Central Nervous System PDF

CENTRAL NERVOUS SYSTEM Dr. Adebayo-Gege EEG  Introduction  Significance  Method of recording  Waves of EEG  Physiology of sleep  EEG during sleep Electroencephalography  is the study of electrical activities of brain.  Electroencephalogram (EEG) is the graphical recording of electr...

CENTRAL NERVOUS SYSTEM Dr. Adebayo-Gege EEG  Introduction  Significance  Method of recording  Waves of EEG  Physiology of sleep  EEG during sleep Electroencephalography  is the study of electrical activities of brain.  Electroencephalogram (EEG) is the graphical recording of electrical activities of brain.  Electrical activity of the brain is complicated when compared to that of a single nerve fiber or neuron.  It is due to the involvement of large number of neurons and synapses.  German psychiatrist Hans Berger was the first one to analyze the EEG waves systematically and hence the EEG waves are referred as Berger waves  is a test used to evaluate the electrical activity in your brain. It can help detect potential problems with brain cell communication.  Electroencephalogram is useful in the diagnosis of neurological disorders and sleep disorders.  EEG pattern is altered in the following neurological disorders:  1. Epilepsy, which occurs due to excessive discharge of impulses from cerebral cortex  2. Disorders of midbrain affecting ascending reticular activating system  3. Subdural hematoma during which there is collection of blood in subdural space over the cerebral cortex. Other functions o Brain tumours o Brain damage from head injury o Brain dysfunction that can have a variety of causes (encephalopathy) o Sleep disorders o Inflammation of the brain (herpes encephalitis) o Stroke o Creutzfeldt-Jakob disease Types of EEG Test Routine EEG Prolonged EEG This may take only 20 to 30 minutes, and is This test usually takes one to two hours, but it can done with standard “activation procedures” last several days if more information about brain that increase the chance of capturing seizure- waves is needed. With a prolonged EEG, it is like discharges or even seizures. The most common to use video to see and hear what common are photic stimulation, happens during unusual brain activity. hyperventilation. and sleep deprivation, Sleep EEG Ambulatory EEG A technician performs an EEG while a patient The patient wears a small, portable device, is asleep, usually over several hours. A sleep connected to electrodes on their scalp, for one EEG provides more information than a to three days. The device records the brain’s routine EEG and is done during a sleep study electrical activity as they go about their daily to evaluate symptoms of a sleep disorder. activities, either awake or asleep. An ambulatory EEG provides more details about your brain activity during a patient’s daily life METHOD OF RECORDING EEG  Electroencephalograph is the instrument used to record EEG.  The electrodes called scalp electrodes from the instrument are placed over unopened skull or over the brain after opening the skull or by piercing into brain.  Electrodes are of two types,  unipolar  bipolar electrodes.  While using bipolar electrodes, both the terminals are placed in different parts of brain.  When unipolar electrodes are used, the active electrode is placed over cortex and the indifferent electrode is kept on some part of the body away from cortex. WAVES OF EEG  Electrical activity recorded by EEG may have synchronized or desynchronized waves.  Synchronized waves are the regular and invariant waves, whereas desynchronized waves are irregular and variant.. Frequency bands  In normal persons, EEG has three frequency bands  1. Alpha rhythm  2. Beta rhythm  3. Delta rhythm.  In addition to these three types of waves,  EEG in children shows theta waves ALPHA RHYTHM  Made of rhythmical waves, which appear at a frequency of 8 to 12 waves/second with the amplitude of 50 µV.  Alpha waves are synchronized waves. Alpha rhythm is obtained in inattentive brain or mind as in drowsiness, light sleep or narcosis with closed eyes.  It is abolished by visual stimuli or any other type of stimuli or by mental effort. So, it is diminished when eyes are opened Alpha Block  Alpha block is the replacement of synchronized alpha waves in EEG by desynchronized and low voltage waves when the eyes are opened. The desynchronized waves do not have specific frequency. It occurs due to any form of sensory stimulation or mental concentration, such as solving arithmetic problems.  Desynchronization is the common term used for replacement of regular alpha  BETA RHYTHM  „Beta rhythm includes high frequency waves of 15 to 60 per second but, the amplitude is low, i.e. 5 to 10 µV.  Beta waves are desynchronized waves. Beta rhythm  is recorded during mental activity or mental tension or  arousal state. It is not affected by opening the eyes.  During higher mental activity or peak performance  Some controversy exists in naming such waves.  Often very high frequency waves are called gamma rhythm. However, many scientists consider these waves as beta rhythm.  „DELTA RHYTHM  Delta rhythm includes waves with low frequency and high amplitude.  These waves have the frequency of 1 to 5 per second with the amplitude of 20 to 200 µV. It is common in early childhood during waking hours.  In adults, it appears mostly during deep sleep.  Presence of delta waves in adults during THETA WAVES  Theta waves are obtained generally in children below 5 years of age.  These waves are of low frequency and low voltage waves.  Frequency of theta waves is 4 to 8 per second and the amplitude is about 10 µV. Physiology of sleep  Sleep is the natural periodic state of rest for mind and body with closed eyes characterized by partial or complete loss of consciousness.  Loss of consciousness leads to decreased response to external stimuli and decreased body movements.  Depth of sleep is not constant throughout the sleeping period. It varies in different stages of sleep. „ SLEEP REQUIREMENT  Sleep requirement is not constant. However, average sleep requirement per day at different age groups is:  1. Newborn infants : 18 to 20 hours  2. Growing children : 12 to 14 hours  3. Adults : 7 to 9 hours  4. Old persons : 5 to 7 hours  PHYSIOLOGICAL CHANGES DURING SLEEP  During sleep, most of the body functions are reduced to basal level. Following are important changes in the body during sleep: „  1. PLASMA VOLUME  Plasma volume decreases by about 10% during sleep. „  2. CARDIOVASCULAR SYSTEM  Heart Rate During sleep, the heart rate reduces. It varies between 45 and 60 beats  3. RESPIRATORY SYSTEM  Rate and force of respiration are decreased. Respiration becomes irregular and Cheyne-Stokes type of periodic breathing may develop. „  4. GASTROINTESTINAL TRACT  Salivary secretion decreases during sleep. Gastric secretion is not altered or may be increased slightly.  Contraction of empty stomach is more vigorous. „  5. EXCRETORY SYSTEM  Formation of urine decreases and specific gravity of urine increases  6. SWEAT SECRETION Sweat secretion increases during sleep. „  7. LACRIMAL SECRETION Lacrimal secretion decreases during sleep.  „8. MUSCLE TONE  Tone in all the muscles of body except ocular muscles decreases very much during sleep. It is called sleep paralysis. „  9. REFLEXES  Certain reflexes particularly knee jerk, are abolished.  Babinski sign becomes positive during deep sleep.  Threshold for most of the reflexes increases. Pupils are constricted. Light reflex is retained. Eyeballs move up and down. „  10. BRAIN  Brain is not inactive during sleep.  There is a characteristic cycle of brain wave activity during sleep with irregular intervals of dreams.  Electrical activity in the brain varies with stages of sleep TYPES OF SLEEP  Sleep is of two types:  1. Rapid eye movement sleep or REM sleep  2. Non-rapid eye movement sleep, NREM sleep or non-REM sleep RAPID EYE MOVEMENT SLEEP – REM SLEEP  Rapid eye movement sleep is the type of sleep associated with rapid conjugate movements of the eyeballs, which occurs frequently.  Though the eyeballs move, the sleep is deep. So, it is also called para doxical sleep.  It occupies about 20% to 30% of sleeping period.  Functionally, REM sleep is very important NON-RAPID EYE MOVEMENT SLEEP – NREM OR NON-REM SLEEP  Non-rapid eye movement (NREM) sleep is the type of sleep without the movements of eyeballs.  