Cerebral Cortex And Speech Najeeb.docx

Anterior root Anterior ramus

trunk

Anterior horn

Internal capsulte (white matter) lentiform nucleus (grey matter)

Thalamus is grey matter

Caudate nucleus (grey matter

Posterior limb internal capsule Corona radiata Medial lemmniscus

Anterior limb internal capsule

Tract of lissaure

Substantia gelatinosa

Lateral spinothalamic for temp and pain

Anterior spinothala mic tract for crude touch

2nd order nurone of crude touch pathway that start from Substantia gelatinosa, they cross to contralateral side to the anterior coloumn

fusion of the spinotectal pathway, anterior spinothalamic tract and lateral spinothalamic tract, fuse together at medulla forming a single bundle called spinal lemniscus

Haydali yal maktoob heya el reticular formation( which is a mix of grey and white matter that extend through out the centre of brain stem

Cingulate gyrus that give emotions to the pain

Fast pain A fibres pain can be easily localized Slow pain dull pain C fibres not easily localized due to the many connections

This for the dorsal spinocerebellar tract

This pic is for the ventral/anterior spinocerebellar pathway

For a summary

RIGHT LESION ABOVE THE CROSSING THEN I WILL LOOSE MOTOR ON LEFT SIDE RIGHT LESION BELOW THE CROSSING THE I WILL LOOSE MOTOR ON RIGHT SIDE (IPSILATERAL

ALL LESION ABOVE CROSSING THEY PRODUCE LOSE OF MOTOR ON CONTRALATERAL SIDE ALL LESION BELOW CROSSING THEY PRODUCE IPSILATERAL MOTOR LOSS

THE ONES IN GREEN ARE THE LOWER MOTOR NEURONE

WERE HE IS POINTING IS FORAMEN LUSHKA, AND ONE IN THE CENTRE IS FORAEMEN MEGENDEE .-----------------------------------------------

EXTRAFUSAL FIBRES MUSCLE SPINDLE AKA INTRAFUSAL FIBRES WHICH HAVE SENSORY NERVE ENDING THAT TAKE INFORMATION FROM MUSCLE SPINDLE AND REPORT THE DEGREE OF STRETECH OF MUSCLE CONTINUSOLY TO THE SPINAL CORD SOME FIBRES GO UP AS PROPIOCEPTION AND SOME FIBRES RETURN BACK VIA ALPHA MOTOR NEURON GTO (GOLGI TENDON ORGAN RECEPTORS) OF THE GOLGI TENDON

MUSCLE SPINDLE ARE STRETCH RECEPTOR, WHEN WE HIT ON THE TENDON THE MUSCLE STRETECHES SO WHEN WE DO DEEP TENDON REFLEX WE PRODUCE A TRANSIENT BRIEF STRETCH IN THE MUSCLE, THEN GO VIA Ia then come back with alpha motor neurone to do muscle contraction SO A DEEP TENDON REFLEX WE ARE ACTUALLY DOING A MUSCLE STRETCH REFLEX

GOLGI TENDON APPARATUS IS NOT STIMULATED IN THIS PATHWAY. SO UNDER WHAT PATHWAY is golgi tendon apparatus are Ib and are stimulated? He keeps on carrying books at what point he can no longer put more weight or carry more book so in order to prevent the muscle damage and tendon damage the golgi tendon apparatus start working and fire when there is too much tension on the muscle and so they start working and inhbit alpha motor neurone firing via inhibitory interneuone

Actually the corticospinal tract they cross and join the alpha motor neurone through an inhibitory interneuron Tone is maintained by the gamma motor neurone activity

