% showed no sign of lateralization. ►Lesions: Speech disorders and depression. The representational hemisphere (non dominant hemisphere) is concerned with the visuospatial relations i.e recognition of faces, objects by their form and musical themes. ►Lesions; Agnosia and euphoria.
- 3. Brain Function: Cerebral Lateralization • Each lobe has special functions
- 4. Right hemisphere functions • Right hemisphere involved in visual-spatial and constructional tasks, emotion and emotional intonation of speech and music. • Right hemisphere is often referred to as the “Minor” Hemisphere • Patients with injury to right cortex often exhibit neglect.
- 5. Neglect
- 6. Mechanism of speech (1) Understanding a written word: Written word is seen by primary visual area & understood by visual association areas → which discharge to angular gyrus to appreciate the meaning of the word → which projects to the Wernicke’s area for interpretation & formation of thoughts. (2) Understanding a spoken word: Spoken word is heard by primary auditory area → which discharges to auditory association areas for understanding the meaning → which projects to Wernicke’s area. If the word is a name , auditory association area discharge to name area then to Wernicke’s area. (3) To express by written words: Wernicke’s area → discharges to hand skill area → which form coordinated hand movements ( with help of basal ganglia & cerebellum) → which projects to primary motor area for hands. (4) To express by spoken words: Wernicke’s area → projects to Broca’s area through arcuate fasciculus → Broca’s area formulates program for vocalization & projects to face area in primary motor cortex.
- 7. Centres of speechCentres of speech (1) Wernicke’s area Comprehension of auditory & visual information. (2) Broca’s area co-ordinates vocalization & is connected to motor cortex to initiate the appropriate movements to produce speech. (3) Hand skills area Lesion of this area leads to motor apraxia or agraphia. (4) Auditory area a. Auditory association areas. Understanding the meaning of spoken words. b. Area for naming objects: (5) Visual areas a. Visual association areas (18-19) b. Angular gyrus; It processes the information from the words that are read so that they can be converted into the auditory forms of words in Wernick’s area.
- 9. AphasiaAphasia Types of aphasia Lesion in Person is unable A) Reiceptive 1.Wernicke’s aphasia Wernicke’s area Understand the meaning of words but talks excessively with neologism 2.Word deafness (auditory) auditory association area To understand the meaning of spoken word.. 3.Word blindness Visual association area Understand written words or letters. 4.Alexia Angular gyrus Understand meaning of written words. B) Expressive 1) lesion in Broca’s area Mild lesions Speech is slow & words are hand to come. Severe lesion Speech is limited to 2 or 3 words which express all emotions e.g OK –NO. 2.Agraphia lesion in Hand skill area, so Person is unable to Express thoughts by written word C) Global Categorical hemisphere (extensive( Produce or understand both spoken & written words.
- 10. Dysartheria Paralysis or Paresis of Muscles • Flaccid: LMN problem – hypernasal, breathy speech and imprecisely articulated consonants • Spastic: UMN – Harsh, strained / strangled speech with slow articulation • Slow low volume monotonus: Basal ganglia lesion (parkinsonism) • Stacato speech: cerebelar lesion
- 11. Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings Dee Unglaub Silverthorn, Ph.D. HUMAN PHYSIOLOGY PowerPoint® Lecture Slide Presentation by Dr. Howard D. Booth, Professor of Biology, Eastern Michigan University AN INTEGRATED APPROACH T H I R D E D I T I O N MEMORY physiology MEMORY physiology DR. RAMADAN MOHAMED AHMED
- 12. Physiology of Memory • Neurons are the basic means of information transfer within the nervous system • Information in the form of a stimulus is detected by a specific type of neuron (sensory neuron). • The information is then passed to an adjacent neuron (interconnecting neuron) and so on till it gets to where it’s going in the brain • It is an electro-chemical process that allows this to happen
- 13. MEMORY This is the ability of the brain to store and recall (i.e. reproduce) information. MEMORY This is the ability of the brain to store and recall (i.e. reproduce) information. 1. Short-term memory: • This is memory that lasts a few minutes to a few hours. The information is introduced in bits one after the other. The capacity of the brain for this type of memory is small, but its recall is rapid. The new information replace the old ones. • One aspect of short-term memory is what is called the "working memory"(= a temporary storage of information used to plan a future action). 2. long-term ( remote) memory : • This is memory that lasts for long times (up to several years). It develops from primary memory by practice or repetition of information. The capacity of • the brain for this type of memory is large, but its recall is slow. • the old information inhibits storage of new ones).