It is also called slow-wave sleep.  Dreams do not occur in this type of sleep and it occupies about 70% to 80% of total sleeping period.  Non-REM sleep is followed by REM sleep NON-RAPID EYE MOVEMENT SLEEP  The NREMsleep is divided into four stages, based on the EEG pattern.  During the stage of wakefulness, i.e. while lying down with closed eyes and relaxed mind, the alpha waves of EEG appear.  When the person proceeds to drowsy state, the alpha waves diminish Stages  Stage I:  Stage of Drowsiness  Alpha waves are diminished and abolished. EEG shows only low voltage fluctuations and infrequent delta waves.  Stage II:  Stage of Light Sleep  Stage II is characterized by spindle bursts at a frequency of 14 per second, superimposed by low voltage delta waves  Stage III:  Stage of Medium Sleep During this stage, the spindle bursts disappear. Frequency of delta waves decreases to 1 or 2 per second and amplitude increases to about 100 µV.  State IV: Stage of Deep Sleep Delta waves become more prominent with low frequency and high amplitude MECHANISM OF SLEEP  Sleep occurs due to the activity of some sleep-inducing centers in brain.  Stimulation of these centers induces sleep.  Damage of sleep centers results in sleeplessness or persistent wakefulness called insomnia. „ SLEEP CENTERS  Complex pathways between the reticular formation of brainstem, diencephalon and cerebral cortex are involved in the onset and maintenance of sleep.  However, two centers which induce sleep are located in brainstem:  1. Raphe nucleus  2. Locus ceruleus of pons.  Recently, many more areas that induce sleep are identified in the brain of animals.  Inhibition of ascending reticular activating system also results in sleep.  1. Role of Raphe Nucleus Raphe nucleus is situated in lower pons and medulla.  Activation of this nucleus results in non- REM sleep. It is due to release of serotonin by the nerve fibers arising from this nucleus. Serotonin induces non-REM sleep.  2. Role of Locus Ceruleus of Pons Activation of this center produces REM sleep.  Noradrenaline released by the nerve fibers arising from locus ceruleus induces REM  Ascending reticular activating system (ARAS) is responsible for wakefulness because of its afferent and efferent connections with cerebral cortex. Inhibition of ARAS induces sleep.  Lesion of ARAS leads to permanent somnolence, i.e. coma  Applied Physiology  „1. INSOMNIA  Insomnia is the inability to sleep or abnormal wakefulness.  It is the most common sleep disorder.  It occurs due to systemic illness or mental conditions such as psychiatric problems, alcoholic addiction and drug addiction. „  2. HYPERSOMNIA  Hypersomnia is the excess sleep or excess need to sleep.  3. NARCOLEPSY AND CATAPLEXY Narcolepsy is the sudden attack of uncontrollable sleep.  Cataplexy is sudden outburst of emotion. Both the diseases are due to hypothalamic disorders 4. SLEEP APNEA SYNDROME  Sleep apnea is the temporary stoppage of breathing repeatedly during sleep. Sleep apnea syndrome is the disorder that involves fluctuations in the rate and force of respiration during REM sleep with short apneic episode.  Apnea is due to decreased stimulation of respiratory centers, arrest of diaphragmatic movements, airway 5. NIGHTMARE  Nightmare is a condition during sleep that is characterized by a sense of extreme uneasiness or discomfort or by frightful dreams. Discomfort is felt as of some heavy weight on the stomach or chest or as uncontrolled movement of the body. After a period of extreme anxiety, the subject wakes with a troubled state of mind. It occurs mostly during REM sleep.  Nightmare occurs due to improper food intake, digestive disorders or nervous NIGHT TERROR  Night terror is a disorder similar to nightmare.  It is common in children.  It is also called pavor nocturnus or sleep terror. The child awakes screaming in a state of fright and semiconsciousness.  The child cannot recollect the attack in the morning. Nightmare occurs shortly after falling asleep and during non-REM sleep. There is no psychological  7. SOMNAMBULISM  Somnambulism is getting up from bed and walking in the state of sleep.  It is also called walking during sleep or sleep walking (somnus = sleep; ambulare = to walk). It varies from just sitting up in the bed to walking around with eyes open and performing some major complex task.  The episode lasts for few minutes to half an hour. It occurs during non-REM sleep.  In children, it is associated with bedwetting or night terror without any psychological  NOCTURNAL ENURESIS Nocturnal enuresis is the involuntary voiding of urine at bed. It is also called or bedwetting. It is common in children. Refer Chapter 57 for details.  „9. MOVEMENT DISORDERS DURING SLEEP Movement disorders occur immediately after falling asleep. Sleep start or hypnic jerk is the common movement disorder during sleep. It is characterized by sudden jerks of arms or legs. Sleep Epilepsy  Epilepsy is a brain disorder characterized by convulsive seizures or loss of consciousness or both.  Convulsion and Convulsive Seizure  Convulsion refers to uncontrolled involuntary muscular contractions.  Convulsive seizure means sudden attack of uncontrolled involuntary muscular contractions.  It occurs due to paroxysmal (sudden and  Epileptic attack develops only when excitability of the neuron is increased, causing excessive neuronal discharge. „ TYPES OF EPILEPSY  Epilepsy is divided into two categories:  1. Generalized epilepsy  2. Localized epilepsy. GENERALIZED EPILEPSY  Generalized epilepsy is the type of epilepsy that occurs due to excessive discharge of impulses from all parts of the brain.  It is also called general onset seizure or general onset epilepsy.  Generalized epilepsy is subdivided into three types:  1. Grand mal  2. Petit mal GRAND MAL  Grand mal is characterized by sudden loss of consciousness, followed by convulsion.  Just before the onset of convulsions, the person feels the warning sensation in the form of some hallucination.  It is called epileptic aura.  Convulsions occur in two stages:  a. Tonic stage  b. Clonic stage. Tonic Stage  Initially, seizure is characterized by tonic contractions of muscle leading to spasm. Spasm causes twisting facial features, flexion of arm and extension of lower limbs Clonic Stage  Clonic convulsions develop after the tonic stage.  This stage is characterized by violent jerky movements of limbs and face due to alternate severe contraction and relaxation of muscles.  At the end of attack, alternative tonic and clonic convulsions are seen.  During the entire period of seizure, tongue may be bitten.  Electroencephalogram (EEG) shows fast waves with a frequency of 15 to 30 per second during tonic stage. Slow and large waves appear during clonic phase. After the attack, slow waves are recorded for some time.  In between seizures, EEG shows delta waves in all types of epileptics. Causes of Grand Mal  Cause of grand mal epilepsy is the excess neural activity in all parts of brain.  Cause for stoppage of attack is neuronal fatigue.  Factors which accelerate the neural activity resulting in grand mal epilepsy are:  i. Strong emotional stimuli  ii. Hyperventilation and alkalosis  iii. Effects of some drugs  iv. Uncontrolled high fever PETIT MAL  In this type of epilepsy, the person becomes unconscious suddenly without any warning.  The unconsciousness lasts for a very short period of 3 to 30 seconds.  Convulsions do not occur. However, the muscles of face show twitchlike contractions and there is blinking of eyes.  Afterwards, the person recovers automatically and becomes normal.  Causes of Petit Mal  Cause of petit mal is not known. It occurs in conditions like head injury, stroke, brain tumor and brain infection. „ PSYCHOMOTOR EPILEPSY  Psychomotor epilepsy is characterized by emotional outbursts such as abnormal rage, sudden anxiety, fear or discomfort.  There is amnesia or a confused mental state for some period. Some persons have the tendency to attack others bodily or rub their own face vigorously. In most cases, the persons are not aware of their activities. Some persons are very well aware of the actions, but still the abnormal actions cannot be controlled. Causes of Psychomotor Epilepsy  Causes of psychomotor epilepsy are the abnormalities  in temporal lobe and tumor in hypothalamus and  other regions of limbic system like amygdala and  hippocampus. „ „LOCALIZED EPILEPSY  Epilepsy that occurs because of excessive discharge of impulses from one part of brain is called localized epilepsy.  