Lower motor neurone

Mass :decrease so become very atrophy Power : decrease more than upper motor neurone Tone: is mainly dependent on gamma motor neurone, if we loose gamma motor nueone so muscle spindle are very relaxed and since they are relaxed they wont give the signal via Ia. So it will be hypotonia and muscle is flaccid Tendon reflex: it is lost (areflexia) or hypoflexia Babinski: babinski if we scratch the outerpart sole of foot there withdrawl reflex in baby which is dorsiflexion this is called upgoing Babinski sign, by the time baby learn walking upper corticospinal motor neurone are myelinated now and are functional then everything is reversed the the baby will not dorsiflex it is will lead to plantar flexion which is downgoing Babinski sign Baniski is downgoing in lower motor neurone aka plantar flexion, or absent in case if the nerve that supply those muscles are lost Fasiculation: present Fibrillation: present

upper motor neurone Mass :maintained or decrease slightly [mass is better maintained here when compared to lower motor nueorne lesion Power : maintained or decrease slightly [power is better maintained here when compared to lower motor nueorne lesion Tone: gamma is over firing and muscle spindle will be contracted so they give more input and Ia fire more and as muscle spindle contract the end of the spindle will be overstretched, so more to Ia, then more to alpha motor neurone and overfiring and hypertonia or rigidity Tendon reflex: hyperreflexia and clonus Babinski: will be upgoing or dorsiflexion Fasciculation: absent in upper motor neurone (fasciulation mean when we are tapping the muscle there is some vissible involuntary contraction, and if they seen in electomyographic studies are called fibrillation Fibrillation: absent

Muscle spasticity(clasp knife) is specil type of hypertonia or special type of rigidity with a phenomen of clasp knife Muscle tone is the tone of muscle (tone of muscle that resist /tone heya 2el resistance, resistance to movment any movment maslan flexion min 6 to7 part 2) Clasp knife or spasticity more reistance that are being faced when trying to extend forearm until the golgi tendon reflex activate and lead to inhibition of alpha motor neurone and it will suddenly extend easily In normal cases it extends without the use of golgi tendon

Another type hypertonia or rigidity is called lead pipe with Parkinson seen with extrapyramidal loss Here the golgi tendon organ reflex is not activated , so through out the movement the resistance will be uniform Lead pipe rigidity + tremor = Cogwheel in parkinson

lesion only in anterior horn, so motor grey matter affected and lower motor neurone are affected so this lesion is motor lesion, its caused by virus poliovirus giving poliomyeleitis to bind with anterior horn cells in spinal cord or motor nerve nuclei in the brainstem; can affet young or old age, clinical features is severe loss of mess, loss of power hypotonia areflexia, fasciulations or fibrlations

Samething few month old infantile age with fh of lesions, and is not due to infection, maybe due to lower motor neurone degenerate, as time pass by more and more lower motor neurone affected, and flaciid paralysis areflexia, muscle atrophy, hypotnia , fascilation fibraltions. And is progressive with no mediacations this is called progressive infantile muscular atrophy aka werdnig Hoffman disorder which is a lower motor neueorne , which can be unilateral but is usally bilateral and is hereditary problem , and clinical presentation is before 1st year of age, and has family history

3rd like the 2nd since both are heridiatry .2nd was infantile, and 3rd was in older stage so the 3rd case is called juvenile heridatery lower motor neurone disease aka kugel berg walendar disease

4. cortical bilateral degeneration of the corticospinal pathway and is heridatery like mutation in the protein involved in the corticospinal pathway, and problem here is in upper motor neurone so clinical

presentation is spastic paralysis , hyperreflexia , Babinski is upgoing and is bilateral upgoing, clonus present , fasiculations will be absent. This is called heridatery spastic paraplegia(paraplegia both lower limbs are involved) and this is due bilateral cortical degnereation of corticospinal pathway

5. some muscle have flacid and some muscle have spastic paralysis Right biceps flaccidity hyporeflexia, left side spascitiy and hyperreflxia. Right lower limb up going Babinski and left side has downgoign Babinski. So this is called motor neurone disease aka amyotrophic lateral scelerosis because it affects both upper motor nueorne for some muscles and lower motor nuerone for some muscles