- 14. Duration of Memory hours Working memory: seconds to minutes •depends on attention and avoiding other stimuli •requires prefrontal cortex seconds years Short-term memory minutes to hours •requires motivation and attention •impaired in confused states •requires processing to be stored as long-term memory •requires temporal lobe structures •involves changes in synaptic strength Long term memory •transferred to diffuse cortical areas •not lost if there are lesions to the hippocampus
- 15. MECHANISMS OF MEMORYMECHANISMS OF MEMORY (A( In short-term memory (a) Activation of reverber-ating circuits. (b) Short-term (post-tetanic) synaptic potentiation. (c) Synaptic sensitization . (d) Long-term potentiation at synapses. (B( In long-term memory: increase in the number of (a) The presynaptic nerve terminals (b) The transmitter vesicles (c) The release sites of the transmitter.
- 16. Reverberating loops • Activity decays • maintained for only a short period of time ~
- 17. CENTRES of memoryCENTRES of memory @ Short-term memory is encoded in the hippocampus. @ Long-term memory • are stored mostly in the neocortex, and the amygdaloid nuclei produce the emotional aspects of memories only.
- 18. CONOLIDATION OF MEMORYCONOLIDATION OF MEMORY DEFINITION • This is the conversion of short-term memory into long-term memory. It requires 5-10 minutes for minimal consolidation and about 4 hours to be complete. MECHANISM OF CONOLIDATION OF MEMORY • This is produced by rehearsal of the information in the mind . It involves new protein synthesis in neurons.
- 19. AMNESIAAMNESIA 1. Retrograde amnesia This is inability to recall memories from the past, specially the more recent events e.g. after certain thalamic lesions and following brain concussion. 2. Anteroqrade amnesia This is inability to form new longterm memories (but the already stored memories are still intact). Its cause is commonly lesions in the hippocampus. 3. Alzheimer disease
- 20. Alzheimer’ s Disease • neurodegenerative disease • amyloid proteins build up and form amyloid plaques (outside cells) • neurofibrilllary tangles inside cells • leads to neuronal death • hippocampus is one of first areas to degenerate, leads to anterograde amnesia • cortex also degenerates early, leads to retrograde amnesia and dementia
- 21. Learning A) Non associative leaning 1) habituation. 2) Sensitization. B) Associative leaning 1) Classical conitioning • 2) Operant conditioning
- 22. Reticular Formation • Located between caudal diencephalon & spinal cord • Network of Overlapping Dendrites and Axons • Input From • Motor Cortex • Basal Ganglia • Cerebellum • Hypothalamus • Vestibular apparatus • Spinothalamic tracts
- 23. RETICULAR FORMATION The Reticular Formation is the oldest part of the brain. It forms a diffuse, multisynaptic, netlike meshwork (reticulum) of widely interconnected neurons in the Tegmentum. The RF is involved in nearly every aspect of brain function including the following: -Homeostasis -Consciousness -Arousal -Pain -Primitive motor control -Muscle tone -Behavioral mechanisms RETICULAR FORMATION
- 25. RETICULAR FORMATION VITAL CENTERS Vital Centers are located in the medulla and pons and control cardiovascular respiratory, and other homeostatic mechanisms. Lesions in these centers are fatal. Examples of RF mediated reflexes are: -Aortic Body -Carotid Body -Aortic Sinus -Carotid Sinus -Respiratory -Cough -Swallowing -Salivary -Vomiting
- 26. Reticular Motor Functions • Facilitatory Reticular Areas • Upper Brainstem (Ascending & descending). • Ascending: Arousal • Descending: Increases Muscle Tone in Extremities • Inhibitory Reticular Areas • Lower and Medial Region of Medulla • Decreases Muscle Tone in Extremities
- 27. Reticular Formation Function • Arousal (Arousal) • Muscle tone Modulation • Pain Processing • Regulation of • Vomiting • Coughing • Cardiovascular Functions • Respiration • Speech Functions
- 29. Reticular Activating System Maintains the conscious, alert state that makes perception possible brainstem reticular formation ascending projection system non-specific thalamic nuclei non-specific thalamocortical projections (diffuse) Activated by sensory information being relayed the the cerebrum
- 30. RETICULAR FORMATION ASCENDING RETICULAR ACTIVATING SYSTEM (ARAS) The midbrain RF gives rise to a tonic ascending barrage of diffuse, nonspecific sensory data called the ARAS. Acting like a battery, the ARAS stimulates the cerebral cortex and maintains the conscious state. Midbrain lesions of ARAS result in Coma. Incomplete lesions may result in Stupor.