It is otherwise known as local or focal epilepsy or local seizure. It involves only a localized area of cerebral cortex or the deeper parts of cerebellum, which are affected by tumor, abscess or vascular defects.  The abnormality starts from a particular Causes of Localized Epilepsy  Localized epilepsy is caused by brain tumor Day 2  Introduction „  histology of cerebral cortex  layers of cerebral cortex  parts of cerebral cortex  lobes of cerebral cortex  cerebral dominance  Cerebral dominance and handedness  brodmann areas  frontal lobe Cerebral Cortex  Cerebral cortex is also called pallidum and it consists of two hemispheres. Surface area of cerebral cortex in human beings is 2.2 sq m.  Both the cerebral hemispheres are separated by a deep vertical fissure (deep furrow or groove).  The Separation is complete anteriorly and posteriorly. But in middle portion, the fissure extends only up to corpus callosum.  Corpus callosum is the broad band of commissural fibers, connecting the two hemispheres.  Surface of the cerebral cortex is characterized by complicated pattern of sulci (singular = sulcus) and Sulcus is a  Histology of brain  „LAYERS OF CEREBRAL CORTEX Cerebral cortex consists of gray matter that surrounds the deeper white matter. It is formed by different types of nerve cells along with their processes and neuroglia. It is not uniform throughout. It is thickest, i.e. 4.5 cm at the precentral gyrus and thinnest at frontal and occipital poles. The cerebral cortex is formed by six layers of structures. Following are the layers from 2. External Granular Layer External granular layer consists of large number of closely packed small cells, which are round, polygonal or triangular in shape. Dendrites of these cells pass into molecular layer. Axons end in the deeper layers. Some axons enter white substance of the hemisphere 3. Outer Pyramidal Layer Outer pyramidal layer is formed by pyramidal cells, which are of two sizes. Medium sized pyramidal cells are in the outer portion and larger pyramidal cells are in deeper portion  4. Internal Granular Layer Like external granular layer, this layer also has closely packed smaller cells, which are stellate type. But, the nerve fibers are more in this layer than in external granular layer. This layer contains many horizontal fibers, which appear as a white strip known as outer strip.  5. Ganglionic Layer or Internal Pyramidal Layer Ganglionic layer or internal pyramidal layer consists of pyramidal cells of graded sizes.  It is well developed in the precentral (motor) cortex.  Pyramidal cells in this region are otherwise known as Betz cells or giant cells.  This layer also contains cells of Martinotti. Martinotti cells are peculiar in that their axons pass outward towards the surface of the cortex.  6. Fusiform Cell Layer Fusiform cell layer is in contact with white matter of cere bral hemisphere. It is composed of closely packed small spindle-shaped cells PARTS OF CEREBRAL CORTEX  Cerebral cortex is divided into two parts based on phylogeny (evolutionary development of a species):  1. Neocortex  2. Allocortex.. Neocortex  Neocortex is the phylogenetically new structure of cerebral cortex. It is also called isocortex or neopallium.  This part forms the major portion of cerebral cortex. Part of the cerebral cortex that has all six layers of structures is called neocortex.  2. Allocortex Allocortex is the phylogenetically oldest structure of cerebral cortex. It has less than six layers of structures. It is divided into two divisions namely, archicortex and paleocortex, which form the parts of limbic system LOBES OF CEREBRAL CORTEX  In each hemisphere, there are three surfaces lateral, medial and inferior surfaces.  Neocortex of each cerebral hemisphere consists of four lobes  1. Frontal lobe  2. Parietal lobe  3. Occipital lobe  4. Temporal lobe.  Lobes of each hemisphere are demarcated by four main fissures and sulci:  1. Central sulcus or Rolandic fissure between frontal and parietal lobe  2. Parieto-occipital sulcus between parietal and occipital lobe  3. Sylvian fissure or lateral sulcus between parietal and temporal lobes  4. Callosomarginal fissure between temporal lobe and limbic area. CEREBRAL DOMINANCE  Cerebral dominance is defined as the dominance of one cerebral hemisphere over the other in the control of cerebral functions.  Both the cerebral hemispheres are not functionally equivalent. Some functional asymmetries are well known. „ CEREBRAL DOMINANCE AND HANDEDNESS  Cerebral dominance is related to handedness, i.e. preference of the individual to use right or left hand.  More than 90% of people are right handed. In these individuals, the left hemisphere is dominant and it controls the analytical process and language related functions such as speech, reading and writing.  Hence, left hemisphere of these persons is called dominant or categorical hemisphere.  Right hemisphere is called representational hemisphere since it is associated with artistic and visuospatial functions like judging the distance, determining the direction, recognizing the tones, etc.  Lesion in dominant hemisphere leads to language disorders.  Lesion in representational hemisphere causes only mild effects like astereognosis.  Left hemisphere is the dominant hemisphere in about 75% of the right-handed persons.  In the remaining left-handed persons, right hemisphere controls the language function.  Some of these persons do not have dominant hemisphere. „ CytoArchitecture :Broadmann area  Brodmann area is a region of cerebral cortex defined on the basis of its cytoarchitecture.  Cytoarchitecture means organization of cells. Brodmann areas were originally defined and numbered in 1909 by Korbinian Brodmann depending upon the laminar organization of neurons in the cortex.  Some of these areas were given specific names based on their functions.  During the period of a century Brodmann areas had been extensively discussed and renamed FRONTAL LOBE OF CEREBRAL CORTEX  Frontal lobe forms one third of the cortical surface. It extends from frontal pole to the central sulcus and limited below by the lateral sulcus.  Frontal lobe of cerebral cortex is divided into two parts:  A. Precentral cortex, which is situated posteriorly  B. Prefrontal cortex, which is situated anterior PRECENTRAL CORTEX  Precentral cortex forms the posterior part of frontal lobe.  It includes the lip of central sulcus, whole of precentral gyrus and posterior portions of superior, middle and inferior frontal gyri.  It also extends to the medial surface.  This part of cerebral cortex is also called excitomotor cortex or area, since the stimulation of different points in this area causes activity of discrete skeletal muscle.  Precentral cortex is further divided into three functional areas  1. Primary motor area  2. Premotor area  3. Supplementary motor area Primary Motor Area  1. Primary motor area extends throughout the precentral gyrus and the adjoining lip of central sulcus.  Areas 4 and 4S are present here.  Structure of primary motor area Though this area has all the six layers, the granular layer is thin.  Special structural feature of this layer is the presence of giant pyramidal cells called Betz cells in ganglionic layer. Connections of primary motor area  Efferent connections  i. Fibers of pyramidal tracts arise from the Betz cells. These fibers synapse with motor neurons in anterior gray horn of opposite side (few fibers reach the same side motor neurons) in spinal cord  ii. Frontopontine fibers from this area reach pontine nuclei of same side  iii. Fibers are also projected to corpus striatum, red nucleus, thalamus, subthalamus and reticular formation  iv. Association fibers connect the primary motor area to other areas of cortex.  Afferent connections  Primary motor area receives fibers from dentate nucleus (cerebellum) via red nucleus and thalamus Functions of primary motor area  Primary motor area is concerned with initiation of voluntary movements and speech.  Area 4 It is a tapering strip of area situated in precentral gyrus of frontal lobe.  