Now moving to the sensory lesions

6. DORSAL Column syndrome: lesion in dorsal coloumn . gracilis fasculitis giving info from lower limbs, cuneatus from upper limb On the right side demyelinating disease since there are high speed pathway associated with fine touch position proprioception vibration. Patient have ipsilateral loss of dorsal coloumn sensation which is 2 point discrimination or tactile discrimination. Sometime maybe bilateral and patient below level of lesion has bilateral loss of of dorsal coloumn sensation and intact anterolateral sensation (anterolateral sensation mean crude touch intact pain temp intact

Spinocerebellar dorsal coloumn sensation, visual and auditory vestibular system all to the cerebellum for steady gait: this is called rhomberg sign were he is dependednt on the visual information to keep his balance

7. spinothalamic tract: anterolateral system that bring pain and temp are affected , so have contralateral loss of pain and temp 1 segment below the lesion since they cross upwards 1 segment upward Dorsol coloumn sesnsation are good

8. dorsal coloumn sensation and lateral coloumn sensation are good Anterior coloum sensation are affected which is for crude touch and pressure Remember both lateral (they cross 1 segment above) and anterior sensation(cross 3-4 segment above) are contralateral

Loss of crude touch pressure 3-4 segment contralateral below level lesion

9.

Lecture 1 Cns consist of brain and spinal cord, the brain has cranial nerves that exit from the inferior surface of brain, and spinal nerves in the spinal cord. The brain consists of grey matter and white matter, the situtuation is reversed in spinal cord. For the motor system there is upper motor neuron that is cortical neuron present in the primary motor cortex giving rise to axon that go down the spinal cord with synapses with internueones, to get down to the lower motor neirone at level anterior horn spinal cord to give the peripheral motor nerve to inervate the muscle. The sensory neuron start from periherphy and go into the brain. The sensoy nerve is a bipolar nerve, the cell body is in dorsal root gangiliin near spinal cord. The peripheral process go to nerve ending in skin while central process go to central cord and goes up to the 2nd afferent neuone several nuclei. Then tertiary sensory neuone in thalamus then go priamary sensory cortex

Sympathetic is t1 to t12 and l1 l2 and give rise sympathetic chain Parasymepthetic has cranial nerve s2 s3 s4 that go to genital Meninges dura (being the outermost) subarchnoid space, arachoid, pia (inner most layer) Ventricles has csf. 2 lateral ventricle with a c shape and tail with anterior and posterior horn and inferior horn and a body, then interventricular foramen of monro to 3 rd ventricle to 4 th ventricle via cerebral aqueduct of syllvius

PHYSIOLOGY NEUROANATOMY AND PATHOLOGY OF SPEECH APHSIAS/DYSPHSIAS: NORMAL VISIAL AUDITIORY CEREBELLUM AND MOTOR SYSTEM AND LOWER AND UPPER MOTOR NEURON, BUT STILL THEY CANT PERFORM LANGAUGE FUNCTION, EITHER THEY CANT UNDERSTAND OR CANT REPEAT WORDS OR BRING OUT THE WORDS. IT CAN COME FROM PROBLEM OF BROCA OR WERNICKE AREA OR THE COMMUNCATION BETWEEN 2 WHICH IS CALLED ARCUATE FASCILAS. IMPARIED OR ABSENT COMMUNICATION BY SPEECH WRITING SIGN WITH NORMAL HEARING AND NORMAL MOTOR SYSTEM, PHONATION AND ARTICULATION IS FINE. TYPE 1 TRUE BROCA APHSIAS OR ANTERIOR APHSIAS OR NON FLUENT APHSIAS OR MUTE APHSIAS OR EXPRESSIVE ASPHSIAS or motor aphasia: LOST BROCA AREA PATIENT STILL ABLE TO READ AND HEAR WELL AND COMPREHEND WELL (WRINECKIE) BUT WHEN HE SPEAKS OUT THE PATIENT KNOWS WHAT HE WANTS TO SAY BUT CANT BRING IT OUT ALSO HE HAS REPITITION PROBLEM. BROCA IS AKA EXPRESIVE AREA. TRUE BROCA HAS OTHER MOTOR DISTURBANCES LIKE HEMIPARALYSIS CONTRALATERAL FACE AND CONTRALATERAL UPPER LIMB WEAKENESS