- 31. Reticular Activating System • Network in brain stem • Arousal, sleep, pain, & muscle tone • Ascending fiber sends signals upward • Arouses and activates cerebral cortex • Controls overall degree of cortical alertness or level of consciousness: • maximum alertness • wakefulness • sleep • coma
- 32. Reticular Activating System Factors affecting RAS activity ►RAS is stimulated by : 1. All sensory signals especially pain & proprioceptive signals. 2. Cortical signals from: areas of emotions & Motor cortex. 3. Sympathomimetic drugs e.g catecholamines & amphetamine. ►RAS is inhibited by: 1. Withdrawal of all sensory signals. 2. Stimulation of sleep centres. 3. general anaesthetic (e.g barbiturates & ether) . 4.Damage of RAS by tumours.
- 33. Reticular Nuclei • Reticularis Gigantocellular • Pontis Oralis and Cudalis • Lateral Reticular Nucleus • Ventral Reticular Nucleus • Paramedial Reticular Nucleus • Interstitial • Raphe • Ceruleus
- 34. Clinical considerations • Disconnection of cortex and basal ganglia from reticular formation • Decerebrate Rigidity • Extensor posturing of all Limbs • Excessive facilitatory impulses • Transection Below Vestibular Nucleus • Flaccid Paralysis • Similar to degeneration of the lower neuron
- 35. Electrical activity of CNS Dr. RAMADAN MOHAMED AHMED
- 36. Evoked potentials Primary evoked potential Secondary evoked potential +ve wave followed by small – ve wave (depolarization followed by repolarization of dendrites & some neurons of cortex). Large prolonged +ve wave, caused by activation of cortical neruons by signals coming from non-specific thalamic nuclei. Localized to brain area at which the sensory pathway terminates. Appears over most of the cortex at the same time. (not localized)
- 37. Spontaneous cortical potentials (electro encephalogram, EEG or brain waves) EPSPs and IPSPs on apical dendrites of cortical pyramidal cells Recording of EEG is done in calm room at comfortable temperature. The subject should be fasting, in complete physical, mental rest & unanesthiatised. In EEG, the frequency of waves in inversely proportional to their amplitude (Voltage).
- 38. Waves of EEG 1. Alpha waves • Regular & rhythmic i.e synchronized (8-13 cycles/second). • Recorded in adults when they are awake, relaxed & their eyes closed. • Recorded most marked in the occipital regions. • Produced by activity of non-specific thalamic nuclei. 2. Beta waves • Irregular, low voltage & rapid i.e dsynchronised (18-30 c/sec.). • Recorded during brain activity e.g when eyes are open or during • sensory stimulation & in infants. • Recorded at the frontal region. • Produced by activation of RAS.
- 39. Waves of EEG 3. Theta waves • Regular & rhythmic i.e synchronized (4-7 cycles/second). • Recorded in adults when early sleep stages), children. • Recorded most marked in the temporal & parietal regions. • Amplitude: 100 mirovolt. 4. Delta waves • Frequency (0.5-4 c/sec.). • Recorded during deep sleep & in brain damage. • Amplitude: 100 mirovolt. • Produced by cortical neurons.
- 40. Brain Activity
- 41. Characterization of the EEG delta (∆): deep sleep, coma. theta (θ): sleep, childhood alpha (α): adult, awake, relaxed, eyes closed, especially over occipital cortex beta (β): awake, alert, aroused, excitement (and REM sleep) infants
- 42. Arousal or alerting response (Alpha block) • Synchronized alpha waves are replaced by beta waves by sensory stimuli or mental concentration on opening the eyes or when solving a problem. • It’s due to stimulation of RAS.
- 43. Clinical uses of EEG recording 1- It helps in determining the sites of tumours. 2- It helps the diagnosis of epilepsy. 3- It helps diagnosis of brain death. 4- It helps to know the stages of sleep.
- 44. SLEEP PHYSIOLOGY • REM favors more fluid thinking than NREM
- 45. Why Sleep? 1- Restore the biochemical and physiological processes of the brain 2- Help brain plasticity necessary for memory State of unconsciousness from which a person can be aroused by sensory stimuli. What is the Sleep?