Broad end lies superiorly at the upper border of hemisphere and most of the efferent fibers of primary motor area arise from this area Function of area 4  Area 4 is the center for movement, as it sends all efferent (corticospinal) fibers of primary motor area.  Through the fibers of corticospinal tracts, area 4 activates the lower motor neurons in the spinal cord.  It activates both α-motor neurons and γ- motor neurons simultaneously by the process called coactivation  Activation of α-motor neurons causes contraction of extrafusal fibers of the muscles.  Activation of γ-motor neurons causes contraction of intrafusal fibers leading to increase in muscle tone. Effect of stimulation of area 4  Electrical stimulation of area 4 causes discrete isolated movements in the opposite side of the body.  The groups of muscles or single isolated muscle may be activated depending upon the area stimulated Localization – homunculus  Muscles of various parts of the body are represented in area 4 in an inverted way from medial to lateral surface.  Lower parts of body are represented in medial surface and upper parts of the body are represented in the lateral surface.  Order of representation from medial to lateral surface: Toes, ankle, knee, hip, trunk, shoulder, arm, elbow, wrist, hand fingers and face. However, parts of the face are not represented in inverted manner  Area 4 is concerned with contraction of discrete muscles.  It sends motor signals to the facial muscles of both sides (bilateral) and the other muscles of the opposite side (contralateral). Lesion of Area 4  Effect of lesion or ablation of area 4 differs in different species.  In cats, the ability to walk is not affected.  In monkeys, there is contralateral flaccid paralysis, hypotonia and loss of reflexes.  Myotatic reflexes(are stretch reflexes that cause muscle contraction after the muscle is stretched). These are local reflex arcs that are used for body posture...) reappear in a short time.  Recovery occurs only in proximal parts of limbs but the digits remain permanently paralyzed.  In man, the symptoms are severe than in monkeys.  In unilateral lesion, paralysis occurs in contralateral side.  Complete paralysis is rare. If both sides are affected, the effect is more severe.  Recovery occurs very slowly.  During recovery, upper parts of body recover first. If area 4 is affected along with area 6, the effect is very severe, causing hemiplegia with spastic paralysis.  Hemiplegia means the paralysis in one half of the body. In spastic paralysis, the muscles undergo spastic contraction due to increased muscle tone. Area 4S  Area 4S is also called suppressor area.  It forms a narrow strip anterior to area 4. It scrutinizes and suppresses the extra impulses produced by area 4 and inhibits exaggeration of movements Premotor Area  Premotor area includes areas 6, 8, 44 and 45.  The premotor area is anterior to primary motor area in the precentral cortex.  The premotor area is concerned with control of postural movements by sending motor signals to axial muscles (muscles near the midline of the body). Structure of premotor area  Premotor area is similar to primary motor area in structure except for the absence of giant pyramidal cells in ganglionic layer. Area 6  is in the posterior portions of superior, middle and inferior frontal gyri.  It is subdivided into 6a and 6b.  It gives origin to some of the pyramidal tract fibers.  The other connections are similar to those of area 4. Functions of area 6  i. It is concerned with coordination of movements initiated by area 4.  It helps to make the skilled movements more accurate and smooth.  ii. It is believed to be the cortical center for extrapyramidal system. Effect of stimulation of area 6  Electrical stimulation of area 6a in human being causes the same effects as the stimulation of area 4. However, the stimulus must be stronger to evoke response from area 6.  The effects of stimulation of this area are:  i. Stimulation of area 6a causes generalized pattern of movements like rotation of head, eyes and trunk towards the opposite side  ii. Stimulation of 6b produces rhythmic, complex coordinated movements involving the muscles of face, buccal cavity, larynx and pharynx. Effect of lesion of area 6  Lesion or removal of area 6 in monkeys leads to loss of skilled movements.  After the lesion, the recovery may occur; but the movements become awkward. It also produces grasping reflexes.  Lesion involving areas 6 and area 4 produces severe symptoms of hemiplegia with spastic paralysis. Area 8  It is called frontal eye field.  It lies anterior to area 6 in the precentral cortex. It is concerned with movements of eyeball.  This area receives afferent fibers from dorsomedial nucleus of thalamus and occipital lobe. It sends efferent fibers to oculomotor nuclei in tegmentum of midbrain. Function of area 8  Frontal eye field is concerned with conjugate movement of eyeballs  This area initiates voluntary scanning movements of eyeballs and it is independent of visual stimuli.  It is also responsible for opening and closing of eyelids, pupillary dilatation and lacrimation. Effect of stimulation of area 8  Stimulation of this area causes conjugate movements of eyeballs to the opposite side.  Effect of lesion of area 8  Lesion of this area turns the eyes to the affected side.  Conjugate movements of eyes are lost.  However, pupils and eyelids are not affected.  In animals, while walking, circular movements occur towards the affected side.  Broca area  Broca area is the motor area for speech. It includes areas 44 and 45.  Broca area is present in left hemisphere (dominant hemisphere) of right-handed persons and in the right hemisphere of left- handed persons.  It is a special region of premotor cortex situated in inferior frontal gyrus.  Area 44 is situated in pars triangularis and 45 in pars opercularis of this gyrus.  effect of lesion of Broca area Lesion in Broca area leads to aphasia 3. Supplementary Motor Area . Supplementary motor area is situated in medial surface of frontal lobe rostral to primary motor area.  Various motor movements are elicited by electrical stimulation of this area like raising the contralateral arm, turning the head and eye and movements of synergistic muscles of trunk and legs function of supplementary motor area  It is suggested that it is concerned with coordinated skilled movements. Although its exact function is still under investigation  Effect of lesion of supplementary motor area  During lesion in this area of human being, the head and eyeballs turn towards the affected side.  Destruction of this area in monkeys causes weak grasping reflexes in contralateral side and bilateral hypertonia of shoulder muscles. But, paralysis is not noticed. „  PREFRONTAL CORTEX OR ORBITOFRONTAL CORTEX  Prefrontal cortex is the anterior part of frontal lobe of cerebral cortex, in front of areas 8 and 44.  It occupies the medial, lateral and inferior surfaces and includes orbital gyri, medial frontal gyrus and the anterior portions of superior, middle and inferior frontal gyri.  Areas present in prefrontal cortex are 9, 10, 11, 12, 13, 14, 23, 24, 29 and 32. Areas 12, 13, 14, 23, 24, 29 and 32 are in medial surface  Areas 9, 10 and 11 are in lateral surface. Connections of Prefrontal Cortex  Afferent fibers  Afferent fibers of prefrontal cortex come from:  1. Dorsomedial nucleus of thalamus  2. Hypothalamus  3. Corpus striatum  4. Amygdala  5. Midbrain.  Areas 23, 24, 29 and 32 receive fibers from anterior nucleus of thalamus.  Area 32 receives fibers from suppressor area of precentral cortex also.  Efferent fibers  Efferent fibers are projected to:  1. Thalamus  2. Hypothalamus  3. Tegmentum  4. Caudate nucleus  5. Pons  6. Temporal lobe of cerebral cortex.  Area 13, along with hippocampus, uncus and amygdala sends fibers to mamillary body of hypothalamus via fornix.  This area is concerned with emotional reactions Functions of Prefrontal Cortex  this area used to be considered as inexcitable to electrical stimulation.  Hence, it was called the silent area or association area.  it has been discovered that it can be stimulated by low voltage electrical stimulus  It causes changes in the activity of digestive, cardiovascular, respiratory and excretory systems and other autonomic functions.  It also causes fear.  Various functions of prefrontal cortex are: 1. It forms the center for the higher functions like emotion, learning, memory and social behavior.  