TYPE 2 TRUE WERNEKIE APHSIAS OR FLEUENT APSHIAS OR RECEPTIVE APHSIAS OR POSTERIOR APHSIAS , SENSORY PROBLEM : CANT UNDERSTAND WHAT OTHERS ARE SAYING, AND SHE CAN TALK SINCE BROCA IS FINE, BUT SHE SPEAKS THINGS THAT ARE NONSENSE AND ARE NOT APPROPRIATELY WRONG USE OF WORDS CALLED PARAPHSIAS AND NEUOLOGIASISM ALSO HERE HE HAS REPITION PROBLEM. WERNKIEKE AKA RECEPTIVE OR COMPREHENSION AREA, ALSO TRUE WERNIEKE VISUAL PATHWAY MAY BE AFFECTED MAY DEVELOP CONTRALATERAL HEMINOPIA

TYPE 3 CONDUCTIVE APHSIAS: REPITITION IS CAUSED BY THE COMMUNICATION BETWEEM BROCA AND WIRNKECIA AREA. HE UNDERSTANDS AND SPEAKS THINGS THAT MAKE SENSE, BUT HE DOESN’T REPEAT TYPE 4 TRANSCORTICAL MOTOR APHSIAS: BROCA PROBLEM WITH NO REPITION PROBLEM, THE BROCA IS DISCONECTED FROM THE SURRONDING CORTEX, HE HAS PROBLEM WITH SPEECH PRODUCTION BUT WHATEVER HE PRODUCED HE CAN REPEAT TYPE 5 TRANSCORTIAL SENSORY APHSIAS: NO REPEITION PROBLEM, WERNICKE PROBLEM, WERNICKE IS DISCONECTED FROM OTHER CORTICAL AREAS, PROBLEM IS IN COMPREHSION WHATEVER PEOPLE ARE SAYING THE PATIENT WONT UNDERSTAND

TYPE 6 MIXED TRANSCORTIAL APHSIAS: BOTH TRANSCORTIAL MOTOR AND TRANSCORTAIL SENSORY APHSIAS WITH NORMAL REPITION. TYPE 7 NOMINAL APHSIAS WE CANT NAME THE THINGS:PROBLEM IS AT MOST POSTERIOR AREA OF WRINKEI (THIS AREA OF DICTORNARY FOR NAMING OF THE OBJECT) IF I SHOW U MARKER U SHOULD SAY MARKER DUE TO THIS AREA. IF SOMEONE SEE MARKER AND SAYS THIS IS CAR HE KNOW THAT IT IS FOR WRITING BUT SAYING THE WRONG NAME. HE CHOOSE THE WRONG NAME FOR OBJECTS, HE COMPREHEND WELL, REPEAT WELL AND BROCA IS GOOD

TYPE 8 GLOBAL APHSIAS: THE WHOLE THING IS GO BROCA WITH WERINKEE AND REPETITION AREA, WE CANT COMPREHEND CANT TALK AND CANT REPEAT

TYPE 9 APHSIAS DUE TO BASAL GANGLIA PROBLEM: THIS IS COMMON IN PARKINSON. REMEMBR THE BASAL GANGLIA (BASAL GAGNLIA HAS MOTOR ACTIVITY) AND THALAMUS AND BROCA WORK TOGETHER. HERE IN THIS TYPE PROBLEM IN BASAL GANGLIA, BROKA IS FINE, CONDUCTIVE AND WERNIEKE IS OK. SO HERE EXTRAPYRAMIDAL IS NOT WORKING WELL ESPECIALLY IN CAUDATE AND PAUTMEN. TONE AND POSTURE ARE A FUNCTION OF BASAL GANGLIA ANTERIOR PART OF BASAL GANGLIA IS SIMILAR TO BROCA WITH NO CHANGE IN OTHER MOTOR PART LIKE CONTRALATERAL FACE AND UPPER LIMB POST PART BASAL GANGLIA IS SIMILAR TO WERNEIKE BUT WITH NO CHANGE IN VISUAL SYSTEM