- 46. Optimum Sleep Required The bigger the animal, the less sleep needed
- 47. How Much Sleep? 1. Newborns : 16 to 18 hours 2. By age 1 : 13 to 14 hours 3. Teenagers : < 9 ½ hours 4. Adults : 8 hours and 20 minutes 5. Seniors : 8 hours
- 48. Sleep – two types Slow-wave sleep (SWS) REM (rapid eye movement sleep), aka paradoxical sleep
- 49. Mechanism of sleep Sleep results from depression of cerebral cortex due to Active inhibition of RAS by: some sleep centres a. Serotonin secreted by raphe nuclei in medulla & lower pons. b. posterior hypothalamus increasing slow wave sleep & REM sleep. c. discharge of cholinergic neurons in pontine reticular formation during REM sleep. d. discharge of noradrenergic neurons in locus ceruleus. e. Some areas in nucleus of tractus solitarius. F. Suprachiasmatic nucleus
- 50. Types of Sleep Types of Sleep Non rapid eye movement (non REM sleep or slow wave sleep) Rapid eye movement (REM) sleep or paradoxical sleep. Occurrence: at start of sleep 80% Duration/ night’s sleep After 4th stage of non REM. 20% About 90 minutes. Duration / cycle About 20 minutes. Eye deviate up & miosis Eye movements Rapid eye movements. Stage1: theta waves Stage 2: appearance of sleep spindles (light sleep) (alternating alpha and theta waves) Stage 3: low frequency & High amplitude delta waves (moderate sleep). Stage4 : very slow large delta Waves (deep sleep). EEG recording Irregular fast low voltage Waves resemble that seen in Alert state Present Sleep talking & walking Absent Absent Dreams & penile erection Present Decrease HR, resp rate & ABP Increase Decrease Ms tone Markedly decreased due to activation of inhibitory reticular area Low Threshold of awaking High
- 51. Coordination of Circadian Rhythms and Sleep
- 52. Sleep Spindles Spindles are caused by activity in the thalamus. It's suspected that when spindles occur, the thalamus is attempting to block brain signals— prompted from external stimuli such as the sound of a crying baby—from reaching other areas of the brain that might disturb sleep.
- 53. 1 2 3 4 5 6 7 8 4 3 2 1 REM AWAKE SleepStages Hours of Sleep REM Stage NREM Normal Sleep Patterns in Young AdultsNormal Sleep Patterns in Young Adults
- 54. REM Sleep • REM: rapid-eye movement • lots of brain activity - EEG shows low voltage fast waves • postural muscles are most relaxed during REM sleep • loose associative thinking • PGO waves - start in the pons → geniculate nucleus of thalamus → occipital cortex
- 55. Metabolic theory of Sleep Sleep-inducing endogenous chemicals: Sleep-inducing peptide (DSIP) - >7 amino acid peptide, high levels after sleep deprivation.
- 56. Thank you!
- 58. Limbic System
- 61. Hippocampal circuit cortex limbic structure hypothalamus thalamus mammillary nuclei hippocampus anterior nucleus cingulate/PHG entorhinal fornix Papez circuit!! mammillo- thalamic tract
- 62. Papez circuit Hippocampus Mammillary body anterior nucleus of the thalamus Cingulate Gyrus Parahippocampal Gyrus Mammillothalamic tract Fornix
- 63. Functions of limbic system:- 1. Olfaction perception & discrimination of olfactory senses. 2. Control of feeding behaviour. Lesions in anygdala → hyperphagia & amniphagia in animals. 3. Control of sexual behviour. Lesions in amygdala → hypersexuality in ♂ animals Leasions in ant hypoth → abolish estrus in ♀ animals. 4. Control of maternal behaviour. Lesions in cingulated gyrus → depress maternal behaviour.
- 64. Functions of limbic system:- 5. Control of emotions i.e fear, rage & placidity. Emotions are feelings associated with autonomic & endocrinal responses. Fear. Is caused by stimulation of amygdaloid nuclei and stim of hypoth. (periventricular nuclei) & Abolished by destruction of amygdala. Rage = violent anger to minor stimuli. It is caused by: Stim of ventromedial nucleus of hypoth. (placidity area). Bilateral destruction of amygdaloid nuclei.
- 65. Functions of limbic system:- 6. Motivation. It is the force that activates a certain behavior to achieve a goal. Stim of the reward system → the subject is motivated to perform tasks & has a sense of pleasure & relaxation. Stim of the punishment system→ the subject feels fear & displeasure & is motivated to avoid the punishment experience. It is present in the lateral portion of the posterior hypoth. Dopamine is the main chemical transmitter in the reward system. Cocaine gives the sense of the well being by ++ the dopamine.
- 66. The Limbic System Electrode implanted in reward center
- 67. Functions of limbic system:- 7. Memory. It is important in storage & consolidation of memory. 8. Learning. It is important in operant conditioning.
Editor's Notes
- #54: Adapted from Berger RJ. The sleep and dream cycle. In: Kales A, ed. Sleep Physiology & Pathology: A Symposium. Philadelphia: J.B. Lippincott; 1969. Used by permission of Lippincott Williams & Wilkins. Breakdown of total time at each stage Stage 1: 5% Stage 2: 50% Stages 3, 4: 20% REM: 20%-25%
- #62: Consider hippo circuit—output via fornix to hypothal, specifically mamm—remember we said mam involved in memory—then info relayed to ant nuc of thal by mamm-thalam tract, thence to cing cortex and through entorhinal back to hippo. Also, intimate connections between hippo and amygdala—allowing for influence of emotions on learning— This is papez circuit—he got circuit right but messed up on function—not really emotion, but is important in laying down of new declarative memories.