Short-term memories are registered here.  2. It is the center for planned actions  3. This area is the seat of intelligence; so, it is also called the organ of mind  4. It is responsible for the personality of the individuals  5. Prefrontal cortex is responsible for the various autonomic changes during emotional conditions, because of its connections with hypothalamus and brainstem. Effect of Lesion of Prefrontal Cortex  Bilateral lesion or removal of prefrontal cortex in human beings does not cause paralysis.  It causes lack of initiation and loss of mental alertness.  Very little or no change occurs in memory, judgment and intelligence Content Content  Higher intellectual functions  facilitating memory  applied physiology  learning  conditioned reflexes  definition  definition  classification  classification and their properties physiological basis of conditioned reflexes  memory   speech  anatomical basis  definition  Physiological basis  mechanism  chemical or molecular basis  development nervous control consolidation  applied physiology  aphasia  classification  dysarthria or anarthria  drugs  dysphonia   stammering Day 3 Higher intellectual function  Higher intellectual functions are very essential/important to make up the human mind.  These functions are also called higher brain functions or higher cortical functions.  The extensive outer layer of gray matter in cerebral cortex is responsible for higher intellectual functions.  Conditioned reflex forms the basis of all higher intellectual functions Learning  Learning is defined as the process by which new information is acquired. It alters the behavior of a person on the basis of past experience. „  CLASSIFICATION OF LEARNING  Learning is classified into two types:  1. Non-associative learning  2. Associative learning.  1. Non-associative Learning  Non-associative learning involves response of a person to only one type of stimulus.  It is based on two factors:  i. Habituation  ii. Sensitization.  i. Habituation  Habituation means getting used to something, to which a person is constantly exposed.  When a person is exposed to a stimulus repeatedly, he starts ignoring the stimulus slowly.  During first experience, the event (stimulus) is novel and evokes a response.  However, it evokes less response when it is repeated.  Finally, the person is habituated to the event (stimulus) and ignores it. ii. Sensitization   Sensitization is a process by which the body is made to become more sensitive to a stimulus. It is called amplification of response.  When a stimulus is applied repeatedly, habituation occurs. But, if the same stimulus is combined with another type of stimulus, which may be pleasant or unpleasant, the person becomes more sensitive to original stimulus.  For example, a woman is sensitized to crying sound of her baby. She gets habituated to different sounds around her and sleep is not disturbed by these sounds.  However, she suddenly wakes up when her baby cries because of sensitization to crying sound of the baby. Thus, sensitization increases the response to an innocuous stimulus when that stimulus is applied after another type of stimulus.  2. Associative Learning  Associative is complex and deep process  It involves learning about relations between two or more stimuli at a time. Classic example of associative learning is the conditioned reflex MEMORY  It is defined as the ability to recall past experience or information.  It is also defined as retention of learned materials.  There are various degrees of memory.  Some memories remain only for few seconds, while others last for hours, days, months or even years together. ANATOMICAL BASIS OF MEMORY  Anatomical basis of memory is the synapse in brain.  Synapse for memory coding is slightly different from other synapses.  Two separate presynaptic terminals are present here.  One of the terminals is primary presynaptic terminal, which ends on postsynaptic neuron as in conventional synapse. This terminal is called sensory terminal, because sensations are transmitted to the postsynaptic neuron through this terminal  Other presynaptic terminal ends on the sensory terminal itself.  This terminal is called facilitator terminal.  When, sensory terminal is stimulated alone without facilitator terminal, the firing from sensory terminal leads to habituation, i.e. the firing decreases slowly. On the other hand, if both the terminals are stimulated, facilitation occurs and the signals remain strong for long period, i.e. for few months to few years. PHYSIOLOGICAL BASIS OF MEMORY  Memory is stored in brain by the alteration of synaptic transmission between  Storage of memory may be facilitated or habituated depending upon many factors, such as neurotransmitter, synaptic transmission, functional status of brain, etc. Facilitation  Facilitation is the process by which memory storage is enhanced.  It involves increase in synaptic transmission and increased postsynaptic activity.  Often, facilitation is referred as positive memory. The process involved in facilitation of memory is called memory sensitization.  Habituation  Habituation is the process by which memory storage is attenuated (attenuation = decrease in strength, effect or value).  It involves reduction in synaptic transmission and slow stoppage of postsynaptic activity.  Sometimes, habituation is referred as negative memory. Is studied in sea snail Basis for Short-term memory  Basic mechanism of memory is the development of new neuronal circuits by the formation of new synapses and facilitation of synaptic transmission.  Number of presynaptic terminals and size of the terminals are also increased. This forms the basis of short-term memory. Basis for Long-term Memory  When neuronal circuit is reinforced by constant activity, memory is consolidated and encoded into different areas of the brain.  This encoding makes memory a permanent or a long-term memory.  Sites of Encoding Hippocampus and Papez circuit (closed circuit between hippocampus, thalamus, hypothalamus and corpus striatum) are the main sites of memory encoding  Frontal and parietal areas are also involved in memory storage.  Experimental Studies of Memory – Aplysia  Most of the experimental studies of memory and learning are based on the research carried out in the sea hare (sea snail) called Aplysia and in rats as well. CHEMICAL OR MOLECULAR BASIS OF MEMORY  Memory Engram  It can be explained by memory engram.  Memory engram is a process by which memory is facilitated and stored in the brain by means of structural and biochemical changes.  Often, it is also called memory trace. Diagram of engram Molecular Basis of Facilitation  In this process, the neurotransmitter serotonin plays major role.  Calcium ions increase the release of serotonin, which facilitates the synaptic transmission to a great extent, leading to memory storage.. Molecular basis of facilitation Molecular Basis of Habituation  Habituation is due to passive closure of calcium channels of terminal membrane.  Hence, the release of transmitter decreases, resulting in decrease in number of action potential in the postsynaptic neuron.  So, the signals become weak and weakening of signals leads to habituation CONSOLIDATION OF MEMORY  The process by which a short-term memory is crystallized into a long-term memory is called memory consolidation.  Consolidation causes permanent facilitation of synapses.  It is possible by rehearsal mechanism, i.e. rehearsal of same information again and again accelerates and potentiates the degree of transfer of short-term memory into long- term memory.  This is what happens in memorizing a poem or a phrase Classification of memory  Memory is classified by different methods, on the basis of various factors.  Short-term Memories  Long-term Memories  1. Short-term memory  Short-term memory is the recalling events that happened very recently, i.e. within hours or days. It is also known as .  Short-term memory may be interrupted by many factors such as stress, trauma, drug abuse, etc.  There is another form of short-term memory called working memory.  It is concerned with recollection of past experience for a very short period, on the basis of which an action is executed. Long-term memory  Long-term memory is the recalling of events of weeks, months, years or sometimes lifetime. It is otherwise called the remote memory.  