TYPE 10 THALAMIC APHSIAS: THALAMUS HAS ANTERIOR MEDIAL AND LATERAL NUCLEI. IN THE LATERAL NUCLEI THERE IS DORSAL AND VENTRAL. IN THE VENTAL ALL 3 CALLED VENTROLATERAL THERE IS ANTERIOR INTERMEDIATE AND POSTERIOR NUCEUS. POSTERIOR IS VENTROPOSTOLATERAL AND VENTROPOSTOMEDIAL. VENTROANTERIOR AND VENTROINTERMEIATE THALAMUS WORK WITH BASAL GANGLIA IN MOTOR SYSTEM. SO MOTOR SYSTEM DISTRIBED AND SPEECH IS DISTRIBED AND SENSORY MAY BE DISTRIBED . FLUENT PARAPHYSICS SPEECH WITH NORMAL REPITITION AND NORMAL COMPREHENSION

TYPE 11: WATER SHED AREAS BETWEEN THE MIDDLE POSTERIOR AND ANTERIOR CEREBRAL ARTERIES PRLONGED HYPOPERFUSION WILL RESULT IN INFARCTION IN THESE AREA CALLED WATERSHED INFARCTS. BROCA AND WERNIEKE OK BUT ARE DISCONECTED FROM SURRONDING CORTEX CAN DEVELOP MOTOR LIKE PROBLEM , BROCA PROBLLEM, SENOSRY APHSYSIA PROBLEM. MIXED APHYSIA TYPE

ALL OF THESE 11 TYPES WERE IN THE DOMINANT HEMISPHERE PROBLEM IN THE NON DOMINANT HEMISPHERE

2 TYPES dYSPROSODIES IN AREAS CORRESPONDING TO BROCA IN NON DOMINANT HEMISPHERE A PERSON WONT BE ABLE TO ADD EMOTIONALITY TO HIS SPEECH THIS IS EXPRESSIVE/ANTERIOR/MOTOR DYSPROSODIES

AREAS CORRESPONING TO WERKNIE IN NON DOMINANT HEMISPHERE A PERSON WONT BE ABLE TO COMPREHENED PR DETECT THE EMOTIONALITY IN OTHER PEOPLE SPEECH THIS IS RECEPTIVE/POSTERIOR/SENSORY DYSPROSODIES

DYSARTHRIAS: DUE TO ARTICULATION PROBLEM WERE WE CANT CONVERT THE SOUND THAT BEEN PREVIOSULY FORMED INTO WORDS. THIS PATHOGLOGY CAN COME FROM CEREBELLUM OR UPPER MOTOR NEURONE FAILURE LIKE IN THE PYRAMIDAL PATHWAYS WITH DEMYLINATION OF CORTICONEUCLAR/CORTICOBULBAR PATHWAY IN MULTIPLE SCLEROSIS, PROBLEM AT UPPER MOTOR NEURONE EXTRAPYARMIDAL PATHWAY LIKE IN PARKINSON,BULBAR PATHWAY PROBLEM PROBLEM IN BULB THE MEDULLA , PROBLEM AT LOWER MOTOR NEURON OR PROBLEM IN MUSCLE AND NEUROMUSCLAR JUNCTION LIKE MYASTHENIA GRAVIS SO INTOTAL DYSARTHRIA CAN BE FROM . CEREBELLUM, PYRAMIDAL AND EXTRAPYRMAIDAL UPPERMOTOR NEURONE CAUSE BOTH PYRAMIDAL AND EXTRAPYRAMIDAL GROUPED TOGETHER AS PSEUDOBULBAR LESION, BULBAR PATHWAY PROBELM BELSE PALSY, OR PROBLEM IN NEURONE MSUCLE . FINALLY NEUROMUSCLAR JUNCTION LIKE MYASTENIA GRAVISU