Examples are, recalling first day of schooling, birthday celebration of previous year, picnic enjoyed last week, etc.  Long-term memory is more resistant and is not disrupted easily. Explicit and Implicit Memories  Physiologically, memory is classified into two types, namely explicit memory and implicit memory.  1. Explicit memory  Explicit memory is defined as the memory that involves conscious recollection of past experience. It consists of memories regarding events, which occurred in the external world around us.  The information stored may be about a particular event that happened at a particular time and place.  Explicit memory is otherwise known as declarative memory or recognition memory. Examples of explicit memory are recollection of a birthday party celebrated three days ago, events taken place while taking breakfast, etc.  Explicit memory involves hippocampus and medial part of temporal lobe. 2. Implicit memory  Implicit memory is defined as the memory in which past experience is utilized without conscious awareness.  It helps to perform various skilled activities properly. Implicit memory is otherwise known as non-declarative memory or skilled memory.  Examples of implicit memory are cycling, driving, playing tennis, dancing, typing, etc. Implicit memory involves the sensory and motor pathways. Memories Depending upon Duration  Depending upon duration, memory is classified into three types:  1. Sensory memory  2. Primary memory  3. Secondary memory. 1. Sensory memory  Sensory memory is the ability to retain sensory signals in sensory areas of brain, for a very short period of few seconds after the actual sensory experience, i.e. few hundred milliseconds.  But, the signals are replaced by new sensory signals in less than 1 second. It is the initial stage of memory. It resembles working memory. 2. Primary memory  Primary memory is the memory of facts, words, numbers, letters or other information retained for few minutes at a time.  For example, after searching and finding telephone number in the directory, we remember the number for a short while. After appreciating beautiful scenery, the details of it could be recalled for some time. Afterwards, it disappears from the memory . Characteristic feature of this type of memory is that the information is available for recall easily from memory store itself.  One need not search or squeeze through the mind, but this memory is easily replaced by new bits of memory, i.e. by looking into another telephone number, the first one may disappear. Secondary memory  Secondary memory is the storage of information in brain for a longer period. The information could be recalled after hours, days, months or years. It is also called fixed memory or permanent memory. It resembles long-term memory. DRUGS FACILITATING MEMORY  Several stimulants for central nervous system are shown to improve learning and memory in animals.  Common stimulants are caffeine, physostigmine, amphetamine, nicotine, strychnine and metrazol.  All these substances mentioned above facilitate the consolidation of memory Applied Physiology  ABNORMALITIES OF MEMORY  1. Amnesia Loss of memory is known as amnesia.  Amnesia is classified into two types:  i. Anterograde amnesia: Failure to establish new long-term memories. It occurs because of lesion in hippocampus.  ii. Retrograde amnesia: Failure to recall past remote long-term memory. It occurs in temporal lobe syndrome.  ( Dementia  Dementia is the progressive deterioration of intellect, emotional control, social behavior and motivation associated with loss of memory. It is an age-related disorder.  Usually, it occurs above the age of 65 years. When it occurs under the age of 65, it is called presenile dementia.  Causes  Dementia occurs due to many reasons.  Most common cause of dementia is Alzheimer disease.  In about 75% of cases, dementia is due to this disease Other common causes of dementia  hydrocephalus,  Huntington chorea,  Parkinson disease,  viral encephalitis,  HIV infection,  hypothyroidism,  hypoparathyroidism,  Cushing syndrome,  alcoholic intoxication,  poisoning by high dose of barbiturate,  carbon monoxide, heavy metals, etc.. Clinical features  Common features are loss of recent memory, lack of thinking and judgment and personality changes.  As the disease progresses, psychiatric features begin to appear.  Motor functions are also affected.  Finally, the patient has to lead a vegetative life without any thinking power.  The person is speechless and is unable to understand anything.  no effective treatment for this disorder.  Physostigmine, which inhibits cholinesterase causes moderate improvement Alzheimer Disease  Alzheimer disease is a progressive neurodegenerative disease.  It is due to degeneration, loss of function and death of neurons in many parts of brain, particularly cerebral hemispheres, hippocampus and pons.  There is reduction in the synthesis of most of the neurotransmitters, especially acetylcholine.  Synthesis of acetylcholine decreases due to lack of enzyme choline acetyltransferase.  Norepinephrine synthesis decreases because of degeneration of locus ceruleus. Dementia is the common feature of this disease Conditioned reflexes  Conditioned reflex is the acquired reflex that requires learning, memory and recall of previous experience.  It is acquired after birth and it forms the basis of learning.  Conditioned reflex is different from unconditioned reflex  Unconditioned reflex is the inborn reflex, which does not need previous experience CLASSIFICATION OF CONDITIONED REFLEXES  Conditioned reflexes are classified into two types:  A. Classical conditioned reflexes  B. Instrumental conditioned reflexes. „ CLASSICAL CONDITIONED REFLEXES  Classical conditioned reflexes are those reflexes, which are established by a conditioned stimulus, followed by an unconditioned stimulus.  Method of Study – Pavlov’s Bell-Dog  Experiments  Various types of classical conditioned reflexes and their properties are demonstrated by the classical belldog experiments (salivary secretion experiments), done by Ivan Pavlov and his associates.  In dogs, the duct of parotid gland or submandibular gland was taken outside through cheek or chin respectively and the saliva was collected by some special apparatus. Apparatus consisted of a funnel, which is sealed over the opening of the duct.  Salivary secretion was measured in drops by means of an electrical recorder TYPES AND PROPERTIES OF CLASSICAL CONDITIONED REFLEXES  Classical conditioned reflexes are classified into two groups according to the properties of reflexes, namely excitation or inhibition:  I. Positive or excitatory conditioned reflexes  II. Negative conditioned reflexes. „  POSITIVE CONDITIONED REFLEXES (EXCITATION OF CONDITIONED REFLEXES) Types of positive conditioned reflexes:  1. Primary conditioned reflex  2. Secondary conditioned reflex  3. Tertiary conditioned reflex. 1. Primary Conditioned Reflex  is the reflex developed with one unconditioned stimulus and one conditioned stimulus.  This reflex is established in the following way.  For instance ; when an individual is feed with food (unconditioned stimulus).  Simultaneously a flash of light (conditioned stimulus) is activated.  If repeated for some days  After the development of reflex, the flash of light (conditioned stimulus) alone causes salivary secretion without food (unconditioned stimulus) Secondary Conditioned Reflex  Secondary conditioned reflex is the reflex developed with one unconditioned stimulus and two conditioned stimuli.  After establishment of a conditioned reflex with one conditioned stimulus, another conditioned stimulus is applied along with the first one.  For example, the animal is fed with food (unconditioned reflex) and simultaneously a flash of light (first conditioned stimulus) and a bell sound (second conditioned stimulus) are applied.  After development of the reflex, bell sound (second conditioned stimulus) alone can cause salivary secretion. Tertiary Conditioned Reflex  In this reflex, a third conditioned stimulus is added and the reflex is established. . Many types of conditioned stimuli associated with sight and hearing were employed by Pavlov. NEGATIVE CONDITIONED REFLEXES (INHIBITION OF CONDITIONED REFLEXES)  The established conditioned reflexes can be inhibited by some factors.  The inhibition is of two types:  1. External or indirect inhibition  2. Internal or direct inhibition. 1 External or Indirect Inhibition .Established conditioned reflex is inhibited by some form of stimulus, which is quite different from the conditioned stimulus. It is not related to conditioned stimulus.  For example, some disturbing factors like sudden entrance of a stranger, sudden noise or a strong smell can abolish the conditioned reflex and inhibit salivary secretion.  This extra stimulus evokes the animal’s curiosity and distracts the attention. According to Pavlov, it evokes an investigatory reflex.  If the extra (inhibitory) stimulus is repeated for some time, its inhibitory effect gets weakened or abolished..Internal or Direct Inhibition  There are four ways in which the established conditioned reflex is abolished by direct or internal factors, which are related to the conditioned stimulus.  i. Extinction of conditioned reflex  ii. Conditioned inhibition  iii. Inhibition by delay or delayed conditioned reflex  iv. Differential inhibition Extinction of conditioned reflex  Extinction is the failure of conditioned reflex.  It occurs if an established conditioned reflex is not reinforced by unconditioned stimulus.  After establishing a conditioned reflex, the conditioned stimulus must be coupled with unconditioned stimulus now and then, i.e. the conditioned stimulus must be reinforced by unconditioned stimulus.  If a conditioned stimulus is given repeatedly several times, without reinforcing it by unconditioned stimulus, there is failure of conditioned reflex.  However, the reflex is not abolished if the unconditioned reflex is also used in between. ii. Conditioned inhibition  is the failure of conditioned reflex due to introduction of an unknown (new) conditioned stimulus.  When a conditioned stimulus like flash of light is effective, if another conditioned stimulus like a bell sound is applied along with this stimulus suddenly, the response does not occur.  Of course, if these two conditioned stimuli are given with unconditioned stimulus (food) repeatedly, the secondary conditioned reflex is developed. iii. Inhibition by delay or delayed conditioned reflex  Inhibition by delay is the absence of response or delayed response that occurs while eliciting a conditioned reflex by delaying the unconditioned stimulus.  While establishing a conditioned reflex, the conditioned stimulus (light or sound) must be followed by unconditioned stimulus (food) immediately.  If the unconditioned stimulus is applied after a long period, response may be absent or delayed.  The reflex is called delayed conditioned reflex. Differential inhibition  is the failure of conditioned reflex that occurs when the conditioned stimulus is altered.  When an animal is trained or conditioned for a particular type of conditioned stimulus and if this stimulus is altered even slightly, the response does not occur.  The animal is able to discriminate the difference. For example, the alteration in frequency of sound or intensity of light abolishes the conditioned reflex INSTRUMENTAL OR OPERANT CONDITIONED REFLEXES  Instrumental conditioned reflexes are those reflexes in which the behavior of the person is instrumental. This type of reflexes is developed by the conditioned stimulus, followed by a reward or a punishment.  The instrumental conditioned reflexes are also called operant conditioned reflexes or Skinner conditioning.  During the development of this type of reflexes, the animal is taught to perform some task, in order to obtain a reward or to avoid a punishment.  The instrumental conditioned reflexes are of several types, such as:  1. Conditioned avoidance reflex  2. Food avoidance reflex  3. Conditioned reward reflex. Conditioned Avoidance Reflex  Conditioned avoidance reflex is the reflex by which the animal is trained to avoid an electric shock, by pressing a bar Food Avoidance Conditioning  If an animal is given a tasty food along with injection of a drug, which produces nausea or sickness, the animal starts avoiding or hating that food.  It is called food aversion conditioning. Conditioned Reward Reflex  If the animal is rewarded by a banana by pressing a bar, the animal repeatedly presses the bar. It is the conditioned reward reflex. Instrumental conditioned reflexes play an important role during the learning processes of a child. These conditioned reflexes are also responsible for the behavior pattern of an individual. „  The physiological basis of conditioned reflexes is by learning and memory Speech  Speech is defined as the expression of thoughts by production of articulate sound, bearing a definite meaning.  It is one of the highest functions of brain.  When a sound is produced verbally, it is called the speech.  If it is expressed by visual symbols, it is known as writing. If visual symbols or written words are expressed verbally, that becomes reading MECHANISM OF SPEECH  Speech depends upon coordinated activities of central speech apparatus and peripheral speech apparatus.  Central speech apparatus consists of higher centers, i.e. the cortical and subcortical centers.  Peripheral speech apparatus includes larynx or sound box, pharynx, mouth, nasal cavities, tongue and lips.  All the structures of peripheral speech apparatus function in coordination with respiratory system, with the influences of motor r areas of the cerebral cortex. „ DEVELOPMENT OF SPEECH  First Stage  First stage in the development of speech is the association of certain words with visual, tactile, auditory and other sensations, aroused by objects in the external world.  Association of words with other sensations is stored as memory. Second Stage  New neuronal circuits are established during the development of speech. When a definite meaning has been attached to certain words, pathway between the auditory area (Heschl area; area 41) and motor area for the muscles of articulation, which helps in speech (Broca area 44) is established.  The child attempts to formulate and pronounce the learnt words. Role of Cortical Areas in the Development of Speech  Development of speech involves integration of three important areas of cerebral cortex:  1. Wernicke area  2. Broca area  3. Motor area. Role of Wernicke area  Understanding of speech begins in Wernicke area that is situated in upper part of temporal lobe.  It sends fibers to Broca area through a tract called arcuate fasciculus. Wernicke area is responsible for understanding the visual and auditory information required for the production of words.  After understanding the words, it sends the information to Broca area. Role of Broca area –  Speech is synthesized in the Broca area.  It is situated adjacent to the motor area, responsible for the movements of tongue, lips and larynx, which are necessary or speech.  By receiving information required for production of words from Wernicke area, the Broca area develops the pattern of motor activities required to verbalize the words.  The pattern of motor activities is sent to motor area. Role of motor area –  Activation of peripheral speech apparatus  By receiving the pattern of activities from Broca area, motor area activates the peripheral speech apparatus.  It results in initiation of movements of tongue, lips and larynx required for speech.  , when the child is taught to read, auditory speech is associated with visual symbols (area 18). Then, there is an association of the auditory and visual areas with the motor area for the muscles of hand.  Now, the child is able to express auditory and visual impressions in the form of written words  NERVOUS CONTROL OF SPEECH  Speech is an integrated and a well-coordinated motor phenomenon.  many parts of cortical and subcortical areas are involved in the mechanism of speech.  Subcortical areas concerned with speech are controlled by cortical areas of dominant hemisphere. In about 95% of human beings, the left cerebral hemisphere is functionally dominant and those persons are right handed.  Following are the motor and sensory cortical areas concerned with speech.  A. Motor Areas  1. Broca area Broca area is also called speech center, motor speech area or lower frontal area. It includes areas 44 and 45.  These areas are situated in lower part of lateral surface of prefrontal cortex. Broca area controls the movements of structures (tongue, lips and larynx) involved in vocalization.  