DYSPHONIA/APHONIA: ABNORMATLITES IN PRODCUTION SOUND EITHER SOUND VOLUME IS LOW OR UNABLE TO MAKE SOUND, PROBLEM CAN BE PROBLEM AT NEUROLOGICAL LIKE RECURRET LARYNGEAL AND VOCAL CORD CANT MOVE OR HIGHER MENTAL DISORDER THE CORTICAL CENTRE THAT CONTROL SOUND PRODUCTION OR PSYCHOLOGIAL OR PROBLEM MUSCLAR OR NEUROMUSCLAR LIKE MYASTEHNIA GRAVIS OR PROBLEM IN RESP AND EXPIRATION (RESP SYSTEM AND LARYNX CANT CORDINATE TO MAKE SOUND Phonation: PRODUCTITON SOUND ARTICULATION: MOVEMENT OF MUSCULECULATRUE OF LIP TONGUE SOFT PALATE PHARYNX SUCH THAT SIMPLE SOUNDS ARE CONVVERTED INTO WORDS, NEUROMUSCLE OF ARTIULATION ARE NERVE 7 9 10 12 AND CONNECTED MUSCLES BOTH TOGETHER THE PHONATION AND ARTICULATION REQURIE CORDINATION WHICH IS A FUNCTION OF THE CEREBELLUM WE CAN SPEAK DURING EXPIRTION ONLY AND NOT DURING INSPIRATION BROCA AREA: CONTROL THE NEUROMUSCLE OF ARTICULATION. BROCA IS CONNECTED TO THE UPPER MOTOR NEURONE OF ARTICULATION THAT THEN CONTROL THE LOWER MOTOR NEURON NORMAL PHYSIOLOGY: WE DEFINE LANGUAGE IS A WAY OF COMMUNICATION OF THOUGHTS AND IDEAS FROM 1 PERSON TO THE OTHER THROUGH SIGNS AND SYMBOLS. LANGAGUE CAN BE BODY LANGUAGE (SIGNS), WRITTEN SIGNS OR VERBAL SIGNS. LANGUAGE IS A HIGH LEVEL FUNCTION NEED INTELLIGENCE. SPEECH IS THE OXYGEN OF THE MIND AND PEOPLE WITH STROKE CANT COMMUNICATE

SPOKEN RIGHT HANDED PATIENT IT IS LEFT HEMISPEREHE DOMINANT LEFT HANDED PATIENT IT IS LEFT HEMISPEREHE DOMINANT (70%) AND 30% RIGHT DOMINANT LESION OF LEFT HEMISPHERE DEVELOPED PARALYSIS ON RIGHT SIDE BOTH HEMISPHERE IS IMPO FOR LANGUAGE LEFT HEMISPHERE (VERBAL HEMISPHERE) IS FOR LISTENING TO POETRY/UNDERSTANDING POETRY (VERBAL TALKING COMPONENT, WORDS AND INTERPRENT AND COMPREHENED VERBAL MEANING AND UNDERSTANDING PROCESSED, AND FORMULATE SENSTENCES BY LEFT SIDE, ALSO CALCULATION BY LEFT HEMISPHERE HEARING MUSIC,DETECT AND ADD EMOTIONALITY, BY ADD NON VERBAL COMPONENTS RIGHT HEMISPHERE WORK. ALSO RIGHT HEMISPHERE FOR DRAWING GEOMTRICAL FIGURE AND INTERNAL AND EXTERNAL ORIETNATION IN THE SPATIAL (LOSS OF SPATIAL ORIENTATION CANT DRESS YOURSELF

PRMARY AREA: AREA 17 VISIAL RECEPTION 2nd AREA 18 VISIAL ANALYSIS AREA 3rd AREA 19 VISIAL RECOGNITION AREA (RECOGNIZING) Both 2nd and 3rd area combined called association area THEN FROM RECOGINTION TO THE WERNIEKE AREA WERNIEKE AREA: IS COMPREHENSION AREA ,FOR UNDERSTANDING LANGUAGE TRUE DECODING AND DEVELOP AN IMAGE IN UR MIND AND MEANING OR IDEA (TRANSLATE VISUAL SYMBOL INTO A WELL DEFINED IDEA