2. Upper frontal motor area Upper frontal motor area is situated in paracentral gyrus over the medial surface of cerebral hemisphere.  It controls the coordinated movements involved in writing B. Sensory Areas  1. Secondary auditory area Secondary auditory area or auditopsychic area includes area 22. It is situated in the superior temporal gyrus. It is concerned with the interpretation of auditory sensation and storage of memories of spoken words.  2. Secondary visual area Secondary visual area or visuopsychic area includes area 18. It is present in angular gyrus of the parietal cortex. This area is concerned with the interpretation of visual sensation and storage of memories of the visual symbols. C. Wernicke Area  Wernicke area is situated in the upper part of temporal lobe.  This area is responsible for the interpretation of auditory sensation. It also plays an important role in speech.  It is responsible for understanding the auditory information about any word and sending the information to Broca area APPLIED PHYSIOLOGY –  DISORDERS OF SPEECH  Speech disorder is a communication disorder characterized by disrupted speech. It is of four types:  I. Aphasia  II. Anarthria or dysarthria  III. Dysphonia  IV. Stammering. „ APHASIA  Aphasia is defined as the loss or impairment of speech due to brain damage (in Greek, aphasia = without speech). It is an acquired disorder and it is distinct from developmental disorders of speech or other speech disorders like dysarthria.   Aphasia is not due to paralysis of muscles of articulation. It is due to damage of speech centers.  Damage of speech centers impairs the expression and understanding of spoken words.  It also affects reading and writing.  Speech function is localized to left hemisphere in most of the people.  Aphasia may be associated with other speech disorders, which also occur due to brain damage. Causes for Aphasia  Usually aphasia occurs due to damage of one or more speech centers, which are situated in cerebral cortex  Damage of speech centers occurs due to: 1. Stroke  2. Head injury  3. Severe blow to head  4. Cerebral tumors  5. Brain infections  6. Degenerative diseases.  Usually, in conditions like head injury, aphasia occurs suddenly and in conditions like infections or cerebral tumors, it develops slowly.  In children, traumatic aphasia can develop by exposure to a horrifying event, without any brain damage. It may be cured with psychological treatment. Types of Aphasia  Aphasia is classified by different methods.  The simple and convenient clinical classification divides aphasia into five types:  1. Broca aphasia  2. Wernicke aphasia  3. Global aphasia  4. Nominal aphasia  5. Other types of aphasia. 1  Broca aphasia . Broca aphasia is the non-fluent speech problem. It occurs due to lesion in left frontal lobe of cerebral cortex.  It is also known as expressive aphasia or anterior aphasia. The affected persons do not complete the sentences because of their inability to construct the sentences.  They often talk in short phrases by omitting small words such as ‘and’, ‘is’, ‘for’, etc.  They make great efforts even to initiate speech. Persons with Broca aphasia are able to understand spoken or written words.  Often, they are affected by weakness or paralysis of right arm or leg. It is due to damage of frontal lobe, which is also responsible for motor activities. Wernicke aphasia  Wernicke aphasia is the speech without any meaning.  It is also called receptive aphasia or posterior aphasia.  Wernicke aphasia occurs due lesion in left temporal lobe. It is characterized by fluent speech.  The affected persons speak long sentences but without any meaning.  They use incorrect or non-existent words and cannot speak sensibly. This type of speech is known as jargon speech.  They are unable to understand others’ speech.  Due to this weakness, they are unaware of their own mistakes while speaking.  Often, they are mistaken as psychiatric patients.  Wernicke aphasia is not associated with paralysis or weakness of muscles because, the injury does not involve the centers concerned with movements. Global aphasia  is the type of aphasia characterized by combined features of Broca aphasia and Wernicke aphasia.  It is due to widespread lesion in speech areas caused by infarction of left cerebral hemisphere. It is the most common type of aphasia.  The affected persons can neither speak nor understand the spoken words. They cannot read and write also. So they have severe communication problems.. Nominal aphasia  Nominal aphasia is the speech disorder characterized by inability in naming the familiar objects.  It is also called anomic aphasia or amnesic aphasia. It is due to lesion in posterior temporal and inferior parietal gyri Other types of aphasia  i. Motor aphasia:  It is the speech disorder caused by the defect in the pathway between left speech areas and excitomotor or precentral cortex).  It is also known as verbal aphasia or dyspraxia or apraxia of speech. It is characterized by difficulty in uttering individual words due to lack of coordination between central speech apparatus (higher cortical centers) and peripheral speech apparatus.  The affected persons are able to decide what to talk. But they cannot pronounce all the words. They are able to pronounce only few monosyllables such as ‘yes’ or ‘no’.  ii. Sensory aphasia:  It is the inability to understand words or symbols.  It is of two types:  a. Auditory aphasia: Inability to understand the spoken words.  It is also called word deafness. It is due to the lesion in secondary auditory area.  b. Visual aphasia: Inability to understand written symbols (difficulty in reading).  It is also called word blindness or dyslexia and it occurs due to the lesion in secondary visual area.  iii. Agraphia:  Agraphia means inability to write. There is no defect in the muscles of the hand concerned with writing. The subject can read and speak.  Agraphia is due to the defect in the connection between the cortical areasconcerned with writing.  Agraphia differs from dysgraphia, which is characterized by distorted writing or writing incorrect letters. Head’s classification of aphasia  Henry Head was the pioneer scientist in the field of speech disorders and he was the first one to classify aphasia. In 1926, he classified aphasia into four types  Types of aphasia  A.Verbal aphasia Inability in formation of words  b.Syntactical aphasia Inability to arrange words in proper sequence  C. Semantic aphasia Inability to recognize the significance of words  D. Nominal aphasia Inability to name the familiar objec DYSARTHRIA OR ANARTHRIA  The term dysarthria refers to disturbed articulation.  Anarthria means inability to speak.  Dysarthria or anarthria is defined as the difficulty or inability to speak because of paralysis or ataxia of muscles involved in articulation.  Psychic aspect of speech is not affected.  The spoken and written words are understood. Causes of Dysarthria  Dysarthria is caused by damage of brain or the nerves that control the muscles involved in speech.  It occurs in conditions like stroke, brain injury, degenerative disease like Parkinson disease and Huntington disease. „).  DYSPHONIA  Dysphonia is a voice disorder.  Often, it is characterized by hoarseness and a sore or a dry throat.  Hoarseness means the difficulty in producing sound while trying to speak or a change in the pitch or loudness of voice.  The voice may be weak, breathy, scratchy or husky.  Causes of Dysphonia  1. Trauma of vocal cords  2. Paralysis of vocal cords  3. Lumps (nodules) on vocal cords  4. Inflammation of larynx  5. Hypothyroidism  6. Stress (psychological dysphonia STAMMERING  Stammering or shuttering is a speech disorder characterized by hesitations and involuntary repetitions of certain syllables or words.  It is also described as a speech disorder in which normal flow of speech is disturbed by repetitions, prolongations or abnormal block or stoppage of sound and syllables.  It is due to the neurological incoordination of speech and it is common in children.  Stammering is associated with some unusual facial and body movements.  Exact cause for stammering is not known.  It is thought that stammering may be due to genetic factors, brain damage, neurological disorders or anxiety